GRIEVE’S MODERN

MUSCULOSKELETAL
PHYSIOTHERAPY
For Elsevier:
Senior Content Strategist: Rita Demetriou-Swanwick
Content Development Specialist: Nicola Lally
Project Manager: Umarani Natarajan
Designer/Design Direction: Miles Hitchen
Illustration Manager: Lesley Frazier
Illustrator: Graphic World Illustration Studio
GRIEVE’S MODERN
MUSCULOSKELETAL
PHYSIOTHERAPY
FOURTH EDITION

Edited by
Gwendolen Jull Dip Phty, Grad Dip Manip Ther, MPhty, PhD, FACP
Emeritus Professor, Physiotherapy, School of Health and Rehabilitation Sciences, University of
Queensland, Brisbane, Australia

Ann Moore PhD, FCSP, FMACP, Dip TP, Cert Ed

Professor of Physiotherapy and Head of the Centre for Health Research, School of Health
Sciences, University of Brighton, UK

Deborah Falla BPhty (Hons), PhD

Professor, Pain Clinic, Center for Anesthesiology, Emergency and Intensive Care Medicine
Professor, Department of Neurorehabilitation Engineering
Universitätsmedizin Göttingen, Georg-August-Universität, Germany

Jeremy Lewis BApSci (Physio), PhD, FCSP

Consultant Physiotherapist, London Shoulder Clinic, Centre for Health and Human Performance,
London, UK
Consultant Physiotherapist, Central London Community Healthcare NHS Trust, UK
Professor (Adjunct) of Musculoskeletal Research, Clinical Therapies, University of Limerick, Ireland
Reader in Physiotherapy, School of Health and Social Work, University of Hertfordshire, UK

Christopher McCarthy PhD, FCSP, FMACP

Consultant Physiotherapist, St Mary’s Hospital, Imperial College Healthcare, UK

Michele Sterling PhD, MPhty, BPhty, Grad Dip Manip Physio, FACP
Director, CRE in Road Traffic Injury
Associate Director, Centre of National Research on Disability and Rehabilitation (CONROD)
Professor, School of Allied Health, Menzies Health Institute Queensland, Griffith University,
Australia

Foreword by
Karim Khan MD, PhD, FASCM
Editor of the British Journal of Sports Medicine
Director, Department of Research & Education, Aspetar Orthopaedic and Sports Medicine Hospital,
Qatar
Professor, Faculty of Medicine, University of British Columbia, Canada

Edinburgh  London  New York  Oxford  Philadelphia  St Louis  Sydney  Toronto 2015
© 2015 Elsevier Ltd. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic
or mechanical, including photocopying, recording, or any information storage and retrieval system,
without permission in writing from the publisher. Details on how to seek permission, further
information about the Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website:
www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).

First edition 1986

Second edition 1994
Third edition 2005

Chapter 44.b: Model B: Linda-Joy Lee. LJ Lee Physiotherapist Corp retains copyright to illustrations.

Chapter 46.b: The Pelvic Girdle: A Look at How Time, Experience And Evidence Change Paradigms:
Diane Lee retains copyright to her own illustrations.

ISBN 978-0-7020-5152-4

Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical treatment
may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds, or experiments described herein. In using such information
or methods they should be mindful of their own safety and the safety of others, including parties for
whom they have a professional responsibility.

With respect to any drug or pharmaceutical products identified, readers are advised to check the most
current information provided (i) on procedures featured or (ii) by the manufacturer of each product to
be administered, to verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of practitioners, relying on their own
experience and knowledge of their patients, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions.

To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume
any liability for any injury and/or damage to persons or property as a matter of products liability,
negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.

The
publisher’s
policy is to use
paper manufactured
from sustainable forests

Printed in China

Last digit is the print number:  9  8  7  6  5  4  3  2

 Contents

Preface to the Fourth Edition ix 9.2 LUMBAR SPINE 101

Acknowledgements x Michael Adams  •  Patricia Dolan
Foreword xi
Contributors xii 10 Tendon and Tendinopathy 106
Plate Section
10.1 TENDON AND TENDON PATHOLOGY 106
Hazel Screen

PA RT I 10.2 MANAGING TENDINOPATHIES 112

Jill Cook  •  Ebonie Rio  •  Jeremy Lewis
1 Introduction to the Text 3
Gwendolen Jull  •  Ann Moore  •  Deborah Falla  •  11 Lifestyle and Musculoskeletal Health 117
Jeremy Lewis  •  Christopher McCarthy  •  Elizabeth Dean  •  Anne Söderlund
Michele Sterling
12 Ageing and the Musculoskeletal System 126
Christopher McCarthy  •  Aubrey Monie  •  Kevin Singer
PA RT I I
SECTION 2.2
ADVANCES IN THEORY AND ADVANCES IN MEASUREMENT
PRACTICE METHODS 136
SECTION 2.1 13 Movement Analysis 137
ADVANCES IN BASIC SCIENCE 7 Aurelio Cappozzo  •  Andrea Cereatti  • 
Valentina Camomilla  •  Claudia Mazzà  • 
Giuseppe Vannozzi
2 The Neurophysiology of Pain and Pain
Modulation: Modern Pain Neuroscience for 14 New Developments in Ultrasound Imaging
Musculoskeletal Physiotherapists 8 in Physiotherapy Practice and Research 144
Jo Nijs  •  Margot De Kooning  •  David Beckwée  •  Peter Vaes
Alan Hough  •  Maria Stokes

3 Neuro-Electrochemistry of Movement 19 15 Advances in Magnetic Resonance

Harsimran Baweja
Imaging (MRI) Measures 153
James Elliott  •  Graham Galloway  • 
4 Postural Control and Sensorimotor Barbara Cagnie  •  Katie McMahon
Integration 28
Ian Loram 16 Musculoskeletal Pain in the Human Brain:
Insights from Functional Brain Imaging
5 Motor Control and Motor Learning 42
Natalie Mrachacz-Kersting  •  Peter Stubbs  •  Sabata Gervasio
Techniques 161
Michael Farrell

6 Interaction between Pain and Sensorimotor

17 Advances in Electromyography 168
Control 53 Deborah Falla  •  Dario Farina
Paul Hodges  •  Deborah Falla

18 Non-Invasive Brain Stimulation in the

7 Neuromuscular Adaptations to Exercise 68
Ross Pollock  •  Stephen Harridge
Measurement and Treatment of
Musculoskeletal Disorders 179
Siobhan Schabrun  •  Caroline Alexander
8 The Peripheral Nervous System and its
Compromise in Entrapment Neuropathies 78
Annina Schmid
19 Musculoskeletal Modelling 187
Mark de Zee  •  John Rasmussen

9 Functional Anatomy 93
20 Quantitative Sensory Testing: Implications
9.1 THE CERVICAL SPINE 93 for Clinical Practice 194
Toby Hall  •  Kathy Briffa  •  Axel Schäfer  • 
Gail Forrester-Gale  •  Ioannis Paneris
Brigitte Tampin  •  Niamh Moloney

v
vi Contents

21 Outcome Measures in Musculoskeletal 28 Pain Management Introduction 262

Practice 202
Jonathan Hill 28.1 THE PATIENT’S PAIN EXPERIENCE 262
Hubert van Griensven

S E CTION 2.3
28.2 EDUCATIONAL APPROACHES TO PAIN
RESEARCH APPROACHES FOR MANAGEMENT 265
MUSCULOSKELETAL James McAuley
PHYSIOTHERAPY 211
28.3 PHYSICAL INTERVENTIONS OF PAIN
22 Clinical Research to Test Treatment MANAGEMENT AND POTENTIAL
Effects 212 PROCESSES 269
Anita Gross  •  Charlie Goldsmith  •  David Walton  •  Kathleen Sluka
Joy MacDermid
29 Spinal Manipulation 277
23 Research Approaches to Musculoskeletal Christopher McCarthy  •  Joel Bialosky  •  Darren Rivett
Physiotherapy 220
30 Neurodynamic Management of the Peripheral
23.1 QUANTITATIVE RESEARCH 221 Nervous System 287
Lieven Danneels Michel Coppieters  •  Robert Nee

23.2 QUALITATIVE RESEARCH 223 31 Therapeutic Exercise 298

Nicola Petty Deborah Falla  •  Rod Whiteley  •  Marco Cardinale  •  Paul Hodges

23.3 MIXED METHODS RESEARCH 224 32 Management of the Sensorimotor System 310
Hubert van Griensven
32.1 THE CERVICAL REGION 310
24 Standardized Data Collection, Audit and Ulrik Röijezon  •  Julia Treleaven
Clinical Profiling 227
Ann Moore 32.2 SENSORIMOTOR CONTROL OF
LUMBAR SPINE ALIGNMENT 315
25 Implementation Research 232 Jaap van Dieën  •  Idsart Kingma  • 
Nienke Willigenburg  •  Henri Kiers
Simon French  •  Sally Green  •  Rachelle Buchbinder  • 
Jeremy Grimshaw
32.3 THE LOWER LIMB 319
Nicholas Clark  •  Scott Lephart

PA RT I I I 33 Consideration of Cognitive and

Behavioural Influences on
ADVANCES IN CLINICAL Physiotherapy Practice 328
SCIENCE AND PRACTICE Justin Kenardy  •  Kim Bennell

34 Adjunct Modalities for Pain 334

S E CTION 3.1
PRINCIPLES OF MANAGEMENT 241 34.1 ELECTROPHYSICAL AGENTS 334
Tim Watson
26 Clinical Reasoning and Models for Clinical
Management 242 34.2 ACUPUNCTURE/DRY NEEDLING 336
Peter Kent  •  Jan Hartvigsen Panos Barlas

27 Communicating with Patients 250 34.3 THE USE OF TAPE IN MANAGING

SPINAL PAIN 339
27.1 PATIENT-FOCUSED PRACTICE AND Jenny McConnell
COMMUNICATION: USE OF
COMMUNICATION IN THE 35 Cautions in Musculoskeletal Practice 342
CLINICAL SETTING 250
Ruth Parry 35.1 MASQUERADERS 343
Susan Greenhalgh  •  James Selfe
27.2 PATIENT EDUCATION:
A COLLABORATIVE APPROACH 254 35.2 HAEMODYNAMICS AND CLINICAL
Lynne Caladine  •  Jane Morris PRACTICE 347
Alan Taylor  •  Roger Kerry
27.3 COMMUNICATING RISK 258
Roger Kerry 35.3 PRE-MANIPULATIVE SCREENING
FOR CRANIOCERVICAL LIGAMENT
INTEGRITY 352
Peter Osmotherly
 Contents vii

SECTION 3.2 44.2 THE THORACIC RING APPROACH™ – A

THE BROADER SCOPE OF WHOLE PERSON FRAMEWORK TO
MANAGEMENT 357 ASSESS AND TREAT THE THORACIC
SPINE AND RIBCAGE 449
36 Supported Self-Management and an Overview Linda-Joy Lee
of Self-Help 358
Ann Moore 44.3 MANAGEMENT OF THE THORACIC
SPINE IN PATIENTS WITH COPD 455
37 Role of Physiotherapy in Lifestyle and Nicola Heneghan
Health Promotion in Musculoskeletal
Conditions 364 45 Lumbar Spine 460
Elizabeth Dean  •  Anne Söderlund
45.1 THE McKENZIE METHOD OF
MECHANICAL DIAGNOSIS AND
38 Musculoskeletal Health in the
Workplace 379 THERAPY – AN OVERVIEW 460
Stephen May  •  Helen Clare
Venerina Johnston  •  Leon Straker  •  Martin Mackey

45.2 MULTIDIMENSIONAL APPROACH FOR

39 Screening 388
THE TARGETED MANAGEMENT OF
LOW BACK PAIN 465
39.1 SCREENING FOR MUSCULOSKELETAL
Peter O’Sullivan  •  Wim Dankaerts  •  Kieran O’Sullivan  • 
DISORDERS 388 Kjartan Fersum
Tania Pizzari  •  Carolyn Taylor
45.3 TREATMENT-BASED CLASSIFICATION
39.2 WHAT IS OUR BASELINE FOR SYSTEM 470
MOVEMENT? THE CLINICAL NEED Julie Fritz
FOR MOVEMENT SCREENING,
TESTING AND ASSESSMENT 394 45.4 MOVEMENT SYSTEM IMPAIRMENT
Gray Cook  •  Kyle Kiesel SYNDROMES OF THE LOW BACK 474
Shirley Sahrmann  •  Linda van Dillen
40 Advanced Roles in Musculoskeletal
Physiotherapy 400 45.5 THE ROLE OF MOTOR CONTROL
Jill Gamlin  •  Maree Raymer  •  Jeremy Lewis TRAINING 482
Paul Hodges

46 The Sacroiliac Joint (Pelvic Pain): Models

PA RT I V of Assessment and Management 488
OVERVIEW OF CONTEMPORARY
46.1 A PERSON-CENTRED BIOPSYCHOSOCIAL
ISSUES IN PRACTICE APPROACH TO ASSESSMENT AND
MANAGEMENT OF PELVIC
SECTION 4.1 GIRDLE PAIN 488
Darren Beales  •  Peter O’Sullivan
INTRODUCTION 409
46.2 THE PELVIC GIRDLE: A LOOK
41 Cervical Spine: Idiopathic Neck Pain 410
AT HOW TIME, EXPERIENCE
Gwendolen Jull  •  Deborah Falla  •  Shaun O’Leary  • 
Christopher McCarthy
AND EVIDENCE CHANGE
PARADIGMS 495
Diane Lee
42 Whiplash-Associated Disorders 423
Michele Sterling  •  Tze Siong Ng  •  David Walton  • 
Ashley Smith 46.3 A CRITICAL VIEWPOINT ON MODELS,
TESTING AND TREATMENT OF
43 Temporomandibular Disorders: PATIENTS WITH LUMBOPELVIC
Neuromusculoskeletal Assessment PAIN 500
Annelies Pool-Goudzwaard
and Management 433
Harry von Piekartz
47 Hip-Related Pain 506
Kay Crossley  •  Alison Grimaldi  •  Joanne Kemp
44 Thoracic Spine: Models of Assessment and
Management 444 48 The Knee: Introduction 522
44.1 CLINICAL EXAMINATION AND 48.1 ACUTE KNEE INJURIES 522
TARGETED MANAGEMENT OF Lee Herrington
THORACIC MUSCULOSKELETAL
PAIN 444
Quentin Scott
viii Contents

48.2 PATELLOFEMORAL PAIN 528 50.5 FROZEN SHOULDER CONTRACTION

Kay Crossley  •  Sallie Cowan  •  Bill Vicenzino SYNDROME 577
Jeremy Lewis
48.3 KNEE OSTEOARTHRITIS 536
Kim Bennell  •  Rana Hinman  •  Melanie Holden  •  51 Elbow 583
George Peat Brooke Coombes  •  Leanne Bisset  •  Bill Vicenzino

49 Ankle Injury 547 52 Wrist/Hand 595

Claire Hiller  •  Kathryn Refshauge Anne Wajon

50 The Shoulder 557

50.1 SHOULDER ASSESSMENT 557 PART V

Eric Hegedus  •  Jeremy Lewis
FUTURE DIRECTIONS
50.2 ROTATOR CUFF TENDINOPATHY AND
SUBACROMIAL PAIN SYNDROME 563 53  Future Directions in Research
Jeremy Lewis  •  Karen Ginn and Practice 609
Gwendolen Jull  •  Ann Moore  •  Deborah Falla  •  Jeremy Lewis  • 
50.3 THE UNSTABLE SHOULDER 568 Christopher McCarthy  •  Michele Sterling
Lyn Watson  •  Tania Pizzari  •  Jane Simmonds  • 
Jeremy Lewis

50.4 POSTERIOR SHOULDER TIGHTNESS 575 Index 611

John Borstad  •  Jeremy Lewis
 Preface to the Fourth Edition

The first edition of Grieve’s Modern Manual Therapy: The wider understanding and appreciation of the associated
Vertebral Column was published in 1986 and its editor was pain, functional impairments and activity limitations.
the late Gregory Grieve. The convention of a roughly 10 Advances in the neurosciences (e.g. the pain sciences,
year period between editions has been preserved for the sensorimotor sciences) as well as the behavioural sciences
fourth edition of this seminal text. Time is needed to have changed practice. The earlier concepts and practices
allow for the furtherance of research and the knowledge of manipulative therapy have grown and developed and
base and for its translation to clinical practice. A review transitioned into more comprehensive methods of man-
of the content of the four editions of this text is not agement. It was therefore time to make the title of this
unexpectedly, witness to the major changes in knowl- fourth edition reflective of contemporary practice. Hence
edge, evidence base, practice and its delivery over the past the name change to Grieve’s Modern Musculoskeletal
30 years. Physiotherapy.
There has been a change in title of the text, from Since the third edition of this text was published, the
Grieve’s Modern Manual Therapy to Grieve’s Modern Mus- physiotherapy world has been saddened by the passing of
culoskeletal Physiotherapy. This change has been made to some of the original leaders in the field, namely Geoffrey
reflect historical development. Physiotherapists have Maitland, Robin McKenzie and Robert (Bob) Elvey. All
been practising manipulative therapy from the early part had a passion for the discipline and for enhanced patient
of the 20th century under successive medical mentors care. We are sure that they along with Gregory Grieve
such as Edgar Cyriax and James Mennell and subse- would be pleased with the way the clinical art and evi-
quently under James Cyriax, John Mennell and the dence base of manipulative and musculoskeletal physio-
leading osteopath, Alan Stoddard. It was in the 1950s therapy has and will continue to develop. This text with
and 1960s that leading physiotherapists developed con- contributions from contemporary researchers and clini-
cepts or methods of manipulative therapy practice that cians is built upon their legacy.
were eagerly sought by the physiotherapy world inter-
nationally. These early concepts placed a major focus GJ
on articular dysfunction. Manipulative therapy and/or AM
manual therapy became a method of management, as
reflected in the title of the earlier editions of this text. DF
The last 20 years in particular have seen quite significant JL
shifts in models of musculoskeletal pain and care which CM
have spurred and directed contemporary practice and
research. Musculoskeletal disorders are now well embed- MS
ded within a biopsychosocial context which provides a Australia, United Kingdom, Germany 2015

ix
 Acknowledgements

There are approximately 140 international researchers second and third editions of Grieve’s Modern Manual
and clinicians who have contributed to this multi- Therapy. We as editors of this fourth edition are very well
authored text and the editors thank them sincerely for aware of your vision for these previous and acclaimed
not only their chapters, but for the years of work and editions. On behalf of the readership, we thank you for
experience behind their words. They are all to be con- your contribution and the massive amount of work and
gratulated on outstanding work. They are often forging time you devoted to this important international text. Fly
new territory that translates into new or better quality high in your (semi) retirement!
assessment and management practices to the benefit of
both the patients and practitioners. You are all making a
significant contribution to musculoskeletal physiotherapy
internationally.
Thanks are also given to the publishers Elsevier, GJ
Oxford and in particular to Rita Demetriou-Swanwick AM
and Veronika Watkins who started the ball rolling and to
Nicola Lally who rolled the ball to the finish line. Thanks DF
are given to all Elsevier staff ‘behind the scenes’ for their JL
work in collating and copy-editing all chapters to bring CM
this complex text to fruition.
Finally, the editors would like to acknowledge the MS
work of Jeffrey Boyling who was the lead editor of the Australia, United Kingdom, Germany 2015

x
 Foreword

If you are a physiotherapist and you see patients of any than a sum of techniques. It captures how physiotherapy
age with musculoskeletal problems then this book is your science and practice have advanced dramatically decade
best value investment. Investment in the broad sense – a over decade since Gregory Grieve launched his almost
valuable way to use your time and cognitive effort. If you 900-page tome in 1986.
teach at any level of a physiotherapy programme, this Today’s 53 chapters codify musculoskeletal physio-
book will broaden your appreciation for your profession therapy that has the power to make a difference in every
no matter how well trained you are. If you are a student, patient encounter. It provides an incontrovertible story-
by definition passionate about health with a spirited love line that physiotherapy benefits from practice-based evi-
of life, you will find this book both a crutch and a ladder. dence and is a solidly evidence-based practice. The
Grieve’s Modern Musculoskeletal Physiotherapy captures comprehensive nature of Grieve’s adds to credibility by
the wisdom of over 100 of the world’s leading physio- demonstrating a body of knowledge that distinguishes
therapists and scientists in related fields. It was created in the musculoskeletal physiotherapy specialisation. As
11 countries. You are holding 500,000 hours of expertise Modern Musculoskeletal Physiotherapy, this ‘extended scope’
in your hands. That would take you 250 years to acquire 4th edition of Grieve’s adds substantial value to an even
solo. broader group of the physiotherapy profession than did
One of the joys of life is being on a steep learning its vertebral column serving predecessors.
curve. It is not marketed the way travel companies On behalf of all those who will benefit from this opus,
promote lounging poolside with a drink. But think of I congratulate and thank the leadership team – Professors
schussing through an alpine forest or conversing fluently Gwen Jull, Ann Moore, Deborah Falla, Jeremy Lewis,
in a new language. Think of any occasion when you have Christopher McCarthy and Michele Sterling – together
gained mastery and you know the buzz of negotiating a with each contributor to this book, for extending and
steep learning curve successfully. very strongly reinforcing the field of modern musculosk-
This revamped edition of Grieve’s guides you to pro- eletal physiotherapy. The multi-year international com-
fessional pleasures. For me, the wisdom and clarity of mitment to Grieve’s reflects the respect the editors have
illustration in Chapter 7 (Neuromuscular adaptations to earned; they inspired, cajoled, and I suspect occasionally
exercise) is just one an example. Chapter 31 (Therapeutic begged, to assemble a physiotherapy dream team. And
exercise) provided a remarkably novel approach for this judging by the team balance, the 5th and 6th editions are
old dog. High quality science mashes up with practical in good hands.
relevance. See Chapter 1 for a concise overview of the
chapters and the innovations.
In the 3rd edition foreword, Lance Twomey wrote Karim Khan, MBBS, PhD, MBA
‘This is a bold book.’ A decade later, Grieve’s 4th edition Director, Department of Research & Education
is not an evolution – it is a revolution. It is a complete Aspetar Orthopaedic and Sports Medicine
synthesis of the different clinically successful physiother- Hospital, Qatar
apy approaches that satisfy patients the world over. It Professor, Faculty of Medicine, University of British
outlines patient-based approaches that are far greater Columbia, Canada

xi
 Contributors

Michael Adams BSc, PhD Kathy Briffa BAppSc(Physiotherapy), Grad Dip Sports
Professor of Biomechanics, Centre for Comparative Physiotherapy, MAppSc (Health Sc), PhD
and Clinical Anatomy, University of Bristol, UK School of Physiotherapy and Exercise Science, Curtin
Visiting Professor, Sir Run Run Shaw Hospital, University, Perth, Australia
Zheijang University, China
Rachelle Buchbinder MBBS (Hons), MSc,
Caroline Alexander PhD, MSc, Grad Dip Phys PhD, FRACP
NIHR Senior Clinical Lecturer, Physiotherapy, Director, Monash Department of Clinical
Imperial College Healthcare NHS Trust Epidemiology, Cabrini Institute
NIHR Senior Clinical Lecturer, Surgery and Cancer, Professor, Department of Epidemiology and Preventive
Imperial College London, UK Medicine, School of Public Health and Preventive
Medicine, Monash University, Melbourne, Australia
Panos Barlas BSc, DPhil, LicAc
School of Health and Rehabilitation,
Keele University, UK Barbara Cagnie PT, PhD
Assistant Professor, Rehabilitation Sciences and
Harsimran Singh Baweja BPT, PhD Physiotherapy, Ghent University, Ghent, Belgium
Assistant Professor, Exercise and Nutritional Sciences,
Physical Therapy, San Diego State University, USA Lynne Caladine EdD, MSc
Head of School, School of Health Professions,
Darren Beales BSc (Physiotherapy), M Manip University of Brighton, UK
Ther, PhD
Research Fellow, School of Physiotherapy and Exercise Valentina Camomilla PhD
Science, Curtin University, Perth, Australia Doctor, Department of Movement, Human and Health
Sciences, University of Rome ‘Foro Italico’, Italy
David Beckwée MSc
Postdoctoral Researcher at the Vrije Universiteit Aurelio Cappozzo PhD
Brussel (Brussels, Belgium) and Teacher at the Professor of Movement, Human and Health Sciences,
Stichting Opleiding Musculoskeletale Therapie University of Rome ‘Foro Italico’, Italy
(SOMT) (Amersfoort, The Netherlands)
Department of Physiotherapy, Vrije University,
Belgium
Marco Cardinale PhD, MSc, BSc
Head of Sports Physiology, Sports Science, Aspire
Academy, Doha, Qatar
Kim Bennell BAppSci (Physio), PhD
Honorary Reader, Computer Science, University
Professor, Department of Physiotherapy, University of
College London, London
Melbourne, Melbourne, Australia
Honorary Senior Lecturer, Medical Sciences,
University of Aberdeen, Aberdeen, UK
Joel E Bialosky PhD, PT
Clinical Assistant Professor, Physical Therapy,
University of Florida, Gainesville, USA Andrea Cereatti PhD
Assistant Professor, Information Engineering Unit,
Leanne Bisset PhD, MPhty (Manipulative), MPhty POLCOMING Department, University of Sassari,
(Sports), BPhty Sassari, Italy
Senior Lecturer, School of Rehabilitation Sciences,
Griffith University, Gold Coast, Australia Helen Clare PhD, MAppSc, GradDipManipTher,
DipPhty
John D Borstad PT, PhD Director of Education, McKenzie Institute
Associate Professor, Physical Therapy, Ohio State International, Wellington, New Zealand
University, Columbus, USA Director, Helen Clare Physiotherapy, Sydney, Australia

xii
 Contributors xiii

Nicholas Clark PhD, MSc, MCSP, MMACP, CSCS Patricia Dolan BSc, PhD
Senior Lecturer in Sport Rehabilitation, School of Reader in Biomechanics, Centre for Comparative and
Sport, Health and Applied Science, St Mary’s Clinical Anatomy, University of Bristol, Bristol, UK
University, Twickenham, London, UK Visiting Professor, Sir Run Run Shaw Hospital,
Zheijang University, Zheijang, China
Gray Cook MSPT, OCS, CSCS
Co-Founder, Functional Movement Systems, Chatham, Jaap van Dieën PhD
UK Professor, Faculty of Human Movement Sciences,
University of Amsterdam, Amsterdam,
Jill Cook PhD, BAppSci The Netherlands
Professor, School of Primary Health Care, Monash
University, Virginia, Australia Linda van Dillen PhD, PT
Associate Director of Musculoskeletal Research,
Professor of Physical Therapy, Professor of
Brooke Coombes BPhty, MPhty, Phd Orthopaedic Surgery, Washington University School
Post-doctorate Research Fellow, Physiotherapy of Medicine in St Louis, St Louis, USA
Division, University of Queensland, Brisbane,
Australia James Elliott PT, PhD
Assistant Professor, Physical Therapy and Human
Michel W Coppieters PhD, PT Movement Sciences, Feinberg School of Medicine,
Professor, Move Research Institute, VU University Northwestern University, Chicago and St Lucia,
Amsterdam, Amsterdam, The Netherlands USA
Honorary Senior Fellow, School of Health and
Sallie Cowan BAppSc (Physio), Grad Dip Manip Rehabilitation Sciences, University of Queensland,
Physio, PhD Brisbane, Chicago and St Lucia, Australia
Senior Research Fellow, Department of Physiotherapy,
University of Melbourne Deborah Falla BPhty (Hons), PhD
Senior Research Fellow, Physiotherapy, St Vincents Professor, Pain Clinic, Center for Anesthesiology,
Hospital, Melbourne Emergency and Intensive Care Medicine
Director, Clifton Hill Physiotherapy, Melbourne, Professor, Department of Neurorehabilitation
Australia Engineering, Universitätsmedizin Göttingen, Georg-
August-Universität, Germany
Kay Crossley PhD, BAppSc (Physio)
School Health Rehab Sciences, University of Dario Farina PhD
Queensland, Brisbane, Australia Professor and Chair, Director of the Department,
Bernstein Center for Computational Neuroscience,
Wim Dankaerts PT, MT, PhD Bernstein Focus Neurotechnology Goettingen,
Musculoskeletal Rehabilitation Research Unit, Department of Neurorehabilitation Engineering,
Department of Rehabilitation Sciences, Faculty of University Medical Center Goettingen, Georg-
Kinesiology and Rehabilitation Sciences, University August University, Germany
of Leuven, Leuven, Belgium
Michael Farrell BAppSc (Phty), MSc, PhD
Senior Research Fellow, Imaging, Florey Institute of
Lieven Danneels PT, PhD Neuroscience and Mental Health
Professor, Department of Physical Therapy and Motor Honorary Senior Research Fellow, Anatomy and
Rehabilitation, Ghent University, Ghent, Belgium Neuroscience, University of Melbourne, Melbourne,
Australia
Elizabeth Dean PhD, MS, DipPT, BA
Professor, Physical Therapy, University of British Kjartan Fersum PhD, MSc, Bsc
Columbia, Vancouver, Canada Researcher, Department of Global Public Health
and Primary Care, University of Bergen, Bergen,
Margot De Kooning MSc Norway
Departments of Human Physiology and Physiotherapy,
Vrije University Gail Forrester-Gale MSc (Manual Therapy),
Faculty of Medicine and Health Sciences, Antwerp BSc Hons (Physiotherapy), PgCertificate Education,
University, Antwerp, Belgium MMACP; MCSP
Senior Lecturer in Physiotherapy, Physiotherapy
Mark de Zee PhD Subject Group, Exercise, Sport and Rehabilitation,
Associate Professor, Department of Health Science and Department of Applied Science and Health,
Technology, Aalborg University, Aalborg, Denmark Coventry University, Coventry, UK
xiv Contributors

Simon French PhD, MPH, BAppSc Jeremy Grimshaw MB ChB, PhD

Assistant Professor, School of Rehabilitation Therapy, Senior Scientist, Clinical Epidemiology Program,
Faculty of Health Sciences, Queen’s University, Ottawa Hospital Research Institute
Kingston, Canada Professor, Department of Medicine, University of
Ottawa, Ottawa, Canada
Julie Fritz PT, PhD
Professor, Physical Therapy, University of Utah, Salt Anita Gross BEcPT, MSc, Grad Dip MT
Lake City, USA Associate Clinical Professor, Rehabilitation Science,
McMaster University
Clinical Lecturer, Physical Therapy, Western
Graham Galloway BSc (H), University, Hamilton, London, Canada
Grad Cert Comp Sci, PhD
Professor, Centre for Advanced Imaging, University of Toby Hall MSc, PhD
Queensland, Brisbane, Australia Adjunct Associate Professor, School of Physiotherapy,
Curtin University of Technology
Jill Gamlin MSc, Grad Dip Phys Senior Teaching Fellow, University of Western
Consultant Physiotherapist, Cambridgeshire, Australia, Perth, Australia,
Cambridge, UK
Stephen Harridge PhD
Sabata Gervasio PhD, MSc EE Professor, Centre of Human and Aerospace
Research Assistant, Health Science and Technology, Physiological Sciences, King’s College London,
Aalborg University, Aalborg, Denmark London, UK

Karen Ginn PhD, MHPEd, GDManipTher, GDPhty Jan Hartvigsen PhD

Professor, Department of Sports Science and Clinical
Associate Professor, Discipline of Biomedical Science,
Biomechanics, University of Southern Denmark
Sydney Medical School, University of Sydney,
Senior Researcher, Nordic Institute of Chiropractic and
Sydney, Australia
Clinical Biomechanics, Odense, Denmark
Charlie Goldsmith BSc, MSc, PhD Eric Hegedus BSBA, MHSc, DPT
Maureen and Milan Ilich/Merck Chair in Statistics for Professor and Chair, Physical Therapy, High Point
Arthritis and Musculoskeletal Diseases, Arthritis University, High Point, USA
Research Centre of Canada
Professor of Biostatistics, Faculty of Health Sciences, Nicola Heneghan PhD, MSc
Simon Fraser University, Richmond, Burnaby and Birmingham, School of Sport, Exercise and
Hamilton Rehabilitation Sciences, University of Birmingham,
Emeritus Professor of Biostatistics, Clinical Birmingham, UK
Epidemiology and Biostatistics, McMaster University,
Canada Lee Herrington PhD, MSc, BSc (Hons)
Senior Lecturer in Sports Rehabilitation, School of
Sally Green PhD, BAppSci (Physiotherapy), Grad Dip Health Sciences, University of Salford
(Manipulative Physiotherapy) Technical Lead Physiotherapist, Physiotherapy, English
Professorial Fellow, School of Public Health and Institute of Sport, Manchester, UK
Preventive Medicine, Monash University, Melbourne,
Australia Jonathan Hill PhD, MSc, BSc
Lecturer in Physiotherapy, Arthritis Research UK
Primary Care Centre, Keele University, Keele, UK
Susan Greenhalgh PhD, MA, GDPhys, (FCSP)
Doctor, Elective Orthopaedics, Bolton NHS
Foundation Trust, Bolton, UK
Claire Hiller PhD, MAppSc, BAppSc
Research Fellow, Faculty of Health Sciences, University
of Sydney, Sydney, Australia
Alison Grimaldi BPhty, MPhty (Sports), PhD
Director, Physiotec Physiotherapy, Brisbane, Australia Rana Hinman BPhysio, PhD
Department of Physiotherapy, School of Health
Hubert van Griensven PhD, MSc (Pain), BSc, DipAc Sciences, University of Melbourne, Melbourne,
Research Fellow, Centre for Health Research, School Australia
of Health Sciences, University of Brighton,
Brighton, UK Paul Hodges PhD, MedDr, DSc, BPhty (Hons)
Consultant Physiotherapist, Department of Director, CCRE Spine, School of Health and
Rehabilitation, Southend University Hospital NHS Rehabilitation Sciences, University of Queensland,
Foundation Trust, Southend, UK Brisbane, Australia
 Contributors xv

Melanie Holden PhD, BSc (Hons) Diane Lee BSR FCAMT

Doctor, Arthritis Research UK Primary Care Centre, Director, Diane Lee & Associates, South Surrey,
Keele University, Keele, UK Canada

Alan Hough PhD, BA (Hons), Grad Dip Phys Linda-Joy Lee PhD, BSc(PT), BSc
Honorary Associate Professor, School of Health Director of Curriculum & Mentorship, Dr Linda-Joy
Professions (NC), Faculty of Health & Human Lee Physiotherapist Corporation, North Vancouver
Sciences (NC), Plymouth University, Plymouth, UK Founder & Director, Synergy Physiotherapy, North
Vancouver, Canada
Venerina Johnston PhD, BPhty (Hons), Grad Cert Honorary Senior Fellow, Physiotherapy, University of
OHS, (Cert Work Disability Prevention) Melbourne, Australia
Academic, Division of Physiotherapy, University of Associate Member, Centre for Hip Health & Mobility,
Queensland, Brisbane, Australia Vancouver, Canada

Gwendolen Jull Dip Phty, Grad Dip Manip Ther, Scott Lephart PhD
MPhty, PhD, FACP Dean and Professor, College of Health Sciences,
Emeritus Professor, Department of Physiotherapy, Endowed Chair of Orthopaedic Research,
School of Health and Rehabilitation Sciences, University of Kentucky
University of Queensland, Brisbane, Australia Lexington, USA

Joanne Kemp MSportsPhysio, BAppSc (Physio) Jeremy Lewis PhD, FCSP

PhD Candidate, School of Health and Rehabilitation Consultant Physiotherapist, London Shoulder Clinic,
Sciences, University of Queensland, Brisbane Centre for Health and Human Performance
Research Associate, Australian Centre of Research into Consultant Physiotherapist, Central London
Injury in Sport and its Prevention (ACRISP), Community Healthcare NHS Trust, UK
Federation University, Ballarat Professor (Adjunct) of Musculoskeletal Research,
Principal Physiotherapist, Bodysystem, Hobart, Clinical Therapies, University of Limerick, Limerick,
Australia Ireland
Reader in Physiotherapy, School of Health and
Justin Kenardy PhD Social Work, University of Hertfordshire, London,
CONROD, University of Queensland, Brisbane, UK
Australia
Ian Loram MA, PhD
Peter Kent BAppSc (Physio), BAppSc (Chiro), Grad Professor of Neuromuscular Control of Human
Dip (Manipulative Physiotherapy), PhD Movement, Cognitive Motor Function Research
Associate Professor, Institute of Sports Science and Group, School of Healthcare Science, Manchester
Clinical Biomechanics, University of Southern Metropolitan University, Manchester, UK
Denmark
Clinical Associate Professor, Institute of Regional James Henry McAuley PhD
Health Research, University of Southern Denmark, Senior Lecturer (Conjoint), Neuroscience Research
Odense, Denmark Australia, School of Medical Sciences, University of
New South Wales, Sydney, Australia
Roger Kerry MSc
Associate Professor, Faculty of Medicine and Health Christopher McCarthy PhD, FCSP, FMACP
Science, University of Nottingham, Nottingham, UK Consultant Physiotherapist, St Mary’s Hospital,
Imperial College Healthcare, London, UK
Henri Kiers MSc
Human Movement Scientist, Physiotherapist, Research Jenny McConnell BAppSci (Phty), Grad Dip Man
Group Lifestyle and Health, University of Applied Ther, M Biomed Eng
Sciences Utrecht, Utrecht, The Netherlands Visiting Senior Fellow, Melbourne University, Australia

Kyle Kiesel PT, PhD Joy MacDermid PhD

Professor, Physical Therapy, University of Evansville, Professor, Rehabilitation Sciences, McMaster
Evansville, USA University, Hamilton, Canada

Idsart Kingma PhD Martin Mackey PhD, MSafetySc,

Associate Professor, Human Movement Scientist, GradDipEducStud(HigherEduc),
Research Institute MOVE, Faculty of Human BAppSc(Physio), BEc
Movement Sciences, VU University Amsterdam, Doctor, Senior Lecturer, Physiotherapy, University of
Amsterdam, The Netherlands Sydney, Sydney, Australia
xvi Contributors

Katie McMahon PhD, Hons, BSc Peter O’Sullivan PhD

Doctor, Centre for Advanced Imaging, University of Professor, Physiotherapy, Curtin University, Perth,
Queensland, Brisbane, Brisbane Australia
Honorary Fellow, Wesley Research Institute, Australia
Ioannis Paneris BSc (Hons), MSc, MCSP, MMACP
Stephen May MA, FCSP, Dip MDT, MSc, PhD Extended Scope Practitioner, Community and
Doctor, Faculty of Health and Wellbeing, Sheffield Medicine, Central Manchester University
Hallam University, Sheffield, UK Hospitals – NHS Foundation Trust, Manchester, UK

Claudia Mazzà PhD Ruth Parry MCSP, MMedSci, PhD

Lecturer, Mechanical Engineering, University of Principal Research Fellow, Supportive, Palliative and
Sheffield, Sheffield, UK End of Life Care Research Group, University of
Nottingham, UK
Niamh A Moloney BPhysio, MManipulative
Therapy, PhD George Peat PhD
Lecturer, Physiotherapy, University of Sydney, Sydney, Professor of Clinical Epidemiology, Arthritis Research
Australia UK Primary Care Centre, Keele University, Keele,
UK
Ann Moore PhD, FCSP, FMACP, Dip TP, Cert Ed
Professor of Physiotherapy and Head of the Centre for Nicola Petty DPT, MSc
Health Research, School of Health Sciences, Principal Lecturer, Centre for Health Research, School
University of Brighton, Brighton, UK of Health Sciences, University of Brighton,
Brighton, UK
Jane Morris Ed D, MA, GradDipPhys, MCSP, PG Cert
HE, FHEA Harry von Piekartz PhD, MSc PT
Deputy Head of School, School of Health Sciences Professor, Department of Movement Science,
University of Brighton, Brighton, UK University of Applied Science, Osnabrück Germany

Natalie Mrachacz-Kersting BSc, MEd, PhD Tania Pizzari PhD, BPhysio (Hons)
Associate Professor, Health Science and Technology, Doctor, Physiotherapy, La Trobe University,
Aalborg University, Aalborg, Denmark Melbourne, Australia

Robert J Nee PT, PhD, MAppSc Ross Pollock BSc, MSc, PhD
Associate Professor, Physical Therapy, Pacific Doctor, Centre of Human and Aerospace Physiological
University, Hillsboro, USA Sciences, King’s College London, London, UK

Jo Nijs PhD, PT, MT Annelies Pool-Goudzwaard PhD, PT, MT

Associate Professor, Pain in Motion Research Group, Senior Researcher, Neuroscience, Faculty of Medicine
Departments of Human Physiology and and Health Sciences, Erasmus MC University,
Rehabilitation Sciences, Faculty of Physical Rotterdam, The Netherlands
Education and Physiotherapy, Vrije Universiteit
Brussel, Brussel, Belgium John Rasmussen MSc, PhD
Professor, Mechanical and Manufacturing Engineering,
Tze Siong Ng BSc (Hons) Physiotherapy, MA Aalborg University, Aalborg, Denmark
(Manual Therapy)
Senior Principal Physiotherapist, Ms, Rehabilitation, Maree Raymer B Phty (Hons), MPhty St (Msk),
National University Hospital, Singapore Masters Health Management
Assistant Program Manager, Statewide Neurosurgical
Shaun O’Leary BPhty(Hons), MPhty(Msk), PhD and Orthopaedic Physiotherapy Screening Clinics
Principal Research Fellow, CCRE (Spinal Pain Injury and Multidisciplinary Service, Physiotherapy, Royal
and Health), University of Queensland, Brisbane, Brisbane and Women’s Hospital, Brisbane, Australia
Australia
Kathryn M Refshauge PhD, MBiomedE,
Peter Osmotherly BSc, Grad Dip Phty, M Med Sci GradDipManipTher, DipTher
Senior Lecturer in Physiotherapy, School of Health Professor, Faculty of Health Sciences, University of
Sciences, University of Newcastle, Newcastle, Sydney, Sydney, Australia
Australia
Ebonie Rio BAppSci, BA Phys (Hons), Masters Sports
Kieran O’Sullivan PhD, M Manip Ther, B Physio Phys, PhD candidate
Lecturer, Department of Clinical Therapies, University PhD Researcher, Physiotherapy Department, Monash
of Limerick, Limerick, Ireland University, Frankston, Australia
 Contributors xvii

Darren A Rivett BAppSc(Phty), GradDipManipTher, Kathleen Sluka PT, PhD

MAppSc(ManipPhty), PhD Professor, Neurobiology of Pain Laboratory, University
Professor of Physiotherapy, School of Health Sciences, of Iowa, Iowa, USA
University of Newcastle, Newcastle, Australia
Ashley Smith PT, PhD(c)
Ulrik Röijezon PhD, PT PhD Student, University of Queensland Director,
Assistant Professor, Department of Health Sciences, Evidence Sport and Spinal Therapy, Calgary,
Luleå University of Technology, Luleå, Sweden Canada, Division of Physiotherapy, NHMRC Centre
of Clinical Excellence Spinal Pain, Injury and Health,
Shirley Sahrmann PT, PhD University of Queensland, Brisbane, Australia
Professor Emeritus, Physical Therapy, Washington
University School of Medicine, St Louis, USA Anne Söderlund PhD, RPT
Professor, Physiotherapy, School of Health, Care and
Siobhan Schabrun PhD, BPhysio (Hons) Social Welfare, Malardalen University, Västerås,
NHMRC Clinical Research Fellow, School of Science Sweden
and Health, University of Western Sydney
Honorary Senior Fellow, School of Health and
Rehabilitation Science, University of Queensland, Michele Sterling PhD, MPhty, BPhty, Grad Dip Manip
Brisbane, Australia Physio, FACP
Associate Director of the Centre of National Research
Axel Meender Schäfer PhD on Disability and Rehabilitation Medicine
Verw Prof, Faculty of Social Work and Health, (CONROD)
University of Applied Science and Art, Hildesheim, Professor in the Centre of Musculoskeletal Research
Germany and the School of Allied Health, Griffith University,
Brisbane, Australia
Annina Schmid PhD, MManipTher,
PT OMT svomp Maria Stokes PhD FCSP
Post Doctoral Research Fellow, Nuffield Department Professor of Musculoskeletal Rehabilitation, Faculty of
of Clinical Neurosciences, Oxford University, Health Sciences, University of Southampton,
Oxford, UK Southampton, UK
School of Health and Rehabilitation Sciences,
University of Queensland, Brisbane, Australia Leon Straker PhD, MSc, BAppSc
Professor of Physiotherapy, School of Physiotherapy
Quentin Scott BPHTY, Post Grad Dip Manip Ther, and Exercise Science, Curtin University, Perth
FACP Australia
Specialist Musculoskeletal Physiotherapist, Milton
Physiotherapy, Brisbane, Australia Peter William Stubbs BSc, MPhty, PhD
Research Officer, Neuroscience Research Australia,
Hazel Screen BEng, MRes, PhD Australia
Reader in Biomedical Engineering and Deputy Post Doctoral Fellow, Research Department, Hammel
Director of Taught Programmes, School of Neurorehabilitation and Research Center, Aarhus
Engineering and Materials Science, Queen Mary University, Aarhus, Denmark
University of London, London, UK
Brigitte Tampin Physio, Grad Dip Manip Ther,
James Selfe PhD, MA, GDPhys, FCSP
Professor of Physiotherapy, School of Sport, Tourism
MSc, PhD
Adjunct Research Fellow, School of Physiotherapy and
and The Outdoors, University of Central Lancashire,
Exercise Science, Curtin University
Preston, UK
Department of Physiotherapy, Sir Charles Gairdner
Hospital, Perth Australia
Jane Simmonds PD, MA, PGDIP, PGCHE,
BAPP(SC), BPE
Professional Lead Physiotherapy, Allied Health and Alan Taylor MCSP, MSc
Midwifery, University of Hertfordshire Lecturer, Physiotherapy and Rehabilitation Sciences,
Clinical Specialist, Hypermobility Unit, Hospital of St University of Nottingham, Nottingham, UK
John and St Elizabeth, London, UK
Carolyn Taylor BAppSc (Exercise & Sports Science),
Kevin P Singer PhD, PT BAppSc (Physiotherapy)
Winthrop Professor, Surgery, University of Western Lecturer in Physiotherapy, La Trobe Rural Health
Australia, Perth, Australia School, La Trobe University, Melbourne, Australia
xviii Contributors

Julia Treleaven BPhty, PhD David Walton BScPT, MSc, PhD

Lecturer, CCRE Spine, Division of Physiotherapy, Assistant Professor, School of Physical Therapy,
University of Queensland, Brisbane, Australia Western University, London, Canada

Lyn Watson BAppSc Physio

Peter Vaes PhD Clinical Shoulder Physiotherapy Specialist, LifeCare,
Head of Department, Rehabilitation Sciences and
Prahran Sports Medicine Centre and Melbourne
Physiotherapy, Vrije University of Brussels, Brussels,
Orthopaedic Group, Prahran, Australia
Belgium
Tim Watson PhD, BSc, FCSP
Giuseppe Vannozzi PhD Professor of Physiotherapy, Department of Allied
University Researcher, Motor, Human and Health Health Professions and Midwifery, University of
Sciences, University of Rome ‘Foro Italico’, Rome, Hertfordshire, Hatfield, UK
Italy
Rod Whiteley PhD
Research & Education Physiotherapist, Rehabilitation
Bill Vicenzino PhD, MSc, BPhty, GradDipSportsPhty Department, Aspetar Sports Medicine Hospital,
Professor, Division of Physiotherapy, School of Health
Doha, Qatar
and Rehabilitation Sciences, University of
Queensland, Brisbane, Australia
Nienke Willigenburg PhD
Post-Doctoral Student, Human Movement Scientist,
Anne Wajon BAppSc (Phty), MAppSc (Phty), PhD Division of Sports Medicine, Sports Health and
Director, Macquarie Hand Therapy, Macquarie Performance Institute, Ohio State University, Ohio
University, Sydney, Australia USA
 PLATE 1
Neural control Motor cortex Sensory cortex
–
SMA

dPM
M1 Thalamus
S1 5 7
PF

–
BG V1
Anterior cerebellum
RN Forward model Inhibition
of afferent
C transmission
RF Predicted
sensory feedback
VN
–
Nucleus Z
Match

Spinal cord
Musculoskeletal Stretch DSCT
mechanics

Iliacus
Clarke’s
column
Motor Spindle
behaviour afferent

Contract
FIGURE 4-2  ■  Sensorimotor pathways through the central
nervous system. The central nervous system is conventionally
viewed as having a hierarchical organization with three levels:
the spinal cord, brainstem and cortex. The spinal cord is the
lowest level, including motor neurons, the final common
pathway for all motor output, and interneurons that integrate FIGURE 4-3  ■  Neural pathways estimating position from sensory
sensory feedback from the skin, muscle and joints with descend- and motor information. Integration of muscle spindle afferents
ing commands from higher centres. The motor repertoire at this with expectations generated from motor output. When the
level includes stereotypical multijoint and even multilimb reflex muscle is stretched, spindle impulses travel to sensory areas of
patterns, and basic locomotor patterns. At the second level, the cerebral cortex via Clarke’s column, the dorsal spinocerebel-
brainstem regions such as the reticular formation (RF ) and ves- lar tract (DSCT ), Nucleus Z, and the thalamus (shown in red).
tibular nuclei (VN) select and enhance the spinal repertoire by Collaterals of DSCT cells project to the anterior cerebellum.
improving postural control, and can vary the speed and quality When a motor command is generated, it leads to co-activation
of oscillatory patterns for locomotion. The highest level of of skeletomotor and fusimotor neurons (shown in blue). A copy
control, which supports a large and adaptable motor repertoire, of the motor command is sent to the anterior cerebellum where
is provided by the cerebral cortex in combination with subcorti- a comparison takes place between the expected spindle
cal loops through the basal ganglia and cerebellum.36 Motor response based on that command and the actual signal pro-
planning and visual feedback are provided through several pari- vided by the DSCT collaterals. The outcome of the match is used
etal and premotor regions. The primary motor cortex (M1) con- to inhibit reafferent activity, preventing it from reaching the
tributes the largest number of axons to the corticospinal tract cerebral cortex. Sites of inhibition could be at Nucleus Z, the
and receives input from other cortical regions that are predomi- thalamus, or the parietal cortex itself. (Reproduced from Proske
nantly involved in motor planning. Somatosensory information and Gandevia.41)
is provided through the primary somatosensory cortex (S1),
parietal cortex area 5 (5) and cerebellar pathways. The basal
ganglia (BG) and cerebellum (C ) are also important for motor
function through their connections with M1 and other brain
regions. RN, Red nucleus; V1, Primary visual cortex; 7, Region
of posterior parietal cortex; dPM, Dorsal premotor cortex; SMA,
Supplementary motor area; PF, Prefrontal cortex. (Reproduced
with modification from Scott.38)
 PLATE 2

Premotor PFC
WM, goals,
if-than scenarios
dl PFC

‘Motor’ BG Behav. gate

vm PFC
‘Cogn.’ BG WM gate
Ventral str. Motiv. gate

Slow RL

DA
Hippocampus
Amygdala Fast learning
Value
arb. associations

FIGURE 4-4  ■  Access of basal ganglia to motivational, cognitive and motor regions for selection and reinforcement learning. The
basal ganglia are a group of interconnected subcortical nuclei that represent one of the brain’s fundamental processing units. Inter-
acting corticostriatal circuits contribute to action selection at various levels of analysis. Coloured projections reflect subsystems
associated with value/motivation (red), working memory and cognitive control (green), procedural and habit learning (blue), and
contextual influences of episodic memory (orange). Sub-regions within the basal ganglia (BG) act as gates to facilitate or suppress
actions represented in frontal cortex. These include parallel circuits linking the BG with motivational, cognitive, and motor regions
within the prefrontal cortex (PFC). Recurrent connections within the PFC support active maintenance of working memory (WM).
Cognitive states in dorsolateral PFC (dlPFC) can influence action selection via projections to the circuit linking BG with the motor
cortex. Dopamine (DA) drives incremental reinforcement learning in all BG regions, supporting adaptive behaviours as a function
of experience. (Reproduced from Frank.22)

Cortical loops Subcortical loops

Sensory Motor Sensory Motor

input Cerebral output input Subcortical output

cortex structures

Striatum Thal Thal SN/GP

SN/GP Striatum
A B
FIGURE 4-5  ■  Cortical and subcortical sensorimotor loops through the basal ganglia. (A) For corticobasal ganglia loops the position
of the thalamic relay is on the return arm of the loop. (B) In the case of all subcortical loops the position of the thalamic relay is on
the input side of the loop. Predominantly excitatory regions and connections are shown in red while inhibitory regions and connec-
tions are blue. Thal, Thalamus; SN/GP, Substantia nigra/globus pallidus. (Reproduced from Redgrave.109)
 PLATE 3

Hammond (1956) Pruszynski et al (2008)

R R
Perturbation
onset
L

5 cm
L

L B
L
Force

Perturbation
onset
20 N
L 2 au
Elbow angle

EMG
EMG

5°
1 mV
SL LL SL LL
20 45 105 100 ms 20 45 105
A Time (ms) C D Time (ms)
FIGURE 4-9  ■  Modulation of fast motor response by prior subject intent. (A) Example of how subjects can categorically modulate the
long-latency (transcortical) stretch response according to verbal instruction. Subjects were verbally instructed to respond to a
mechanical perturbation with one of two verbal instructions (‘resist’/‘let go’). The upper panel depicts force traces from individual
trials aligned on perturbation onset and labelled according to the instruction. The bottom panel is the corresponding muscle activity,
which shows modulation in the long-latency stretch response (LL) but not the short-latency (spinal) stretch response (SL). (B) Example
of how subjects can continuously modulate their long-latency stretch response in accordance with spatial target position. Subjects
were instructed to respond to an unpredictable mechanical perturbation by placing their hand inside one of the five presented
spatial targets. Each plot represents exemplar hand kinematics as a function of target position. Subjects began each trial at the filled
black circle, and the black diamond indicated final hand position. The small arrows indicate the approximate direction of motion
caused by the perturbation. (C) Temporal kinematics for the elbow joint aligned on perturbation onset. (D) Pooled EMG aligned on
perturbation onset and normalised to pre-perturbation muscle activity. Note that the long-latency stretch response exhibits graded
modulation as a function of target position. (Reproduced from Pruszynski and Scott.27)
 PLATE 4

Vasti EMG 1

EMG
Hz Hz

(mV)
5
8.7 6.5
A
Discharge rate
B

Discharge
rate (Hz)

1 mV
C Derecruitment
10 ms
20 D
New recruitment
0
Vasti EMG 2
EMG
(mV)

3
9.5 7.1
E
Discharge rate
F
Discharge
rate (Hz)

20 New recruitment
G
0 500 ms

$ %
-8° 15°
39°
44°

No pain
Pain

& '
FIGURE 6-3  ■  Redistribution of muscle activity in acute pain. (A) During acute pain activity of motor units is redistributed within and
between muscles. (B) Fine-wire electromyography (EMG) recordings are shown during contractions performed at identical force
before (left) and during (right) pain for two recording sites in the vasti muscles. The time of discharge of individual motor units is
displayed below the raw EMG recordings. The template for each unit is shown. Pain led to redistribution of activity of the motor
units. Units A and E discharged at a slower rate during pain. Units B and C stopped discharging during pain and units F and G,
which were not active prior to pain, began to discharge only during pain. These changes indicate that the participant maintained
the force output of the muscle, by using a different population of motor units (i.e. redistribution of activity within a muscle). 
(C) Knee extension task. (D) The direction of force used by the participants to match the force during contractions with and without
pain differed between trials. During pain, participants generated force more medially or laterally than in the pain-free trials. 
(A, B Redrawn from data from Tucker et al.;26 C, D redrawn from data from Tucker et al.64)
 PLATE 5

Start Mid End

Cranial 40

30

Control 20

10

Caudal 0 mV
Medial Lateral

30

20
Low back pain

10

$ %
0 mV
FIGURE 6-4  ■  Reduced redistribution of muscle activation in low back pain. Although healthy individuals redistribute muscle activity
to maintain the motor output in the presence of fatigue, this is not observed in people with low back pain. (A) A 13 × 5 grid of
electromyography electrodes was placed over the lumbar erector spinae in a group of healthy controls and people with chronic low
back pain to assess the spatial distribution of erector spinae activity and change in the distribution during performance of a repeti-
tive lifting task for ~200 second. (B) Representative topographical maps of the root mean square EMG amplitude from the right
lumbar erector spinae muscle for a person with low back pain and a control. EMG maps are shown for the start, mid and end of a
repetitive lifting task. Areas of blue correspond to low EMG amplitude and dark red to high EMG amplitude. Note the shift (redis-
tribution) of activity in the caudal direction as the task progresses but for the control subject only. (Reprinted with permission from
Falla et al.17)
 PLATE 6
12
12 (0°)

9 (270°) 3 (90°)

9 3

Baseline
Control
$ % 6 Pain

BIO ANC BME BLA

BIA TLA TLO DME

PEC DAN DPO LAT

&

DAN DPO DAN DPO

' (
FIGURE 6-5  ■  Changes in muscle activity vary between individuals when challenged by pain, with no few consistent changes across
participants. (A) Pain-free volunteers (n=8) performed multijoint reaching in the horizontal plane using a manipulandum, with the
starting point at the centre of the circle. The subject had to reach the 12 targets depicted in A with each reaching movement lasting
1 second followed by a 5 second rest period at the target position before returning to the centre point over 1 second. Subjects
performed the task at baseline, and following the injection of isotonic (control) and hypertonic (painful) saline. Saline was injected
into the right anterior deltoid (DAN) muscle. (B) Representative example of endpoint trajectories recorded from one subject during
the baseline (blue), control (magenta), and painful (red) conditions. Note that pain did not affect the kinematics of this controlled
task. (C) Directional tuning of the EMG envelope peak value recorded from 12 muscles during the baseline (blue), the control
(magenta), and pain (red) conditions. The ‘shrinking’ of the pain curves of the DAN muscle was due to a consistent decrease of the
EMG activity of this muscle across subjects. Other muscles also change their activity, however the direction of change was different
across subjects, demonstrating the variability in subject response. For example, the activity of the posterior deltoid (DPO), increased
during pain in three subjects while it decreased in five subjects, so that on average it was unchanged. (D) Representative data from
a single subject showing a decrease in DAN activity with a simultaneous increase in DPO activity during pain. (E) In contrast, rep-
resentative data from another subject shows that decreased DAN activity occurred together with a decrease in DPO activity during
pain. ANC, Anconeus; BIA, Brachialis; BIO, Brachioradialis; BLA, Lateral head of the biceps brachii; BME, Medial head of the biceps
brachii; DME, Medial deltoid; LAT, Latissimus dorsi; PEC, Pectoralis major; TLA, Lateral head of the triceps brachii; TLO, Long head
of the triceps brachii. (Reprinted with permission from Muceli et al.3)
 PLATE 7

Motor cortex
(M1)

Medulla

Corticospinal
Vertex tract
(Cz) $ TMS over scalp grid
Spinal cord

' MEPs superimposed

over scalp sites % Abdominal muscle
EMG recordings

& MEP recorded at each site

( Motor cortical map

) Relationship between cortical map
5
4 and onset in arm movement task
Healthy
4
LBP
3 3
CoG-lateral (cm)

1 2

Cz 1 2 3 4 5 1

r = 0.57 p <0.001
0
-100 -50 0 50 100
Relative onset of TrA (ms)
FIGURE 6-7  ■  Changes in motor cortex organization in low back pain. (A) Transcranial magnetic stimulation (TMS) was applied
according to a grid over the motor cortex to stimulate the corticospinal pathway. (B) Electromyography was recorded from the
transversus abdominis (TrA) muscle. (C) Motor evoked potentials (MEP) were recorded from stimuli applied at each point on the
grid. (D) The amplitude of MEPs is larger when stimulation is applied to the cortical region with neural input to the muscle.
(E) The gradient from low (blue) to high (light green) MEP amplitude is shown relative to the vertex (Cz). White/blue dots indicate
the centre of the region with input to TrA in healthy participants, and the grey/orange indicates that for people with a history of
LBP. The centre is positioned further posterior and lateral in the LBP group, providing evidence of reorganization of the motor cortex.
(F) The degree of reorganization was correlated with the delay of the onset of activation of TrA EMG during an arm movement task.
 PLATE 8

$ %

FIGURE 8-4  ■  Patients with CTS have elongated nodes of Ranvier. (A) Normal nodal architecture of a dermal myelinated fibre shown
by a distinct band of voltage-gated sodium channels (pNav, blue) located in the middle of the gap between the myelin sheaths
(green, myelin basic protein [MBP]). Paranodes are stained with contactin associated protein (Caspr, red). (B) A dermal myelinated
fibre of a patient with carpal tunnel syndrome demonstrating an elongated node with an increased gap between the myelin sheaths.
Voltage-gated sodium channels are dispersed within the elongated node.

$ % &
FIGURE 8-5  ■  Patients with CTS have a loss of small fibres. (A) Cross-section through a healthy skin taken on the lateropalmar aspect
of the second digit. The dermal–epidermal junction is marked with a faint line with the epidermis located on top. Axons are stained
with protein gene product 9.5 (a panaxonal marker, red) and cell nuclei are stained with DAPI (blue). There is an abundancy of nerve
fibres in the subepidermal plexus as well as inside papillae (arrowheads). Many small fibres pierce the dermal–epidermal junction
(arrows). (B) Skin of an age- and gender-matched patient with carpal tunnel syndrome (CTS) demonstrates a clear loss of intraepi-
dermal nerve fibres and a less dense subepidermal plexus. (C) Graph confirms a substantial loss of intraepidermal nerve fibres (per
mm epidermis) in patients with CTS (p < 0.0001, mean and standard deviations).
 PLATE 9

$ CD68

% CD68 / GFAP

FIGURE 8-6  ■  Experimental mild nerve compression induces a local immune-inflammatory reaction intraneurally as well as in con-
nective tissue. Longitudinal sections through non-operated (left) and mildly compressed (right) sciatic nerves of rats. (A) Top panel
shows the presence of resident CD68+ macrophages in a non-operated nerve (left) and an intraneural activation and recruitment of
macrophages beneath a mild nerve compression (right). (B) The activation and recruitment of CD68+ macrophages (red) within the
epineurium following mild nerve compression (right) compared to a healthy nerve (left). Schwann cells are stained in green with
glial fibrillary acid protein (GFAP).
 PLATE 10

A 20.00 um B 20.00 um

FIGURE 10-5  ■  Histological sections, viewed with a Nikon Eclipse 80i, from the energy-storing equine superior digital extensor tendon.
Images compare (A) a healthy tendon and (B) a tendinopathic tendon. Note the aligned and ordered matrix in the healthy tendon,
and clearly differentiated interfascicular matrix. By contrast, the tendinopathic sample shows the disordered matrix, rounded cells
and increased cellularity. (Photographs taken in Professor Peter Clegg’s laboratory, University of Liverpool.33)
 PLATE 11

Flexion Flexion
50 50

FwLSF 40 FwRSF FwLSF 40 FwRSF

30 30

20 20

10 20s 10
30s
LSF 0 RSF 40s LSF 0 RSF
50s
60s

EwLSF EwRSF EwLSF EwRSF

A Extension B Extension
FIGURE 12-3  ■  The decline in range of motion in all planes, observed when using the combined movement examination of the lumbar
spine. F, flexion; FwRSF, flexion with right side flexion; RSF, right side flexion; EwRSF, extension with right side flexion; E, exten-
sion; EwLSF, extension with left side flexion; LSF, left side flexion; FwLSF, flexion with left side flexion.
 PLATE 12

FIGURE 14-1  ■  Types of image display. (C) Colour Doppler.

 PLATE 13

FIGURE 15-3  ■  An example of whole body magnetic resonance imaging using a three-dimensional semi-automated segmentation
algorithm where the quantification of specific muscle volume and fat infiltration can be realized. (Images are courtesy of Dr Olof
Dahlqvist-Leinhard, Linköping University, Sweden; Advanced MR Analytics http://amraab.se/).

$ %

FIGURE 15-4  ■  Magnetic resonance (fat only) image of the right plantar (red) and dorsiflexors (blue) in (A) subject with incomplete
spinal cord injury and (B) subject with chronic whiplash-associated disorder. Note the increased signal throughout the plantar/
dorsiflexors in both subjects, suggestive of fatty infiltrates. Note: The posterior tibialis is highlighted in green.
 PLATE 14

$ %

FIGURE 15-5  ■  Anatomically defined regions of interest (ROIs) on the (A) magnetization transfer (MT) and (B) non-MT-weighted image
over the ventromedial and dorsolateral (green in colour plate, arrows in this figure) primarily descending motor pathways and the
dorsal column (red in colour plate, circled in this figure) ascending sensory pathways of the cervical spinal cord. The non-
magnetization transfer (non-MT) scan (B) is identical except that the MT saturation pulse is turned off and run as a separate
co-registered acquisition. The MTR is calculated on a voxel-by-voxel basis using the formula of: MTR = 100*(non-MT − MT)/
non-MT.
 PLATE 15

A B C D E
FIGURE 16-1  ■  (A) A midline sagittal view of the brain is provided to show the location of the brainstem, which is enclosed within
the dashed box. (B) The brainstem outlined in panel A is enlarged and transverse lines indicate the axial level of images displayed
in the remaining panels. The z-value refers to the distance in mm inferior to the anterior commissure. (C) An axial slice through the
midbrain shows pain activations encompassing the ventrolateral regions of the periaqueductal grey. The aqueduct is visible on the
image as a dark oval region at the midline between the symmetrical activations. (D) The parabrachial regions are incorporated within
the pain activations on this axial slice at the upper level of the pons. (E) An axial slice through the upper (rostral) part of the medulla
also cuts through the lowest portion of the pons (grey tissue highest in the panel). The pain activation overlays the midline nucleus
raphe magnus, which is the human homologue of the rostroventral medulla in animals.
 PLATE 16

A B

C D

E F

FIGURE 16-2  ■  (A) A three-dimensional rendering of the left hemisphere of human brain is traversed by two yellow lines that indicate
the positions of axial slices shown in panels C and E. The z-values are the distances in mm of the lines above the anterior commis-
sure. (B) The hemispheres are viewed from above to show the position of a sagittal slice 2 mm into the left hemisphere (x = −2)
and a coronal slice 20 mm posterior to the anterior commissure (y = −20). The slices appear in panels D and F. (C) Pain activation
commonly occurs in the insula and prefrontal cortex (PFC). Regions within the basal ganglia, such as the putamen can also show
pain activation. (D) The thalamus is the projection site of inputs from the spinothalamic tract. The ventroposterior lateral nuclei of
the thalamus project to the primary (SI) and secondary (SII) somatosensory cortices. (E) The midcingulate cortex (MCC) almost
invariably activates in association with pain. The primary somatosensory cortex (SI) is less consistently activated during noxious
stimulation. Pain activation in the posterior parietal cortex (PPC) predominates in the right hemisphere for stimuli on either side of
the body, although the left PPC can also activate during pain. (F) The midcingulate cortex (MCC) is a midline structure that is proxi-
mal to, and has connections with, the supplementary motor area (SMA).
 PLATE 17

Fibromyalgia Control
0–5 s 55–60 s 0–5 s 55–60 s
Cranial 140

120

100

80
y-axis

60

40

20

0 µV
Caudal
Medial x-axis Lateral
FIGURE 17-6  ■  Topographical mapping of muscle activity. Representative topographical maps (interpolation by a factor 8) of the EMG
root mean square value from the right upper trapezius muscle for a person with fibromyalgia and a control subject. Maps are shown
for the first and last 5 seconds of a 60-degree sustained shoulder abduction contraction. Areas of blue correspond to low EMG
amplitude and dark red to high EMG amplitude. Note the shift of activity in the cranial direction as the task progresses but for the
control subject only. (Reprinted with permission from Falla et al.111)
 PLATE 18

400 µV

300 µV

200 µV

100 µV

0 µV

20 10.0
19
Discharge rate

18 Force
17
16 7.5
15 pps
15 10 pps

Force (% MVC)
14 Time 5 pps
13
12 5.0
MU number

11
10
9
8 2.5
7
6
5
4 0
3
2
1
1 2 3 4 5 6 7 8 9 10 11 12
A Time (s)

15
Discharge rate (pps)

16 10
5
MU number

15
15 10
5
1 2 3 4 5 6 7 8 9 10 11 12
B Time (s)
FIGURE 17-7  ■  Extraction of single motor unit discharge patterns from high-density surface EMG. (A) Motor unit discharge patterns
during an increasing (6 seconds) and decreasing (6 seconds) force isometric contraction (to 10% of the maximum) of the abductor
pollicis brevis muscle, as estimated from surface EMG recordings obtained with a 13 × 5 electrode grid. Each dot indicates a motor
unit discharge at a time instant. The grey thick line represents the exerted muscle force. The upper panel depicts the root mean
square EMG map under the electrode grid during the same muscle contraction. RMS values were calculated from signal epochs of
1-s duration. (B) The discharge times of two motor units from (A) are shown on a larger vertical scale to illustrate the discharge
rate modulation during the contraction. MU: motor unit. (Reprinted with permission from Merletti et al.119)
 PLATE 19

Most muscles are

12%
relatively
11% unaffected
10%

9%

Muscle active state

8%

7%

X 6%

5%

4%

3%

2% A few muscles are

FIGURE 19-3  ■  Model of human lifting a load with spine and hip 1% significantly
flexion. The model is developed in the AnyBody Modelling Sys- 0%
affected
0.00 0.10 0.20 0.30 0.40 0.50 0.60 0.70 0.80 0.90 1.00
temTM and comprises more than 1000 individually activated
Fraction of movement
muscles. The colour shading of the muscles indicates the level
of activity. X indicates the x-direction of the global coordinate FIGURE 19-5  ■  The effect of a gradual 15° pelvic lateral tilt on
system. muscle activation in the lumbar spine.

FIGURE 19-6  ■  Alteration of muscle forces (illustrated by the thickness of each fascicle) from symmetrical standing (left) to 10° pelvic
lateral tilt (right).
 PLATE 20

$ %
FIGURE 19-7  ■  Model of the cervical spine with (A) all the muscle and (B) the six fascicles of the semispinalis cervicis on the right
side.

100 30
T1C2 T1C2
90
T2C3 T2C3
80 25
T3C4 T3C4
70
T4C5 20
T4C5
Activity (%)

60
Force (N)

50 T5C6 T5C6
15
40 T6C7 T6C7
30 10
20
5
10
0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5
Time (s)
Time (s)
FIGURE 19-8  ■  The predicted activity of the six fascicles of the
semispinalis cervicis during ramped extension. FIGURE 19-9  ■  The predicted force in the six fascicles of the
semispinalis cervicis during ramped extension.
 PLATE 21

800

700 C2C1
C3C2
600
C4C3
C5C4
500
C6C5
Force (N)

400 C7C6
T1C7
300

200

100

0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5
Time (s)
FIGURE 19-10  ■  The predicted reaction forces between the vertebrae in the cervical spine during ramped extension.
 PLATE 22

Diaphragm
(C3–5)

Heart
(C8–T4)

Pancreas Stomach
(T6–10) (T6–10)
Gall bladder Liver
(T7–8) (T7–8)

Bladder Kidney
(T11–L1) (T10–L1)

FIGURE 35-1  ■  Common sites of visceral pain referral.5,6

 PLATE 23

FIGURE 37-4  ■  Health Improvement Card. (Source: Health Improvement Card. World Health Professions Alliance. Reprinted with permis-
sion. <http://www.ifpma.org/fileadmin/content/Publication/2011/ncd_Health-Improvement-Card_web-1.pdf>.22)
PLATE 24

Figure 37-4. Cont’d

PA RT I

1
This page intentionally left blank
 C H A P T E R 1 

Introduction to the Text

Gwendolen Jull  •  Ann Moore  •  Deborah Falla  • 
Jeremy Lewis  •  Christopher McCarthy  •  Michele Sterling

The theory and practice of musculoskeletal physiother- which include consideration of and attention to psycho-
apy have grown and changed quite markedly in the logical or social moderators. The original manual therapy
decade following the publication of the third edition of or manipulative therapy approaches have metamorphosed
this seminal text. This fourth edition aims to reflect this into musculoskeletal physiotherapy and this is recognized
change and present some of the advances that have by the change in title of this text.
occurred in both the science and evidence base pertaining A second change is the expansion of the focus of the
to the diagnosis and management of musculoskeletal dis- text from the vertebral column to the entire musculo­
orders. The text also explores issues that will face clini- skeletal system. In this edition, both the spine and
cians and researchers over the next decade. extremities are considered for the first time. This was a
Several changes have been made in presenting this logical progression of the scope of the text as the rele-
fourth edition. Firstly, there has been a name change vance of much of the basic, behavioural and clinical sci-
from ‘Grieve’s Modern Manual Therapy: The Vertebral ences and indeed the principles of practice are not
Column’ to ‘Grieve’s Modern Musculoskeletal Physiotherapy’. confined to one body region. There can certainly be
This is to reflect the evolution in knowledge, models of peculiarities in the nature of the disorders and their man-
diagnosis and contemporary practice. The original agement in the various regions of the body and this has
manipulative therapy concepts developed in the 1950s been respected, particularly in the section which over-
and 1960s by physiotherapists such as Geoffrey Maitland views contemporary issues in practice (Part IV).
and Freddy Kaltenborn were presented essentially, as The third change is in the nature of the content of the
complete systems of assessment and management of mus- text. The aims in assembling this multi-authored text
culoskeletal disorders. Painful musculoskeletal disorders were to capture some of the advances in the science and
were regarded broadly as manifestations of abnormal practices made in the last decade relevant to musculo­
movement and articular dysfunction. Such concepts set skeletal physiotherapy, to look futuristically at emerging
physiotherapists on a path of detailed analysis of the areas as well as presenting some of the current issues in
‘symptoms and signs’ of a patient’s musculoskeletal dis- practice. Initially, emphasis is placed on the advances in
order, which were interpreted on predominantly kinesio- the sciences underpinning musculoskeletal physiotherapy
logical, biomechanical and neurophysiological bases, practice, where there is commentary on topics such as
taking the individual patient into account. It was recog- pain, movement, motor control, the interaction between
nized even then that the patho-anatomical model was not pain and motor control as well as neuromuscular adapta-
very helpful in designing manipulative therapy manage- tions to exercise. There is also consideration of applied
ment programmes. Health professionals were first chal- anatomical structure as well as the current and future
lenged about the inadequacy and limitations of regarding field of genetics in musculoskeletal pain. A new section
illness only on a biological basis by Engel in 1977,1 who of the text highlights the important area of measurement
introduced the concept of a biopsychosocial model. A and presents the scope of current and emerging measure-
decade later, Waddell2 presented for consideration a new ments for investigating central and peripheral aspects
clinical model for the treatment of low back pain which relating to pain, function and morphological change. It
embraced the biopsychosocial principles. It spurred a is important for clinicians to be intelligent and discrimi-
massive volume of research internationally to understand nating consumers of research. A section of the text has
psychological and social moderators and mediators not therefore been devoted to discussing some contemporary
only of back pain, but of all chronic musculoskeletal dis- research approaches including quantitative and qualita-
orders. There has also been a surge of research into the tive methods to gather, test and examine treatment effects
neurosciences pertaining to, for example, pain, move- in their broadest interpretation. Importantly, transla-
ment and sensorimotor function in musculoskeletal dis- tional research is discussed, the process which ensures
orders. The knowledge gained through this research that evidence-based practices which are developed in the
has had and is having a profound influence on physio- research environment genuinely make change in clinical
therapists’ approaches to the diagnosis and management practice and policy/procedures.
of musculoskeletal disorders. The original concepts of A sizeable portion of this text is devoted to the prin-
manipulative therapy have grown to embrace new ciples and broader aspects of management that are appli-
research-generated knowledge. There have been expan- cable to musculoskeletal disorders of both the spine
sions in practice to embrace the evidence for, for example, and periphery. A range of topics have been chosen for
the superiority of multimodal management approaches this section to reflect the scope of musculoskeletal
3
4 PART I

physiotherapy practice. Topics presented include models presentation of discussion of topics pertaining to the
for management prescription, communication and pain upper and lower extremities. It is not possible to provide
management, as well as contemporary principles of man- the full scope of management for any region and this
agement for the articular, nervous and sensorimotor was not the intention of this text. Rather, this section
systems. Recognizing the patient-centred and inclusive presents selected issues in current practice for a particular
nature of contemporary musculoskeletal practice, there region or condition or the most topical approaches to
is discussion about how physiotherapists may include the diagnosis and management of a region. A critical
cognitive behavioural therapies in the management of review of the evidence or developing evidence for
people with chronic musculoskeletal disorders. In this approaches is provided and areas for future work are
broader context, self-management, occupational health, highlighted. It is recognized that some topics or fields
lifestyle and health promotion and musculoskeletal of practice are not discussed, even in a text of this size.
screening are presented as is the place of adjuvant physi- It is hoped nevertheless, that the reader gains a good
cal modalities in pain management. A chapter is also understanding and appreciation of contemporary mus-
devoted to cautions in musculoskeletal practice of which culoskeletal physiotherapy.
all clinicians must be aware. Over the last decade, there
has been development of advanced practice roles for
some musculoskeletal physiotherapists and these differ- REFERENCES
ent models of practice are discussed.
1. Engel GL. The need for a new medical model: a challenge for bio-
Part IV of the text concentrates on contemporary medicine. Science 1977;196:129–36.
issues in clinical practice. All regions of the spine are 2. Waddell G. A new clinical model for the treatment of low-back pain.
presented and, as mentioned, novel to this edition is Spine 1987;12:632–44.
 PA RT I I

ADVANCES IN THEORY
AND PRACTICE

5
This page intentionally left blank
 SECTION 2 . 1

ADVANCES IN BASIC SCIENCE

Basic science is essential science and provides the founda- sensorimotor disturbances in musculoskeletal pain is
tion for the development of evidence-based therapeutic offered. It is valuable for clinicians to understand treat-
strategies. Over the past two decades in particular, there ment effects, and a chapter presents exercise-induced
has been a surge in basic science in the field of musculo- neuromuscular adaptations with a focus on the muscle
skeletal physiotherapy which has led to developments and structural and neural adaptations to both strength and
advances in this discipline. Contemporary interventions endurance training. Then follows a collection of chapters
for musculoskeletal disorders are no longer arbitrarily where other aspects of the musculoskeletal system vital
applied but rather are grounded on scientific discoveries to clinical practice are presented, including contempo-
in the field of musculoskeletal health and injury. rary research into the peripheral nervous system in func-
This Section brings together the views of some tion and dysfunction, functional anatomy, and the area
eminent experts in this field and presents 11 chapters that continues to attract considerable interest, namely
which review research into basic mechanisms related to tendon health and pathology. The Section concludes
musculoskeletal health, pain and movement that are fun- with chapters dealing with important contemporary
damental to musculoskeletal physiotherapy practice. First issues in musculoskeletal health and pain, namely, the
is a vital update on pain physiology where knowledge has role that genetics and lifestyle play in the development
increased enormously over the past decade. Modern pain of chronic pain and the effects of ageing on the muscu-
neuroscience is used by the clinician for diagnostic and loskeletal system.
therapeutic purposes. The next collection of chapters There have been tremendous advances in our under-
covers the basic sciences that are essential to understand standing of musculoskeletal health and injury in recent
when assessing movement and muscle dysfunction and years and the current state of knowledge is provided
prescribing exercise. It presents the important areas of within this Section. An ongoing aim is to translate the
muscle neurophysiology, the sensorimotor mechanisms benefits of advances in the basic sciences to the treatment
underlying postural control and recent research relating of musculoskeletal disorders. Much knowledge is already
to motor control and motor learning. The interaction being implemented in the contemporary management of
between pain and sensorimotor function is explored, and musculoskeletal disorders as seen in Section 4 of this text.
a contemporary theory for the effect of pain on senso-
rimotor function and potential mechanisms underlying

7
 CHAPTER 2 

The Neurophysiology of Pain and

Pain Modulation: Modern Pain
Neuroscience for Musculoskeletal
Physiotherapists
Jo Nijs  •  Margot De Kooning  •  David Beckwée  •  Peter Vaes

INTRODUCTION potentials that can be interpreted by the brain as pain.

These include the skin, muscles, tendons, muscle fascia,1
Anatomy, arthrokinematics and neurophysiology are tra- part of the menisci, ligaments, joint capsules, (osteochon-
ditionally viewed as the key basic sciences for musculo- dral) bone and the nervous system itself. Besides
skeletal physiotherapy. Neurophysiology is important for low-threshold sensory receptors, important for touch
understanding how the brain controls body movements (including texture and shape) and proprioception, high-
and how neuromuscular control can become a potential threshold sensory receptors are available and respond to
part of the treatment in patients with musculoskeletal strong heat, cold and mechanical or chemical stimuli.
pain. In addition, the neurophysiology of pain is impor- Given their high threshold they respond preferentially,
tant for musculoskeletal physiotherapy. but certainly not exclusively, to noxious stimuli and are
Modern pain neuroscience has evolved spectacularly therefore called nociceptors. Many such nociceptors
over the past decades. Here we explain the basic princi- respond to multiple stimulus modalities (i.e. heat, cold,
ples of modern pain neuroscience, from the musculosk- mechanical or chemical stimuli), making them polymodal
eletal tissues to the brain, and from the brain down the nociceptors.
spinal cord back to the tissues. It will be explained that Each of the nociceptors is connected to an ion channel
not all pain arises from damage in the musculoskeletal that opens once the nociceptor is activated by a stimulus
system, that all pain is in the brain, and that musculosk- (e.g. chemicals released from cell rupture). This allows
eletal physiotherapists can apply modern pain neurosci- for the stimulus (often tissue damage or one that holds
ence for diagnostic, communicational and therapeutic the capacity to cause tissue damage such as a pin prick)
purposes. In addition, specific information for better to be converted into an electrical current: first a gradual
understanding (the underlying mechanisms of) musculo- potential, followed by an action potential. For instance,
skeletal diagnosis and therapy is provided. in patients where the neck muscles become highly tensed
The chapter begins with a very brief overview of acute due to physical (over)use, mechanical pressure builds
pain neurophysiology, followed by various key mecha- up inside the neck muscles, which causes the polymodal
nisms involved in neuroplasticity (i.e. wind-up, long-term nociceptors to open their connecting ion channels, which
potentiation, central sensitization) and pain modulation results in an influx of positive charges in the neurons,
(descending nociceptive inhibition and facilitation). An generating an action potential (physiological response
important part of the chapter is dedicated to the pain due to usual use). Following overuse and in cases of
(neuro)matrix, and several ‘boxes’ throughout the chapter local inflammation, chemicals like potassium ions, his-
highlight the translation of modern pain neuroscience to tamine, serotonin, prostaglandins, pro-inflammatory
clinical practice. cytokines and substance P are released from damaged
tissue or produced by immune cells or sensory neurons.
These chemicals lower the stimulus thresholds of the
THE NEUROPHYSIOLOGY OF nociceptors significantly, which increases the chance of
MUSCULOSKELETAL PAIN: FROM generating action potentials. This results in increased
sensitivity to pain (recall you cannot even touch the
TISSUE NOCICEPTION TO THE PAIN skin of an acutely injured joint without triggering
NEUROMATRIX more pain).
Regardless of whether or not the sensitivity of the
Many tissues hold the capacity to alert the central nervous nociceptor is altered, the action potential arising from
system of (potential) danger, and hence to produce action nociceptors can be transported by two types of nerve
8
 2  The Neurophysiology of Pain and Pain Modulation 9

fibres: Aδ and C fibres. Fast pain is transmitted from the TEMPORAL SUMMATION AND WIND-UP
tissue to the central nervous system via Aδ fibres, which
are small, myelinated nerve fibres with a high conduction It is important to understand that not all nociceptive
speed. Fast pain is typically described by patients as sharp signals are perceived as pain, and not every pain sensation
and localized, while slow (C-fibre) pain is duller and more originates from nociception. Nevertheless, acute pain
diffuse, but lasts much longer. C fibres are small, unmy- almost always originates from nociceptors in somatic or
elinated nerve fibres with a low conduction speed. visceral tissue. However, when the nociceptors keep on
Both Aδ and C fibres are primary sensory nerve fibres. ‘firing’ nociceptive impulses, the dorsal horn neurons
Sensory information enters the central nervous system may become hypersensitive.5,6 This increased neuronal
in the spinal cord, where these nerve fibres synapse on responsiveness is accomplished by neurotransmitters (e.g.
secondary afferent nerve fibres. These synapses are glutamate, aspartate and substance P) that modulate the
highly modulated by local (interneurons) and top-down postsynaptic electric discharges with further transmission
(descending or brain-orchestrated) neurons, implying to supraspinal sites (thalamus, anterior cingulate cortex,
that not all action potentials entering the spinal cord will insular cortex and somatosensory cortex) via ascending
enter the brain (and hence not all action potentials arising pathways.5 The neurotransmitters initiate increased post-
from nociceptors trigger pain). This modulation of synaptic responses by triggering hyperexcitability of
incoming danger messages is further detailed below N-methyl-D-aspartate (NMDA) receptor sites of second-
(under the heading ‘Brain-orchestrated pain modula- order neurons in the dorsal horn (Fig. 2-1). This mecha-
tion’). If the action potential from the primary afferent nism is related to temporal summation of second pain or
neuron is transferred to the secondary afferent neuron in wind-up. Wind-up refers to the progressive increase of
the dorsal horn, then the incoming message will cross the electrical discharges from the second-order neuron in the
body’s midline in the spinal cord and can ascend to spinal cord in response to repetitive C-fibre stimulation,
the brain, more precisely the thalamus, which spreads the and is experienced in humans as increased pain.7,8
message to several other brain regions involved in the Wind-up is part of the process known as central
pain (neuro)matrix (see below and Fig. 2-2). Even when sensitization.9
the action potential makes it to the brain, it still remains
unconscious until the brain has processed it. This implies
that the various brain areas involved in processing the BRAIN-ORCHESTRATED PAIN
incoming messages, together referred to as the pain MODULATION
matrix, will decide whether or not the signals should be
interpreted as threatening to the body’s homeostasis or The brain orchestrates top-down pain-modulatory
not (pain or no pain). systems that are able to facilitate or inhibit nociceptive

BOX 2-1  The Nervous System as Source of Nociception and Pain:

Neuropathic Pain Highlights for Clinicians
It is not only the musculoskeletal system that can generate Addressing the clinical signs of neuropathic pain, the loca-
nociception: the nervous system itself can be a source of tion of neuropathic pain is neuroanatomically logical, imply-
nociception. Neuropathic pain is defined as ‘pain arising as ing that all neuropathic pains are perceived within the
a direct consequence of a lesion or disease affecting the somato- innervation territory of the damaged nerve, root, or pathway
sensory system’.2 Neuropathic pain can be both peripheral due to the somatotopic organization of the primary somato-
(i.e. located in a nerve, dorsal root ganglion or plexus) sensory cortex.4 Patients with neuropathic pain often describe
and central (i.e. located in the brain or spinal cord). In pain as burning, shooting, or pricking. Finally, sensory testing
the neuropathic pain definition, the term lesion points to is of prime importance for the diagnosis of neuropathic pain.2
the often available evidence from diagnostic investigations This includes testing of the function of sensory fibres with
(e.g. imaging, neurophysiology, biopsies, laboratory tests) simple tools (e.g. a tuning fork for vibration, a soft brush for
to reveal an abnormality (such as scar tissue) of the nervous touch and cold/warm objects for temperature), which typically
system. Alternatively, lesion may refer to posttraumatic or assess the relation between the stimulus and the perceived
postsurgical damage to the nervous system. For example, sensation.4 Several options arise here, all suggestive of neuro-
about 27% of patients develop chronic postsurgical pain pathic pain: hyperaesthesia, hypoaesthesia, hyperalgesia,
following total hip or knee arthroplasty, but neuropathic hypoalgesia, allodynia, paraesthesia, dysaesthesia, aftersensa-
pain is rare, accounting for 5.7% of all chronic pain tions, etc. Again, the location of the sensory dysfunction
patients.3 This implies that following total hip or knee should be neuroanatomically logical. The presence of neuro-
arthroplasty, damage to a peripheral nerve is rarely identi- pathic pain does not exclude the possibility of central sensiti-
fied. Further addressing the neuropathic pain definition, zation pain (i.e. hyperexcitability of the central nervous system
the term disease refers to the underlying cause of the lesion, as often seen in chronic musculoskeletal pain – this concept
which is often clear: postherpetic neuralgia, cancer, stroke, is further detailed below) or vice versa. In fact, some patients
vasculitis, diabetes mellitus, genetic abnormality, neurode- evolve from neuropathic pain with severe but local signs and
generative disease, etc. Finally, somatosensory refers to infor- symptoms, to a widespread pain condition that cannot be
mation about the body per se including visceral organs, explained by neuropathic pain solely. In such cases, central
rather than information about the external world (e.g. sensitization might account for the evolution to a widespread
vision, hearing, or olfaction). pain condition.
10 PART II  Advances in Theory and Practice

BOX 2-2  Translating the Neurophysiology

↑ C-fibre of Temporal Summation and
transmission NMDAr Wind-Up to Clinical Practice
activated
How can we translate these findings to clinical practice? Is it
required to translate these findings to clinical practice? This
question relates to how wind-up is possibly created/facilitated
by musculoskeletal treatment. Here we provide a viewpoint.
When musculoskeletal physiotherapists apply hands-on
techniques, and by doing so eliciting compression and
hereby deliver identical nociceptive stimuli to the skin,
↑ Synaptic Ca2+ entry muscles or joint capsules more often than once every 3
excitability in dorsal seconds, they are likely to trigger this mechanism of pain
over long horn amplification.10 In line with this reasoning, musculoskeletal
distance neurons physiotherapists should be aware that the vicinity of myo-
fascial trigger points differs from normal muscle tissue by its
lower pH levels (i.e. more acid), increased levels of substance
P, calcitonin gene-related peptide and pro-inflammatory
cytokines (i.e. tumour necrosis factor alpha and interleukine-
Signalling
1β), each of which has its role in increasing pain sensitivity.11–13
cascades
Sensitized muscle nociceptors are more easily activated and
FIGURE 2-1  ■  The neurophysiology of temporal summation and may respond to normally innocuous and weak stimuli such
wind-up. NMDAr, N-methyl D-aspartate receptors; ca2+, calcium as light pressure and muscle movement.11,12 All this becomes
ions. even more important when one realizes how crucial it is to
limit the time course of afferent stimulation of peripheral
nociceptors. Indeed, tissue injury healing and focal pain
recovery should occur within a period of approximately 3
input from the periphery.15 This implies that all nocicep- months to prevent development of chronic widespread
tive stimuli arising from muscles, joints, skin or viscera pain.14 Progression towards chronic widespread pain is asso-
are modulated in the spinal cord, more specifically the ciated with injuries to deep tissues which do not heal within
dorsal horn. Incoming messages (nociceptive stimuli) several months.14
from the periphery enter the spinal cord in the dorsal
horn where they synapse with secondary afferent neurons
that have the capacity to send the messages to the brain.
‘Have the capacity’ implies that they do not always sensitization of dorsal horn spinal cord secondary
do that. These synapses are modulated by top-down neurons.17 Sustained arousal is likely to maintain sensiti-
(descending) neurons, which can either result in inhibi- zation of the brain circuitry involved in central sensitiza-
tion (descending inhibition) or augmentation (descend- tion pain.18 It is important for clinicians to realize that
ing facilitation) of the incoming messages. In the case of pain cognitions like fear of movement and catastrophiz-
the former, nociceptive stimuli may ‘die’ in the dorsal ing are not only of importance in patients with chronic
horn, implying that nociceptive stimuli will not result in pain, but may even be crucial at the stage of acute/
pain. In such cases the person will never become aware subacute musculoskeletal disorders.19
of the nociception that has occurred. Descending facilita-
tion implies that incoming messages are amplified and
that the threshold in the dorsal horn for sending incom-
Descending Nociceptive Inhibition
ing messages to the brain is lower than normal. Stimulation of certain regions of the midbrain facilitates
In summary, the brain controls a brake (descending extremely powerful descending pain-modulating path-
inhibition) and an accelerator (descending facilitation). ways that project, via the medulla, to neurons in the
Both modulatory mechanisms are further explained dorsal horn that control the ascending information in the
below, starting with descending facilitation. nociceptive system.20 These pain-inhibitory pathways
arise mainly from the periaquaductal grey matter and the
rostral ventral medulla in the brainstem.20 The descend-
Descending Nociceptive Facilitation ing inhibitory pathways apply neurotransmitters such as
Output from the brainstem (i.e. nuclei in the mesence- serotonin16 and noradrenaline. The main descending
phalic pontine reticular formation) activates descending inhibitory action to the spinal dorsal horn is noradrener-
pathways from the rostral ventromedial medulla that gic. In the dorsal horn, norepinephrine, through its
enhances nociceptive processing at the level of the spinal action on alpha-2A-adrenoceptors, suppresses the release
dorsal horn.16 Descending facilitatory pathways are not of excitatory transmitters from central terminals of
demonstrably involved during nociceptive processing in primary afferent nociceptors.21 In addition it may
the normal state. suppress postsynaptic responses of spinal pain-relay
Catastrophizing, avoidance behaviour and somatiza- neurons.21 One function of the descending inhibitory
tion are factors that have been shown to prevent effective pathway is to ‘focus/target’ the excitatory state of the
descending inhibition, and at the same time they activate dorsal horn neurons by suppressing surrounding neuro-
descending facilitation.17 Together, this may result in nal activity,22 a role attributed to the ‘diffuse noxious
 2  The Neurophysiology of Pain and Pain Modulation 11

inhibitory controls’ phenomenon.23 In case of central • The primary and secondary somatosensory cortex,
sensitization and chronic widespread pain these descend- which is the primary area responsible for identifying
ing pain-inhibitory pathways are malfunctioning.24–27 the location of the pain in the body (i.e. the sensory-
Exercise is a physical stressor that activates descending discriminative aspect of pain). The more attention
nociceptive inhibition, a mechanism often referred to one pays to the painful stimulus/painful region, the
as exercise-induced endogenous analgesia.28 In some more activity is observed in the primary somatosen-
patients with chronic musculoskeletal pain (including sory cortex.37 The amount of activity in the somato-
chronic whiplash-associated disorders29 and fibromyal- sensory cortex correlates with pain intensity in those
gia30), exercise does not activate endogenous analgesia. with central sensitization pain.38
Other populations such as people with chronic low back • One key brain area involved in the pain (neuro)
pain, do have a normal endogenous analgesic response to matrix is the amygdala (the upper part of Fig. 2-2
exercise.31 illustrates its deep location in the brain), often
Likewise, manual joint mobilizations have been shown referred to as the fear-memory centre of the brain:
to activate descending nociceptive inhibition. For • The amygdala has a key role in negative emotions
instance, animal research indicates that joint mobilization and pain-related memories.39 In addition to the
reduces postoperative pain by activation of the peripheral amygdala, the anterior cingulate cortex takes part
opioid pathway32 and the involvement of the adenosiner- of the central fear network in the brain.40,41
gic system.33 Likewise, unilateral joint mobilization • Recent research supports the cardinal role of the
reduces bilateral hyperalgesia induced by chronic muscle amygdala as a facilitator of chronic pain develop-
or joint inflammation in animal models.34 In humans, ment, including sensitization of central nervous
there is level A evidence for a significant effect of spinal system pain pathways.39,40,42–45
manipulative therapy on increasing pressure pain thresh- • In line with this is the finding that the amygdala,
olds at the remote sites of stimulus application supporting as well as the somatosensory cortex and insula,
a potential central nervous system mechanism (i.e. activa- shows less activity during pain delivery in case
tion of descending nociceptive inhibition).35 of positive treatment expectations.46 This is an
Until now we have learned how the brain tries to important message for clinicians: it is advocated
control what information comes in and what stays out. to question the patient’s treatment expectations.
Next, let us have a look at what happens when nociceptive
messages enter the brain. For a proper understanding of
modern pain neuroscience, it is important to understand
that incoming nociceptive messages, when they first enter
the brain, are still not perceived consciously. At this
point, we are not even aware of them. The brain will now S
M 1
start processing the nociception. For the processing of 1
incoming nociceptive messages, the brain uses several
brain regions that co-work to decide whether or not the
ACC
nociceptive messages will be interpreted as dangerous or
not (i.e. painful or not). When the brain decides that the P
messages are dangerous, then it will produce pain and it F INSU
will let the same brain regions decide how much pain (pain C
THAL
severity) is produced. Although a specific role is attrib-
uted to each of these brain regions (see below), they do CEREB
not function independently from one another; they PAG
co-work and communicate closely. Together this brain
circuitry is called the pain matrix or pain neuromatrix
(first proposed by Melzack to explain phantom pain36).

THE PAIN NEUROMATRIX

All pain is in the brain. The brain can produce pain
without nociception and vice versa, which holds tremen-
dous potential for musculoskeletal clinicians working
with patients in pain. The brain produces pain by activat-
ing a circuitry: a number of brain regions that become
active all together when a person is in pain (Fig. 2-2).
These brain regions differ between individuals and pos- Amygdala
sibly even for one individual in different circumstances, Hippocampus
but they differ the most when comparing acute versus
FIGURE 2-2  ■  The pain neuromatrix. ACC, anterior cingulate
chronic pain. Nevertheless, the following brain regions cortex; CEREB, cerebellum; INSU, insula; M1, primary motor
are generally accepted as being involved in pain cortex; PAG, periaqueductal grey; PFC, prefrontal cortex; S1,
sensations: primary somatosensory cortex; THAL, thalamus.
12 PART II  Advances in Theory and Practice

Positive treatment expectations not only increase BOX 2-3  Long-Term Pain Memories are
the likelihood of a positive treatment outcome, often Apparent in Patients with
it also implies less activity in key areas involved Chronic Musculoskeletal Pain
in the pain neuromatrix. This should motivate
clinicians to address negative treatment expecta- Kinesiophobia or fear of movement is seldom applicable to
tions, for instance by increasing treatment expec- all kinds of physical activity, but rather applies to certain
tations during therapeutic pain neuroscience movements (e.g. neck extension in patients postwhiplash,
education. overhead smashes in patients with shoulder impingement
• Movement therapy in musculoskeletal pain: Of syndrome, or forward bending in patients with low back
major relevance for providing exercise therapy to pain). Even though these movements provoked pain in the
(sub)acute phase, or even initiated the musculoskeletal pain
patients with chronic musculoskeletal pain is the
disorder (e.g. the pain initiated following an overhead
amygdala’s role in pain memories and, more pre- smash), they are often perfectly safe to perform in a chronic
cisely, in memories of painful movements. There- stage. The problem is that the brain has acquired a long-
fore the amygdala closely collaborates with the term pain memory, associating such movements with danger/
hippocampus and the anterior cingulate cortex threat. Even preparing for such ‘dangerous’ movements is
(Fig. 2-2). Even though nociceptive pathology enough for the brain to activate its fear-memory centre and
has often long subsided, the brains of patients hence to produce pain (without nociception) and employ
with chronic musculoskeletal pain have typically an altered (protective) motor control strategy.48 Exercise
acquired a protective pain memory,47 which can therapy can address this by applying the ‘exposure without
be defined as a memory of movements that once danger’ principle.47 This implies addressing patients’ percep-
tions about exercises, before and following performance of
elicited pain and prevents people from perform-
exercises and daily activities. This way, therapists try to
ing that ‘dangerous’ movement. For movements decrease the anticipated danger (threat level) of the exercises
that once provoked pain, this implies protective by challenging the nature of and reasoning behind their
behaviours like antalgic postures, antalgic move- fears, assuring the safety of the exercises, and increasing
ment patterns (including altered motor control), confidence in a successful accomplishment of the exercise.
or even avoidance of such movements (fear of Such treatment principles are in line with those applied by
movement). psychologists during graded exposure in vivo,49 a cognitive
• The thalamus is important for sending the incom- behaviour treatment that has yielded good outcomes in
ing (nociceptive) messages to other brain regions, patients with chronic low back pain,50,51 complex regional
including those listed above. In addition, the pain syndrome type I,52 whiplash pain,53 and work-related
upper limb pain54 (level B evidence). Studies examining
(sensory) thalamus, together with the periaqueduc-
whether musculoskeletal physiotherapists are capable of
tal grey (see below) is used as a target for deep brain applying such treatment principles are warranted.
stimulation in patients with neuropathic pain,55 Recent experimental (basic) pain research reveals that
illustrating its role in descending analgesia. More extinction training during reconsolidation of threat memory
precisely, the thalamus and the periaqueductal grey is more effective than classical extinction training (i.e. expo-
closely interact (i.e. activity in the periaqueductal sure in vivo).41 Extinction training results in increased con-
grey inhibits the sensory thalamus and activation of nectivity between the prefrontal cortex and the amygdala,
the sensory thalamus activates the periaqueductal which implies that the prefrontal cortex inhibits the expres-
grey).56 The thalamus activity differs in those with sion of pain memories by the amygdala. Precise timing of
chronic pain: it shows less activity on the contralat- such extinction training (exposure in vivo principles) to coin-
cide with pain memory reconsolidation (e.g. imagery of the
eral side.37 A functional magnetic resonance imaging
movement that injured the shoulder or lower back) results
study showed increased anterior thalamic activity in in a disconnection between the prefrontal cortex and the
those with central sensitization compared to the amygdala.41 This altered brain connectivity may be impor-
normal state.38 tant for enabling extinction training to more permanently
• The brain stem, which includes several key regions ‘rewrite’ the original pain memory. In clinical practice, this
for orchestrating top-down pain inhibition (or would imply that immediately before performing the threat-
endogenous analgesia). The brainstem has been ening exercise or activity, we ask our patients to think back
identified as one of the key regions for the mainte- to the movement that once injured the painful body part (or
nance of central sensitization pain in humans, with to the accident that triggered the musculoskeletal pain dis-
increased brainstem activity in those with central order). However, before translating these basic pain research
findings into clinical practice, more studies using pain
sensitization compared to the normal state.38 Within
memory reconsolidation are required, including studies
the brainstem the mesencephalic pontine reticular showing that extinction training during reconsolidation of
formation has been identified as a particularly threat memory is more effective than classical extinction
important region showing increased activity in training also applies to clinical pain (i.e. studies in patients
central sensitization.38 The increased brainstem with musculoskeletal pain), and not only to experimental
activity, and more specifically the mesencephalic pain in healthy subjects.
pontine reticular formation, in central sensitization
pain may reflect increased descending facilitation.
Another (mid)brain stem area of importance is the
periaqueductal grey, which – together with the dor-
solateral prefrontal cortex – is another key centre
for activating top-down endogenous analgesia.55,56
 2  The Neurophysiology of Pain and Pain Modulation 13

Finally, different classes of neurons important for expectations for subsequent pain experiences (e.g.
top-down pain inhibition have been identified in the in response to treatments or daily activities). This
rostral ventromedial medulla; ON-cells are known is not soft science, but neuroscience: expectancies
to promote nociception, and OFF-cells to suppress shape pain-intensity processing in the central
nociception.57 nervous system, with strong effects on nocicep-
• The anterior cingulate cortex, an area important tive portions of insula, cingulate and thalamus.64
for the affective-motivational aspects of pain, includ- Expectancy effects on subjective experience are
ing empathy and social exclusion. also driven by responses in other regions like the
• The anterior cingulate cortex does not seem to dorsolateral prefrontal cortex and the orbitofron-
be involved in coding stimulus intensity or loca- tal cortex.64 Naturally, these brain regions largely
tion, but participates in both the affective and overlap with brain regions identified as playing a
attentional concomitants of pain sensation.37 pivotal role in placebo analgesia, such as the ante-
• Studies have shown that social exclusion evokes rior cingulate cortex, anterior insula, prefrontal
social pain in excluded individuals, and neuroim- cortex and periaqueductal grey.65
aging studies suggest that this social pain is asso- • The insula, a brain region that has a role in the
ciated with activation of the dorsal anterior emotional component of every pain sensation, but
cingulate cortex, with further regulation of social also contributes to the sensory-discriminative aspect
pain being reflected in activation of the right ven- of pain.37
trolateral prefrontal cortex.58,59 Thus, the brain
areas that are activated during the distress caused
by social exclusion are also those activated during CENTRAL SENSITIZATION
physical pain.60 The pain of a broken heart is now
an evidence-based metaphor for explaining to Central sensitization is defined as ‘an augmentation of
patients that all pain is in the brain, and that pain responsiveness of central pain-signalling neurons to input
does not rely on tissue damage (cf. therapeutic from low-threshold mechanoreceptors’.67 While periph-
pain neuroscience education). eral sensitization is a local phenomenon that is important
• With respect to empathy for pain, a core network for protecting damaged tissue during the early phases
consisting of bilateral anterior insular cortex and post injury, central sensitization means that central pain-
medial/anterior cingulate cortex has been identi- processing pathways localized in the spinal cord and the
fied.61 For obtaining a modern understanding of brain become sensitized. Indeed, the process of central
pain, it is important to realize that activation in sensitization is neither limited to the dorsal horn, nor to
these areas overlaps with activation during directly pain amplification of afferent impulses. Central sensitiza-
experienced pain. tion encompasses altered sensory processing in the brain
• The prefrontal cortex, an area responsible for the and malfunctioning of pain-inhibitory mechanisms.
cognitive-evaluative dimension of pain: Coding of the mechanism of wind-up involves multiple
• The prefrontal cortex is important for anticipa- brain sites, including somatosensory (thalamus, anterior
tion and attention (vigilance) to pain and pain- insula, posterior insula, primary somatic sensory cortex,
provoking situations, which brings us to pain secondary somatic sensory cortex), cognitive-evaluative/
memories/previous painful experiences. For the affective (anterior cingulate cortex and prefrontal cortex)
latter, the prefrontal cortex closely communicates and pain-modulating regions (rostral anterior cingulate
with the amygdala and the hippocampus. All cortex).68 The elevated central nervous system reactivity
together these brain areas can be viewed as the inhibits functioning of regulatory pathways for the auto-
‘pain memories circuitry’. nomic, endocrine and the immune systems.69
• The dorsolateral part of the prefrontal cortex has
been identified as a key region involved in
descending nociceptive inhibition/endogenous
BOX 2-4  The Overlap between the Pain
analgesia mediated by opioids.62 Therefore, the
Neuromatrix and the Brain Regions
dorsolateral prefrontal cortex has become a
Involved in Movement Control
popular target for transcranial magnetic brain
stimulation,62 a non-invasive electrotherapy treat- For musculoskeletal physiotherapists it is important to
ment for chronic (neuropathic) pain and depres- realize that frequent activation in motor-related areas
sion. In case of more intense pain levels, pain such as the striatum, cerebellum and supplementary motor
catastrophizing is associated with decreased activ- area has been observed during (experimental) pain.37 These
ity in several brain regions involved in top-down areas are increasingly accepted as parts of the pain (neuro)
pain inhibition like the dorsolateral prefrontal matrix. In line with this is the finding that healthy subjects
cortex and the medial prefrontal cortex.63 display a relation between pain catastrophizing and brain
• Pain anticipation, or pain expectancies, can con- activity in regions involved in motor response and motor
planning (i.e. thalamus, putamen and premotor cortex).63
tribute to determining the intensity of pain. This implies that the pain neuromatrix partly overlaps
Indeed, expectancies have pain-modulatory with brain regions involved in movement control,66 partly
effects and they closely relate to placebo effects. explaining why people who are in pain present with move-
This is a powerful tool in clinical practice: clini- ment dysfunctions.
cians can increase or decrease the patient’s
14 PART II  Advances in Theory and Practice

In those with central sensitization pain, the pain BOX 2-5  Recognition of Central
neuromatrix is likely to be overactive: increased activity Sensitization Pain in
is present in brain areas known to be involved in acute Musculoskeletal Pain Patients
pain sensations and emotional representations like the
insula, anterior cingulate cortex and the prefrontal For recognizing central sensitization pain in musculoskeletal
cortex.70 An overactive pain neuromatrix also entails pain patients with conditions like osteoarthritis, low back
brain activity in regions not involved in acute pain pain, or lateral epicondylalgia, the following clinical signs
sensations, including various brain stem nuclei, dorso- and symptoms can be of use. Central sensitization pain is
lateral frontal cortex and the parietal associated cortex.70 typically characterized by disproportionate pain, implying
Research findings also suggest a specific role of the that the severity of pain and related reported or perceived
disability (e.g. restriction and intolerance to daily life activi-
brainstem for the maintenance of central sensitization
ties, to stress, etc.) are disproportionate to the nature and
in humans.38 extent of injury or pathology (i.e. tissue damage or structural
Furthermore, long-term potentiation of neuronal synapses impairments). In addition, patient self-reported pain distri-
in the anterior cingulate cortex,71 nucleus accumbens, bution, as identified from the clinical history and/or a body
insula and the sensorimotor cortex, as well as decreased chart, often reveals a large pain area with a non-segmental
gamma-aminobutyric acid-neurotransmission72 represent distribution (i.e. neuroanatomically illogical), or pain varying
two mechanisms contributing to the overactive pain neu- in (anatomical) location/travelling pain, including to ana-
romatrix. Long-term potentiation implies that synapses tomical locations unrelated to the presumed source of noci-
become much more efficient: a single action potential ception. Finally, a score of 40 or higher on part A of the
will lead to more presynaptic release of neurotransmit- Central Sensitization Inventory,89 which assesses symptoms
common to central sensitization, provides a clinically rele-
ters, combined with more postsynaptic binding of
vant guide to alert healthcare professionals to the possibility
neurotransmitters. This results in more efficient com- that a patient’s symptom presentation may indicate the pres-
munication between neurons and even brain regions. ence of central sensitization.90
This mechanism of long-term potentiation makes it pos-
sible for us to understand that the circuitry of different
brain regions will be more easily (and longer) activated
in those with chronic compared to acute pain. Long-term
potentiation is one of the key mechanisms contributing seems rational to target therapies at the central nervous
to central sensitization. system rather than muscles and joints. More precisely,
The decreased availability of neurotransmitters like modern pain neuroscience calls for treatment strategies
gamma-aminobutyric acid72 (GABA) is a second mecha- aimed at decreasing the sensitivity of the central nervous
nism contributing to the overactive pain neuromatrix. system (i.e. desensitizing therapies). Therapeutic pain
GABA is an important inhibitory neurotransmitter. Less neuroscience education (Box 2-6) might be part of such
available GABA neurotransmission, which can be the a desensitizing approach to musculoskeletal pain, but
result of long-term stress, implies increased excitability further study is required to support this viewpoint.
of central nervous system pathways.
In acute musculoskeletal pain, the main focus for
treatment is to reduce the nociceptive trigger. For that DOES THE AUTONOMIC NERVOUS
we have several non-pharmacological treatment options, SYSTEM INFLUENCE PAIN?
including hands-on manual therapy and exercise therapy.
Such a focus on peripheral pain generators is often effec- The autonomic nervous system, together with the
tive for treatment of (sub)acute musculoskeletal pain.73–76 hypothalamus–pituitary–adrenal axis, accounts for the
In patients with chronic musculoskeletal pain, ongoing body’s stress response systems. Pain is a stressor that
nociception rarely dominates the clinical picture. Chronic activates the stress response systems, but at the same time
musculoskeletal pain conditions like osteoarthritis,77 the stress response systems can influence pain through
rheumatoid arthritis,78 whiplash,26,79,80 fibromyalgia,9,81 several neurophysiologic mechanisms. It goes like this:
low back pain,82 pelvic pain,83 and lateral epicondylitis,84 once pain becomes apparent, the body activates its stress
are often characterized by brain plasticity that leads to response systems, including the autonomic nervous
hyperexcitability of the central nervous system (central system and the hypothalamus–pituitary–adrenal axis.
sensitization) or vice versa. Cumulating evidence sup- Given the threatening nature of pain, it seems logical to
ports the clinical importance of central sensitization in understand that the body responds to pain with its ‘fight
patients with chronic musculoskeletal pain.85–88 Still, not or flight’ system. This leads to increases in stress hor-
all patients with one of the above-mentioned diagnoses mones like (nor)adrenaline and cortisol, which exert anal-
have central sensitization pain. Box 2-5 provides a brief gesic effects at the level of the brain (e.g. noradrenaline
overview on how to recognize central sensitization pain is an important neurotransmitter for enabling descending
in clinical practice. nociceptive inhibition15) and spinal cord (e.g. cortisol
In such cases, musculoskeletal physiotherapists need in the dorsal horn). The dorsal horn neurons contain
to think and treat beyond muscles and joints.91 Within glucocorticoid receptors, having pain-inhibitory capac-
the context of the management of chronic pain, it is ity.102 Thus, a normal response to stress is pain inhibition.
crucial to consider the concept of central pain mecha- Stress is a natural pain killer.
nisms like central sensitization.92 Hence, in patients with However, many of our patients with musculoskeletal
chronic musculoskeletal pain and central sensitization it pain experience the reverse: stress aggravates pain rather
 2  The Neurophysiology of Pain and Pain Modulation 15

BOX 2-6  Translating Modern Pain lead to lowered sensory and pain thresholds.105 Enhanced
Neuroscience to Practice: sympathetic activation affects muscle spindle function,
Therapeutic Pain Neuroscience muscle microcirculation and muscle contractile proper-
Education in Musculoskeletal ties, and consequently might even contribute to the
Physiotherapy Practice development of central sensitization and chronic pain.106
The theoretical framework provided above under-
The presence of central sensitization implies that the brain scores the importance of addressing stress management
produces pain, fatigue and other ‘warning signs’ even in patients with chronic musculoskeletal pain. Stress
when there is no real tissue damage or nociception. How management programs target the cognitive emotional
can musculoskeletal physiotherapists translate our current component of central sensitization pain.
understanding of pain neuroscience to clinical practice in The involvement of dysfunction in the autonomic
patients with (chronic) musculoskeletal pain? The first thing nervous system (e.g. enhanced activity of the sympathetic
to do is to explain to patients what pain is, and that all pain
nervous system) has been found in chronic widespread
is in the brain. Therapeutic pain neuroscience education
enables patients to understand the controversy surrounding pain syndromes characterized by central sensitization
their pain, including the lack of objective biomarkers or (e.g. fibromyalgia107–109), but not in all patients with
imaging findings. One of the main goals of therapeutic pain chronic widespread pain or central sensitization. Study-
neuroscience education is changing pain beliefs through the ing the relation between the autonomic nervous system
reconceptualization of pain. The focus is convincing patients and chronic widespread pain in a large sample (n = 1574),
that pain does not per se result from tissue damage. Pain a dysregulation of the autonomic nervous system, includ-
neuroscience education is generally welcomed very posi- ing the balance between sympathetic and parasympa-
tively by patients.93,94 We and other groups have shown that thetic nervous system activity, was found to be unrelated
face-to-face sessions of therapeutic pain neuroscience educa- to the presence of chronic widespread pain.110 Also, no
tion, in conjunction with written educational material, are
relation between a dysregulated sympathetic tone and
effective for changing pain beliefs and improving health
status in patients with various chronic pain disorders (level pain intensity was present. But in persons experiencing
A evidence),93,94 including those with chronic spinal pain.95– chronic widespread pain, lower parasympathetic activity
100
More specifically, therapeutic pain neuroscience educa- was associated with higher pain intensity suggesting that
tion is effective for improving maladaptive pain beliefs, and intense pain is a chronic stressor interfering with the
decreasing pain and disability in patients with chronic parasympathetic activity.110
pain.95–99 However, the effects are small and education is In more localized pain conditions (e.g. lower back
insufficient as a sole treatment.94 Practice guidelines for pain111) there is no clear evidence of the involvement of
therapeutic pain neuroscience education are available.93,94 dysfunctions in the autonomic nervous system. In chronic
Interestingly, one study revealed that therapeutic pain low back pain, not pain but the perceived disability was
neuroscience education improves descending pain inhibition
related to parasympathetic activity. Cardiac sympathetic
(i.e. conditioned pain modulation) in patients with fibromy-
algia.101 Larger studies should confirm these early findings, activation and parasympathetic withdrawal are caused by
but if confirmed they point towards a remarkable mind– psychological stressors,112 suggesting that it is not the
body interaction, and moreover one that can be influenced perceived pain as such, but how the patient reacts (i.e.
by physiotherapists. what interpretations they give to painful stimuli) to the
pain that may be the key link between the physical and
mental aspects experienced.111 Such observations indicate
that interactions between the autonomic nervous system
and pain are modulated by the pain neuromatrix.
than inhibiting pain. Indeed, stress triggers a switch in Similar conclusions can be drawn in patients with
second messenger signalling for pronociceptive immune chronic whiplash-associated disorders. In the acute stage
mediators in primary afferent nociceptors, possibly diminished vasoconstrictive response as an indication of
explaining pain and stress-induced symptom flares/ sympathetic nervous system activation has a predictive
exacerbations as typically seen in those with chronic mus- value for the transition from acute to chronic whiplash-
culoskeletal pain.103 In addition, stress activates the dor- associated disorders.113 It has been hypothesized that
somedial nucleus of the hypothalamus and subsequent increased acute autonomic activity and variations in
activation of ON-cells plus suppression of OFF-cells104 hypothalamus–pituitary–adrenal axis activity after a (car)
(recall that ON- and OFF-cells are different types of accident would predict an increased likelihood of subse-
neurons in the ventromedial medulla; ON-cells are quently developing whiplash-associated disorders.102
known to promote nociception and OFF-cells to sup- However, the autonomic response to painful stimuli did
press nociception57). Together these central nervous not differ in chronic whiplash-associated disorders com-
system changes can result in stress-induced hyperalgesia pared to healthy controls.114 The autonomic nervous
(augmented nociceptive facilitation and suppressed system activity or reactivity to pain appeared unrelated
nociceptive inhibition) instead of analgesia.104 Likewise, to either pain thresholds or endogenous analgesia.114
chronic exercise stress has detrimental effects on GABA However a subgroup of patients with chronic whiplash-
neurotransmission both at the spinal and supraspinal associated disorders suffering from moderate post-
level, resulting in generalized hyperalgesia and disinhibi- traumatic stress demonstrated a reduced sympathetic
tion of the hypothalamic–pituitary–adrenal axis.72 reactivity to pain. This suggests that disturbances in the
Focussing on the role of the sympathetic branch of the autonomic nervous system are not a general feature in
autonomic nervous system, sympathetic activation may chronic whiplash, but instead might be a trait of a
16 PART II  Advances in Theory and Practice

subgroup experiencing a prolonged state of stress after from active myofascial trigger points. Arch Phys Med Rehabil
the impact event.114 With respect to the hypothalamus– 2008;89(1):16–23.
14. Vierck CJ Jr. Mechanisms underlying development of spatially
pituitary–adrenal axis, cortisol (one of the major stress distributed chronic pain (fibromyalgia). Pain 2006;124(3):
hormones and output product of the axis) did not differ 242–63.
either at baseline, nor following cognitive tests in patients 15. Millan MJ. Descending control of pain. Prog Neurobiol 2002;
with chronic whiplash-associated disorders versus healthy 66(6):355–474.
16. Suzuki R, Morcuende S, Webber M, et al. Superficial NK1-
controls.115 expressing neurons control spinal excitability through activation
of descending pathways. Nat Neurosci 2002;5(12):1319–26.
17. Zusman M. Forebrain-mediated sensitization of central pain path-
CONCLUSION ways: ‘non-specific’ pain and a new image for MT. Man Ther
2002;7(2):80–8.
18. Ursin H, Eriksen HR. Sensitization, subjective health complaints,
Pain neuroscience has evolved spectacularly over the past and sustained arousal. Ann N Y Acad Sci 2001;933:119–29.
20 years. It is becoming increasingly recognized that 19. Swinkels-Meewisse IE, Roelofs J, Schouten EG, et al. Fear of
musculoskeletal physiotherapy can benefit from pain movement/(re)injury predicting chronic disabling low back pain:
neuroscience. With respect to diagnosis, musculoskeletal a prospective inception cohort study. Spine 1976;31(6):658–64.
20. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neurosci-
physiotherapists rely on pain neuroscience for the clas- ence. Sunderland: Sinauer Associations; 1997.
sification of nociceptive versus neuropathic versus central 21. Pertovaara A. Noradrenergic pain modulation. Prog Neurobiol
sensitization pain.116,117 At the communicational level, 2006;80(2):53–83.
musculoskeletal therapists can explain pain neuroscience 22. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in
to patients with (chronic) musculoskeletal pain. This pain. Science 2000;288(5472):1765–9.
23. Le Bars D, Villanueva L. Electrophysiological evidence for the
strategy is known as therapeutic pain neuroscience edu- activation of descending inhibitory controls by nociceptive affer-
cation and aims at ‘retraining’ the patient’s pain neuro- ent pathways. Prog Brain Res 1988;77:275–99.
matrix.66 More importantly, it prepares the patient for 24. Staud R, Robinson ME, Price DD. Isometric exercise has opposite
a modern neuroscience approach to musculoskeletal effects on central pain mechanisms in fibromyalgia patients com-
pared to normal controls. Pain 2005;118(1–2):176–84.
physiotherapy, including hands-on treatment,10 exercise 25. Price DD, Staud R, Robinson ME, et al. Enhanced temporal sum-
therapy,28,118 and behavioural interventions49 that are mation of second pain and its central modulation in fibromyalgia
inspired by advances in pain neuroscience. patients. Pain 2002;99(1–2):49–59.
26. Banic B, Petersen-Felix S, Andersen OK, et al. Evidence for spinal
cord hypersensitivity in chronic pain after whiplash injury and in
REFERENCES fibromyalgia. Pain 2004;107(1–2):7–15.
1. Taguchi T, Yasui M, Kubo A, et al. Nociception originating from 27. Daenen L, Nijs J, Roussel N, et al. Dysfunctional pain inhibition
the crural fascia in rats. Pain 2013;154(7):1103–14. in patients with chronic whiplash-associated disorders: an experi-
2. Treede RD, Jensen TS, Campbell JN, et al. Neuropathic pain: mental study. Clin Rheumatol 2012;32(1):23–31.
redefinition and a grading system for clinical and research pur- 28. Nijs J, Kosek E, Van Oosterwijck J, et al. Dysfunctional endog-
poses. Neurology 2008;70(18):1630–5. enous analgesia during exercise in patients with chronic pain: to
3. Haroutiunian S, Nikolajsen L, Finnerup NB, et al. The neuro- exercise or not to exercise? Pain Physician 2012;15(Suppl. 3):
pathic component in persistent postsurgical pain: a systematic ES205–13.
literature review. Pain 2013;154(1):95–102. 29. Van Oosterwijck J, Nijs J, Meeus M, et al. Lack of endogenous
4. Haanpää MTR. Diagnosis and classification of neuropathic pain. pain inhibition during exercise in people with chronic whiplash
Pain Clinical Updates 2010;XVII(7). associated disorders: an experimental study. J Pain 2012;13(3):
5. Staud R, Smitherman ML. Peripheral and central sensitization in 242–54.
fibromyalgia: pathogenetic role. Curr Pain Headache Rep 30. Kosek E, Ekholm J, Hansson P. Modulation of pressure pain
2002;6(4):259–66. thresholds during and following isometric contraction in patients
6. Baranauskas G, Nistri A. Sensitization of pain pathways in the with fibromyalgia and in healthy controls. Pain 1996;64(3):
spinal cord: cellular mechanisms. Prog Neurobiol 1998;54(3): 415–23.
349–65. 31. Meeus M, Roussel NA, Truijen S, et al. Reduced pressure pain
7. Mendell LM, Wall PD. Responses of single dorsal cord cells to thresholds in response to exercise in chronic fatigue syndrome but
peripheral cutaneous unmyelinated fibres. Nature 1965;206: not in chronic low back pain: an experimental study. J Rehabil
97–9. Med 2010;42(9):884–90.
8. Staud R, Robinson ME, Price DD. Temporal summation of 32. Martins DF, Bobinski F, Mazzardo-Martins L, et al. Ankle joint
second pain and its maintenance are useful for characterizing mobilization decreases hypersensitivity by activation of peripheral
widespread central sensitization of fibromyalgia patients. J Pain opioid receptors in a mouse model of postoperative pain. Pain
2007;8(11):893–901. Med 2012;13(8):1049–58.
9. Meeus M, Nijs J. Central sensitization: a biopsychosocial explana- 33. Martins DF, Mazzardo-Martins L, Cidral-Filho FJ, et al. Ankle
tion for chronic widespread pain in patients with fibromyalgia joint mobilization affects postoperative pain through peripheral
and chronic fatigue syndrome. Clin Rheumatol 2007;26(4): and central adenosine A1 receptors. Phys Ther 2013;93(3):
465–73. 401–12.
10. Nijs J, Van Houdenhove B. From acute musculoskeletal pain to 34. Sluka KA, Skyba DA, Radhakrishnan R, et al. Joint mobilization
chronic widespread pain and fibromyalgia: application of pain reduces hyperalgesia associated with chronic muscle and joint
neurophysiology in manual therapy practice. Man Ther 2009; inflammation in rats. J Pain 2006;7(8):602–7.
14(1):3–12. 35. Coronado RA, Gay CW, Bialosky JE, et al. Changes in pain sen-
11. Shah JP, Phillips TM, Danoff JV, et al. An in vivo microanalytical sitivity following spinal manipulation: a systematic review and
technique for measuring the local biochemical milieu of human meta-analysis. J Electromyogr Kinesiol 2012;22(5):752–67.
skeletal muscle. J Appl Physiol 1985;99(5):1977–84. 36. Wall B, Melzack R, editors. Textbook of Pain. 3rd ed. London:
12. Shah JP, Gilliams EA. Uncovering the biochemical milieu of myo- Churchill-Livingstone; 1994.
fascial trigger points using in vivo microdialysis: an application of 37. Peyron R, Laurent B, Garcia-Larrea L. Functional imaging of
muscle pain concepts to myofascial pain syndrome. J Bodyw Mov brain responses to pain. A review and meta-analysis. Neurophysiol
Ther 2008;12(4):371–84. Clin 2000;30(5):263–88.
13. Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with 38. Lee MC, Zambreanu L, Menon DK, et al. Identifying brain
pain and inflammation are elevated in sites near to and remote activity specifically related to the maintenance and perceptual
 2  The Neurophysiology of Pain and Pain Modulation 17

consequence of central sensitization in humans. J Neurosci 2008; 62. Taylor JJ, Borckardt JJ, George MS. Endogenous opioids mediate
28(45):11642–9. left dorsolateral prefrontal cortex rTMS-induced analgesia. Pain
39. Li Z, Wang J, Chen L, et al. Basolateral amygdala lesion inhibits 2012;153(6):1219–25.
the development of pain chronicity in neuropathic pain rats. PLoS 63. Seminowicz DA, Davis KD. Cortical responses to pain in healthy
ONE 2013;8(8):e70921. individuals depends on pain catastrophizing. Pain 2006;120(3):
40. Kattoor J, Gizewski ER, Kotsis V, et al. Fear conditioning in an 297–306.
abdominal pain model: neural responses during associative learn- 64. Atlas LY, Wager TD. How expectations shape pain. Neurosci
ing and extinction in healthy subjects. PLoS ONE 2013; Lett 2012;520(2):140–8.
8(2):26. 65. Kong J, Kaptchuk TJ, Polich G, et al. Placebo analgesia: findings
41. Schiller D, Kanen JW, Ledoux JE, et al. Extinction during recon- from brain imaging studies and emerging hypotheses. Rev Neu-
solidation of threat memory diminishes prefrontal cortex involve- rosci 2007;18(3–4):173–90.
ment. Proc Natl Acad Sci U S A 2013;110(50):20040–5. 66. Puentedura EJ, Louw A. A neuroscience approach to managing
42. Hadjikhani N, Ward N, Boshyan J, et al. The missing link: athletes with low back pain. Phys Ther Sport 2012;13(3):
enhanced functional connectivity between amygdala and viscero- 123–33.
ceptive cortex in migraine. Cephalalgia 2013;29:29. 67. Meyer RA, Campbell IT, Raja SN. Peripheral neural mecha-
43. Kim JY, Kim SH, Seo J, et al. Increased power spectral density in nisms of nociception. In: Wall PD, Melzack R, editors. Text-
resting-state pain-related brain networks in fibromyalgia. Pain book of Pain. 3rd ed. Edinburgh: Churchill Livingstone; 1995.
2013;154(9):1792–7. p. 13–44.
44. Schwedt TJ, Schlaggar BL, Mar S, et al. Atypical resting-state 68. Staud R, Craggs JG, Robinson ME, et al. Brain activity related to
functional connectivity of affective pain regions in chronic temporal summation of C-fiber evoked pain. Pain 2007;129(1–2):
migraine. Headache 2013;53(5):737–51. 130–42.
45. Simons LE, Moulton EA, Linnman C, et al. The human amygdala 69. Bell IR, Baldwin CM, Schwartz GE. Illness from low levels of
and pain: evidence from neuroimaging. Hum Brain Mapp environmental chemicals: relevance to chronic fatigue syndrome
2014;35(2):527–38. and fibromyalgia. Am J Med 1998;105(3A):S74–82.
46. Schmid J, Theysohn N, Gass F, et al. Neural mechanisms mediat- 70. Seifert F, Maihofner C. Central mechanisms of experimental and
ing positive and negative treatment expectations in visceral pain: chronic neuropathic pain: findings from functional imaging
a functional magnetic resonance imaging study on placebo and studies. Cell Mol Life Sci: CMLS 2009;66(3):375–90.
nocebo effects in healthy volunteers. Pain 2013;16(13):381–3. 71. Zhuo M. A synaptic model for pain: long-term potentiation in the
47. Zusman M. Mechanisms of musculoskeletal physiotherapy. Phys anterior cingulate cortex. Mol Cells 2007;23(3):259–71.
Ther Rev 2004;9:39–49. 72. Suarez-Roca H, Leal L, Silva JA, et al. Reduced GABA neuro-
48. Tucker K, Larsson AK, Oknelid S, et al. Similar alteration of transmission underlies hyperalgesia induced by repeated forced
motor unit recruitment strategies during the anticipation and swimming stress. Behav Brain Res 2008;189(1):159–69.
experience of pain. Pain 2012;153(3):636–43. 73. Grunnesjo MI, Bogefeldt JP, Blomberg SI, et al. A randomized
49. Vlaeyen JWSMS, Linton SJ, Boersma K, et al. Pain-related fear. controlled trial of the effects of muscle stretching, manual therapy
In: Exposure-Based Treatment of Chronic Pain. USA: IASP Press and steroid injections in addition to ‘stay active’ care on health-
Seattle; 2012. p. 196. related quality of life in acute or subacute low back pain. Clin
50. Leeuw M, Goossens ME, van Breukelen GJ, et al. Exposure Rehabil 2011;25(11):999–1010.
in vivo versus operant graded activity in chronic low back 74. Surenkok O, Aytar A, Baltaci G. Acute effects of scapular mobili-
pain patients: results of a randomized controlled trial. Pain zation in shoulder dysfunction: a double-blind randomized
2008;138(1):192–207. placebo-controlled trial. J Sport Rehabil 2009;18(4):493–501.
51. Vlaeyen JW, de Jong J, Geilen M, et al. The treatment of fear of 75. Brantingham JW, Cassa TK, Bonnefin D, et al. Manipulative and
movement/(re)injury in chronic low back pain: further evidence multimodal therapy for upper extremity and temporomandibular
on the effectiveness of exposure in vivo. Clin J Pain 2002; disorders: a systematic review. J Manipulative Physiol Ther
18(4):251–61. 2013;36(3):143–201.
52. de Jong JR, Vlaeyen JW, Onghena P, et al. Reduction of pain- 76. Struyf F, Nijs J, Mollekens S, et al. Scapular-focused treatment in
related fear in complex regional pain syndrome type I: the applica- patients with shoulder impingement syndrome: a randomized
tion of graded exposure in vivo. Pain 2005;116(3):264–75. clinical trial. Clin Rheumatol 2013;32(1):73–85.
53. de Jong JR, Vangronsveld K, Peters ML, et al. Reduction of pain- 77. Lluch Girbes E, Nijs J, Torres-Cueco R, et al. Pain treatment for
related fear and disability in post-traumatic neck pain: a replicated patients with osteoarthritis and central sensitization. Phys Ther
single-case experimental study of exposure in vivo. J Pain 2013;93(6):842–51.
2008;9(12):1123–34. 78. Meeus M, Vervisch S, De Clerck LS, et al. Central sensitization
54. de Jong JR, Vlaeyen JW, van Eijsden M, et al. Reduction of pain- in patients with rheumatoid arthritis: a systematic literature
related fear and increased function and participation in work- review. Semin Arthritis Rheum 2012;41(4):556–67.
related upper extremity pain (WRUEP): effects of exposure in 79. Sterling M. Differential development of sensory hypersensitivity
vivo. Pain 2012;153(10):2109–18. and a measure of spinal cord hyperexcitability following whiplash
55. Gray AM, Pounds-Cornish E, Eccles FJ, et al. Deep brain stimu- injury. Pain 2010;150(3):501–6.
lation as a treatment for neuropathic pain: a longitudinal study 80. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, et al. Central
addressing neuropsychological outcomes. J Pain 2013;15(3): hypersensitivity in chronic pain after whiplash injury. Clin J Pain
283–92. 2001;17(4):306–15.
56. Wu D, Wang S, Stein JF, et al. Reciprocal interactions between 81. Staud R. Evidence of involvement of central neural mechanisms
the human thalamus and periaqueductal gray may be important in generating fibromyalgia pain. Curr Rheumatol Rep 2002;4(4):
for pain perception. Exp Brain Res 2013;232(2):527–34. 299–305.
57. Carlson JD, Maire JJ, Martenson ME, et al. Sensitization of pain- 82. Roussel NA, Nijs J, Meeus M, et al. Central sensitization and
modulating neurons in the rostral ventromedial medulla after altered central pain processing in chronic low back pain: fact or
peripheral nerve injury. J Neurosci 2007;27(48):13222–31. myth? Clin J Pain 2013;29(7):625–38.
58. Yanagisawa K, Masui K, Furutani K, et al. Does higher general 83. Kaya S, Hermans L, Willems T, et al. Central sensitization in
trust serve as a psychosocial buffer against social pain? An NIRS urogynecological chronic pelvic pain: a systematic literature
study of social exclusion. Soc Neurosci 2011;6(2):190–7. review. Pain Physician 2013;16(4):291–308.
59. Eisenberger NI, Lieberman MD, Williams KD. Does rejection 84. Fernandez-Carnero J, Fernandez-de-Las-Penas C, de la Llave-
hurt? An FMRI study of social exclusion. Science 2003; Rincon AI, et al. Widespread mechanical pain hypersensitivity as
302(5643):290–2. sign of central sensitization in unilateral epicondylalgia: a blinded,
60. Panksepp J. Neuroscience. Feeling the pain of social loss. Science controlled study. Clin J Pain 2009;25(7):555–61.
2003;302(5643):237–9. 85. Smart KM, Blake C, Staines A, et al. Self-reported pain severity,
61. Lamm C, Decety J, Singer T. Meta-analytic evidence for common quality of life, disability, anxiety and depression in patients classi-
and distinct neural networks associated with directly experienced fied with ‘nociceptive’, ‘peripheral neuropathic’ and ‘central sen-
pain and empathy for pain. Neuroimage 2011;54(3):2492–502. sitisation’ pain. The discriminant validity of mechanisms-based
18 PART II  Advances in Theory and Practice

classifications of low back (+/−leg) pain. Man Ther 2012;17(2): collision: integrating the potential role of stress response systems
119–25. into a biopsychosocial model. Psychosom Med 2005;67(5):
86. Sterling M, Jull G, Vicenzino B, et al. Sensory hypersensitivity 783–90.
occurs soon after whiplash injury and is associated with poor 103. Khasar SG, Burkham J, Dina OA, et al. Stress induces a switch of
recovery. Pain 2003;104(3):509–17. intracellular signaling in sensory neurons in a model of general-
87. Jull G, Sterling M, Kenardy J, et al. Does the presence of sensory ized pain. J Neurosci 2008;28(22):5721–30.
hypersensitivity influence outcomes of physical rehabilitation for 104. Martenson ME, Cetas JS, Heinricher MM. A possible neural basis
chronic whiplash? – A preliminary RCT. Pain 2007;129(1–2): for stress-induced hyperalgesia. Pain 2009;142(3):236–44.
28–34. 105. Caceres C, Burns JW. Cardiovascular reactivity to psychological
88. Coombes BK, Bisset L, Vicenzino B. Thermal hyperalgesia dis- stress may enhance subsequent pain sensitivity. Pain 1997;
tinguishes those with severe pain and disability in unilateral lateral 69(3):237–44.
epicondylalgia. Clin J Pain 2012;28(7):595–601. 106. Passatore M, Roatta S. Influence of sympathetic nervous system
89. Mayer TG, Neblett R, Cohen H, et al. The development and on sensorimotor function: whiplash associated disorders (WAD)
psychometric validation of the central sensitization inventory. as a model. Eur J Appl Physiol 2006;98(5):423–49.
Pain Pract 2012;12(4):276–85. 107. Martinez-Lavin M, Hermosillo AG, Mendoza C, et al. Ortho-
90. Neblett R, Cohen H, Choi Y, et al. The Central Sensitization static sympathetic derangement in subjects with fibromyalgia.
Inventory (CSI): establishing clinically significant values for iden- J Rheumatol 1997;24(4):714–18.
tifying central sensitivity syndromes in an outpatient chronic pain 108. Raj SR, Brouillard D, Simpson CS, et al. Dysautonomia among
sample. J Pain 2013;14(5):438–45. patients with fibromyalgia: a noninvasive assessment. J Rheumatol
91. Nijs J, Roussel N, Paul van Wilgen C, et al. Thinking beyond 2000;27(11):2660–5.
muscles and joints: therapists’ and patients’ attitudes and beliefs 109. Furlan R, Colombo S, Perego F, et al. Abnormalities of cardiovas-
regarding chronic musculoskeletal pain are key to applying effec- cular neural control and reduced orthostatic tolerance in patients
tive treatment. Man Ther 2012;18(2):96–102. with primary fibromyalgia. J Rheumatol 2005;32(9):1787–93.
92. Gifford L, Butler D. The integration of pain sciences into clinical 110. Barakat A, Vogelzangs N, Licht CM, et al. Dysregulation of the
practice. J Hand Ther 1997;10:86–95. autonomic nervous system and its association with the presence
93. Louw A, Diener I, Butler DS, et al. The effect of neuroscience and intensity of chronic widespread pain. Arthritis Care Res
education on pain, disability, anxiety, and stress in chronic mus- 2012;64(8):1209–16.
culoskeletal pain. Arch Phys Med Rehabil 2011;92(12):2041–56. 111. Gockel M, Lindholm H, Niemisto L, et al. Perceived disability
94. Nijs J, Paul van Wilgen C, Van Oosterwijck J, et al. How to but not pain is connected with autonomic nervous function among
explain central sensitization to patients with ‘unexplained’ chronic patients with chronic low back pain. J Rehabil Med 2008;
musculoskeletal pain: practice guidelines. Man Ther 2011;16(5): 40(5):355–8.
413–18. 112. Cacioppo JT, Malarkey WB, Kiecolt-Glaser JK, et al. Heteroge-
95. Van Oosterwijck J, Nijs J, Meeus M, et al. Pain neurophysiology neity in neuroendocrine and immune responses to brief psycho-
education improves cognitions, pain thresholds, and movement logical stressors as a function of autonomic cardiac activation.
performance in people with chronic whiplash: a pilot study. Psychosom Med 1995;57(2):154–64.
J Rehabil Res Dev 2011;48(1):43–58. 113. Sterling M, Jull G, Vicenzino B, et al. Physical and psychological
96. Moseley GL. Evidence for a direct relationship between cognitive factors predict outcome following whiplash injury. Pain 2005;
and physical change during an education intervention in people 114(1–2):141–8.
with chronic low back pain. Eur J Pain 2004;8(1):39–45. 114. De Kooning M, Daenen L, Cras P, et al. Autonomic response to
97. Moseley GL. Widespread brain activity during an abdominal task pain in patients with chronic whiplash associated disorders. Pain
markedly reduced after pain physiology education: fMRI evalua- Physician 2013;16(3):E277–85.
tion of a single patient with chronic low back pain. Aust J Phys- 115. Meeus M, Van Oosterwijck J, Ickmans K, et al. Interrelationships
iother 2005;51(1):49–52. between pain processing, cortisol and cognitive performance in
98. Moseley GL. Joining forces – combining cognition-targeted chronic whiplash-associated disorders. Clin Rheumatol 2014;
motor control training with group or individual pain physiology [Epub ahead of print].
education: a successful treatment for chronic low back pain. J Man 116. Nijs J, Van Houdenhove B, Oostendorp RA. Recognition of
Manip Ther 2003;11:88–94. central sensitization in patients with musculoskeletal pain: applica-
99. Moseley GL, Nicholas MK, Hodges PW. A randomized con- tion of pain neurophysiology in manual therapy practice. Man
trolled trial of intensive neurophysiology education in chronic low Ther 2010;15(2):135–41.
back pain. Clin J Pain 2004;20(5):324–30. 117. Smart KM, Blake C, Staines A, et al. The Discriminative validity
100. Moseley GL. Combined physiotherapy and education is effica- of ‘nociceptive,’ ‘peripheral neuropathic,’ and ‘central sensitiza-
cious for chronic low back pain. Aust J Physiother 2002;48(4): tion’ as mechanisms-based classifications of musculoskeletal pain.
297–302. Clin J Pain 2011;27(8):655–63.
101. Van Oosterwijck J, Meeus M, Paul L, et al. Pain physiology educa- 118. Nijs J, Meeus M, Cagnie B, et al. A modern neuroscience approach
tion improves health status and endogenous pain inhibition in to chronic spinal pain: combining pain neuroscience education
fibromyalgia: a double-blind randomized controlled trial. Clin J with cognition-targeted motor control training. Phys Ther
Pain 2013;29(10):873–82. 2014;94(5):730–8.
102. McLean SA, Clauw DJ, Abelson JL, et al. The development of
persistent pain and psychological morbidity after motor vehicle
 C H A P T E R 3 

Neuro-Electrochemistry
of Movement
Harsimran Baweja

the cytoplasmic and extracellular fluid. In the presence of

EDITOR’S INTRODUCTION a stimulus, an action potential momentarily eliminates
the negative resting membrane potential and creates a
In this chapter the author, a neuro physiologist
positive potential. Action potentials are the signals that
and physical therapist, has provided the reader
relay information along the axons from one structure to
with a detailed description of the complex
another within the nervous system. These information-
neuro-electrochemistry underpinning
packed neural signals arise due to ionic fluctuations, the
movement. Descriptions of the neural pathways
selective permeability of the membranes to different
or ‘circuitry’ involved in movement are detailed
species of ions and the uneven circulation of these ions
elsewhere in this book; however, it is easy to
across excitable membranes.
forget the sophisticated neural physiology that
In order to comprehend muscle activation by the
is involved in the propagation, direction and
nervous system, it is important to review a few basic
conveyance of signals within these circuits. The
physical principles underlying ‘neuro-electrochemistry’.
neuro-electrochemical interactions within the
These principles deal with the presence and flow of
nerve and those of synaptic transmission are
electric charge through electrical conductors2,3 within
described in detail. It is hoped that this chapter
the nervous system. These help one appreciate the flow
will remind us that our understanding of the
of current along the excitable membranes, which enable
neurophysiology of movement must start at an
the interaction of contractile proteins in muscles on a
electrochemical level.
grander scale.

Multiple levels of the nervous system collaborate for the

neurophysiological control of movement – how the FUNDAMENTAL PRINCIPLES
nervous system controls the actions of muscles to pro­ UNDERLYING NEURO-
duce human motion is akin to biomechanical principles.
Several processes occur concurrently and in synchrony
ELECTROCHEMISTRY
for activation signals to be generated by the neural tissues, Electrical Potential and Current
leading to muscle contraction and production of forces
for movement to be executed. At the most fundamental Electrical potential is the difference between charged
functional level of all, this is the motor unit. A motor unit particles at any two points on a current-carrying conduc­
consists of the anterior horn cell in the spinal cord, its tor and is the cause of current flow. Very often it is
motor neuron and all the muscle fibers it supplies.1 The interchangeably referred to as voltage, electromotive
motor unit and its properties are discussed in greater force or simply ‘potential difference’. Electrical potential
depth later in this book. The objective of this chapter is is measured in volts (V or ΔV for potential difference),
to provide insight into the neuronal electrochemical which is defined as the amount of work (Joules; J) required
physiology underlying the operation of excitable mem­ to move one coulomb (C) of charge (Q) between any two
branes on nerves, motor units and thereafter muscles in points in a circuit (equation 1):
a global sense. This chapter includes the physiological
properties of excitable membranes, resting membrane V = J /C [1]
potential, action potentials and their propagation and
transmission across the synapses. Current is the rate at which the charged particles move
Information is transmitted across nerve cells because between two points on an electrical conductor with a
of the electrical signals produced within them. One would potential difference. Opposing charges move towards
then assume that neurons are good conductors of elec­ each other. That is charges with a negative polarity move
tricity, but they are not. Rather, the system has mecha­ towards areas of positive polarity and vice versa. Current
nisms set in place for producing these signals simply on (I) is measured in amperes (A) and is defined as the
the movement of ions across the nerve cell membranes. amount of charge (Q) crossing a given point on a conduc­
Typically, excitable membranes generate a negative tor in one second (time; t) (equation 2):
potential, called the resting membrane potential. This is
measured by recording the potential difference between I = Q /t [2]
19
20 PART II  Advances in Theory and Practice

We can compute the electrical potential of a ‘neuronal’ In the nervous system, neurons act as batteries storing
battery if we know the ionic concentrations on either side potential energy (E) because of charged particles across
of the membrane. This forms the electrochemical basis their membranes. The difference in polarity and concen­
for the resting membrane potential, which is discussed in tration gradient of the ions present on either side of the
greater depth, in the next section. membrane leads to an electrical potential difference. The
Nernst equation describes this electrical potential within
a neuronal ‘battery’ as (equation 6):
Conductance
The electrical conductance (G) of an electrical conductor RT [ concentration of ions ]outside
is the ease at which an electric current passes through it. E= ln
Electrical conductance is measured in Siemens (S).
zF [ concentration of ions ]inside
[6]
Simply put, conductance is dependent upon the length RT [ concentration of ions ]outside
= 2.303 log10
(L) and the cross-sectional area (A) of the conductor and zF [ concentration of ions ]inside
the conductivity (proportionality constant; σ) of the
material. This relation is described as equation 3:
where, R = gas constant, T = absolute temperature
A (Kelvins), z = valence (electrical charge) of the ions and
G =σ [3]
L F = Faraday constant (i.e., the amount of electric charge
contained in one mole of a univalent ion). Given that at
Resistance room temperature and normal atmospheric pressure (at
sea level):7
The inverse of conductance is resistance. The electrical
resistance (R) is the opposition to the passage of an elec­ RT /zF ≅ 26 mV /z [7]
tric current through an electric conductor. Electrical
resistance shares some theoretical equivalents with the one can work out the electric potential difference across
mechanical notion of friction. The SI unit of electrical a membrane if the ionic concentrations inside and outside
resistance is the ohm (Ω). Resistance is the inverse of the cell are known. Let us consider that the concentration
conductance and is dependent upon the same factors as gradient of K+ outside the cell is ten times lesser than its
conductance. These are length of the conductor, concentration inside the cell. Inputting this together with
its cross-sectional area and the proportionality equation 6 into equation 7 for K+:
constant called resistivity (ρ). This relation is described
in equation 4: 26 mV [1]
EK = 2.303 ∗ log10 outside [8]
R=ρ
L
[4]
zK [10]inside
A
The valance of z for K+ is +1 and log 1/10 equals −1.
Ohm’s law asserts an essential relation between the resis­ Solving for the equilibrium potential (EK) and rewriting
tance, electrical potential and the current in an electrical the equation 8 above:
conductor. Ohm’s law states that the current through a
conductor between two points is directly proportional to EK ≅ 60* − 1 ≅ −60 mV [9]
the potential difference across the two points.4 In this
relation resistance is the constant of proportionality, The fundamental characteristic of voltage is that nega­
giving us the following (equation 5): tively charged ions move towards a higher voltage and
positively charged ions move towards lower voltages.
I = V /R [5] Consequently, the current in an electrical conductor
always flows from higher voltage to lower voltage. In
where I is the current through a conductor. The SI unit some cases, current can flow from a lower voltage to a
for current is ampere (A), and R is the resistance of the higher voltage, but only at the expense of energy to push
conductor, measured in units of ohms.5 the positively charged ions against a higher potential gra­
Taken together, these are some of the fundamental dient. From a biophysical point of view, this flow occurs
constructs6 underlying the electrophysiological proper­ due to the difference in ionic gradient across the mem­
ties of excitable membranes and neurons. For example, branes. These occur as a result of specific membrane
neurons can be classified as fast-conducting and slow- permeability for potassium, sodium, calcium, chloride
conducting depending on their length, cross-sectional and bicarbonate ions, which result from changes in
area and degree of myelination. The following sections functional activity of various ion channels and ion
discuss the electrochemical processes underlying some of transporters.
these principles. In summary, the membrane permeability for potas­
sium is high, causing potassium ions to flow from the
intracellular cytoplasm into the extracellular fluid carry­
RESTING MEMBRANE POTENTIAL ing out a positive charge. Once the movement of potas­
sium ions is balanced by the build-up of a negative charge
The relatively inert membrane potential of electrically on the inner surface of the membrane, resting membrane
silent cells is known as the resting membrane potential. potential is established.8-17
 3  Neuro-Electrochemistry of Movement 21

the voltmeter records the voltage from outside the mem­

Experimentally Measuring brane. The generator is used to deliver a current pulse
the Membrane Potential through the membrane and the corresponding change in
the transmembrane potential is recorded by the voltme­
The most popular electrophysiological method used to ter. The advantages of performing voltage clamping
measure membrane potential is the voltage clamp method include: (a) it eliminates the capacitive current (e.g. syn­
(Fig. 3-1).18 Its name is derived from the ability to measure aptic potentials); (b) the current flow is proportional to
potential difference across voltage-gated ionic channels. the number of open channels (i.e. membrane conduc­
Essentially, a voltage clamp allows the experimenter tance); and (c) it offers control over the opening and
to control the membrane voltage and measure the closing of transmembrane ionic channels.19-23
transmembrane current required to maintain that The experimentally derived values of physiologically
voltage.19-23 important ionic equilibrium potentials across the squid
In the early 1940s, Kenneth Cole24 came up with the nerve cell membranes for K+, Na+, and Cl− are −75, +55
notion of voltage clamping. He tested the hypothesis that and −60 mV, respectively.41 The resting membrane poten­
a cell’s membrane potential could be experimentally tial of nerve cells is approximately −65 mV. Over a series
maintained by using pair of electrodes and a feedback of seminal experiments, Hodgkin and Katz42,43 suggested
circuit, and discovered that it was feasible to do so. It was that the membrane potential at rest is negative because:
with the help of this technique that Hodgkin and Huxley (a) the excitable membranes at rest are more permeable
conducted a series of seminal experiments13,17,25-38 con­ to K+ than other physiologically important ion species;
tributing to our basic understanding of the resting mem­ and (b) the ionic concentration of K+ inside the neuron
brane potential and action potential.Together, their work is greater than outside. Therefore, at rest the net ionic
led to Hodgkin and Huxley being conferred the Nobel polarity inside a cell membrane is negative. The trans­
Prize in Physiology and Medicine in 1963.39,40 membrane ionic gradients equilibrium and transport is
In its simplest form, a voltage clamp consists of a two- maintained by the Na+/K+ pump (commonly known as
electrode pair apparatus. A pair of electrodes is connected the sodium–potassium pump). This is discussed in greater
to a current generator and a pair is connected to a volt­ detail in the next section.
meter. A stimulating electrode from the current genera­
tor and a recording electrode from the voltmeter are
placed inside the cell. The second electrode from the
Sodium–Potassium Pump
current generator is placed outside the cell and acts as The resting membrane potential across excitable mem­
the ground electrode, while the second electrode from branes and nerve cells is established by the Na+/K+

Current
generator Voltmeter

Cytoplasm

Extracellular fluid

FIGURE 3-1  ■  Representation of a voltage clamp setup. A voltage clamp consists of a pair of electrodes each connected to a current
generator and a voltmeter. A stimulating electrode from the current generator and a recording electrode from the voltmeter are
placed inside the cell. The other electrode from the current generator is placed outside the cell and acts as the ground electrode,
while the one from the voltmeter records the voltage from outside the membrane. The generator is used to deliver a current pulse
through the membrane and the corresponding change in the membrane potential is recorded by the voltmeter. (Adapted from Adrian
RH, Chandler WK, Hodgkin AL. Voltage clamp experiments in skeletal muscle fibres. J Physiol 1966;186(2):51P–2P.)
22 PART II  Advances in Theory and Practice

Extracellular fluid one permeant species of ions crossing the membrane at

Cl Na
Cl Na Cl any given instance. Therefore, in 1943, David Goldman
Cl Cl Na developed what is now known as the Goldman equa­
Na
tion.44 This equation accounts for not only the concen­
Cl Cl
Na Na Na K
Na Cl tration gradients of multiple permeant ionic species, but
also the relative permeability of the membrane to these
 
ions. A simple version of the Goldman equation for Na+,
K+, HCO3− and Cl− can be written as (equation 10):

Sodium–potassium
PNa [ Na ]outside + PK [ K ]outside
pump + PHCO [ HCO ]inside + PCl [Cl ]inside
V = 60 log10 [10]
PNa [ Na ]inside + PK [ K ]inside
 
+ PHCO [ HCO ]outside + PCl [Cl ]outside

K Where, V is the transmembrane voltage and P is the rela­

K
K K K
tive permeability of the membrane to these ions. It looks
K K K K similar to the Nernst equation and is an extension of it
to account for all the ionic species and their membrane
Cytoplasm permeability. It is important to note that the valence (z)
has been eliminated, consequently inverting the concen­
FIGURE 3-2  ■  The sodium–potassium pump. The sodium–
potassium pump is a transmembrane antiporter molecule trations of the anions (HCO3− and Cl−) relative to the
present on the phospholipid bilayer membrane. It helps the cations (Na+ and K+).
bidirectional transport of K+ and Na+ ions across the membrane. So far, it has been assumed that neurons maintain
(Adapted from Hall JE, Guyton AC. Textbook of Medical Physiology. steady ionic concentration gradients across their excitable
St. Louis, Mo: Elsevier Saunders; 2006.)
membrane surfaces. But ions are never in a state of
electrochemical homeostasis; rather resting membrane
(sodium–potassium pump; Fig. 3-2). The separation and potential is a bit noisy in vivo. Unless nerve cells can
transport of potassium (K+) and relatively immobile restore the ions displaced during current flow during
bicarbonate (HCO3−) ions from the intracellular cyto­ neural signalling and the constant ionic escape that
plasm, and the sodium (Na+) and chloride (Cl−) ions in occurs at rest, there will be a steady dissipation of the
the extracellular fluid causes a concentration gradient concentration gradients creating an imbalance. A group
across the membranes. Because of concentration gradi­ of plasma membrane proteins known as active transport­
ents, a cell cannot maintain the passive diffusion of ers maintain the ionic concentration and gradient. Active
sodium and potassium ions in and out of the membrane transporters do this by forming complex molecules which
indefinitely. This is where the Na+/K+ pump comes in to they translocate and slowly supply energy in the form of
play. It is a transmembrane antiporter molecule present ion concentration gradients across the membranes. In the
on the phospholipid bilayer membrane. The primary case of a stimulus, the opening of ionic channels rapidly
mechanistic function of the Na+/K+ pump as a protein disintegrates this stored energy to being the cascade of
embedded in the membrane is that it can return Na+ and processes involved in generating and transmitting the
K+ ions to their regions of higher concentrations. The action potential.
protein has binding sites for Na+ and ATP inside the cell
and K+ on the outside of the cell. The Na+/K+ pump
actively transports different ions across excitable mem­ ACTION POTENTIAL AND
branes in opposite directions by expending one molecule ITS PROPAGATION
of energy (ATP). The Na+/K+–ATPase enzyme promotes
the transport of K+ out of the cell and Na+ into the cell. We have established that bidirectional exchange of ions
The equilibrium potential for K+ is around −78 mV is the ionic basis for the production and occurrence of
and is the primary driver for the resting membrane the membrane potential. This exchange occurs as a func­
potential. But the resting membrane potential is typically tion of the membrane’s permeability to various ions on
around −65 mV. This suggests that the other ions such as either side. For the generation of an action potential
Cl−, Na+ and HCO3− also contribute towards the resting within a neuronal cell, it is the interplay of these pro­
membrane potentials, but to a proportionally smaller cesses that underlies neuronal signalling. The reversal of
extent than K+. Because of the greater concentration gra­ polarity inside the cell (due to an influx of excessive Na+
dient of Na+ in the extracellular fluid, the net ionic move­ by the Na+/K+ pump) relative to outside of the cell is
ment of Na+ is inwards. This deposit of Na+ within the referred to as depolarization. This typically requires an
intracellular cytoplasm generates a lesser negative charge activation signal to trigger the influx of Na+ via the Na+/
inside the cell than the equilibrium potential of K+. Con­ K+ pump. The return to resting membrane polarity
sequently, the resting membrane potential is sustained due to an increase in the K+ efflux is known as
due to a relatively constant influx of Na+ and efflux of K+ repolarization.
across the nerve cell membrane. This would also imply An action potential is an all-or-none event. This
that the Nernst equation is simplistic as it only considers means that the voltage threshold has to be breached
 3  Neuro-Electrochemistry of Movement 23

 depolarization (change in polarity). During the rising

phase, the depolarizing membrane potential momentarily
becomes positive with respect to the extracellular fluid,
causing greater positive potential to be recorded and is
Overshoot called an overshoot. The peak of the overshoot cor­
Repolarization responds with the closure of the sodium channels, thus
0 mV causing a fall in the potential (seen as the downward
Depolarization limb of the action potential in Fig. 3-3). This rapid
Threshold decline in the membrane potential back to negative
voltage polarity is known as repolarization. Repolarization
–65 mV
reflects the rapid intake of K+ ions back into the cyto­
plasm. Similar to the overshoot, during repolarization
Refractory
period
excessive K+ intake leads to an undershoot (below the
resting membrane potential). This undershoot is known
as the after hyperpolarization or refractory period. The
 beauty of the refractory period is that it is difficult to
FIGURE 3-3  ■  A representative action potential and its phases. elicit another action potential during this phase. This
The initial depolarization, overshoot, repolarization and hyper- is because as an action potential moves along the nerve
polarization (refractory period). The grey-dotted line indicates axon, it leaves behind it the Na+ channels inactivated
an arbitrary threshold potential. If the ionic imbalance leads to
a potential generation greater than this voltage an action poten-
and K+ channels activated for a brief time. Hence, the
tial will be generated. This is the all-or-none principle. (Adapted period is defined by the time necessary to reactivate
from Hodgkin AL, Huxley AF. A quantitative description of mem- the Na+ channels to open up and the K+ channels to
brane current and its application to conduction and excitation in close down. This limits the number of action potentials
nerve. J Physiol 1952;117(4):500–44.) that can be generated per unit time by a given cell.
This is also the physiological phenomenon accounting
for the unidirectional flow of current in nerve cells.
by an activation signal to cause the cascade of events An intriguing concept of action potential generation
that lead to an action potential. This can then be is its all-or-none nature. This means the action potential
repeated once every few milliseconds until there is an will not initiate below a certain membrane potential,
activation signal (stimulus) providing the drive to alter known as the threshold potential. The initial triggering
the resting state. stimulus could be a synaptic input or an external electric
An action potential arises from the temporary reversal current that facilitates the spread of an action potential
of the membrane potential due to an increase in the down the axon. The ionic channels mediating the rapid
permeability to Na+.30 The concurrent activation of reversal of the membrane permeability are voltage-gated
many synapses leads to the activation of the ionic channels. These channels do not activate and open up
channels necessary to cause the reversal of the mem­ completely unless a criterion voltage has been achieved
brane polarity – depolarization. So the resting membrane on the outside of the membrane.There is a range of sub­
potential that is originally negative now starts to become critical depolarization, where the rate of Na+ influx is less
positive. This continues until the Na+ channels are open, than the rate of K+ efflux from within the cell (recall the
creating an influx of Na+. Once the ionic channels resting membrane is favourably permeable to K+ and
transporting Na+ into the cell close, the membrane requires the efflux of K+ for depolarization). So there
permeability to K+ is restored – repolarization and would be a certain level – the threshold – at which the
the ionic balance returns the potential to resting mem­ efflux matches the influx leading to an unstable equilib­
brane potential. These are the sequence of events that rium above the resting membrane potential. Theoreti­
occur within a neuronal cell during the generation of cally, an action potential would occur if at this point there
an action potential. This action potential is then quickly was a net increase of Na+ inwards; on the contrary, repo­
transmitted along the axon.10,13,17,24-38,42,43,45-57 larization would occur if there was a net gain of K+ inside
the membrane. Therefore a threshold is defined as the
depolarizing membrane potential at which the ionic
Decomposing an Action Potential potential of Na+ entering is equal to that of K+ exiting
Action potentials have a characteristic waveform that the cell.58
can be divided into phases. Each phase marks a particular
ionic event leading to a change in the voltage across
the membrane, rendering a characteristic waveform to
Action Potential Propagation
the action potential. Figure 3-3 describes the typical The voltage-dependent mechanisms underlying the gen­
waveform of an action potential. There are four basic eration of action potentials are also responsible for their
parts to an action potential – the initial depolarization, transmission (Fig. 3-4). This means an action potential
overshoot, repolarization and hyperpolarization (refrac­ will propagate if there is a directional displacement of
tory period). A stimulus triggers the action potential the transient membrane potential reversal across the
by causing a rapid and transient reversal of the perme­ nerve axon.
ability to Na+ into the cytoplasm. This causes a rise in A depolarizing trigger such as a postsynaptic potential
the membrane potential and is known as the initial or an experimentally induced current injected into the
24 PART II  Advances in Theory and Practice

Node of Ranvier

Direction of action
Axon
Potential propagation
Myelin

   

   

FIGURE 3-4  ■  Representation of action potential transmission along a myelinated neuronal axon. The transmission of action potentials
along the axons of nerve fibers is facilitated by passive conductance due to the potential difference between the electrically active
sites of the action potential and the inactive sites in the direction of propagation on the axon. (Adapted from Dodge FA, Frankenhaeuser
B. Membrane currents in isolated frog nerve fibre under voltage clamp conditions. J Physiol 1958;143(1):76–90.)

membrane causes the local depolarization of the excitable A NOTE ON SYNAPTIC TRANSMISSION
membrane. This leads to the opening of voltage-gated
Na+ channels in that area (e.g. node of Ranvier on an An activation signal is necessary for an action potential
axon). The opening of these channels leads to a transient to develop and propagate through the axon of a nerve
increase on the influx of Na+, depolarizing the membrane cell. This activation signal needs to possess the charge
potential enough to breach the threshold initiating an necessary to depolarize the cell membrane and cause
action potential in that area. A small quantity of the the cascade of events leading to the generation and
current generated by the action potential flows passively propagation of the action potential mentioned in the
along the axon by electronic conductance. This means previous sections of this chapter. These activation
that Na+ does not move along the axon, but transfers its signals are generated at and propagated via synapses:
charge to neighbouring particles passively. This passive the functional connections between nerve cells which
current flow causes the depolarization of membrane allow the flow of information across the length of
potential in the adjacent node of Ranvier (on an axon). the nervous system. Based on the specialized modus
Thus, the local depolarization initiates an action poten­ operandi, synapses are fundamentally classified into
tial in this node, repeating the cascade of events in an electrical and chemical synapses. While electrical syn­
ongoing cycle until the length of the axon is traversed. apses allow for the direct flow of current via gap
Consequently, the transmission of action potentials junctions, chemical synapses cause the flow of current
entails the organized current flow in two ways: active through neurotransmitter secretion across the synaptic
currents flowing through voltage-gated ion channels and junction.
passive flow of current through conductance. In the case of an electrical synapse, the presynaptic and
The electrochemical mechanisms explained above postsynaptic membranes are lined with pairs of commu­
render the following principal properties to the propaga­ nicating ion channels that are separated by a microscopic
tion of action potentials: (a) the propagation to action gap of 2–3 nanometers. The term gap junction is used to
potentials is also an all-or-none event. This means that describe this space in an electrical synapse (Fig. 3-5). For
the magnitude of the action potentials measured across the postsynaptic membrane to depolarize there needs to
the length of its transmission remains constant; (b) due be an action potential traversing the presynaptic neuron
to the refractory nature of the involved ion channels, and ample pairs of ionic channels and gap junctions to
action potential propagation is unidirectional; and (c) cause a sufficient transfer of the current to change the
action potentials have a measurable conduction velocity. postsynaptic membrane threshold.59 The advantages of
The conduction velocity is dependent on the thickness of having electrical synapses are that they allow for two-way
the axon, number of ionic channels lining the nodes of communication within neurons. They work by high
Ranvier, the state of neuronal myelination and the length passive conductance of ionic current from one neuron to
of the axon. The rate of transmission is measureable by another along the series. The flow of current is very rapid
placing recording electrodes at varying distances on the compared with chemical synapses. One of the most
axon. The mechanism of action potential propagation is important functions of electrical synapses is their role in
comprehensible if one understands the generation of emergency situations. Because of the speed of transmis­
action potentials, the passive flow of current in conduc­ sion across an electrical synapse, onset of the elicited
tors and axons and the functioning of voltage-gated ionic motor response is very rapid, as needed in life-saving
channels. circumstances.60
 3  Neuro-Electrochemistry of Movement 25

Presynaptic
neuron

Gap junction

Neurotransmitter

Postsynaptic
neuron

FIGURE 3-5  ■  Representations of an electric synapse. The presynaptic and postsynaptic membranes are lined with pairs of commu-
nicating ion channels that are separated by gap junctions. (Adapted from Hall JE, Guyton AC. Textbook of Medical Physiology. St. Louis,
Mo: Elsevier Saunders; 2006.)

Chemical synapses use neurotransmitters to convey potentials proportional to the quantum of received
information from one neuron to another.61-63 The ‘gaps’ neurotransmitter in the postsynaptic neuron. In brief,
in chemical synapses are considerably larger (~20–40 this is the mechanism of interneuronal transfer of
nanometers) than in electrical synapses and are known as information.
synaptic clefts. Characteristic of these synapses are syn­
aptic vesicles that store the chemical neurotransmitters.
The release of the neurotransmitter from a synaptic SUMMARY
vesicle occurs on the arrival of the action potential at the
presynaptic end of the synapse.64 The incoming action Excitable membranes on neural tissue generate electricity
potential causes the opening of the Ca2+ voltage-gated to transport signals across the nervous system and other
channels at the presynaptic end.65 Consequently, the cells. These signals are generated due to changes in the
increase of Ca2+ concentration in the presynaptic termi­ transmembrane resting potential. The resting membrane
nal mobilizes the vesicles towards the presynaptic mem­ potential arises due to membrane permeability to physi­
brane, where they fuse and release neurotransmitter into ologically important ion species which cause a transmem­
the cleft.66-68 This release process is known as exocytosis.69 brane ionic gradient. Specifically, the resting membrane
Upon reaching the postsynaptic membrane the neu­ potential results from predominant membrane permea­
rotransmitter binds with specific binding sites on the bility to K+. Action potentials are voltage-gated events
membrane. This causes the change in the conductance that occur due to a transient reversal of the membrane
(increase or decrease) of the membrane potential in the permeability to Na+. Upon the closure of these Na+ chan­
postsynaptic neuron – causing excitation or inhibition nels the membrane potential reverts to its K+ permeabil­
based on the nature of the signal. Due to the cascade of ity, causing repolarization. As this is a voltage-gated
events that occur for transmission to complete across a event, momentarily during repolarization, another action
chemical synapse, the speed of transmission is relatively potential cannot be elicited from the same site on the
slower than across electrical synapses. Furthermore, syn­ membrane.
aptic vesicles release neurotransmitters in fixed quanti­ Action potentials and their properties have been
ties, also known as quanta.70 This produces membrane studied for years via a technique called voltage clamping
26 PART II  Advances in Theory and Practice

developed in the 1940s. It allows for the control and IUPAC recommendations. 2nd ed. Oxford [England]; Malden, MA,
regulation of the transmembrane potentials in a labora­ USA: Blackwell Science; 1997.
8. Baker PF, Hodgkin AL, Shaw TI. The effects of changes in internal
tory setting. Significant scientific work using this tech­ ionic concentrations on the electrical properties of perfused giant
nique has established that the ionic gradients and their axons. J Physiol 1962;164:355–74.
transmembrane potentials are the basis of the all-or-none 9. Frankenhaeuser B, Hodgkin AL. The effect of calcium on the
nature of action potentials. The transmission of action sodium permeability of a giant nerve fibre. J Physiol 1955;128(2):
40–1P.
potentials along the axons of nerve fibres is facilitated by 10. Frankenhaeuser B, Hodgkin AL. The after-effects of impulses in
passive conductance due to the potential difference the giant nerve fibres of Loligo. J Physiol 1956;131(2):341–76.
between the electrically active sites of the action potential 11. Frankenhaeuser B, Hodgkin AL. The action of calcium on the
and the inactive sites in the direction of propagation on electrical properties of squid axons. J Physiol 1957;137(2):218–44.
the axon. 12. Hawkins RD, Abrams TW, Carew TJ, et al. A cellular mechanism
of classical conditioning in Aplysia: activity-dependent amplifica­
Interneuronal communication and transmission of tion of presynaptic facilitation. Science 1983;219(4583):400–5.
action potential occurs via specialized junctions between 13. Hodgkin AL. The membrane resistance of a non-medullated nerve
neurons. These junctions are called synapses. Based on fibre. J Physiol 1947;106(3):305–18.
their specialized mechanism of information transfer 14. Hodgkin AL. Ionic movements and electrical activity in giant nerve
fibres. Proc R Soc Lond B Biol Sci 1958;148(930):1–37.
within the neural circuit, they are broadly categorized 15. Hodgkin AL, Horowicz P. The influence of potassium and chloride
into electrical and chemical synapses. In electrical syn­ ions on the membrane potential of single muscle fibres. J Physiol
apses, the passive yet direct flow of current across the gap 1959;148:127–60.
junctions is the mechanism of transmission. Transmission 16. Hodgkin AL, Horowicz P. The effect of sudden changes in ionic
across these synapses is a very rapid event and plays a concentrations on the membrane potential of single muscle fibres.
J Physiol 1960;153:370–85.
functional role in evoking a quick motor response during 17. Hodgkin AL, Huxley AF. Resting and action potentials in single
life-threatening situations. In the case of chemical syn­ nerve fibres. J Physiol 1945;104(2):176–95.
apses, there is a cascade of events leading up to the release 18. Dodge FA, Frankenhaeuser B. Membrane currents in isolated frog
of neurotransmitters into the synaptic cleft. Neurotrans­ nerve fibre under voltage clamp conditions. J Physiol 1958;143(1):
76–90.
mitters are released in fixed amounts – quanta. Upon 19. Adrian RH, Chandler WK, Hodgkin AL. Voltage clamp experi­
their binding with sites in the postsynaptic membrane, ments in skeletal muscle fibres. J Physiol 1966;186(2):51P–2P.
information is transmitted to the next neuron. This 20. Adrian RH, Chandler WK, Hodgkin AL. Voltage clamp experi­
process is relatively slower when compared with electrical ments in striated muscle fibers. J Gen Physiol 1968;51(5):188–92.
synapses. This is the fundamental basis of how informa­ 21. Adrian RH, Chandler WK, Hodgkin AL. Voltage clamp experi­
ments in striated muscle fibers. J Gen Physiol 1968;51(Suppl.
tion is generated and transferred across the whole nervous 5):188S+.
system. 22. Adrian RH, Chandler WK, Hodgkin AL. Slow changes in potas­
sium permeability in skeletal muscle. J Physiol 1970;208(3):
645–68.
SUGGESTED READING 23. Adrian RH, Chandler WK, Hodgkin AL. Voltage clamp experi­
Cole KS. Membranes, Ions and Impulses: A Chapter of Classical ments in striated muscle fibres. J Physiol 1970;208(3):607–44.
Biophysics. Berkeley, CA: University of California Press; 1968. 24. Cole KS. Mostly membranes (Kenneth S. Cole). Annu Rev Physiol
Hodgkin AL. The Conduction of the Nervous Impulse. Springfield, 1979;41:1–24.
IL: Charles C. Thomas; 1967. 25. Hodgkin AL, Huxley AF. Potassium leakage from an active nerve
Hodgkin AL. Chance and Design. Cambridge: Cambridge University fibre. Nature 1946;158:376.
Press; 1992. 26. Hodgkin AL. The effect of potassium on the surface membrane of
Junge D. Nerve and Muscle Excitation. 3rd ed. Sunderland, MA: an isolated axon. J Physiol 1947;106(3):319–40.
Sinauer Associates; 1992. 27. Hodgkin AL. The local electric changes associated with repetitive
Katz B. Nerve, Muscle, and Synapse. New York: McGraw-Hill; 1966. action in a non-medullated axon. J Physiol 1948;107(2):165–81.
28. Hodgkin AL, Katz B. The effect of calcium on the axoplasm of
giant nerve fibers. J Exp Biol 1949;26(3):292–4, pl.
REFERENCES 29. Hodgkin AL, Katz B. The effect of temperature on the electrical
1. Buchthal F, Schmalbruch H. Motor unit of mammalian muscle. activity of the giant axon of the squid. J Physiol 1949;109(1–2):
Physiol Rev 1980;60(1):90–142. 240–9.
2. Esty W, Millikan RA, McDougal WL. American Technical Society. 30. Hodgkin AL, Katz B. The effect of sodium ions on the electrical
Elements of Electricity. Chicago: American Technical Society; activity of giant axon of the squid. J Physiol 1949;108(1):37–77.
1937. 31. Hodgkin AL, Nastuk WL. Membrane potentials in single fibres of
3. Esty W, Millikan RA, McDougal WL. American Technical Society. the frog’s sartorius muscle. J Physiol 1949;108(3):Proc, 42.
Elements of Electricity: A Practical Discussion of the Fundamental 32. Hodgkin AL. Conduction of the nervous impulse: some recent
Laws and Phenomena of Electricity and Their Practical Applica­ experiments. Br Med Bull 1950;6(4):322–5.
tions in the Business and Industrial World. Chicago: American 33. Hodgkin AL, Huxley AF. Propagation of electrical signals along
Technical Society; 1944. giant nerve fibers. Proc R Soc Lond B Biol Sci 1952;140(899):
4. Ohm GS. Die GalvanischeKette, Mathematisch. Berlin: T. H. 177–83.
Riemann; 1827. 34. Hodgkin AL, Huxley AF. A quantitative description of membrane
5. Millikan RA, Bishop ES. American Technical Society. Elements of current and its application to conduction and excitation in nerve.
electricity. Chicago: American Technical Society; 1917. J Physiol 1952;117(4):500–44.
6. American Technical Society. Cyclopedia of Applied Electricity; A 35. Hodgkin AL, Huxley AF. The dual effect of membrane potential
General Reference Work on Direct-Current Generators and on sodium conductance in the giant axon of Loligo. J Physiol
Motors, Storage Batteries, Electrochemistry, Welding, Electric 1952;116(4):497–506.
Wiring, Meters, Electric Light Transmission, Alternating-Current 36. Hodgkin AL, Huxley AF. The components of membrane conduc­
Machinery, Telegraphy, etc. Chicago: American Technical Society; tance in the giant axon of Loligo. J Physiol 1952;116(4):473–96.
1914. 37. Hodgkin AL, Huxley AF. Currents carried by sodium and potas­
7. McNaught AD, Wilkinson A. International Union of Pure and sium ions through the membrane of the giant axon of Loligo.
Applied Chemistry. Compendium of Chemical Terminology: J Physiol 1952;116(4):449–72.
 3  Neuro-Electrochemistry of Movement 27

38. Hodgkin AL, Huxley AF. Movement of sodium and potassium ions 55. Hodgkin AL. Chance and design in electrophysiology: an informal
during nervous activity. Cold Spring Harb Symp Quant Biol account of certain experiments on nerve carried out between 1934
1952;17:43–52. and 1952. J Physiol 1976;263(1):1–21.
39. Hodgkin, Huxley and Eccles. Medical Nobelists for 1963. Med 56. Kandel ER. Small systems of neurons. Sci Am 1979;241(3):66–76.
Serv J Can 1964;20:191–5. 57. Kandel ER. Cellular insights into behavior and learning. Harvey
40. [Winners of the 1963 Nobel Prize in Medicine)]. Orv Hetil Lect 1979;73:19–92.
1963;104:2477–8. 58. Huxley AF. Hodgkin and the action potential 1935–1952. J Physiol
41. Hodgkin AL. The relation between conduction velocity and the 2002;538(Pt 1):2.
electrical resistance outside a nerve fibre. J Physiol 1939;94(4): 59. Galarreta M, Hestrin S. Electrical synapses between GABA-
560–70. releasing interneurons. Nat Rev Neurosci 2001;2(6):425–33.
42. Hodgkin AL, Huxley AF, Katz B. Measurement of current-voltage 60. Bennett MV. Electrical synapses, a personal perspective (or history).
relations in the membrane of the giant axon of Loligo. J Physiol Brain Res Brain Res Rev 2000;32(1):16–28.
1952;116(4):424–48. 61. Curtis DR, Phillis JW, Watkins JC. The chemical excitation of
43. Hodgkin AL. A note on conduction velocity. J Physiol 1954;125(1): spinal neurones by certain acidic amino acids. J Physiol 1960;
221–4. 150:656–82.
44. Goldman DE. Potential, impedance, and rectification in mem­ 62. Curtis DR, Phillis JW, Watkins JC. Chemical excitation of spinal
branes. J Gen Physiol 1943;27(1):37–60. neurones. Nature 1959;183(4661):611–12.
45. Hodgkin AL. Evidence for electrical transmission in nerve: Part I. 63. Changeux JP. Chemical signaling in the brain. Sci Am 1993;269(5):
J Physiol 1937;90(2):183–210. 58–62.
46. Cole KS, Hodgkin AL. Membrane and protoplasm resistance in 64. Murthy VN, De Camilli P. Cell biology of the presynaptic terminal.
the squid giant axon. J Gen Physiol 1939;22(5):671–87. Annu Rev Neurosci 2003;26:701–28.
47. Hodgkin AL, Rushton WA. The electrical constants of a crustacean 65. Adler EM, Augustine GJ, Duffy SN, et al. Alien intracellular
nerve fibre. Proc R Soc Med 1946;134(873):444–79. calcium chelators attenuate neurotransmitter release at the squid
48. Hodgkin AL, Huxley AF. Potassium leakage from an active nerve giant synapse. J Neurosci 1991;11(6):1496–507.
fibre. J Physiol 1947;106(3):341–67. 66. Miledi R. Transmitter release induced by injection of calcium ions
49. Hodgkin AL, Keynes RD. Sodium extrusion and potassium absorp­ into nerve terminals. Proc R Soc Lond B Biol Sci 1973;183(73):
tion in Sepia axons. J Physiol 1953;120(4):46P–7P. 421–5.
50. Hodgkin AL, Keynes RD. The mobility and diffusion coefficient 67. Schweizer FE, Ryan TA. The synaptic vesicle: cycle of exocytosis
of potassium in giant axons from Sepia. J Physiol 1953;119(4): and endocytosis. Curr Opin Neurobiol 2006;16(3):298–304.
513–28. 68. Sudhof TC. The synaptic vesicle cycle: a cascade of protein-protein
51. Hodgkin AL, Keynes RD. The potassium permeability of a giant interactions. Nature 1995;375(6533):645–53.
nerve fibre. J Physiol 1955;128(1):61–88. 69. Heuser JE, Reese TS, Dennis MJ, et al. Synaptic vesicle exocytosis
52. Hodgkin AL, Keynes RD. Active transport of cations in giant axons captured by quick freezing and correlated with quantal transmitter
from Sepia and Loligo. J Physiol 1955;128(1):28–60. release. J Cell Biol 1979;81(2):275–300.
53. Hodgkin AL, Horowicz P. Movements of Na and K in single 70. Del Castillo J, Katz B. Quantal components of the end-plate poten­
muscle fibres. J Physiol 1959;145(2):405–32. tial. J Physiol 1954;124(3):560–73.
54. Caldwell PC, Hodgkin AL, Keynes RD, et al. The effects of inject­
ing ‘energy-rich’ phosphate compounds on the active transport of
ions in the giant axons of Loligo. J Physiol 1960;152:561–90.
 CHAPTER 4 

Postural Control and

Sensorimotor Integration
Ian Loram

SUMMARY shanks, thighs, pelvis, spine, thorax, neck and head such
that standing is temporarily possible with no muscle
Sensorimotor integration is central to sustained control activity.3,5,6 Passive stabilization through alignment, or
of configuration (postural control). This chapter consid­ through contact with external surfaces (e.g. floor, wall,
ers postural sensorimotor integration at the level of the table or chair), reduces the control and attentional
whole system, which includes concurrent perceptual, demands of maintaining configuration. However, even
executive and motor processes. These mechanisms allowing for passive stabilization, the free-standing
provide a basis for physiotherapeutic practice. Multiple upright aligned body is mechanically unstable. In the
sensory modalities are combined with prior personal absence of sensory feedback even small departures from
experience and converged to a set of movement possi­ alignment will cause the body to fall.2,7-13 During accurate
bilities. From these possibilities, control priorities are alignment, the active muscular forces required to balance
selected and passed to the motor system which generates gravity are minimal. The time taken to fall from the
coordinated inhibition and excitation of the entire mus­ aligned configuration increases exponentially with the
cular system. Within a main perception–selection–motor accuracy of the initial alignment.2,14-16 Hence, upright
feedback loop, two levels of mechanism work together. configuration is achieved most economically and most
The slow intentional system acting through central selec­ stably when alignment is controlled accurately.
tion and optimization pathways (e.g. basal ganglia, pre­ Neural regulation is essential for postural control.
motor and prefrontal cortex, cerebellum) allows sequential Mechanical instability alone means sensorimotor feed­
optimization, selection and temporal inhibition of alter­ back is required. Furthermore, daily life requires sensory
native possibilities up to a maximum rate of two to four and mechanical engagement with external objects and
selections per second. The fast habitual-reflexive system social engagement with other people: the required con­
acting through previously facilitated transcortical, brain figurations are many and difficult to predict beyond a
stem and spinal pathways implements coordinated short time scale. Pre-computing motor solutions and
responses to environmental stimuli with a latency as low storing them in a retrievable fashion is appropriate when
as 50–100 ms. The main perception–selection–motor the controlled ‘system’ and necessary constraints do not
loop provides a mechanism for amplifying or diminishing change.17 Pre-computed building blocks of motor control
maladaptive perceptions and selections. Restoration of known as motor primitives are stored within the motor
maladapted function requires re-education of the central cortex, brain stem and spinal cord. The sensorimotor
processes of perception and selection. system retrieves and combines these primitive compo­
nents in the construction of posture and movement.18-20
However, through fatigue, development and ageing the
POSTURAL CONTROL human system changes. Local pain, injury and irritation
cause people to limit the ranges of desired configurations.
Posture simply means configuration of the body. The These altered limits may be required swiftly and may
human body comprises multiple segments along a kine­ also evolve gradually. Constraints on configuration and
matic chain which includes feet, shanks, thighs, pelvis, control strategy change with the need to catch, pick up
spine, thorax, arms, neck and head. There are many pos­ and hold objects, look at computer monitors, communi­
sible configurations. Some configurations require little cate with other people, evade dangerous objects and
muscular energy to maintain whereas others require a generally negotiate the mechanical environment. Pre-
great deal. In choosing a configuration one is constrained computed solutions alone are insufficient. This kind of
to provide the effort required to balance that configura­ control, to handle changing constraints, requires flexibil­
tion. The postural task is to maintain these segments in ity for computing new motor solutions in the moment
a desired configuration or choose some other control of activity.21 Constructing new motor solutions in the
priority which allows configuration to adjust as required. moment of activity requires selection, recombination of
Passive structures, including joint surface, ligaments existing possibilities and temporal inhibition of non-
and inactive muscle, provide some degree of postural selected alternatives.22 Thus within a main feedback loop
control.1-3 For example, muscle naturally becomes stiffer retaining executive control of posture, the human pos­
when it is still and that stiffness dispels during move­ tural system requires two kinds of feedback: a fast loop
ment,2,4 thus assisting maintenance of configuration for implementing pre-computed control, and a slow loop
without impeding movement. It is possible to align the for implementing control which is reconstructed during
28
 4  Postural Control and Sensorimotor Integration 29

activity. The human nervous system has sensorimotor Neural control

pathways corresponding to both loops.23 In this chapter SMA
these loops are named as habitual-reflexive (fast) and
intentional (slow). In control theory, the general para­ dPM
M1
digm which provides time for selection and optimization PF
S1 5 7
within the main feedback loop is known as intermittent
control.17,23,24 The continuous paradigm (e.g. servo
control, continuous optimal control) has been the main­ V1
BG
stay of postural and motor control since early physiologi­
cal investigation into postural reflexes,25,26 and since the
RN
1960s from investigation of sensorimotor integration.27
The more recently developed intermittent control para­ C
digm includes and extends the explanatory power of the RF
better known continuous paradigm.23,24 VN
To summarize, postural mechanisms provide sustained
control of an unstable multisegmental structure in known
and unpredicted circumstances. This control requires
neural integration of multiple sensory modalities with
multiple possible goals and constraints. Spinal cord
Musculoskeletal
mechanics
SENSORIMOTOR INTEGRATION
Sensorimotor integration is central to postural control. Iliacus
Postural control can be understood as a main feedback
loop combining concurrent elements of perception,
selection and motor control23,28 (Fig. 4-1) implemented Motor
through a range of neural pathways (Fig. 4-2). behaviour

Perception
The person receives multiple channels of information
through their eyes, ears, skin, muscles, joints and other
internal sources. Perception is the interpretive process of FIGURE 4-2  ■  Sensorimotor pathways through the central
sensory analysis. Sensory information is uncertain and nervous system. The central nervous system is conventionally
potentially ambiguous. Sensory accuracy and confidence viewed as having a hierarchical organization with three levels:
are improved by integrating information between sensory the spinal cord, brainstem and cortex. The spinal cord is the
lowest level, including motor neurons, the final common
modalities, and by combining sensory information with pathway for all motor output, and interneurons that integrate
prior experience in a process described mathematically as sensory feedback from the skin, muscle and joints with descend-
Bayesian state estimation.29-34 Prior personal experience ing commands from higher centres. The motor repertoire at this
influences the earliest stages of neural sensory represen­ level includes stereotypical multijoint and even multilimb reflex
patterns, and basic locomotor patterns. At the second level,
tation through to later stages of perceptual decision brainstem regions such as the reticular formation (RF ) and ves-
making.29 Through integrative analysis all sensory chan­ tibular nuclei (VN) select and enhance the spinal repertoire by
nels are converged to a smaller number of possibilities improving postural control, and can vary the speed and quality
for movement stored as action representations in the of oscillatory patterns for locomotion. The highest level of
frontal cortex.23,35 control, which supports a large and adaptable motor repertoire,
is provided by the cerebral cortex in combination with subcorti-
cal loops through the basal ganglia and cerebellum.36 Motor
Selection planning and visual feedback are provided through several pari-
etal and premotor regions. The primary motor cortex (M1) con-
From the current possibilities, priorities are selected for tributes the largest number of axons to the corticospinal tract
and receives input from other cortical regions that are predomi-
postural and motor action. This response selection nantly involved in motor planning. Somatosensory information
is provided through the primary somatosensory cortex (S1),
parietal cortex area 5 (5) and cerebellar pathways. The basal
ganglia (BG) and cerebellum (C ) are also important for motor
Perception Selection Motor function through their connections with M1 and other brain
regions. RN, Red nucleus; V1, Primary visual cortex; 7, Region
of posterior parietal cortex; dPM, Dorsal premotor cortex; SMA,
Supplementary motor area; PF, Prefrontal cortex. For colour
FIGURE 4-1  ■  Perception–selection–motor feedback loop. Senso- version see Plate 1. (Reproduced with modification from Scott.38)
rimotor integration forms a feedback loop in which selected
motor control influences sensory analysis, perception and
future selection. This feedback loop provides a mechanism for
amplifying or diminishing the consequences of maladaptive
selections.
30 PART II  Advances in Theory and Practice

process acts through central selection and optimization Motor cortex Sensory cortex
pathways such as those within the basal ganglia and cer­ –
ebellum22,36 and allows sequential optimization, selection
and temporal inhibition of alternative possibilities up
Thalamus
to a maximum low rate of two to four selections per
second.23,28,37
–
Motor Control
Anterior cerebellum
Using parameters passed from the selection process, the
motor system produces coordinated inhibition and exci­ Forward model Inhibition
of afferent
tation of the entire set of muscles, joints and implements transmission
control of configuration. These selections are executed Predicted
through the slow and fast pathways working together sensory feedback
within the main perception–selection–motor feedback –
loop. The slow intentional pathway provides control Nucleus Z
Match
which is reformulated and executed sequentially within
the main feedback loop with a variable latency of
180–500 ms.28,37 Using preselected parameters, the fast
loop acting through transcortical, brain stem and spinal Stretch DSCT
pathways implements coordinated habitual-reflexive
responses to environmental stimuli with a latency as low
as 50–100 ms.5
The results of motor control generate sensory input
which is interpreted, thus completing the feedback loop. Clarke’s
The feedback loop is a dynamic system. Thus all mal­ column
adapted features of postural control (symptoms) evolve Spindle
through time, either constructively or destructively afferent
depending on whether feedback is mathematically nega­
tive or positive.

SENSORY INTEGRATION Contract

Combination of sensory signals with prior expectation

occurs centrally in areas including the mid-brain and
cerebral cortex.30,39,40 For example, the posterior parietal
cortex receives input from the three sensory systems that FIGURE 4-3  ■  Neural pathways estimating position from sensory
enable localization of the body and external objects in and motor information. Integration of muscle spindle afferents
space: the visual system, the auditory system and the with expectations generated from motor output. When the
muscle is stretched, spindle impulses travel to sensory areas of
somatosensory system. The posterior parietal cortex also the cerebral cortex via Clarke’s column, the dorsal spinocerebel-
receives input from the cerebellum which is increasingly lar tract (DSCT ), Nucleus Z, and the thalamus (shown in red).
thought to generate expected sensory signals from known Collaterals of DSCT cells project to the anterior cerebellum.
motor commands20 (Fig. 4-3). Much of the output of the When a motor command is generated, it leads to co-activation
posterior parietal cortex goes to areas of the frontal motor of skeletomotor and fusimotor neurons (shown in blue). A copy
of the motor command is sent to the anterior cerebellum where
cortex.20 a comparison takes place between the expected spindle
For postural control, the visual, vestibular, proprio­ response based on that command and the actual signal pro-
ceptive and cutaneous modalities work together to esti­ vided by the DSCT collaterals. The outcome of the match is used
mate where parts of the body are in relation to one to inhibit reafferent activity, preventing it from reaching the
cerebral cortex. Sites of inhibition could be at Nucleus Z, the
another and the external world. These senses are com­ thalamus, or the parietal cortex itself. For colour version see
monly stated to be redundant, since postural control is Plate 1. (Reproduced from Proske and Gandevia.41)
possible with one or more modalities missing. However
estimation is more accurate and more robust when dif­
ferent senses are combined.40,42 A weighted combination
of signals from all sensory modalities is combined with retina, the world appears stationary because your nervous
copies of motor signals passing through central neural system knows that you are stationary relative to the
networks trained by prior experience to produce equiva­ ground and knows that you have moved your eyes rather
lent expected sensory signals (Fig. 4-3).20,41,43-45 This inte­ than believe the external world has moved.46
gration enables the nervous system to use all its available Vision provides powerful sensory input to posture and
information and knowledge to resolve potential conflicts balance,47-49 illustrated by its famous ability in ‘moving
of interpretation.43,44 For example, when you move your room’ experiments to make young children fall over.50,51
eyes causing the image of the world to move across your Vision signals movement of the external world relative to
 4  Postural Control and Sensorimotor Integration 31

the eye via optic flow of the visual field across the whole particularly the muscle spindles, form a ‘proprioceptive
retina.52,53 Estimation of body movement from retinal chain’ crossing all articulations between the eyes, feet
information requires knowledge of eye-in-head move­ and hands which functionally links the eye muscles
ment, knowledge of head-on-neck movement and other to the foot and hand muscles.43,67-69 Along the
joint movement down the kinematic chain.54,55 For proprioceptive–kinematic chain, information accumu­
example, when fixing the fovea on stationary targets, lates from the source of sensory information to the
together rotation of eye-in-head and head-on-neck signal mass segment whose location needs to be controlled.
movement of the head and trunk relative to the external For postural control, the head and ground (or other
target. Visual sensitivity to postural sway is high, allowing supporting surface) source two lines of accumulating
detection of sway about the ankle joint of only ~0.1 sensory information:
degree,52,56 but this sensitivity decreases as distance to the • Head-referenced information: Proprioception is
visual target increases.52,53 Closing one’s eyes illustrates essential for extracting body motion from visual and
both an immediate reduction in stability and also that vestibular sensation of head movement.54 The main
normally postural control without vision is possible. mass of the body lies within or close to the trunk
Vestibular organs including the semicircular canals and and the primary articulation defining trunk location
otoliths register rapid rotation and translation of the from the head is the neck. Proprioception of the
head, respectively.57-59 While commonly thought to sense neck is substantial and well connected with the ves­
acceleration, these organs contain substantial internal tibular and visual system68,70-73 and provides the first,
viscous damping, which means they measure damped most predictive estimate of body location. This esti­
acceleration that more closely resembles velocity.46 Ves­ mate of body location is improved through proprio­
tibular sensitivity to postural sway is an order of magni­ ception of additional joints along the extended
tude lower than vision and requires postural rotations proprioceptive-kinematic chain.
about the ankle joint of approximately ~1 degree. Similar • Ground-referenced information: Proprioception
to vision, extraction of body motion from sensed head alone can extract body motion relative to the ground
movement requires knowledge of head orientation with or other supporting surface. When supported only
respect to the trunk.57-60 Similar to vision, postural control on the ground through the feet, the primary articu­
is possible with vestibular loss, but balance is less robust lation defining body location is the ankle joints, and
and falls are more likely.61-64 However, vestibular organs during free standing, ankle rotation alone provides
provide compelling sensory input of larger, faster head a good estimate of centre of mass location,7,8 which
movements relevant to falls and balance. Most impor­ is improved through adding knowledge of articula­
tantly, whereas vision alone cannot distinguish motion tions further along the chain from the ground refer­
relative to the ground (self-motion) from motion of ence. Consequently, proprioception of ankle rotation
external objects relative to the eye (world motion), ves­ is highly sensitive (~0.1 degree).56 Single joint
tibular sensation alone provides an absolute measure of muscles crossing the ankle such as the soleus and
self-motion albeit motion of the head in space. Vestibular to a lesser extent the tibialis anterior are richly
sensation is important for resolving ambiguity resulting endowed with muscle spindles.7,74,75
from visual and proprioceptive sensation.44 To summarize, vision (with eye proprioception) and
Proprioception provides the sense of relative position vestibular sensation give movement of the head, and
and movement between neighbouring parts of the body. movement of the body requires measurement of neck
The sensory information derives mainly from sensory rotation. Movement of the body can be measured directly
receptors associated with skeletal striated muscles (spin­ relative to the ground. For both of these proprioception
dles, Golgi tendon organs), less so from joints, and is is vital.
combined with cutaneous receptors signalling skin stretch Pressure registered through the feet signals the mean
and pressure.41,43 Proprioception does not provide any location and strength of the contact support force. During
particular sensations, but provides knowledge of the posi­ free-standing postural control, accelerations are low and
tion and movement of our limbs and body.41 If there is the ground contact force position signals the anterior–
any sensation, this usually relates to a difference between posterior and mediolateral location of the gravitational
what is expected and what has actually occurred.41 In force vector and thus of the whole body centre of mass
contrast to vision and vestibular sensation, loss of pro­ position. Thus, under normal conditions, sensation
prioception is instantly devastating for motor and pos­ through the sole contributes to estimation of the centre
tural control.65 For example, in a rare case of large-fibre of mass location relative to the foot. This estimate is
sensory neuropathy, the individual (I. W.) has no sensa­ important, since balance requires maintaining the centre
tion of cutaneous light touch and no movement/position of mass within the base of support.76
sense below the neck: without vision he has no knowledge Proprioception provides knowledge of the kinematic
of where his limbs and body are in space.60 Following this chain. In unconstrained movements, proprioceptive
loss, motor control, posture, movement and learning information provides relatively accurate estimates of limb
new control have only been possible when deliberately position. So-called active proprioception, in which the
using direct vision of the limbs for guidance and forward person moves their own limb, does not provide better
planning.65,66 estimates of limb position than passive proprioception in
Estimation of body configuration and motion is a which the limb is moved for the participant.77 During
multimodal process integrating proprioception, vision multijoint movement,78 proprioceptive information is
and vestibular input.54 The proprioceptive organs, thought to be used in the translation of higher-level
32 PART II  Advances in Theory and Practice

movement goals into joint-based motor commands55 and knowledge of probable external sensory input influencing
also to provide local reflexive stabilization of joints.79-81 perceptual inference: we expect light to come from above
However, there are limits to the accuracy of proprio­ rather than below, faces to be convex and not concave,
ception, particularly for slow changes in position.41 and objects in the world to move slowly rather than fast.
Muscle spindles are highly sensitive to change in muscle Illusions aside, we easily forget that our perception does
length and like most sensory cells tend to habituate to not provide an absolute impression of the sensory world.
constant conditions that limit their capability to sense We cannot tickle ourself because our prior knowledge of
absolute values of joint angles.41 Tendon compliance, our action cancels the self-generated sensation of tickle.89
which is high under postural conditions of low forces, and If we support the dead weight of an external body part
muscle slack, dependent on the previous history of con­ such as an arm or leg, these are surprisingly heavy, yet
traction, both mean that muscle length and change in we do not sense our own weight which is cancelled by
muscle length can be poorly related to joint angle.6,7,41,74,82,83 our prior expectation. Perhaps only when emerging from
Thixotropy, namely the tendency of muscle to become the swimming pool when our expectation has partially
stiff when still,84,85 means that joint rotation transmits less adapted, do we partially sense our weight. We tend to
effectively into muscle length change under postural con­ perceive difference from expectation rather than sensory
ditions, and this is compounded by the changes in muscle information directly.41,89
length caused by fluctuating muscle activity which can be It might be thought this Bayesian process of combin­
an order of magnitude larger than those caused by joint ing prior belief with sensory input to create a perception
rotation.6,74 The sense of position, as identified by posi­ is confined to higher-order neural areas. However, data
tion-matching tasks, shows that proprioception can be show that prior expectations can modify sensory repre­
substantially disturbed by the previous history of move­ sentations in the early visual cortex29 and even in the
ment, contraction, muscle slack, thixotropy and exer­ retina.90 Prior expectations modify sensory processing at
cise.41 Proprioception becomes markedly less sensitive the earliest stages by affecting not only the amplitude of
during co-activation across joints41 and passive spindles neural responses or their sharpness, but also by changing
are more sensitive to movements than when fusimotor the contents of sensory representations.91 In other words,
neurons are contracting.41,74,86 During voluntary muscle prior expectations affect what is represented, rather than
contraction skeletal-motor and fusimotor neurons con­ just how well things are represented.29
tract together (‘α-γ co-activation’). Hence these findings With respect to the control of posture, perception
are at odds with the common view that proprioception is of the current environment concerns more than con­
more accurate under active than passive conditions.41 figuration alone. This element is missed in analyses that
These factors, very well reviewed by Proske and Gande­ view postural control as only a low-level dedicated
via,41 highlight three main facts: (a) proprioception pro­ control of configuration isolated from wider perceptual
vides limited absolute accuracy; (b) sense of limb position factors. Asking people to stand ‘naturally’ for a photo­
is more complex than simple measurement of joint angles graph is an easy way to demonstrate the influence of
through sensory organs; and (c) accuracy of propriocep­ perceptual factors on postural control. In an increasingly
tion is influenced by motor control (e.g. co-activation, established paradigm,92-96 the effect of these perceptual
activity). To illustrate (b), the perceptual sense of owner­ factors is illustrated by experiments in which the per­
ship (i.e. distinguishing our own body from the external ceived risk to life is manipulated by comparing postural
world) depends primarily on proprioception, but is also control at exposed height with control at ground level.
highly plastic given appropriate stimuli.41 Expectation of At exposed height, the altered visual environment
position through central sense of effort and prior experi­ changes the visual input necessary for the control of
ence are integral to the sense of position.41 The effect of balance: the distance to visual targets increases, decreas­
(c) is that the current postural control strategy has con­ ing visual sensitivity of postural sway with the conse­
sequences for the quality of position sense, which thus quence that postural sway increases.47,52 However, at
influences motor planning, translation of higher-level height, awareness of risk also influences visual input
movement goals into joint-based motor commands and even to the extent that spatial dimensions perceived as
therefore motor control. This is a feedback loop, a dangerous are perceived to be greater than they are.97-99
dynamic system, in which quality of position sense can Experiment has shown that in response to postural threat,
be amplified or diminished over time. knowledge of danger rather than current visual environ­
ment was the dominant cause of cautious gait and
elevated physiological arousal.95 The disturbing control
Perception of locomotion, balance and autonomic response occurred
The main point of this section is to emphasize the increas­ at a level that integrates cognition and prior experience
ingly accepted idea that prior personal experience influ­ with sensory input.95 This disturbed control results in
ences sensory analysis of sensory information.87,88 The changes of sustained postural configuration as well as
postural task is to control configuration appropriately higher levels of co-activation and greater restriction of
with respect to perception of the environment and the movement.94,95,100
current intentions of the person within that environment. However, while sensory input through vision and pro­
Perception is not solely determined by the input from prioception are both modifiable by perceptual factors, the
our senses but it is strongly influenced by our expecta­ same appears not to be true for the vestibular system.94
tions.29 As introduced by Kok and colleagues,29 many Galvanic vestibular stimulation of participants who were
perceptual illusions are explained as the result of prior highly motivated to minimize sway because they were
 4  Postural Control and Sensorimotor Integration 33

perturbed at height, showed little change in the initial, which are maintained weakly within the prefrontal and
pure vestibular response, even though there were strong premotor cortex (Fig. 4-4).22,35,106,107 If selected for expres­
differences in the later response that integrates balance- sion, these parallel action possibilities have the possibility
relevant sensory feedback from all modalities. Pure ves­ of being amplified by corresponding columns within the
tibular sensory input and the immediate reflexive response thalamus.35
appears to lie largely outside of cognitive and emotive
control.101 Unlike somewhat ambiguous signals from the
other senses (e.g. vision, proprioception), the semicircu­
Selection
lar canals provide an unambiguous signal of head rota­ Consistent with all vertebrates,103,109 the human nervous
tion.58 It is probably important for survival that these system contains centralized mechanisms for switching
vestibular reflexes cannot be interfered with. The reflex­ between alternative possibilities for motor control. Ana­
ive vestibular-balance responses can be trusted even tomically and functionally, there is convergence of anal­
though fearful participants may not trust their own ysed sensorimotor input, contextual, perceptual and
mechanisms.94 motivational input into and through the basal ganglia.109
Input to the basal ganglia from all major sources, the
cerebral cortex, limbic structures and the thalamus are
Generation of Action Possibilities topographically ordered.109,110 Inputs to ventromedial
Sensory analysis provides the information needed to sectors come from structures in which competing behav­
regulate motor output. In the context of postural control, ioural goals may be represented (prefrontal cortex, amyg­
people normally think of reflexes as being the underlying dala, hippocampus), while the connections of dorsolateral
and primitive mechanism that transforms sensory input sectors are from regions that guide movements (e.g.
into motor output. Reflexes provide rapid, environmen­ sensory and motor cortex) (Fig. 4-4). As summarized by
tally triggered responses similar in kind and easily mis­ Redgrave,109 basal ganglia outputs contact regions of the
taken for habitual automated habitual responses.102 The thalamus that project back to those regions of cortex
biological process of decision making and adaptation providing original inputs. Similarly, basal ganglia outputs
involves generation of multiple possibilities, selection, to the brainstem tend to target those regions that provide
and reinforcement of selections which are rewarded by indirect input to the basal ganglia (Fig. 4-5). Projections
valued outcomes. Mechanisms implementing this process from the basal ganglia output nuclei to the thalamus and
of decision making extend through vertebrates,103 inver­ brainstem are also topographically ordered. Neurons in
tebrates,104 even to the level of individual cells.105 Thus the basal ganglia output nuclei have high tonic firing rates
biological mechanisms of decision making are just as (40–80 Hz). This activity ensures that target regions of
primitive as reflexes.104 Neurophysiological recording the thalamus and brainstem are maintained under a tight
shows that sensory analysis converges to the simultane­ and relatively constant inhibitory control. Reduction of
ous, active representation in the frontal cortex of multiple inhibitory output releases associated target regions in the
possibilities for action.106-108 Action possibilities include thalamus and brainstem (e.g. superior colliculus) from
representations for movement, thought, simple or com­ normal inhibitory control.23,35,109 Topologically, in a spiral
plex action, control priorities or cognitive processes architecture using successive connections between the

FIGURE 4-4  ■  Access of basal ganglia to motiva-

tional, cognitive and motor regions for selection Premotor PFC
and reinforcement learning. The basal ganglia WM, goals,
are a group of interconnected subcortical nuclei if-than scenarios
that represent one of the brain’s fundamental
processing units. Interacting corticostriatal cir- dl PFC
cuits contribute to action selection at various
levels of analysis. Coloured projections reflect
subsystems associated with value/motivation
(red), working memory and cognitive control ‘Motor’ BG Behav. gate
vm PFC
(green), procedural and habit learning (blue), ‘Cogn.’ BG WM gate
and contextual influences of episodic memory
(orange). Sub-regions within the basal ganglia Ventral str. Motiv. gate
(BG) act as gates to facilitate or suppress actions
represented in frontal cortex. These include par- Slow RL
allel circuits linking the BG with motivational,
cognitive, and motor regions within the prefron- DA
tal cortex (PFC). Recurrent connections within Hippocampus
the PFC support active maintenance of working
memory (WM). Cognitive states in dorsolateral Amygdala Fast learning
Value
PFC (dlPFC) can influence action selection via arb. associations
projections to the circuit linking BG with the
motor cortex. Dopamine (DA) drives incremen-
tal reinforcement learning in all BG regions,
supporting adaptive behaviours as a function of
experience. For colour version see Plate 2.
(Reproduced from Frank.22)
34 PART II  Advances in Theory and Practice

Cortical loops Subcortical loops

Sensory Motor Sensory Motor

input Cerebral output input Subcortical output

cortex structures

Striatum Thal Thal SN/GP

SN/GP Striatum
A B
FIGURE 4-5  ■  Cortical and subcortical sensorimotor loops through the basal ganglia. (A) For corticobasal ganglia loops the position
of the thalamic relay is on the return arm of the loop. (B) In the case of all subcortical loops the position of the thalamic relay is on
the input side of the loop. Predominantly excitatory regions and connections are shown in red while inhibitory regions and connec-
tions are blue. Thal, Thalamus; SN/GP, Substantia nigra/globus pallidus. For colour version see Plate 2. (Reproduced from
Redgrave.109)

limbic, associative and sensorimotor territories, the basal Cortex

ganglia are organized to allow progressive selection of an
overall goal, actions to achieve a selected goal and move­
ments to achieve a selected action.103,109,111 Striatum
The basal ganglia act as a system that dynamically and
adaptively gates information flow in the frontal cortex, Hyper-direct Indirect Direct
and from the frontal cortex to the motor system.35,36,109 pathway pathway pathway
The basal ganglia are richly anatomically connected to Thalamus
the frontal cortex and the thalamocortical motor system SNc/VTA
via several distinct but partly overlapping loops.22,35
Through hyper-direct, indirect and direct pathways, this
system provides centralized mechanisms for generalized GPe
inhibition, specific inhibition and specific facilitation of
action possibilities represented in the frontal cortex (Fig.
4-6).22,35,103,112 As described by Cohen and Frank,35 the STN GPi/SNr
basal ganglia system does not directly select which action
to ‘consider’, but instead modulates the activity of Excitation
already active representations in cortex. This functional­ Inhibition
Brainstem
ity enables the cortex to weakly represent multiple poten­ Dopamine modulation
tial actions in parallel; the one that first receives a ‘go’ FIGURE 4-6  ■  Simplified illustration of basal ganglia anatomy
signal from basal ganglia output is then provided with based on a primate brain. The basal ganglia comprise two princi-
sufficient additional excitation to be executed. Lateral pal input nuclei, the striatum and the subthalamic nucleus (STN),
and two principal output nuclei, the substantia nigra pars reticu-
inhibition within thalamus and cortex act to suppress lata (SNr) and the internal globus pallidus (GPi ) (primates). The
competing responses once the winning response has been external globus pallidus (GPe) is principally an intrinsic structure
selected by the basal ganglia circuitry.22,35 that receives most of its afferents from and provides efferent
Mechanisms of response selection also lie within the connections to other basal ganglia nuclei. Finally, dopaminergic
prefrontal and premotor cortex.113,114 While these mecha­ neurones in substantia nigra (pars compacta) (SNc) and the adja-
cent ventral tegmental area (VTA) provide other basal ganglia
nisms are the subject of much current research, a general nuclei, principally the striatum, with important modulatory
conclusion is that together, these striatal (basal ganglia) signals.109 The hyper-direct, direct and indirect pathways from
and prefrontal systems provide both selection and rein­ the striatum have net effects of generalized inhibition, specific
forcement learning (i.e. progressive facilitation of those disinhibition and specific inhibition on the cortex, respectively.
(Reproduced with modification from Yin and Knowlton.102)
responses which achieve valued outcomes and progres­
sive inhibition of those responses which achieve undesired
outcomes).22,35,102 While selection and reinforcement of During learning, humans select responses flexibly
rewarded selections is associated with the basal ganglia depending on whether the anticipated outcome is desir­
system, refinement and adaptation of the possibilities able. With reinforcement of selections that are rewarded,
available for selection is associated with the cerebellum responses can become habitual. With sufficient facilita­
within cortico–cerebellar–cortico loops that match equiv­ tion, corticocortical associations can become sufficiently
alent cortico–basal ganglia–cortico loops (Fig. 4-7).36 strong to elicit automatized transcortical responses even
 4  Postural Control and Sensorimotor Integration 35

Reward
propensity Input 1 Input 2 Error

Basal ganglia Cerebral Cerebellum

cortex

Pattern Pattern
Embodiment Amplification Refinement
classification formation

Output
FIGURE 4-7  ■  Complementary basal ganglia and cerebellar loops for selection-reinforcement learning and optimization. An individual
cortical area together with its loops through basal ganglia and cerebellum form a powerful computational structure that has been
dubbed a distributed processing module (DPM).115 DPMs communicate with each other via the cortical–cortical connections. There
are on the order of a hundred DPMs in the human brain, forming a large-scale neural network. The figure shows the selection (clas-
sification) and refinement operations posited for each DPM. Net excitatory pathways are shown with closed arrows, net inhibitory
pathways with open arrows and the grey diamonds signify neuromodulatory and training inputs. (Reproduced from Houk et al.36)

Perception Selection Motor

Slow
All possible tasks
All other sensory input Refractory
SA response MS
planner

Cord

SA MS 

Spinal
Fast

Body
Sensory Mechanical Muscle
system Muscles
output activations

FIGURE 4-8  ■  Overall scheme of sensorimotor integration. For postural control there is an overall feedback loop relating perception,
selection and motor control. Perception requires sensory analysis integrating all sensory modalities with prior experience (SA).
Acting through central pathways such as the basal ganglia loops, selections are made. Recent evidence suggests selection converges
to a serial process with a maximum rate of two to four selections per second (Refractory Response Planner).23 The motor system
(MS) translates selected goals, actions, movements and control priorities into coordinated motor output. Within a slow feedback
loop restricted to the voluntary bandwidth of control (2 Hz) the motor system generates coordinated motor responses sequentially
from each new selection. With a fast loop restricted to a higher bandwidth (>10 Hz) acting through transcortical, brain stem and
spinal pathways, the motor system uses selected parameters to modulate habitual-reflexive feedback.23,37,123

before striatal gating signals occur, thus bypassing the Selection represents executive function. This execu­
basal ganglia loop (see Fig. 4-5).22,102,116-119 Functionally, tive function is required for choosing postural goals,
physiological reflexes, reflexes formed through operant control priorities and movements required to maintain
conditioning, and habitual responses share the same those goals.28 The configuration to be maintained, or
characteristic of being elicited rapidly by environmental parameters such as peripheral feedback thresholds which
stimuli without regard to the current value of the outcome. determine the resulting configuration, are selected.
Hence these are described collectively as habitual reflex­ Implicit or explicit choices are made between different
ive22,102 and in the overall scheme of sensorimotor inte­ control priorities. For example, does the selected control
gration are implemented through the fast feedback loop allow flexible adjustment of configuration, or does it
(Fig. 4-8). minimize movement at the ankle, knee and hip joints?
36 PART II  Advances in Theory and Practice

Evidence supports a normal tendency is to allow sway These responses are modulated by preceding factors,
within safe limits and minimize muscular effort.9 including explicit external instructions, the implicit
However, normal standing conceals a large inter- behavioural context including the current posture and
individual range in leg control strategies. Commonly, leg task goals, and by the external environment including
configuration is maintained stiffly.120 Less commonly, a the direction of the gravitational-acceleration vector and
bilateral, low-stiffness, energy-absorbing strategy utiliz­ location of objects (Fig. 4-9).27 These responses are
ing the available degrees of freedom is shown.120 These environmentally triggered, without taking consequences
inter-individual differences indicate the range of possi­ into account within the feedback loop: they are reflexive
bilities available for progression with development and in the sense of having environmental causality according
skill acquisition, and also for decline with age, disease, to previously made choices. These responses are coher­
injury, and fear. Consistent with feedback around the ent with environmental stimuli to a frequency of 10  Hz
perception–selection–motor loop (see Fig. 4-1), it is or more.124 The fast loop corresponds to automated,
suggested that the individual coordination strategy has habitual and reflexive control.22,35,102 Although functional,
diagnostic and prognostic potential in relation to the fast loop alone is not adequate to reject disturbance,
perceptual–posture–movement–fall interactions.100,120 is highly variable and is not fully sustained.125 Fully
Recent emerging evidence shows how executive func­ adequate, accurate and sustained control requires the
tion is required for ongoing adjustments in the mainte­ combined operation of both fast and slow feedback
nance of posture. Experimentation demonstrates loops.
substantial refractoriness up to 0.5 seconds in the imple­
mentation of postural tasks such as adjusting the position
of the body and maintaining balance.23,28,121 Refractori­
The Slow Loop
ness is the increased delay in selecting and forming one The slow loop corresponds to intentional control limited
response before the previous selection and formation of to the low bandwidth of 1–2 Hz.13,28,37,121,123,126 Within
the previous response has been completed.23 The impli­ this bandwidth there is flexibility within the feedback
cation is that for postural control, sensory input con­ loop to reselect the control priorities, goals, internal and
verges to a sequential single channel process involving external constraints at a maximum rate of two to four
optimization, selection and temporal inhibition of alter­ times per second.15,23,28,37,121,123,127 There is recent evidence
native responses prior to motor output.23,28 In the overall that reselection and execution of postural goals proceeds
scheme of sensorimotor integration (Fig. 4-8), refractori­ as a sequential process along a single channel of
ness (selection) occurs through the slow loop. This evi­ control.28,121 The slow loop ensures that control of posture
dence highlights the fact that control of posture requires can be voluntarily reprogrammed whenever necessary.
operation of the slow intentional feedback loop.23 For example, when balance is challenged unexpectedly
precipitating a fall, the fast system provides response
within 60–120 ms, and the slow system allows intentional
MOTOR CONTROL response within 180 ms.23,126 When habitual control is
perceived to have undesirable consequences, habitual
The executive selection process produces parameters control can be inhibited and reprogrammed.128 It is
which relate to the chosen tasks (e.g. standing, standing hypothesized that this slow loop passes through the basal
and looking, standing, looking and pointing, or standing, ganglia.22,23,28,119 The relative contribution of the slow and
looking, pointing and talking). The motor system gener­ fast loops is currently a matter of research and debate,
ates coordinated patterns of muscle inhibition and activa­ though evidence is emerging that the slow loop is domi­
tion through approximately 700 distinct muscles or nant in postural balance as well as visually guided manual
muscular regions acting across multiple joints.122 control.23,28,37,121,129 The hallmark of the slow loop is that
As shown in Figure 4-8, the motor system operates it explains power within motor output signals coherent
through fast and slow feedback loops.22,102,119 The slow, with unpredictable disturbances limited to below 1–2 Hz
intentional feedback loop is characterized by refractori­ and this accounts for the majority of power in postural
ness.23,28,121 To reiterate this key point, refractoriness is control.13,23
the increased delay in selecting and forming one response The motor system receives integrated sensory input
before the previous selection has been completed.23 from the vestibular nuclei and different sensory areas of
Refractoriness is absent from the fast, automatic feedback the cerebral cortex such as the posterior parietal cortex.
loop. From the selection processes, the motor system also
receives the task-related parameters which tell the motor
system what kind of coordination, feedback control and
The Fast Loop muscles synergies to generate. The motor system includes
Much accumulated evidence summarized by Pruszynski more preliminary organizing function within motor parts
and Scott27 demonstrates the power and sophistication of the basal ganglia system, the supplementary motor
of transcortical reflexes which are a class of fast-acting area, the premotor cortex and cerebellum, and influences
responses, of latency (~60–120 ms), triggered by inte­ muscle activations through the pyramidal and extrapyra­
grated environmental stimuli including joint rotations, midal systems.130 The pyramidal motor system transmits
visual, cutaneous and vestibular sensations. Pathways directly from the motor cortex, through upper motor
mediating these responses pass through the cortex and neurons within the corticospinal tract. Upper motor
are influenced by many brain regions, including the neurons terminate within the anterior horn of the spinal
cerebellum, posterior parietal cortex and frontal cortex.27 cord mostly on interneurons and to a lesser extent directly
 4  Postural Control and Sensorimotor Integration 37

Hammond (1956) Pruszynski et al (2008)

R R
Perturbation
onset
L

5 cm
L

L B
L
Force

Perturbation
onset
20 N
L 2 au

Elbow angle

EMG
EMG

5°
1 mV
SL LL SL LL
20 45 105 100 ms 20 45 105
A Time (ms) C D Time (ms)
FIGURE 4-9  ■  Modulation of fast motor response by prior subject intent. (A) Example of how subjects can categorically modulate the
long-latency (transcortical) stretch response according to verbal instruction. Subjects were verbally instructed to respond to a
mechanical perturbation with one of two verbal instructions (‘resist’/‘let go’). The upper panel depicts force traces from individual
trials aligned on perturbation onset and labelled according to the instruction. The bottom panel is the corresponding muscle activity,
which shows modulation in the long-latency stretch response (LL) but not the short-latency (spinal) stretch response (SL). (B) Example
of how subjects can continuously modulate their long-latency stretch response in accordance with spatial target position. Subjects
were instructed to respond to an unpredictable mechanical perturbation by placing their hand inside one of the five presented
spatial targets. Each plot represents exemplar hand kinematics as a function of target position. Subjects began each trial at the filled
black circle, and the black diamond indicated final hand position. The small arrows indicate the approximate direction of motion
caused by the perturbation. (C) Temporal kinematics for the elbow joint aligned on perturbation onset. (D) Pooled EMG aligned on
perturbation onset and normalised to pre-perturbation muscle activity. Note that the long-latency stretch response exhibits graded
modulation as a function of target position. For colour version see Plate 3. (Reproduced from Pruszynski and Scott.27)

on lower motor neurons. Lower motor neurons directly control posture by innervating extensor muscles in the
innervate muscles as motor units. The pyramidal system legs and trunk muscles.130
is concerned specifically with discrete voluntary skilled While the motor system is complex, there is structure
movements, such as precise movement of the fingers and and organization to the generation of motor output.
toes. The more ancient extrapyramidal motor system Firstly, while motor output is executed through multiple
includes all motor tracts other than the corticospinal muscles crossing multiple joints, the motor output
(pyramidal) tract, including parts of the rubrospinal, achieves a small number of concurrent goals: thus motor
reticulospinal, vestibulospinal and tectospinal tracts. The output is organized along a small number of synergistic
rubrospinal tract, thought to be small in humans com­ patterns of muscle activation related to the small number
pared with primates, is responsible for large muscle of concurrent task goals.28,131-133 There is increasing evi­
movement as well as fine motor control, and it terminates dence that motor output is constructed from a repertoire
primarily in the cervical spinal cord, suggesting that it of motor primitives which are stored in the cortex, brain
functions in upper limb, but not in lower limb, control. stem and spinal cord for retrieval and use in the genera­
The reticulospinal tract descends from the reticular for­ tion of movements.19,20,108,132,134-137 Secondly, there is
mation in two tracts, medullary and pontine, to act on temporal organization to motor output. Activation of
the motor neurons supplying the trunk and proximal muscles proceeds sequentially from proximal reference
limb muscles. It functions to coordinate automatic move­ or stabilizing segments to distal segments. This principle
ments of locomotion and posture, facilitate and inhibit is observed in the so-called anticipatory postural adjust­
voluntary movement and influence muscle tone. The ves­ ments where, for example, activation of leg and trunk
tibulospinal tract originates in the vestibular nuclei, muscles precedes activation of arm muscles in reaching
receives additional input from the vestibulocerebellum, movements.138-140 The ground provides the reference
and projects down to the lumbar spinal cord. It helps to or stabilizing segment. During reaching movements
38 PART II  Advances in Theory and Practice

activation proceeds temporally from the trunk to the eventually symptoms of focal dystonia.146,147 If the biome­
end of the arm.141 The trunk–head axis provides the chanical loading on bone and soft tissue are inappropri­
reference-stabilizing segment. During balance perturba­ ate, then wear, tear, compression, stretch, inflammation
tions involving sudden translation of the floor, activation and inappropriate regeneration are likely.148-150 These
proceeds temporally from the leg to the trunk,142 and consequences are subject to feedback through the
in this case the ground provides the reference or stabi­ perception–selection–motor-perception feedback loop.
lizing segment. These observations support the idea that Feedback acts to cumulatively amplify or diminish con­
posture is prior to movement. Posture is prior to move­ sequences (symptoms). This process can explain the evo­
ment both temporally and hierarchically in that control lution through time of postural problems, fear of falling
of the reference segment precedes and sets the boundary and problems consequent on poor postural control. If the
conditions for control of the end segments. Thus for individual believes their inappropriate control is the right
control of the hands, head, vocal organs and internal solution (misconception), they increase their inappropri­
respiratory muscles there is a kinematic basis to the ate response to worsening symptoms: that provides
observation143 that control of the trunk–head axis is destructive (mathematically positive) feedback. Thus two
primary. For balance relative to the ground, there is a factors determine the progression of symptoms: (a) the
basis in which control of the legs is primary. concept the person has of their own control; and
To summarize (Fig. 4-8), two levels of mechanism (b) whether that control is highly facilitated (automatic)
work together within a main perception–selection–motor or flexible (intentional).128
feedback loop. The slow system acting through central Within the sensorimotor loop (see Fig. 4-1), the motor
selection and optimization pathways (e.g. basal ganglia, and sensory processes proceed automatically. Thus there
premotor and prefrontal cortex, cerebellum) allows are two possibilities for re-education leading to improved
online sequential planning, selection and temporal inhi­ function. First, individuals can be given new information.
bition of alternative possibilities up to a maximum rate External feedback of postural and motor control can
of two to four events per second. The fast system acting provide new input, either verbally, by educative manipu­
through transcortical, brain stem and spinal pathways lation, or using visual-audio-haptic technology.128 Dis­
allows implementation of coordinated habitual, reflexive cussion and reformulation of perceptions can generate
responses to environmental stimuli with a latency as low new possibilities for thought and movement. However, if
as 50–100 ms according to preselected goals. postural control is so facilitated that selection proceeds
automatically before striatal selection processes can inter­
vene, then change is unlikely. Hence transfer of control
PRINCIPLES APPLICABLE FOR from the fast to the slow loop is required to allow postural
PHYSIOTHERAPEUTIC PRACTICE control to reformulate along more constructive lines.143
This transfer requires training targeted at improving
Sensorimotor integration occurs at the level of the whole inhibition of highly facilitated postural control.128 This
system. While understanding of sensorimotor integra­ training may be more effective if it targets areas early in
tion is still evolving, we can consider principles relevant the natural temporal kinematic progression of control.
to preventing decline and improving function. To summarize, restoration of function related to sen­
Postural control can be considered as a perception– sorimotor integration requires that neurophysiological
selection–motor feedback loop (see Fig. 4-1). Perception and neuromuscular mechanisms are working, and beyond
relevant to postural control integrates prior personal that requires re-education of the central processes of per­
experience with sensory information from the eyes, ears, ception and selection which drive postural control.
proprioception and skin. Prior experience biases sensory
information: thus postural control is sensitive to expecta­ Acknowledgements
tions including fears of what is required. Furthermore,
postural control is likely highly facilitated, proceeding Appreciation is offered to Martin Lakie, Alison Loram
automatically from environmental stimuli without current and Cornelis van de Kamp for their invaluable feed­
evaluation of the consequences of the control adopted. back improving this chapter and additionally to Peter
The selected postural control has consequences. For Gawthrop and Henrik Gollee for their collaborative
example, increased co-activation limits proprioceptive contribution to the advances in understanding sensori-
sensitivity.41 Reduced quality of position sense will impair motor integration.
the translation of higher-level movement goals into joint-
based motor commands. Increased joint stiffness limits
possibilities for adjusting balance such as when required REFERENCES
to prevent a fall.120,144 Restriction of joint movement 1. MacConaill MA, Basmajian JV. Muscles and Movements: A Basis
for Human Kinesiology. New York: Krieger; 1977. p. 400.
limits the amount, variability and asynchronicity of infor­ 2. Loram ID, Maganaris CN, Lakie M. The passive, human calf
mation gained through joint movement, and thus limits muscles in relation to standing: the non-linear decrease from short
motor learning including the possibility for learning range to long range stiffness. J Physiol 2007;584(Pt 2):661–75.
highly differentiated, skilled and economical control.145 PubMed PMID: 17823209. Pubmed Central PMCID: 2277155.
Unvaried, repetitive, synchronous control in which atten­ 3. Kelton IW, Wright RD. The mechanism of easy standing by man.
Aust J Exp Biol Med 1949;27:505. PubMed PMID: http://www
tion is paid to the task is known to cause poor even .nature.com/icb/journal/v27/n5/abs/icb194949a.html.
harmful adaptation within the nervous system, including 4. Loram ID, Maganaris CN, Lakie M. The passive, human calf
reduced differentiation of sensory receptive fields and muscles in relation to standing: the short range stiffness lies in the
 4  Postural Control and Sensorimotor Integration 39

contractile component. J Physiol 2007;584(Pt 2):677–92. PubMed 28. Van De Kamp C, Gawthrop P, Gollee H, et al. Interfacing sensory
PMID: 17823208. Pubmed Central PMCID: 2277144. input with motor output: does the control architecture converge
5. Basmajian JV, De Luca C. Muscles Alive : Their Functions Revealed to a serial process along a single channel? Front Comput Neurosci
by Electromyography. Baltimore: Williams & Wilkins; 1985. 2013;7:[2013-May-9]; English.
6. Di Giulio I, Maganaris CN, Baltzopoulos V, et al. The proprio­ 29. Kok P, Brouwer GJ, van Gerven MAJ, et al. Prior expectations
ceptive and agonist roles of gastrocnemius, soleus and tibialis bias sensory representations in visual cortex. J Neurosci 2013;
anterior muscles in maintaining human upright posture. J Physiol 33(41):16275–84. PubMed PMID: 24107959.
2009;587(Pt 10):2399–416. PubMed PMID: 19289550. Pubmed 30. Berniker M, Kording K. Bayesian approaches to sensory integra­
Central PMCID: 2697307. tion for motor control. Wiley Interdisciplinary Reviews-Cognitive
7. Loram ID, Maganaris CN, Lakie M. Active, non-spring-like Science 2011;2(4):419–28. WOS:000298176400006.
muscle movements in human postural sway: how might paradoxi­ 31. Bays PM, Wolpert DM. Computational principles of sensorimo­
cal changes in muscle length be produced? J Physiol 2005;564 tor control that minimise uncertainty and variability. J Physiol
(Pt 1):281–93. PubMed PMID: 15661825. Pubmed Central 2007;578(Pt 2):387–96. PubMed PMID: 17008369.
PMCID: 1456051. 32. Butz MV, Belardinelli A, Ehrenfeld S. Modeling body state-
8. Loram ID, Lakie M. Direct measurement of human ankle stiffness dependent multisensory integration. Cogn Process 2012;13:S113–
during quiet standing: the intrinsic mechanical stiffness is insuf­ 16. PubMed PMID: 22806661.
ficient for stability. J Physiol 2002;545(Pt 3):1041–53. PubMed 33. Angelaki DE, Gu Y, DeAngelis GC. Visual and vestibular cue
PMID: 12482906. Pubmed Central PMCID: 2290720. integration for heading perception in extrastriate visual cortex.
9. Kiemel T, Zhang Y, Jeka JJ. Identification of neural feedback for J Physiol 2011;589(4):825–33. PubMed PMID: 20679353.
upright stance in humans: Stabilisation rather than sway minimi­ 34. Fetsch CR, Turner AH, DeAngelis GC, et al. Dynamic reweight­
zation. J Neurosci 2011;31(42):15144–53. PubMed PMID: ing of visual and vestibular cues during self-motion perception.
22178153. J Neurosci 2009;29(49):15601–12. PubMed PMID: 20007484.
10. Kiemel T, Elahi AJ, Jeka JJ. Identification of the plant for upright 35. Cohen MX, Frank MJ. Neurocomputational models of basal
stance in humans: multiple movement patterns from a single ganglia function in learning, memory and choice. Behav Brain Res
neural strategy. J Neurophysiol 2008;100(6):3394–406. PubMed 2009;199(1):141–56.
PMID: 18829854. 36. Houk JC, Bastianen C, Fansler D, et al. Action selection and
11. Casadio M, Morasso PG, Sanguineti V. Direct measurement of refinement in subcortical loops through basal ganglia and cerebel­
ankle stiffness during quiet standing: implications for control lum. Philos Trans R Soc Lond B Biol Sci 2007;362(1485):1573–
modelling and clinical application. Gait Posture 2005;21(4):410. 83. PubMed PMID: 17428771.
PubMed PMID: 15886131. 37. van de Kamp C, Gawthrop PJ, Gollee H, et al. Refractoriness in
12. Magnus R. Der Korperstellung. Berlin: Springer; 1924. sustained visuo-manual control: Is the refractory duration intrinsic
13. Peterka RJ. Sensorimotor integration in human postural control. or does it depend on external system properties? PLoS Comput
J Neurophysiol 2002;88(3):1097. PubMed PMID: 12205132. Biol 2013;9(1):e1002843.
14. Loram ID. Mechanisms for human balancing of an inverted pen­ 38. Scott SH. Optimal feedback control and the neural basis of voli­
dulum using the ankle strategy [PhD]. University of Birmingham; tional motor control. Nat Rev Neurosci 2004;5(7):532–46.
2003. 39. Kording KP, Wolpert DM. Probabilistic mechanisms in senso­
15. Loram ID, Lakie M. Human balancing of an inverted pendulum: rimotor control. Novartis Found Symp 2006;270:191–8, discus­
position control by small, ballistic-like, throw and catch move­ sion 198–202, 232–7. PubMed PMID: 16649715.
ments. J Physiol 2002;540(Pt 3):1111–24. PubMed PMID: 40. Kording KP, Wolpert DM. Bayesian integration in sensorimo­
11986396. Pubmed Central PMCID: 2290269. tor learning. Nature 2004;427(6971):244–7. PubMed PMID:
16. Asai Y, Tasaka Y, Nomura K, et al. A model of postural control 14724638.
in quiet standing: Robust compensation of delay-induced instabil­ 41. Proske U, Gandevia SC. The proprioceptive senses: their roles in
ity using intermittent activation of feedback control. PLoS ONE signalling body shape, body position and movement, and muscle
2009;4(7):PubMed PMID: 19584944. force. Physiol Rev 2012;92(4):1651–97. [Epub 2012/10/18];
17. Ronco E, Arsan T, Gawthrop PJ. Open-loop intermittent feed­ PubMed PMID: 23073629. eng.
back control: Practical continuous-time GPC. IEE Pmc.-Contml 42. Shadmehr R, Mussa-Ivaldi S. Biological learning and control:
Theory Appl 1999;146(5):426–34. PubMed PMID: 10.1049/ How the brain builds representations, predicts events, and makes
ip-cta:19990504. decisions. Cambridge, MA, USA: MIT Press; 2012.
18. Roh J, Cheung VCK, Bizzi E. Modules in the brain stem 43. Proske U, Gandevia SC. The kinaesthetic senses. J Physiol
and spinal cord underlying motor behaviors. J Neurophysiol 2009;587(17):4139–46. PubMed PMID: 19581378.
2011;106(3):1363–78. PubMed PMID: 21653716. 44. van der Kooij H, Jacobs R, Koopman B, et al. An adaptive model
19. Flash T, Hochner B. Motor primitives in vertebrates and inverte­ of sensory integration in a dynamic environment applied to human
brates. Curr Opin Neurobiol 2005;15(6):660–6. PubMed PMID: stance control. Biol Cybern 2001;84(2):103–15. PubMed PMID:
16275056. 11205347.
20. Hardwick RM, Rottschy C, Miall RC, et al. A quantitative meta- 45. Stein BE, Stanford TR. Multisensory integration: current issues
analysis and review of motor learning in the human brain. Neu­ from the perspective of the single neuron. Nat Rev Neurosci
roimage 2013;67:283–97. PubMed PMID: 23194819. English. 2008;9(4):255–66. PubMed PMID: 18354398.
21. Bernstein NA, Latash LL, Turvey MT. On Dexterity and its 46. Carpenter RHS. Neurophysiology. 3rd ed. London: Hodder
Development. Mahwah: New Jersey Lawrence Erlbaum Associ­ Arnold; 1995.
ates; 1996. p. 3. 47. Paulus WM, Straube A, Brandt T. Visual stabilisation of posture
22. Frank MJ. Computational models of motivated action selection in – physiological stimulus characteristics and clinical aspects. Brain
corticostriatal circuits. Curr Opin Neurobiol 2011;21(3):381–6. 1984;107(DEC):1143–63. PubMed PMID: 6509312.
PubMed PMID: 21498067. 48. Peterka RJ, Benolken MS. Role of somatosensory and vestibular
23. Loram I, van de Kamp C, Lakie M, et al. Does the motor system cues in attenuating visually induced human postural sway. Exp
need intermittent control?. Exerc Sport Sci Rev 2014;42:117. Brain Res 1995;105(1):101–10. PubMed PMID: 7589307.
PubMed PMID 24819544: DOI 10.1249/JES.0000000000000018. 49. Paulus W, Straube A, Brandt TH. Visual postural performance
24. Gawthrop P, Loram I, Lakie M, et al. Intermittent control: a after loss of somatosensory and vestibular function. J Neurol Neu­
computational theory of human control. Biol Cybern 2011;104(1– rosurg Psychiatry 1987;50(11):1542–5. PubMed PMID: 3501001.
2):31–51. PubMed PMID: 21327829. WOS:000287851400003. 50. Foster EC, Sveistrup H, Woollacott MH. Transitions in visual
25. Sherrington CS. Integrative action of the nervous system. Cam­ proprioception: A cross-sectional developmental study of the
bridge: Cambridge University Press; 1947. effect of visual flow on postural control. J Mot Behav 1996;
26. Sherrington CS. Integrative action of the nervous system. London: 28(2):101–12. PubMed PMID: 12529212.
Constable; 1906. 51. Lee D, Aronson E. Visual proprioceptive control of standing in
27. Pruszynski JA, Scott SH. Optimal feedback control and the long- human infants. Percept Psychophys 1974;15(3):529–32. English.
latency stretch response. Exp Brain Res 2012;218(3):341–59. 52. Paulus W, Straube A, Krafczyk S, et al. Differential-effects of
PubMed PMID: 22370742. retinal target displacement, changing size and changing disparity
40 PART II  Advances in Theory and Practice

in the control of anterior posterior and lateral body sway. Exp 76. Kavounoudias A, Roll R, Roll JP. Foot sole and ankle muscle
Brain Res 1989;78(2):243–52. PubMed PMID: 2599035. inputs contribute jointly to human erect posture regulation.
53. Paulus WM, Straube A, Brandt T. Visual stabilisation of posture: J Physiol 2001;532(3):869. PubMed PMID: 11313452.
physiological stimulus characteristics and clinical aspects. Brain 77. Capaday C, Darling WG, Stanek K, et al. Pointing to oneself:
1984;107:1143. PubMed PMID: 6509312. active versus passive proprioception revisited and implications
54. Graziano MSA. Where is my arm? The relative role of vision and for internal models of motor system function. Exp Brain Res
proprioception in the neuronal representation of limb position. 2013;229(2):171–80. PubMed PMID: 23756602.
Proc Natl Acad Sci U S A 1999;96(18):10418–21. PubMed PMID: 78. Sainburg RL, Ghilardi MF, Poizner H, et al. Control of limb
10468623. dynamics in normal subjects and patients without proprioception.
55. Sober SJ, Sabes PN. Multisensory integration during motor J Neurophysiol 1995;73(2):820–35. PubMed PMID: 7760137.
planning. J Neurosci 2003;23(18):6982–92. PubMed PMID: 79. Riemann BL, Lephart SM. The sensorimotor system, part I: The
12904459. physiologic basis of functional joint stability. J Athl Train 2002;
56. Fitzpatrick R, McCloskey DI. Proprioceptive, visual and vestibu­ 37(1):71–9. PubMed PMID: 16558670.
lar thresholds for the perception of sway during standing in 80. Mergner T. A neurological view on reactive human stance control.
humans. J Physiol 1994;478(Pt 1):173. PubMed PMID: 7965833. Ann Rev Control 2010;34(2):177–98. PubMed PMID: WOS:
57. Cathers I, Day BL, Fitzpatrick RC. Otolith and canal reflexes in 000285491500001.
human standing. J Physiol 2005;563(1):229. PubMed PMID: 81. Mergner T, Maurer C, Peterka RJ. A multisensory posture control
15618274. model of human upright stance. In: Prablanc C, Pelisson D, Ros­
58. Fitzpatrick RC, Day BL. Probing the human vestibular system setti Y, editors. Neural Control of Space Coding and Action Pro­
with galvanic stimulation. J Appl Physiol 2004;96(6):2301. duction. Progress in Brain Research. 1422003. 2003. p. 189–99.
PubMed PMID: 15133017. 82. Loram ID, Maganaris CN, Lakie M. Paradoxical muscle move­
59. Wardman DL, Taylor JL, Fitzpatrick RC. Effects of galvanic ves­ ment during postural control. Med Sci Sports Exerc 2009;
tibular stimulation on human posture and perception while stand­ 41(1):198–204. PubMed PMID: 19092688.
ing. J Physiol 2003;551(3):1033. PubMed PMID: 12865505. 83. Loram ID, Maganaris CN, Lakie M. Paradoxical muscle move­
60. Day BL, Cole J. Vestibular-evoked postural responses in the ment in human standing. J Physiol 2004;556(Pt 3):683–9. PubMed
absence of somatosensory information. Brain 2002;125:2081–8. PMID: 15047776. Pubmed Central PMCID: 1664994.
PubMed PMID: 12183353. 84. Lakie M, Walsh EG, Wright GW. Resonance at the wrist dem­
61. Creath R, Kiemel T, Horak F, et al. The role of vestibular and onstrated by the use of a torque motor: an instrumental analysis
somatosensory systems in intersegmental control of upright of muscle tone in man. J Physiol 1984;353:265–85. PubMed
stance. J Vestib Res 2008;18(1):39–49. PubMed PMID: 18776597. PMID: 6481624.
62. Buchanan JJ, Horak FB. Vestibular loss disrupts control of head 85. Lakie M, Vernooij CA, Osborne TM, et al. The resonant compo­
and trunk on a sinusoidally moving platform. J Vestib Res nent of human physiological hand tremor is altered by slow vol­
2001;11(6):371. PubMed PMID: 12446963. untary movements. J Physiol 2012;590(10):2471–83. PubMed
63. Allum JH, Honegger F, Schicks H. The influence of a bilateral PMID: 22431335.
peripheral vestibular deficit on postural synergies. J Vestib Res 86. Wise AK, Gregory JE, Proske U. The responses of muscle spin­
1994;4(1):49–70. PubMed PMID: MEDLINE:8186863. dles to small, slow movements in passive muscle and during fusi­
64. Black FO, Wade SW, Nashner LM. What is the minimal vestibu­ motor activity. Brain Res 1999;821(1):87–94. [Epub 1999/03/05];
lar function required for compensation? Am J Otol 1996;17(3):401. PubMed PMID: 10064791. English.
PubMed PMID: 8817017. 87. Kersten D, Mamassian P, Yuille A. Object perception as Bayesian
65. Cole J. Pride and a Daily Marathon The MIT Press. 1995. inference. Annu Rev Psychol 2004;55:271–304. PubMed PMID:
66. Cole JD, Sedgwick EM. The perceptions of force and of move­ 14744217. English.
ment in a man without large myelinated sensory afferents below 88. Helmholtz H. Handbuch der physiologischen optik. Leipzig: L.
the neck. J Physiol 1992;449:503–15. PubMed PMID: 1522522. Voss; 1867.
67. Kavounoudias A, Gilhodes JC, Roll R, et al. From balance regula­ 89. Bays PM, Wolpert DM, Flanagan JR. Perception of the conse­
tion to body orientation: two goals for muscle proprioceptive quences of self-action is temporally tuned and event driven. Curr
information processing? Exp Brain Res 1999;124(1):80–8. PubMed Biol 2005;15(12):1125–8. PubMed PMID: 15964278.
PMID: 9928792. 90. Tong F, Meng M, Blake R. Neural bases of binocular rivalry.
68. Roll R, Velay JL, Roll JP. Eye and neck proprioceptive messages Trends Cogn Sci 2006;10(11):502–11. PubMed PMID: 16997612.
contribute to the spatial coding of retinal input in visually oriented 91. Murray SO, Boyaci H, Kersten D. The representation of per­
activities. Exp Brain Res 1991;85(2):423–31. PubMed PMID: ceived angular size in human primary visual cortex. Nat Neurosci
1893990. 2006;9(3):429–34. PubMed PMID: 16462737.
69. Karnath HO. Subjective body orientation in neglect and the 92. Adkin AL, Frank JS, Carpenter MG, et al. Fear of failing modifies
interactive contribution of neck muscle proprioception and ves­ anticipatory postural control. Exp Brain Res 2002;143(2):160.
tibular stimulation. Brain 1994;117:1001–12. PubMed PMID: PubMed PMID: 11880892.
7953584. 93. Carpenter MG, Frank JS, Silcher CP. Surface height effects on
70. Armstrong B, McNair P, Taylor D. Head and neck position sense. postural control: a hypothesis for a stiffness strategy for stance.
Sports Med 2008;38(2):101–17. [Epub 2008/01/19]; PubMed J Vestib Res 1999;9(4):277. PubMed PMID: 10472040.
PMID: 18201114. eng. 94. Osler CJ, Tersteeg MCA, Reynolds RF, et al. Postural threat dif­
71. Ivanenko YP, Grasso R, Lacquaniti F. Effect of gaze on postural ferentially affects the feedforward and feedback components of the
responses to neck proprioceptive and vestibular stimulation in vestibular-evoked balance response. Eur J Neurosci 2013;38(8):
humans (vol 519, pg 301, 1999). J Physiol 1999;519(3):923. 3239–47.
PubMed PMID: 10432359. 95. Tersteeg MCA, Marple-Horvat DE, Loram ID. Cautious gait in
72. Taylor JL, McCloskey DI. Proprioception in the neck. Exp Brain relation to knowledge and vision of height: is altered visual
Res 1988;70(2):351–60. [Epub 1988/01/01]; PubMed PMID: information the dominant influence? J Neurophysiol 2012;
3384037. eng. 107(10):2686–91. PubMed PMID: 22378173.
73. Karnath HO, Sievering D, Fetter M. The interactive contribution 96. Carpenter MG, Frank JS, Silcher CP, et al. The influence of
of neck muscle proprioception and vestibular stimulation to postural threat on the control of upright stance. Exp Brain Res
subjective straight ahead orientation in man. Exp Brain Res 2001;138(2):210. PubMed PMID: 11417462.
1994;101(1):140–6. PubMed PMID: 7843292. 97. Stefanucci JK, Proffitt DR. The roles of altitude and fear in the
74. Loram ID, Lakie M, Di Giulio I, et al. The consequences of short- perception of height. J Exp Psychol Hum Percept Perform
range stiffness and fluctuating muscle activity for proprioception 2009;35(2):424–38. PubMed PMID: 19331498.
of postural joint rotations: the relevance to human standing. 98. Clerkin EM, Cody MW, Stefanucci JK, et al. Imagery and fear
J Neurophysiol 2009;102(1):460–74. PubMed PMID: 19420127. influence height perception. J Anxiety Disord 2009;23(3):381–6.
75. Voss H. [Tabulation of the absolute and relative muscular spindle PubMed PMID: 19162437.
numbers in human skeletal musculature]. Anat Anz 1971;129(5):562– 99. Stefanucci JK, Storbeck J. Don’t look down: Emotional arousal
72. PubMed PMID: 4260484. Tabelle der abosluten und relativen elevates height perception. J Exp Psychol Gen 2009;138(1):131–
Muskelspindelzahlen der menschlichen Skelettmuskulatur. 45. PubMed PMID: 19203173.
 4  Postural Control and Sensorimotor Integration 41

100. Tersteeg M. Locomotion and stance at height [PhD]. Manchester: 125. Marsden CD, Merton PA, Morton HB, et al. Reliability and effi­
Manchester Metropolitan University; 2012. cacy of the long-latency stretch reflex in the human thumb.
101. Guerraz M, Day BL. Expectation and the vestibular control of J Physiol 1981;316( JUL):47–60. PubMed PMID: 7320877.
balance. J Cognit Neurosci 2005;17(3):463–9. PubMed PMID: 126. Loram ID, Lakie M, Gawthrop PJ. Visual control of stable and
15814005. unstable loads: what is the feedback delay and extent of linear
102. Yin HH, Knowlton BJ. The role of the basal ganglia in habit time-invariant control? J Physiol 2009;587(Pt 6):1343–65.
formation. Nat Rev Neurosci 2006;7(6):464–76. PubMed PMID: 19171654. Pubmed Central PMCID: 2675002.
103. Redgrave P, Prescott TJ, Gurney K. The basal ganglia: 127. Loram ID, Maganaris CN, Lakie M. Human postural sway results
a vertebrate solution to the selection problem? Neurosci­ from frequent, ballistic bias impulses by soleus and gastrocnemius.
ence 1999;89(4):1009–23. [Epub 1999/06/11]; PubMed PMID: J Physiol 2005;564(Pt 1):295–311. PubMed PMID: 15661824.
10362291. eng. Pubmed Central PMCID: 1456055.
104. Brembs B. Towards a scientific concept of free will as a biological 128. Loram A. A scientific investigation into violin playing: diagnosis
trait: spontaneous actions and decision-making in invertebrates. of musculo-kinematic coordination patterns and methodology for
Proceedings of the Royal Society B: Biological Sciences 2010;[2010 reducing interference with performance [MSc Dissertation].
December 15]. London: UCL/MMU; 2013.
105. Balazsi G, van Oudenaarden A, Collins JJ. Cellular decision 129. Loram ID, van de Kamp C, Gollee H, et al. Identification of
making and biological noise: from microbes to mammals. Cell intermittent control in man and machine. J R Soc Interface
2011;144(6):910–25. [Epub 2011/03/19]; PubMed PMID: 2012;9(74):2070–84. PubMed PMID: 22491973.
21414483. Pubmed Central PMCID: PMC3068611, eng. 130. Kandel E, Schwartz J, Jessell T. Principles of Neural Science. 4th
106. Cisek P, Kalaska JF. Neural correlates of reaching decisions in ed. New York: McGraw-Hill; 2000.
dorsal premotor cortex: Specification of multiple direction choices 131. Castelo Oliveira AS, Gizzi L, Kersting UG, et al. Modular organi­
and final selection of action. Neuron 2005;45(5):801–14. PubMed sation of balance control following perturbations during walking.
PMID: 15748854. J Neurophysiol 2012;108(7):1895–906. PubMed PMID: 22773783.
107. Cisek P. Integrated neural processes for defining potential actions 132. Delis I, Chiovetto E, Berret B. On the origins of modularity in
and deciding between them: A computational model. J Neurosci motor control. J Neurosci 2010;30(22):7451–2. PubMed PMID:
2006;26(38):9761–70. PubMed PMID: 16988047. 20519519.
108. Rizzolatti G, Luppino G. The cortical motor system. Neuron 133. Latash ML. Motor synergies and the equilibrium-point hypothesis.
2001;31(6):889–901. PubMed PMID: 11580891. Motor Control 2010;14(3):294–322. PubMed PMID: 20702893.
109. Redgrave P. Basal ganglia. J Scholarpedia 2007;2(6):1825. 134. Hart CB, Giszter SF. A neural basis for motor primitives in the
110. Voorn P, Vanderschuren L, Groenewegen HJ, et al. Putting a spin spinal cord. J Neurosci 2010;30(4):1322–36. PubMed PMID:
on the dorsal-ventral divide of the striatum. Trends Neurosci 20107059.
2004;27(8):468–74. PubMed PMID: 15271494. 135. Lockhart DB, Ting LH. Optimal sensorimotor transformations
111. Haber SN, Fudge JL, McFarland NR. Striatonigrostriatal path­ for balance. Nat Neurosci 2007;10(10):1329–36. PubMed PMID:
ways in primates form an ascending spiral from the shell to the 17873869.
dorsolateral striatum. J Neurosci 2000;20(6):2369–82. PubMed 136. Chvatal SA, Macpherson JM, Torres-Oviedo G, et al. Absence of
PMID: 10704511. postural muscle synergies for balance after spinal cord transection.
112. Mink JW. The basal ganglia: focused selection and inhibition of J Neurophysiol 2013;110(6):1301–10. PubMed PMID: 23803327.
competing motor programs. Prog Neurobiol 1996;50(4):381–425. 137. Bizzi E, Cheung VC. The neural origin of muscle synergies. Front
[Epub 1996/11/01]; PubMed PMID: 9004351. eng. Comput Neurosci 2013;7:[2013-April-29]; English.
113. Jiang YH, Kanwisher N. Common neural substrates for 138. Belen’kii VE, Gurfinkel VS. Pal’tsev EI. [Control elements of
response selection across modalities and mapping paradigms. voluntary movements]. Biofizika 1967;12(1):135–41. PubMed
J Cognit Neurosci 2003;15(8):1080–94. PubMed PMID: PMID: 5623488.
14709228. 139. Krishnan V, Aruin AS, Latash ML. Two stages and three compo­
114. Dux PE, Ivanoff J, Asplund CL, et al. Isolation of a central bottle­ nents of the postural preparation to action. Exp Brain Res
neck of information processing with time-resolved fMRI. Neuron 2011;212(1):47–63. PubMed PMID: 21537967.
2006;52(6):1109–20. PubMed PMID: 17178412. 140. Ahmed AA, Wolpert DM. Transfer of dynamic learning across
115. Houk J. Models of basal ganglia. Scholarpedia 2007;2(10):1633. postures. J Neurophysiol 2009;102(5):2816–24. PubMed PMID:
116. Beiser DG, Hua SE, Houk JC. Network models of the basal 19710374.
ganglia. Curr Opin Neurobiol 1997;7(2):185–90. PubMed PMID: 141. Vandenberghe A, Bosmans L, De Schutter J, et al. Quantifying
9142759. individual muscle contribution to three-dimensional reaching
117. Frank MJ. Dynamic Dopamine Modulation in the Basal Ganglia: tasks. Gait Posture 2012;35(4):579–84. PubMed PMID: 22410130.
A Neurocomputational Account of Cognitive Deficits in Medi­ 142. Horak FB, Nashner LM. Central programming of postural
cated and Nonmedicated Parkinsonism. J Cognit Neurosci 2005; movements – Adaptation to altered support-surface configura­
17(1):51–72. [2005/01/01]. tions. j neurophysiol 1986;55(6):1369. pubmed pmid: 3734861.
118. Frank MJ, Claus ED. Anatomy of a decision: Striato-orbitofrontal 143. Door B. Towards perfect posture. London. Orion 2003;155.
interactions in reinforcement learning, decision making, and 144. Loram I, editor. Control Strategy in Postural-manual Interac­
reversal. Psychol Rev 2006;113(2):300–26. PubMed PMID: tions: is the Priority Posture or Configuration? Natal, Brazil: ISB;
16637763. 2013.
119. Ashby FG, Ennis JM, Spiering BJ. A neurobiological theory of 145. Seidler RD. Neural correlates of motor learning, transfer of learn­
automaticity in perceptual categorisation. Psychol Rev 2007; ing, and learning to learn. Exerc Sport Sci Rev 2010;
114(3):632–56. PubMed PMID: 17638499. 38(1):3–9. doi:10.1097/JES.0b013e3181c5cce7.
120. Di Giulio I, Baltzopoulos V, Managanaris CN, et al. Human 146. Blake DT, Byl NN, Cheung S, et al. Sensory representation
standing: does the control strategy pre-program a rigid knee? abnormalities that parallel focal hand dystonia in a primate
J Appl Physiol 2013;2013. model. Somatosens Mot Res 2002;19(4):347–57. PubMed PMID:
121. Van de Kamp C, Gawthrop P, Gollee H, et al., editors. Refracto­ 12590836.
riness in a whole-body human balance task. Trondheim, Norway: 147. Byl NN, Merzenich MM, Jenkins WM. A primate genesis model
ISPGR; 2012. of focal dystonia and repetitive strain injury: I. Learning-induced
122. Tortora, Gerard, Grabowski. Principles of Anatomy and Physiol­ dedifferentiation of the representation of the hand in the primary
ogy. Harper Collins College Publishers; 1996. somatosensory cortex in adult monkeys. Neurology 1996;47(2):508–
123. Loram ID, Gollee H, Lakie M, et al. Human control of 20. [Epub 1996/08/01]; PubMed PMID: 8757029. eng.
an inverted pendulum: Is continuous control necessary? Is inter­ 148. Cailliet R. Cailliet R, editor. Soft Tissue Pain and Disability. 3rd
mittent control effective? Is intermittent control physiological? ed. Philadelphia: Davis; 1996.
J Physiol 2011;589(2):307–24. PubMed PMID: 21098004. 149. Cailliet R. Cailliet R, editor. Neck and Arm Pain. 3rd ed. Phila­
124. Evans CM, Fellows SJ, Rack PM, et al. Response of the normal delphia: FA Davis Company; 1991.
human ankle joint to imposed sinusoidal movements. J Physiol 150. Cailliet R. Low Back Pain Syndrome. 4th ed. Philadelphia:
1983;344(1):483. PubMed PMID: 6655591. F.A.Davis Company; 1988. p. 34.
 CHAPTER 5 

Motor Control and

Motor Learning
Natalie Mrachacz-Kersting  •  Peter Stubbs  •  Sabata Gervasio

higher centres have a certain expectation of the appropri-

INTRODUCTION ate sensory information that should be generated when a
particular motor programme is executed. This is well
From the basic idea to move, to the planning and execu- documented by the fact that artificially induced reflexes
tion of movement, the nervous system must achieve the are differently modulated within and across tasks. Closed-
feat of activating the muscles that produce the selected loop control systems are based on the assumption that
movement and control these movements in an appropri- sensory feedback is part of the control system. Thus, the
ate temporal and spatial manner. Temporal precision feedback is used by the central nervous system (CNS) to
refers to the onset and offset of activity, whereas the continuously adjust movement parameters and ensure
spatial aspects relate to the resulting excursions of the that the final goal is achieved. Despite these distinctions,
bony attachments such that meaningful movements are most movement patterns are more complex than ‘open’
produced, accounting for the environmental conditions, or ‘closed’ systems and therefore may not be solely part
the position of the body within the environment and the of an open- or closed-looped control system.
cognitive and physical abilities of the individual. In doing In an attempt to understand how an individual gener-
so, the nervous system must choose between approxi- ates a movement that by nature is constrained by factors
mately 640 muscles and 360 joints and provide the appro- within the individual (structural or functional, e.g. body
priate combination of these to produce the desired weight, shape, height, emotional and cognitive states),
outcome. There are often a number of ways to produce the environment (gravity, temperature, wind, etc.) and
the desired outcome (degrees of freedom). For example, the task (e.g. goal of the task, implements to be manipu-
a soccer player may be required to pass the ball under a lated, rules of the game, etc.), theories of motor control
variety of conditions but the final goal remains the same. have been developed. Such theories could aid the practi-
Specifically in the context of rehabilitation where skills tioner to understand the variables that affect motor skill
such as walking need to be retrained, the question arises: performance and through this provide a basis for effective
What is normal? The problem of redundancy in relation development and implementation of rehabilitation
to patients may be perceived as an advantage, since it strategies.
allows flexibility when the degrees of freedom are reduced.
However, it may also be associated with non-optimal
(mal)adaptive strategies limiting the efficiency/normality THEORIES OF MOTOR CONTROL
of the movement.
To study motor control is to appreciate the degrees of 1. Reflex theory: Reflexes are generally perceived as
freedom problem and the strategies the body, brain and stereotypical events where a specific stimulus leads
mind employ to overcome these problems. An additional to a specific response (i.e. when the patellar tendon
complication in the study of motor control arises from is tapped by a hammer, the lower leg extends). It is
the way that any movement may be initiated or con- now understood that reflexes are not as invariant as
trolled once commenced. Evidence supports the notion originally perceived, as the same sensory stimulus
of at least two types of control: (a) open loop or feed may produce a different behaviour depending on
forward which generally implies no sensory feedback; and the context and task. Sir Charles Sherrington sug-
(b) closed loop or feedback which has sensory feedback gested that reflexes are the building blocks of
as part of the controller system. complex behaviours. However, research on deaf-
Open-loop control systems encompass fast, ballistic ferented animals as well as humans has demon-
movements where no time is available to receive, extract strated that it is possible to control movement
and evaluate the sensory feedback resulting from the without sensory feedback.1,2 This does not under-
movement. In such a system it is assumed that sensory mine the importance of local reflex circuits, as we
information is absent; however, sensory information is know they are integrated into complex behaviour
conveyed to higher centres in the resting state providing and thus form an integral part of movement control.
relevant information about the position of the joints, 2. Hierarchical theory: Hughlings Jackson believed that
limbs and the individual as a whole in the environment. higher centres within the nervous system control
Without such knowledge, the nervous system would be the lower centres and a top-down approach governs
unable to correctly select the appropriate motor pro- all movement. It is now generally acknowledged
gramme to execute the desired movement. Furthermore, that although spinal reflexes are under the influence
42
 5  Motor Control and Motor Learning 43

of higher structures (e.g. modulation of reflexes programming theory is still the predominate theory of
during tasks), the sensory information that trig- motor control.6,7
gered the reflex is fed back to the higher centres In the following sections, several recent and new
that adjust their output. A multisegmental control aspects relating to motor control and motor learning will
exists where each level within the nervous system be presented that are intended to complement the exist-
can act on the other levels. ing knowledge. Motor control and motor learning can
3. Motor programming theory: According to Lashley a occur at cortical, subcortical and spinal levels, and sensory
motor program is ‘… a generalized schemata of information is often required for motor control and
action which determines the sequence of specific learning to occur. More specifically, three broad concepts
acts’.3 He spent his career searching for the place will be examined. (a) Sensory feedback from muscle,
within the cerebral cortex where the memory trace tendon and cutaneous receptors forms an integral part of
for movement resides and, demonstrated in seminal normal voluntary movement and is integrated with higher
laboratory experiments on rats, that memory (and levels of control. (b) Sensory feedback as part of a reflex
learning) was impaired in direct proportion to loop is not fixed and can be conditioned to allow improved
the degree of cerebral cortex destroyed.4,5 Richard voluntary control in both healthy and impaired popula-
Schmidt refined Lashley’s initial ideas by proposing tions. The necessity for higher-level input to allow these
a generalized motor programme that controls changes will be presented. (c) Sensory feedback from
classes of actions rather than individual movements. receptors forms an integral part, not only in the execution
For example, if a person writes their name using the of already learned movements, but as a key component
right or left hand, foot or even mouth, the general- in the relearning and acquisition of new motor skills fol-
ized motor programme allows one to perform these lowing a CNS insult or musculoskeletal injury.
tasks such that any person inspecting the written
word would recognize the person’s handwriting.
The generalized motor programme represents a SENSORY FEEDBACK AS AN INTEGRAL
pattern of a movement containing fixed elements PART OF MOTOR CONTROL
(invariant features such as relative time of phases of
a movement that remain the same from trial to trial) It has been known for a long time that proprioceptive
and flexible elements (parameters that are adjusted feedback contributes to the activation of muscles and thus
depending on the demands of the specific situation, the control of movement in both animals and humans.
e.g. the speed of a movement). During learning (or Proprioceptors encompass a group of sensory receptors,
relearning) of movement skills, the individual con- including muscle spindles, Golgi tendon organs, joint
siders four pieces of information to develop a and skin receptors, that convey knowledge about the
schema: (a) the initial conditions (start of the move- position of our limbs to the higher centres that integrate
ment); (b) the response parameters (speed, size, the acquired sensory information and select the correct
etc.); (c) sensory consequences of the movement; motor programme for task execution. Thus, even though
and (d) the response outcome. proprioceptive feedback may be too slow to adjust an
4. Dynamic systems theory: Nikolai Bernstein believed ongoing fast ballistic movement, such as a tennis serve,
that there is not one solution for one movement it is a necessary part of the initial motor planning. There-
problem, rather a movement pattern is produced as fore there are elements of feedforward and feedback
a function of the changing constraints placed upon control required in movement control.
it – these are the structural, environmental and task An example of this is when we pick up an object. In
constraints mentioned previously. Constraints act this case we are able to exert the correct force such that
as control parameters when they lead to any change the object is not crushed or slips from our hands. We are
in the movement. Control parameters (e.g. direc- able to determine the pre-controlled motor programme
tion, force, speed and perceptual information) are based on vision (for the opening of the hand to grip) and
variables that move the system (you) into a new prior experience allowing us to apply an initial force
attractor state. The acquisition of motor skills can (feedforward control) and then adjust this force based on
be seen as finding the optimum values accounting the immediate characteristics of the object itself (feed-
for control parameters (constraints) that will meet back control). When subjects grip large objects, they
the demand of the task for each individual. For apply more force than comparatively smaller objects of
example, following an injury to the lower leg, the the same weight, based on previous experience. Despite
patient will display a given gait pattern as a result this, subjects perceive the smaller object, of the same
of the constraints imposed on the system. The leg weight, as being heavier, but once the object is lifted, the
strength of the patient serves as a control parame- grip force is modified based on the characteristics of the
ter. As the leg of the patient becomes stronger there object itself. When an object with a rough lifting surface
are changes in the walking pattern meaning that the is lifted, it is gripped with less force than an object of the
increases in leg strength have caused a phase shift same mass but with a slippery surface. In addition, the
and a new gait (attractor state) self-organizes. force is modulated such that the object is gripped with a
Currently, the opinions on which theory will prevail are force slightly greater than the force in which the object
divided. Some contend that aspects of the motor pro- will be dropped (see Johnsson & Westling8 for a review).
gramme theory will be subsumed into the dynamic This is likely due to feedback mechanisms arising from
systems theory. However, at this point, the motor peripheral receptors in the hand. In these examples, both
44 PART II  Advances in Theory and Practice

feedforward and feedback control contribute to motor

planning and motor control. Under normal conditions, a
simple task such as picking up an object can be achieved
with little thought and concentration. When there is a
lack of feedback such as in patients with large fibre neu-
ropathy, and subsequently impaired movement control,
accuracy and adaptability to alterations in the environ-
mental constraints are diminished.9,10 However, some
degree of movement persists in these patients even in the
absence of visual feedback (often used as a compensatory
mechanism). Rothwell et al.10 investigated a patient with
impaired sensory control, largely confined to the sensory
fibres, and noted that the patient may retain the ability
to produce different levels of force when asked.10 The
patient was as accurate as normal subjects when perform-
ing fast ballistic movements of the thumb, although only
when he had received prior training using visual feed-
back. In addition, since the patient was not successful at
everyday living tasks (e.g. holding objects such as pens,
cups, coins, buttoning his shirt, judging weights of objects
if his eyes were closed), it is questionable whether he
would have been able to perform as well on such ballistic
movements if the environmental constraints were altered.
FIGURE 5-1  ■  The actuator system developed by Andersen and
Sinkjær is attached to the subject via specialized casts. The
SENSORY FEEDBACK DURING subject can move his/her ankle joint freely and the actuator can
LOCOMOTION be programmed to suddenly extend or flex the ankle joint at any
time during the gait cycle.
During walking, sensory feedback from muscle receptors
and tendon organs is required for (a) normal movement
control and (b) generating appropriate reactions follow- step cycle to the next (Fig. 5-3A). These small adjust-
ing an unexpected disturbance such as an obstacle or ments do not result in a synchronized reflex response,
uneven ground surface. Many studies investigating but rather in small enhancements or reductions in the
sensory feedback in humans use electrical stimulation and EMG signal of the SOL (Fig. 5-3B). It became evident
base conclusions on motor control and motor learning that group Ia afferents are responsible for the increased
on the reaction of the muscle following this. However, muscle activity during slight dorsiflexion enhancements
electrically stimulating the muscle is not representative imposed such as occurs when walking up an incline,17
of a true ‘physiological’ stimulus. Sinkjær and colleagues11 whereas group II afferents are the main contributors to
created a specialized actuator system that mechanically the decrements in activity seen during the imposed
stretches the ankle joint, allowing the assessment of reduction movements.18
motor control and motor learning following a ‘physio- As we have just described how homonymous feedback
logical’ stretch of the muscle during walking. contributes to the activation of the muscle itself during
This actuator (Fig. 5-1)11 was attached to the ankle walking, likewise, following an unexpected disturbance,
joint of subjects in such a way that they could walk proprioceptive feedback is used to adjust the activity of
freely. When a sudden plantarflexion movement was the muscle(s) of the same limb,15,19 opposite limb,20–23 and
applied during the stance phase of gait, thus unloading between lower and upper limbs.24 This mechanism allows
the soleus (SOL) muscle, the electromyographic (EMG) the body to make the necessary adjustments enabling the
activity of the SOL was significantly reduced (Fig. 5-2B) body to remain upright (and not fall).
while there was no effect on the antagonist tibialis ante- It is well known that afferent feedback produces inter-
rior (Fig. 5.2C).12 This was the first indication that limb reflexes that are relevant for postural stability.25 For
sensory feedback arising from tendon organs or muscle instance, when a unilateral rotation of the hip or knee
afferents forms part of the normal activation of that joint is imposed during walking, bilateral responses in the
muscle, up to 50% depending on the phase of the gait leg muscles are observed. It was suggested that the
cycle. Subsequent publications from that group provided purpose of these responses is to restore normal physio-
further conclusive evidence to show that force-sensitive logical movement following the perturbation.26 Studies
feedback from group Ib afferents contributes to the involving other unilateral perturbations, such as treadmill
normal locomotor muscle activity during the stance acceleration or deceleration (while one leg is on the
phase of walking.13–16 This group also investigated the treadmill) or peripheral nerve electrical stimulation, have
role of small changes in the ankle angle. Using the unique reported bilateral muscle responses that are specific to
actuator system, small enhancements and reductions of the type of perturbation and dependent on when the
the ankle joint may be imposed that are within the natural perturbation occurs during the gait cycle.27 Functionality
variability of the ankle angular movements from one is often inferred based on the observations in the EMG
 5  Motor Control and Motor Learning 45

10
Position (Deg) Normal step
5 Imposed reduction
Imposed enhancement
0

–5

–10

–15

–20
5°
–25
A 200 ms
A
70
Soleus EMG (µV)
60

50

40 20 µV

30 200 ms

20

10

0
B

180
Anterior tibialis EMG (µV) B
160
140 FIGURE 5-3  ■  (A) The position of the ankle joint under normal
(black trace), sudden imposed reduction (light grey trace) or
120 enhancement (dark grey trace). (B) The resulting electromyo-
100 graphic activity of the soleus shows no reflex response but
rather reduced or enhanced activity.
80
60
We have observed that the stimulation of the tibial
40
nerve of one leg (at the popliteal fossa) at the end of
20 the swing phase, elicited a facilitatory response in
0 the contralateral gastrocnemius lateralis (Fig. 5-4A).22
–200 –100 0 100 200 300 400 500 600
Recordings from pressure-sensitive insoles inserted into
Time (ms)
C the shoe of the subject revealed that this response elicited
FIGURE 5-2  ■  (A) The position of the ankle joint under normal a shift of the CoP under the contralateral foot toward the
(thick trace) and sudden plantarflexion (thin trace) conditions medial and anterior direction (Fig. 5.4B and C), and
during walking. The resulting electromyographic activity of the consequently increased the pressure at the level of the
(B) soleus and (C) tibialis anterior. first metatarsal head. The stance phase of the stimulated
leg was significantly shorter in the step following the
stimulation. The crossed responses observed in the
triceps surae might therefore be a method to accelerate
activity; however, the reflex action on the basis of muscle the propulsion phase of the contralateral leg and prepare
activity and actual joint function may not be correlated. it for a faster step in the event that the stimulated leg is
To alleviate this, studies further investigate the kinemat- not able to sustain the body. This result provides direct
ics and kinetics following joint perturbations and again evidence of the role of interlimb reflexes in postural
infer function and dysfunction from these. However, control and dynamic stability.
most of these studies lack relevance to current clinical Afferent feedback and its role within reflex pathways
practice and are therefore inaccessible to many clinicians. was for a long time considered to be non-modifiable.
Recently, we have applied a novel method to investigate Thus, although afferent feedback is modulated during
changes in the centre of pressure (CoP) after evoking different tasks, it was thought that all conditions being
interlimb reflexes. These measures are frequently used in equal, the response observed would be similar in latency
clinics to evaluate balance and postural control28 and and magnitude. It was through some observations on
therefore increase relevance of this type of research to animals by Di Gorgio29,30 that led Wolpaw and col-
the clinician and clinical populations. leagues31 to the idea that reflex pathways could be trained
46 PART II  Advances in Theory and Practice

200 control subjects and patients with spinal cord injuries,

and showed that in humans, as in animals, the H-reflex
cGL sEMG (mV)

150 pathway could be altered.34 The alterations in the H-reflex

Swing phase
size also lead to functionally beneficial alterations in the
100 modulation of the SOL activity during dynamic activities
in both the healthy and individuals with spinal cord in-
50 juries.34,35 This latter result is of particular importance
when considering the role that reflexes have during
0
A 0 10 60 70 80 90 100 dynamic movements (as outlined in the previous section).
Here, reflexes not only contribute to the overall stiffness
50 of a joint, but their function changes dynamically
CoP displacement (mm)

throughout activities such as walking, running and sprint-

Lateral
45 ing. For example, the ankle extensors are stretched under
Swing phase

the weight of the body during the stance phase of loco-

40 motion and the stretch reflex may assist the force produc-
tion during this phase. The muscles are also stretched

Medial
35
during the early swing phase, and without suppression of
30 this reflex, the stretch reflex could extend the ankle and
may cause foot drop.36–39 Appropriate phase-dependent
0 10 60 70 80 90 100 modulation of spinal reflexes is thus necessary during
B
dynamic tasks. Training these reflexes as described above,
200
is a completely novel approach as a possible therapeutic
CoP displacement (mm)

intervention in humans, despite 30 years of successful

Anterior

animal studies.32,40–43
Swing phase

150 Recent studies have investigated whether it is possible

to also condition the stretch reflex of the SOL, as shown
Posterior

100 for the human biceps brachii muscle.44–46 This stretch

reflex is more ‘physiological’ when compared to the elec-
trically evoked H-reflex. In particular, this work evalu-
50
ated whether the alteration in the size of the stretch reflex
0 10 60 70 80 90 100 has functional implications for healthy subjects. The pro-
C Time (% ipsilateral gait cycle) tocol of this work is depicted in Figure 5-5. Ankle dorsi-
FIGURE 5-4  ■  Gastrocnemius lateralis EMG (A), centre of pres- flexion movements were imposed using a unique ankle
sure (CoP) displacement under the contralateral foot in the perturbator while the subjects were seated (Fig. 5-6A).
medial–lateral (B) and in the anterior–posterior direction (C) for The activity of the SOL was quantified by the amount of
n = 1 subject. Grey and black traces indicate data when a stimu-
lation occurred and the control condition (no stimulation) EMG (bottom trace of Fig. 5-5). Generally, three bursts
respectively. After the stimulation, indicated by the dashed of activity can be visualized that are termed the short-,
black line, a short-latency facilitation was observed in the gas- medium- and long-latency reflex (or M1, M2 and M3 in
trocnemius EMG, followed by a medial anterior shift of the CoP. some studies). After six baseline sections, subjects were
The onset of the shift in CoP is indicated by the dashed 
grey line.
required to either up- or down-condition the short-
latency component in the following 24 conditioning ses-
sions (Fig. 5-6). A screen placed in front of the subject
and that the spinal cord, much like the brain, was capable provided visual feedback (shown as bars) relating to the
of learning. activity level of the SOL and the size of the SOL stretch
reflex following each imposed ankle dorsiflexion stretch
(Fig. 5-6B). The shaded areas in the figure represent the
SENSORY FEEDBACK AS PART OF A window in which the SOL background activity and the
REFLEX LOOP IS NOT STEREOTYPED stretch reflex size must be maintained by the subject.
During control trials, this area is set as large as possible
Wolpaw and colleagues (see Wolpaw32 for a review) have as the subject is not training to modify the size. For a
demonstrated that training of a simple reflex pathway, successful conditioning trial, the bar is depicted as green
such as the electrically evoked H-reflex, in animal prepa- while unsuccessful trials result in a red bar.
rations, can significantly alter the response to the stimu- Following up-conditioning, the size of the SOL stretch
lus – either increasing or decreasing the reflex depending reflex is significantly enhanced while it is significantly
on the protocol implemented. This is accompanied by decreased following down-conditioning (Fig. 5-6B).
significant alterations in function as observed in lesioned Importantly, this alteration also led to modifications in
animals.32 For example, when the H-reflex was down- tasks unrelated to the training. For example, subjects
conditioned, such that over time the reflex excitability were asked to perform drop jumps from a 30 cm height,
was trained to decrease, the activity of the SOL during landing on one foot and the excursion of the
locomotion was reduced, whereas when it is up- CoP was quantified (Fig. 5-7). Subjects trained to
conditioned the activity was increased.33 In 2009, Wolpaw up-condition the SOL stretch reflex decreased their CoP
and colleagues applied this type of training to healthy excursion from touchdown for a duration of 1 minute.
 Baseline Conditioning
Sessions

B C C
1 1 24

Trials Mmax 75 conditioned 75 conditioned 75 conditioned Mmax

stretch reflexes stretch reflexes stretch reflexes

600
Rectified EMG (uV)

Single Trial
400

200

0
0 50 100
Time after stretch (ms)
FIGURE 5-5  ■  The protocol. Subjects attend six baseline sessions during which they are exposed to 245 single trials consisting of
imposed ankle dorsiflexion movements. They only receive feedback on the background level of soleus activity which they maintain
at approximately 5% of the maximum activation. In the following 24 sessions, subjects are conditioned to either increase (up-condition)
or decrease (down-condition) the size of the soleus stretch reflex following the imposed ankle dorsiflexions. The activity of the
soleus muscle following a single imposed dorsiflexion is depicted in the lower trace. Several peaks may be seen that are separated
by the vertical dashed lines. Subjects receive feedback on only the first burst.

Control stretch reflex Stretch reflex

Trial: 15

Abs size (µV)

Background EMG Stretch reflex Up
success
Abs size (µV)
EMG (µV)

Stretch reflex
up-conditioning

Stretch reflex
Abs size (µV)

Success rate: 100% Up

failure

Conditioned stretch reflex

Stretch reflex
Trial: 72
Abs size (µV)

Background EMG
Down
success
EMG (µV)

Stretch reflex
down-conditioning

Stretch reflex

Success rate: 66.67%

Abs size (µV)

Down
failure

A B
FIGURE 5-6  ■  (A) The unique ankle perturbator. Subjects are seated comfortably with both feet on separate foot plates. The enlarged
figure on the left visualizes the foot position and fixation. A screen placed in front of the subject provides feedback to the subject
relating to both the activity level of the soleus muscle as well as on the size of the soleus stretch reflex following each imposed
ankle dorsiflexion. (B) The visual feedback on the screen is comprised of two parts, the background EMG and the stretch reflex size
both shown as bars. The shaded areas represent the window in which the soleus background activity and the stretch reflex size
must be maintained by the subject. During control trials, this area is set as large as possible since the subject is not training to
modify the size. During up-conditioning trials, this area is above a criterion level based on the baseline sessions while for the down-
conditioning trials it is below this criterion level. When the subject has a successful conditioning trial, the bar is depicted as green
(light grey in the figure) while unsuccessful trials result in a red (dark grey in the figure) bar. This provides for immediate feedback
to the subject for each single trial performed.
48 PART II  Advances in Theory and Practice

Pre up-conditioning
Post up-conditioning

200 µV

20 ms

Pre down-conditioning
Post down-conditioning

50

40
Anterior–posterior CoP displacement (mm)

30

20

Pre up-conditioning
10 Post up-conditioning

–10

–20

–30
–30 –20 –10 0 10 20 30
C Medio-lateral CoP displacement (mm)
FIGURE 5-7  ■  (A) The soleus stretch reflex prior to (black trace) and following (grey trace) 24 sessions of up-conditioning. The grey
shaded area represents the duration of the short-latency component of the soleus stretch reflex which was the target for the con-
ditioning, (B) as in (A) but following 24 sessions of down-conditioning. (C) Excursions of the centre of pressure (CoP) during landing
on one leg from a height of 50 cm. Data are the best of three trials in n = 1 prior to (black trace) and following (grey trace)
up-conditioning.
 5  Motor Control and Motor Learning 49

This indicates an improved balance control. The func- neurofeedback methods allow the user to control his/her
tional benefits from conditioning the H-reflex and the own brain activity by using immediate visual feedback on
stretch reflex continue to be explored. The indications their respective brain state (by electroencephalographic
are strong that this type of intervention can provide [EEG] recordings). EEG activity of the user is measured
an alternative strategy for improved motor control continuously while he/she imagines performing a specific
following musculoskeletal injury. However, despite the task (also called motor imagery) that normally leads to a
success of conditioning reflexes in both human and painful sensation (e.g. reaching movement if the condi-
animal studies, exact mechanisms causing up- and down- tion is lateral epicondylalgia). During motor imagery, the
regulation are unknown and more research is required to brain activity is shown to the user via a screen and he/she
investigate the underlying neural mechanisms involved. is instructed to control specific brain waves known to be
altered during the experience of pain as a form of mal-
adaptive plasticity. The correct level of brain activation
SENSORY FEEDBACK IS A KEY is rewarded in two ways: (a) the user receives immediate
positive visual feedback on their performance; and (b)
COMPONENT IN MOTOR (RE)LEARNING pain sensation is reduced. Thus neurofeedback may
Chronic Pain States reverse maladaptive plasticity as the user learns to modu-
late his/her brain activity.
The mechanisms of chronic musculoskeletal pain are not In order to successfully use neurofeedback methods, it
fully understood, and thus management of chronic mus- is imperative to understand which signals are affected
culoskeletal pain is often sub-optimal. One of the reasons during chronic musculoskeletal pain. Studies investigat-
for such a mismatch is the fact that facilitations in the ing EEG oscillations in central neuropathic pain56,57 and
CNS pain mechanisms are not accounted for. CNS struc- musculoskeletal pain58 have been restricted to resting
tures play a key role in the development and experience state EEG or motor imagery. However, the effect on the
of chronic pain resulting from conditions (e.g. lateral EEG waves when the person is performing the task may
epicondylalgia).47 Human pain models have been devel- be different. In addition, motor imagery can enhance
oped to mimic chronic pain states and we now know that pain and thus may not be as useful when treating patients
significant maladaptive plasticity (i.e. negative alterations with chronic pain resulting from musculoskeletal prob-
in the connections within the brain) occurs in a chronic lems such as lateral epicondylalgia. Performing the move-
musculoskeletal pain state. This may detrimentally alter ment may in these cases be more appropriate.
motor control affecting the activation of the CNS.48–50
Imaging studies51,52 have contributed to the localization
of brain areas affected by pain and those that are altered
Central Nervous System Lesions
through application of treatments. However, these tech- The Hebbian rule of associativity has also been applied
niques often have a poor temporal resolution, require to retrain patients following a CNS lesion. For instance,
large and expensive equipment and confine the patient to chronic stroke patients were asked to attempt a simple
a restricted environment such that occurrence of pain dorsiflexion movement of the ankle joint and the related
under dynamic conditions cannot be investigated. A electrical activity over the motor cortex was recorded
recent review highlighted several non-pharmacological using scalp electrodes.59 The signal in this case is charac-
treatments designed to restore normal brain function terized by a slow negative potential (Fig. 5-7), termed
concomitantly with a reduction of chronic pain.53 These movement-related cortical potential, which is generated
include repetitive transcranial magnetic stimulation, in every movement or imagined movement, though in
transcranial direct current stimulation and neurofeed- the latter case it is of smaller amplitude. It has been
back. The central idea behind restoring brain activity shown that when a peripheral stimulus is timed such that
patterns is to avoid maladaptive alterations that may lead the afferent volley (the sensory feedback) arrives during
to secondary problems (i.e. altered movement patterns the peak negative phase, which, represents the time of
when performing a task that will induce pain in other movement onset, plasticity is induced. Thus in both
areas thus adding to the problem rather than relieving it). healthy60,61 and chronic stroke patients,59 the pairing of
In order to retrain the brain and induce a relearning motor attempt or imagination and peripheral nerve stim-
of the correct movement patterns (and thereby reverse ulation lead to significant enhancements in the output
maladaptive cortical reorganization), the mechanisms of motor cortex to the target muscle, as assessed by
behind learning need to be satisfied. The current belief changes in the amplitude of the motor evoked potential
is that plasticity can only be induced appropriately if the following non-invasive transcranial magnetic stimulation
relevant neural structures are activated in a correlated (TMS). In chronic stroke patients, an enhancement in
manner (‘neurons that fire together, wire together’).54 As dynamic task performance such as walking speed and foot
such, any treatment targeting the final output stage of the tapping frequency accompanies the alterations in motor
brain to activate the muscles that produce the movement evoked potential size59 (Fig. 5-8)
(e.g. the motor cortex) must be designed so that the A recent study investigated if task imagination can be
correct temporal activation is satisfied. Repetitive trans­ temporally combined with afferent information gener-
cranial magnetic stimulation and transcranial direct ated by a passive movement to alter M1 output.62 Thus,
current stimulation have a poor spatial target resolution in this case, both the peripheral input and the central
such that many brain areas surrounding the target area command are generated by a physiological activation of
are activated upon stimulation.55 On the contrary, the relevant neural structures. Subjects were asked to
50 PART II  Advances in Theory and Practice

Execution of dorsiflexion combined with modalities that have a central component

movement and require the patient’s conscious attention are more
successful at inducing permanent improvements in func-
tion compared to any single method applied alone.64–67

10 µV CONCLUSIONS
A 1s Motor learning and control is a complex topic and many
studies are being conducted to induce motor learning and
improve motor control. Although previous research has
investigated simple movements with non-physiological
Imagination of dorsiflexion
stimuli, with the advent of more sophisticated technolo-
movement gies for the assessment and interpretation of movement,
we are now moving into the realm in which more complex
movements are being altered or retrained for longer
periods of time. This will therefore have implications in
rehabilitation, motor learning and motor unlearning (in
the case where people have adapted pathologically fol-
lowing an injury). Due to the number of methods used
to induce motor learning and assess motor control, it is
Peak negativity
difficult to know which is best and if one should be used
B indicating task onset preferentially over another. The limits of the clinical
setting, the abilities and preferences of the patient as well
FIGURE 5-8  ■  Scalp recordings over the vertex using non-
invasive electrodes. The movement-related cortical potential as the knowledge and skills of the clinician will dictate
during (A) execution and (B) imagination of a simple dorsiflex- the most feasible treatment regimen. When is it best to
ion task. The most negative peak, signals the onset of task treat the patient? What is the optimal dosage for maximal
execution (vertical dashed line). Data are the average of 50 benefit? Will the effects be maintained for weeks, months
consecutive trials in n = 1.
or permanently following the intervention? When is the
neural system most capable of recovery? What medica-
self-select when to imagine the task which was detected tion should be taken/avoided to assist in motor learning?
by a computerized algorithm. Once the algorithm A lot of these questions require long-term studies using
detected that a movement was being imagined, it trig- clinical trials that are both time consuming and expen-
gered a motorized orthotic device that passively moved sive. Further research and larger clinical trials are required
the joint as if the movement had been executed rather to consolidate and disseminate the research that has been
than imagined. The detection accuracy of the algorithm and continues to be conducted in this area.
was approximately 73%, thus not all imagined trials
resulted in a subsequent movement by the orthosis; yet
the motor evoked potential increased significantly fol- REFERENCES
lowing only 50 imaginations and remained enhanced 30 1. Grillner S. Locomotion in vertebrates: central mechanisms and
minutes after the cessation of the intervention. The study reflex interaction. Physiol Rev 1975;55(2):247–304.
2. Pearson KG, Misiaszek JE, Hulliger M. Chemical ablation of
thus demonstrates that significant learning is possible sensory afferents in the walking system of the cat abolishes the
even if the correlation between two inputs is not always capacity for functional recovery after peripheral nerve lesions. Exp
given. The question arises: How many correlated repeti- Brain Res 2003;150(1):50–60.
tions are required to ensure long-term potentiation 3. Lashley K. The problem of serial order in behaviour. In: Jeffress
LA, editor. Cerebral Mechanisms in Behaviour. New York: Wiley;
(LTP)-like changes are induced? This is not an easy 1951. p. 112–31.
question as a variety of protocols have been implemented 4. Franz SI, Lashley KS. The retention of habits by the rat after
and these lack consistency in, amongst other things, destruction of the frontal portion of the cerebrum. Psychobiol
parameters such as the number of repetitions (for a 1917;1(1):3–18.
review see Ziemann et  al.63). These may be beneficial in 5. Passingham RE, Stephan KE, Kotter R. The anatomical basis of
functional localisation in the cortex. Nat Rev Neurosci
subjects with musculoskeletal conditions that lack the 2002;3(8):606–16.
strength to perform a movement properly. 6. Li KY. Examining contemporary motor control theories from the
Nevertheless, the most recent studies imply that affer- perspective of degrees of freedom. Aust Occup Ther J 2013;60(2):
ent input in combination with central commands either 138–43.
7. Magill R, Anderson D. Motor Learning and Control: Concepts and
elicited naturally or through artificial means, lead to Applications. 10th ed. Singapore: McGraw-Hill Education; 2011.
motor learning. This is not to infer that techniques using 8. Johnsson R, Westling G. Afferent signals during manipulative tasks
either only afferent feedback (e.g. functional electrical in humans. In: O Franzen JW, editor. Information Processing in
stimulation, dual motor point stimulation) or central the Somatosensory System. Macmillan Press; 1991. p. 25–48.
input (e.g. repetitive transcranial magnetic stimulation, 9. Sanes JN, Mauritz KH, Evarts EV, et al. Motor deficits in patients
with large-fibre sensory neuropathy. Proc Natl Acad Sci U S A
theta burst stimulation) have no effect on plasticity. 1984;81(3):979–82.
However, in the past few years, clinical trials suggest that 10. Rothwell JC, Traub MM, Day BL, et al. Manual motor perfor-
a multimodal approach where afferent feedback is mance in a deafferented man. Brain 1982;105(Pt 3):515–42.
 5  Motor Control and Motor Learning 51

11. Andersen JB, Sinkjær T. An actuator system for investigating elec- 36. Capaday C, Stein RB. Difference in the amplitude of the human
trophysiological and biomechanical features around the human soleus H reflex during walking and running. J Physiol 1987;392:
ankle joint during gait. IEEE Trans Rehabil Eng 1995;3(4): 513–22.
299–306. 37. Capaday C, Stein RB. Amplitude modulation of the soleus H-reflex
12. Sinkjær T, Andersen JB, Ladouceur M, et al. Major role for sensory in the human during walking and standing. J Neurosci 1986;6(5):
feedback in soleus EMG activity in the stance phase of walking in 1308–13.
man. J Physiol 2000;523(Pt 3):817–27. 38. Schneider C, Lavoie BA, Capaday C. On the origin of the soleus
13. Mazzaro N, Grey MJ, Sinkjær T, et al. Lack of on-going adapta- H-reflex modulation pattern during human walking and its task-
tions in the soleus muscle activity during walking in patients dependent differences. J Neurophysiol 2000;83(5):2881–90.
affected by large-fibre neuropathy. J Neurophysiol 2005;93(6): 39. Nielsen JF, Andersen JB, Barbeau H, et al. Input-output properties
3075–85. of the soleus stretch reflex in spastic stroke patients and healthy
14. Grey MJ, Nielsen JB, Mazzaro N, et al. Positive force feedback in subjects during walking. Neurorehabilitation 1998;10:151–66.
human walking. J Physiol 2007;581(1):99–105. 40. Wolpaw JR. Operant conditioning of primate spinal reflexes: the
15. af Klint R, Cronin NJ, Ishikawa M, et al. Afferent contribution to H-reflex. J Neurophysiol 1987;57(2):443–59.
locomotor muscle activity during unconstrained overground human 41. Wolpaw JR, O’Keefe JA. Adaptive plasticity in the primate spinal
walking: an analysis of triceps surae muscle fascicles. J Neuro- stretch reflex: evidence for a two-phase process. J Neurosci
physiol 2010;103(3):1262–74. 1984;4(11):2718–24.
16. af Klint R, Mazzaro N, Nielsen JB, et al. Load rather than length 42. Chen XY, Wolpaw JR. Operant conditioning of H-reflex in freely
sensitive feedback contributes to soleus muscle activity during moving rats. J Neurophysiol 1995;73(1):411–15.
human treadmill walking. J Neurophysiol 2010;103(5):2747–56. 43. Wolpaw JR, Lee CL. Memory traces in primate spinal cord pro-
17. Mazzaro N, Grey MJ, Sinkjær T. Contribution of afferent feedback duced by operant conditioning of H-reflex. J Neurophysiol
to the soleus muscle activity during human locomotion. J Neuro- 1989;61(3):563–72.
physiol 2005;93(1):167–77. 44. Wolf SL, Segal RL. Conditioning of the spinal stretch reflex: impli-
18. Mazzaro N, Grey M, do Nascimento O, et al. Afferent-mediated cations for rehabilitation. Phys Ther 1990;70(10):652–6.
modulation of the soleus muscle activity during the stance phase of 45. Segal RL, Wolf SL, Catlin PA, et al. Uncoupling of human short
human walking. Exp Brain Res 2006;173(4):713–23. and long latency stretch reflex responses with operant conditioning.
19. af Klint R, Nielsen JB, Cole J, et al. Within-step modulation of leg Restor Neurol Neurosci 2000;17(1):17–22.
muscle activity by afferent feedback in human walking. J Physiol 46. Wolf SL, Segal RL. Reducing human biceps brachii spinal stretch
2008;586(19):4643–8. reflex magnitude. J Neurophysiol 1996;75(4):1637–46.
20. Stubbs PW, Mrachacz-Kersting N. Short-latency crossed inhibi- 47. Coombes BK, Bisset L, Vicenzino B. A new integrative model of
tory responses in the human soleus muscle. J Neurophysiol lateral epicondylalgia. Br J Sports Med 2009;43(4):252–8.
2009;102(6):3596–605. 48. Schabrun SM, Jones E, Kloster J, et al. Temporal association
21. Stubbs PW, Nielsen JF, Sinkjær T, et al. Phase modulation of the between changes in primary sensory cortex and corticomotor
short-latency crossed spinal response in the human soleus muscle. output during muscle pain. Neuroscience 2013;235:159–64.
J Neurophysiol 2011;105(2):503–11. 49. Schabrun SM, Hodges PW. Muscle pain differentially modulates
22. Gervasio S, Farina D, Sinkjær T, et al. Crossed reflex reversal short interval intracortical inhibition and intracortical facilitation
during human locomotion. J Neurophysiol 2013;109(9):2335–44. in primary motor cortex. J Pain 2012;13(2):187–94.
23. Stevenson AJ, Geertsen SS, Andersen JB, et al. Interlimb commu- 50. Graven-Nielsen T, Arendt-Nielsen L. Assessment of mechanisms
nication to the knee flexors during walking in humans. J Physiol in localised and widespread musculoskeletal pain. Nat Rev Rheu-
2013;591(Pt 19):4921–35. matol 2010;6(10):599–606.
24. Zehr EP, Haridas C. Modulation of cutaneous reflexes in arm 51. Wiech K, Preissl H, Birbaumer N. Neuroimaging of chronic pain:
muscles during walking: further evidence of similar control mecha- phantom limb and musculoskeletal pain. Scand J Rheumatol Suppl
nisms for rhythmic human arm and leg movements. Exp Brain Res 2000;113:13–18.
2003;149(2):260–6. 52. Wiech K, Preissl H, Birbaumer N. [Neural networks and pain
25. Dietz V. Do human bipeds use quadrupedal coordination? Trends processing. New insights from imaging techniques]. Anaesthesist
Neurosci 2002;25(9):462–7. 2001;50(1):2–12.
26. Dietz V, Colombo G, Muller R. Single joint perturbation during 53. Jensen MP, Hakimian S, Sherlin LH, et al. New insights into neu-
gait: neuronal control of movement trajectory. Exp Brain Res romodulatory approaches for the treatment of pain. J Pain 2008;
2004;158(3):308–16. 9(3):193–9.
27. Berger W, Dietz V, Quintern J. Corrective reactions to stumbling 54. Hebb DO. The Organisation of Behaviour: A Neuropsychological
in man: Neuronal co-ordination of bilateral leg muscle activity Theory. Mahwah, NJ: Lawrence Erlbaum Associates Inc; 1949.
during gait. J Physiol 1984;357:109–25. 55. Lontis ER, Voigt M, Strujik JJ. Focality assessment in transcranial
28. Palmieri R, Ingersoll C, Stone M, et al. Centre-of-pressure param- magnetic stimulation with double and cone coils. J Clin Neuro-
eters used in the assessment of postural control. J Sport Rehabil physiol 2006;23(5):462–71.
2002;11:51–66. 56. Vuckovic A, Hasan MA, Fraser M, et al. Dynamic oscillatory sig-
29. DiGiorgio A. Azione del cervelletto-neocerebellum-sul tono pos- natures of central neuropathic pain in spinal cord injury. J Pain
turale degli arti e localizzazioni cerebellari dell’animale rombence- 2014;15(6):645–55.
falico. Arch Fisiol 1942;42:25–79. 57. Michels L, Moazami-Goudarzi M, Jeanmonod D. Correlations
30. DiGiorgio A. Persistenza nell’animale spinale, di asymmetrie pos- between EEG and clinical outcome in chronic neuropathic pain:
turali e motorie di origine cerebellare: I, II, III. Arch Fisiol 1929; surgical effects and treatment resistance. Brain Imaging Behav
27:518–80. 2011;5(4):329–48.
31. Wolpaw JR. Activity-dependent spinal cord plasticity in health and 58. Chang PF, Arendt-Nielsen L, Graven-Nielsen T, et al. Psycho-
disease. Annu Rev Neurosci 2001;24(1):807–43. physical and EEG responses to repeated experimental muscle pain
32. Wolpaw JR. Spinal cord plasticity in acquisition and maintenance in humans: pain intensity encodes EEG activity. Brain Res Bull
of motor skills. Acta Physiol 2007;189(2):155–69. 2003;59(6):533–43.
33. Chen Y, Chen XY, Jakeman LB, et al. The interaction of a new 59. Mrachacz-Kersting N, Niazi IK, Jiang N, et al. A novel brain-
motor skill and an old one: H-reflex conditioning and locomotion computer interface for chronic stroke patients. ICNR Conference,
in rats. J Neurosci 2005;25(29):6898–906. Nov 2012; Toledo, Spain, 2012.
34. Thompson AK, Chen XY, Wolpaw JR. Acquisition of a simple 60. Mrachacz-Kersting N, Kristensen SR, Niazi IK, et al. Precise tem-
motor skill: Task-dependent adaptation plus long-term change in poral association between cortical potentials evoked by motor
the human soleus H-reflex. J Neurosci 2009;29(18):5784–92. imagination and afference induces cortical plasticity. J Physiol
35. Thompson A, Abel BM, Wolpaw JR. Soleus H-reflex modulation 2012;590(Pt 7):1669–82.
during locomotion in people with chronic incomplete spinal cord 61. Niazi IK, Mrachacz-Kersting N, Jiang N, et al. Peripheral electri-
injury. Abstract Viewer/Itinerary Planner. San Diego: Society for cal stimulation triggered by self-paced detection of motor intention
Neuroscience; 2010. Online.; San Diego 2010 p. Program Number enhances motor evoked potentials. IEEE Trans Neural Syst Rehabil
82.11. Eng 2012;20(4):595–604.
52 PART II  Advances in Theory and Practice

62. Xu R, Jiang N, Mrachacz-Kersting N, et al. An EEG controlled 65. Turner DL, Murguialday AR, Birbaumer N, et al. Neurophysiol-
motorised ankle-foot orthosis induces neural plasticity with minimal ogy of robot-mediated training and therapy: A perspective for
training. IEEE Trans Biomed Eng 2014;61(7):2092–101. future use in clinical populations. Front Neurol 2013;4.
63. Ziemann U, Paulus W, Nitsche MA, et al. Consensus: Motor cortex 66. Hubli M, Dietz V. The physiological basis of neurorehabilitation–
plasticity protocols. Brain Stimulation 2008;1(3):164–82. locomotor training after spinal cord injury. J Neuroengineering
64. Daly JJ, Zimbelman J, Roenigk KL, et al. Recovery of coordinated Rehabil 2013;10:5.
gait: Randomized controlled stroke trial of functional electrical 67. Belda-Lois JM, Mena-del HS, Bermejo-Bosch I, et al. Rehabilita-
stimulation (FES) versus no FES, with weight-supported treadmill tion of gait after stroke: a review towards a top-down approach.
and over-ground training. Neurorehabil Neural Repair 2011; J Neuroeng Rehabil 2011;8:66.
25(7):588–96.
 CHAPTER 6 

Interaction Between Pain and

Sensorimotor Control
Paul Hodges  •  Deborah Falla

interpretation of the position and movement of the body,

INTRODUCTION features of the environment, and the body’s interaction
with the environment. It includes all of the central pro-
Changes in sensorimotor control are an almost obliga- cessing involved in interpretation of motor requirements,
tory feature of musculoskeletal conditions. Evidence for planning of appropriate responses and interpretation of
modification of motor and/or sensory functions has been the success of output. This interaction between input,
reported for a broad array of conditions, and these output and processing is impacted by emotions, experi-
changes have become common targets for rehabilitation. ences and context, which is particularly pertinent to
It has been assumed that sensorimotor changes are rel- consider when attempts are made to understand the func-
evant for the development, perpetuation or recurrence tion of the sensorimotor system in a person experiencing
of pain and/or injury. It is timely to reflect on this pain. As a consequence of the breadth and scope of sen-
assumption. sorimotor control it is somewhat overwhelming to con-
Current evidence suggests that sensorimotor changes sider, in a patient sitting in front of you, how and where
may be both a cause and a consequence of pain and/or the sensorimotor system might be modified, whether this
injury, and the relevance of these changes for symptoms can be changed, and where to start. A starting point is
varies between individuals. For some it may be a major to consider the nature of the presenting sensorimotor
factor and the key target for treatment, whereas for change (e.g. poor ability to detect motion or inability to
others it may be an epiphenomenon (i.e. present, but activate a muscle) and then, in combination with an
without impact on the clinical condition). Although early understanding of optimal sensorimotor control and clini-
theories proposed stereotypical changes in sensorimotor cal reasoning, build a clinical hypothesis to explain the
function, it is apparent that individual variation is a patient’s presentation.
characteristic of most musculoskeletal conditions. This Out of the complexity of sensorimotor control arise
is observed in experimental conditions1–3 and in the several key issues that are particularly relevant when
identification of subgroups in clinical practice.4,5 The addressing musculoskeletal conditions (Box 6-1). A first
aim of this chapter is to present the state-of-the-art principle is that movements generally involve compo-
understanding of sensorimotor control and to review nents that are task directed and components that are
how and why it changes in musculoskeletal conditions. postural, but the relative importance varies between func-
This requires consideration of an overarching theory to tions.7,8 When throwing a ball, the arm action to propel
explain sensorimotor dysfunction to aid conceptualiza- the ball requires postural control of the axioscapular
tion of the relevance of sensorimotor control for pain region and trunk as both a stable base for the limb muscles
and recovery. to generate torque as well as to maintain orientation of
the segments with respect to each other, and of the body
with respect to gravity/environment. The division
between postural and task-orientated elements of move-
SENSORIMOTOR DYSFUNCTION IN ment can be blurred;9 in running, activity of the trunk
muscles is necessary for progression through space and
MUSCULOSKELETAL PAIN postural control. Pain could impact on the task-directed
Sensorimotor Control or postural component, or both.
A second key principle is that function requires a
Sensorimotor control refers to all of the sensory and balance between movement and stiffness.10 The relative
motor elements that underpin an individual’s potential importance placed on each varies between tasks (gait
to move in, interact with and experience the environ- requires movement of the spine for shock absorption,
ment.6 It includes the output that arises from any element load transfer and energy minimization,11 whereas lifting
of the nervous system that contributes to motor function, 100 kg from the floor requires restriction of spine move-
from the spinal cord to the deep brain structures ment12), but all tasks require some element of each.
(e.g. basal ganglia), brain stem, cerebellum and cortex. Even maintenance of a static upright standing posture
It includes any sensory input that contributes to involves some movement (e.g. small movements occur in
53
54 PART II  Advances in Theory and Practice

BOX 6-1  Key Principles of Sensorimotor available from more than one source). The nervous
Control system relies on multiple sources of sensory information,
and places ‘weight’ or emphasis on the most trustworthy
• Functional movement involves components that are task source.23 This provides opportunity for the nervous
directed and components that are postural system to reweight to an alternative source when one is
• Function requires a balance between movement and stiffness no longer available, but can also lead to problems if it
• Function depends on the interaction between the passive relies on an inaccurate source.
elements, active system and sensor/controller The sixth and potentially most important feature of
• Motor function is inherently variable sensorimotor control is that of individual variation. No
• Multiple sources of sensory information are available to
two individuals use their body in the same way and this
guide and control movement
• Sensorimotor control varies between individuals variation is particularly apparent in the presence of pain
and injury.1 Although many aspects of motor function
may be fundamentally similar between individuals,
many are not and depend on the individual’s anatomy/
biomechanics (e.g. anthropometry, muscle fibres, fascial
conjunction with breathing to counteract the disturbance network, mass, muscle strength), the individual’s experi-
from the mechanics of breathing when standing erect).13,14 ence and exposure to movements/environments, and the
Pain and injury may be characterized by too much stiff- influence of an individual’s psychosocial/cognitive fea-
ness or too much movement, depending on the patient, tures (e.g. perceived capacity of their body, motivation,
the function or the context (e.g. whether the environ- experiences, beliefs about the consequence of a move-
ment is threatening).15 ment). In the presence of pain, what is ‘ideal’ for one
A third principle is that the overall motor function person may not be so for another. Although some cluster-
depends on the interaction between the passive elements, ing of features may be present, and different patient sub-
active system and sensor/controller. As defined by Panjabi,16 groups or phenotypes have been identified that provide
all are important for maintenance of control as each guidance for selection of treatments,5,24 within these sub-
contributes to stiffness and guidance of movement. Mod- groups there is large potential for variation.25
ification of any element will have repercussions for sen- Consideration of these key principles of sensorimotor
sorimotor control and the interaction between them is control assists interpretation of the changes in motor
necessary to consider when building a clinical picture of control identified in people with pain and injury. The
a patient’s presentation. For instance, change in passive following section outlines the breadth of changes that
stiffness of a joint will necessitate changes in motor have been reported and builds a conceptual model to
control (e.g. increased ankle stiffness will require changes understand and reconcile these changes.
in coordination of the knee, hip and spine to enable gait),
changes in the capacity of a muscle to generate force will
require compensation elsewhere (e.g. rapid atrophy of Relationship Between Pain, Injury and
multifidus may underlie changes in activation of other
back muscles to compensate or a change in position to
Sensorimotor Dysfunction
enable greater contribution by passive elements1,17), and Sensorimotor changes in the presence of pain and/or
changes in motor control strategy have repercussions for injury present across a spectrum from subtle changes
the other systems (e.g. enhanced muscle co-contraction, in sharing of load between synergist muscles1,3 or the
potentially related to fear of pain, requires compensation distribution of activity within a muscle,26,27 to a com-
at other segments18). plete avoidance of movement or function;28 from a
A fourth principle is that motor function is inherently subtle change in threshold to perceive a sensory input29
variable. There are multiple ways to achieve a goal involv- to a complete reorganization of the sensory represen-
ing different combinations of muscle activity, different tation of the body segment30 (Fig. 6-1). Early models
coordination between body segments and multiple pos- predicted a systematic increase in muscle activity to
sible control strategies.19,20 This redundancy (multiple protect a painful region with subsequent pain provoked
ways to achieve the same outcome) has both positive and by muscle ischaemia secondary to the muscle ‘spasm’
negative aspects. Variability can be helpful as variation in (vicious cycle theory31), or a reduced amplitude of
movement ‘shares’ the load around structures so that one movement or force secondary to a systematic reduc-
tissue is not repeatedly loaded,20 it enables compensation tion of excitability of muscles that produce a painful
when one option is no longer available21 and it allows trial movement and increased excitability of the antagonist
and error, which is required for learning.22 These pro- muscles (pain adaptation theory32). Although there are
cesses are compromised and may underpin problems if examples that support these hypotheses, these models
variation is limited. If variation is excessive it can be a fail to explain the diversity and complexity of individual
problem if it leads to lack of control, or if it leads to an change in sensorimotor control. New theories have
option that achieves the task’s goal but with an unneces- been developed that consider the key principles of
sary cost (e.g. increased energy demand or greater tissue sensorimotor control and are inclusive of not only
load20). Thus, both too little and too much variation may the individual variation in sensorimotor dysfunction
be harmful. in pain and injury, but also the potential role of these
A fifth principle is that the sensory system includes redun- changes in development and/or perpetuation of pain
dancy (information about movement and position is and injury (Fig. 6-1).15,33
 6  Interaction Between Pain and Sensorimotor Control 55

Discrete Accumulated load

excessive load (posture, function, etc.)

Load exceeds tissue tolerance

Sensitized nervous system

Psychosocial features
Fear/attitudes/beliefs
Real or threatened
nociceptive input/pain/injury
Mismatch between motor
output – sensory output
Mechanism:
Changes in
sensorimotor
system Subtle changes in Major changes in
(Motor cortex motor behaviour motor behaviour
[excitability/ (redistributed activity within (avoidance of
organization], sensory and between muscles) movement)
cortex, cognitive-
emotional,
sensory integration, Changed motor output/
sensorimotor mismatch mechanical behaviour:
brain stem, spinal Change – stiffness, force direction,
cord [e.g., inhibition/ load distribution, variability,
excitation] receptor injury force and movement amplitude
muscle, etc.)

Short-term benefit: Long-term consequences:

Protection of the injured/painful Increase potential for injury
region – ↓muscle activity/stress, and/or nociceptor provocation
↓movement, ↓potential for error injured tissue and other body
segments – ↑load, invariable
load, ↓shock absorption,
deconditioning

FIGURE 6-1  ■  Contemporary theory of interaction between pain, injury and motor adaptation. Changes in sensorimotor control can
be a cause or outcome of injury and/or nociceptor discharge/pain. Initial tissue damage may be caused by a major loading event
or repeated lower loading. Changes in sensorimotor control that range from subtle modification of movement to complete avoid-
ance of function can be mediated by a range of mechanisms at multiple sites in the sensory and motor systems. The variable and
individual specific modified sensorimotor control can have positive (often short-term outcomes aimed at immediate relief and pro-
tection) and negative outcomes (often longer-term changes) and these can underlie persistence and recurrence of pain.

Pain and/or Injury: The Cause or which they are located is damaged.38–40 It may change the
Consequence of Sensorimotor Dysfunction control of movement either at a spinal level (e.g. reflex
inhibition secondary to modified afferent input41) or
The initial mechanisms for development of injury and/or higher centres (e.g. selection of a solution to protect the
pain are diverse and can include a single event that over- injured segment1).
loads the tissues, or an accumulation of load that exceeds Sensorimotor deficits could contribute to the develop-
the capacity of the tissues over time.34 Whether an indi- ment of injury/pain if, for example: (a) the strategy of
vidual develops injury/pain from an event depends on the movement/muscle activation involves components that
load, the frequency and the individual’s tissue qualities load the tissues excessively (e.g. compromised activation
(Fig. 6-1). Trauma can initiate this process when tissue of the medial vasti muscles leading to sub-optimal control
tolerance is exceeded by a single high load (e.g. whiplash of patella glide42); (b) the muscles are unable to meet or
injury35) or repetitive cyclical low load (e.g. repetitive sustain the requirement of the task leading to sub-optimal
trunk flexion leads to an inflammatory response in spine tissue loading (e.g. lack of endurance of multifidus in
ligaments36). Injury to the tissue has several important rowers with back pain43); (c) inaccurate sensory informa-
and diverse consequences. It may become a source of tion about the movement leading to inaccurate control
peripheral nociceptive input. Peripheral effects such as (e.g. Brumagne et al.23); or (d) the movement involves too
inflammation and central mechanisms may underpin sen- much (e.g. greater stride-to-stride variability, represent-
sitization of this input.37 It may not only compromise the ing increased fluctuations in dynamic thoracic and pelvic
passive or active control of the injured region if the oscillations in low back pain44) or too little variability
trauma has led to failure of ligaments or muscle injury (e.g. low variation of leg kinematics predicts injury in
(e.g. torn anterior cruciate ligament), but also affect runners20). There are many other examples. A range of
sensory function if the sensory receptors or the tissue in possible factors could lead to sub-optimal sensorimotor
56 PART II  Advances in Theory and Practice

behaviour, which subsequently presents as a risk factor Sensorimotor Dysfunction in Pain and/or
for development of injury/pain. At the trunk this could Injury Across a Spectrum from ‘Subtle’ to
include modified demand of respiratory45 and continence ‘Major’ Adaptations
functions46 of the trunk muscles with a subsequent effect
on the quality of spine control. Other options include Why are pain and movement linked? In the presence of
habitual postures or movement patterns (e.g. early lumbar acute injury and/or pain, if the nervous system concludes
rotation during hip rotation47), or modified function there is a threat to the tissues, then movement is the
induced by the environment (e.g. repetitive use of a primary mechanism by which the nervous system can
device48). react to reduce that threat. This motor adaptation may
There are alternative theories regarding the relation- be as simple as a flexor withdrawal reflex to move away
ship between sensorimotor changes and pain. For from a noxious input,60 or as complex as a change in
instance, several authors argue that the experience of pain movement pattern of the whole body to compensate for
may result from mismatch between the sensory input the reduced contribution by the painful segment (e.g. hip
regarding a body part or a movement and the movement external rotation, decreased stance time and trunk lateral
or position that is expected.49 Such mismatch could arise flexion to avoid loading the ankle in dorsiflexion during
from modification of the internal representation of the stance after an ankle sprain). Such changes may be rele-
body (body schema), afferent information from the vant in the short term when there is potential risk to the
periphery,50,51 or corrupted motor output52 or motor tissue as it heals. Although early theories predicted a
organization.53 Although the exact mechanisms are as yet systematic and uniform increase or decrease in activ-
unclear, it has been speculated that such mismatch may ity,31,32 clinical observations and more recent experimen-
underlie neurodegenerative change and pain.54 tal evidence point to individual variation in response from
It is also important to note that the original mecha- ‘subtle’ to ‘major’ adaptations (Fig. 6-1).15
nism for a person to develop injury and pain in the Some individuals modify their movement in a major
first instance may be different from the reason that way such as the complete avoidance of a movement or
it is maintained. Although excessive load from a trau- function, or avoidance of participation in activity.28
matic event or sub-optimal mechanics from less than Although this change in behaviour ultimately achieves a
ideal sensorimotor control may be the initial stimulus similar goal to that achieved by the more subtle adapta-
for tissue damage, nociceptive input and pain, the tions (i.e. unloading of the painful or injured tissue), the
mechanism(s) underpinning the persistence or recur- underlying mechanisms are likely to be different. There
rence of pain may be very different. There will be is considerable literature linking these major avoidant
cases where nociceptive input and load continue to be strategies to a range of psychosocial features such as cata-
relevant, with peripheral nociceptive input continuing strophizing and fear avoidance.28,61
to drive the experience of pain.55 Peripheral nociceptive At the other end of the spectrum are more subtle
input can maintain central sensitization.56 In these cases changes in the manner in which movement/forces are
continued sensorimotor dysfunction is likely to have produced in the presence of pain and/or injury. Such
direct relevance for recovery. The alternative is that protective adaptations can be characterized by redistribu-
persistence and recurrence may be mediated by psy- tion of muscle activity to enhance stability (e.g. enhanced
chosocial issues (e.g. catastrophization and worker muscle co-contraction in back pain (Fig. 6-2),1 neck
support are factors in the transition to chronicity in pain62 and knee osteoarthritis63), redistribution of muscle
back pain,57 and moderate post-traumatic stress symp- activity within and between muscles to change distribu-
toms predict poor outcome following a whiplash tion of load on structures (Fig. 6-3)3 or modify the direc-
injury58), central and peripheral sensitization,37 or the tion of force (Fig. 6-3),64 reduced variability to limit the
development of secondary issues from sub-optimal tissue potential for error,48,65,66 unloading of a limb,67 reduced
loading related to the ‘new’ movement pattern adopted force/movement amplitude,68 increased motion at adja-
after the initial exposure to nociceptive input/pain (e.g. cent joints to compensate for reduced movement of the
development of back pain secondary to modified gait injured part,17,18 redistribution of muscle activity away
in low limb injury59). In these cases tissue load and from a painful region,69 failure to redistribute muscle
nociceptive input from the initial injury may have little activity when it is normally present to compensate for
to do with maintenance of the pain state, and treat- fatigue (Fig. 6-4),17 and more deterministic (less random)
ment is more likely to be effective if it is targeted to structure of the variability in accessory (non-task-related)
other issues. angular movement,70 which indicates less random vari-
Regardless of whether changes in sensorimotor control ability in the underlying muscle activation pattern
are the cause or consequence of pain, when a patient (Fig. 6-5).
presents for management of their clinical condition this Redistribution of muscle activity is particularly
is most commonly motivated by the presence of pain and common in musculoskeletal conditions of the spine,
they have already entered the cycle with pain reinforcing which is a region with many muscles available for func-
sensorimotor dysfunction or motivating new adaptations, tion.10 As a component of this redistribution of activity,
and sensorimotor dysfunction reinforcing sub-optimal there is substantial evidence for reduced activation of the
loading on the originally injured tissues or those of deeper muscles such as transversus abdominis52,71 and
other body regions as a consequence of compensatory multifidus72,73 in the lumbar region, and the deep cervical
mechanisms. flexor and extensor muscles in the neck.74,75 These muscles
 6  Interaction Between Pain and Sensorimotor Control 57

OE

RA
OI

TES
LD

LES

$ % &

RA r OE r OI r LD r TES r LES r RA l OE l OI l LD l TES l LES l

350 S1
S2
330 S3
310 S4
Stability index (Nm/rad)

S5
290
270
* S6
S7
S8
250 * S9
230 S10
S11
210 S12
190 S13
S14
170
S15
150 S16
Pre-pain Pain S17

' (
FIGURE 6-2  ■  Muscle activity is redistributed during acute pain to increase spine protection, but the pattern varies between individu-
als. (A) Recordings of electromyography (EMG) were made with 12 pairs of surface electrodes to record from superficial muscle
sites. (B) Healthy participants moved slowly forwards and backwards in a semi-seated position. (C) Trials were performed before
and during acute pain that was induced by injection of hypertonic saline into the longissimus muscle. (D) Stability of the spine
(estimated using an EMG-driven mathematical model) was increased during pain. (E) Changes in EMG are shown individually for
12 muscles in 17 participants. Black indicates increased EMG during pain, grey indicates decreased EMG, white indicates no change.
Although there was a net increase in spine stability during pain (D), this was achieved by individual specific patterns of modulation
of EMG activity. Each person used a different solution to protect the painful region. l, Left; LD, Latissimus dorsi; LES, Lumbar erector
spinae; OE, Obliquus externus abdominis; OI, Obliquus internus abdominis; r, Right; RA, Rectus abdominis; TES, Thoracic erector
spinae. (Figure redrawn from data from Hodges et al.1)

have a unique capacity to contribute to control of inter- is some evidence for a high prevalence of increased acti-
segmental motion by virtue of their segmental attach- vation of the sternocleidomastoid muscle in neck pain,85
ments (enabling fine intersegmental control76–79) and and obliquus externus abdominis and/or long erector
limited torque-generating capacity (enabling control spinae in low back pain,21,86,87 but this is not universal.
throughout range of motion without compromising Although a review of the back pain literature could iden-
dynamic function76,80). Reduced contribution of the tify no consistent patterns,84 a recent study with experi-
deeper muscles to spine control is characterized by mentally induced acute low back pain showed that despite
delayed activation;52,73,81 reduced activation71,74 and the variation in muscle activation, all but a few partici-
replacement of the usual tonic activation with phasic pants had a net increase in activity that resulted in aug-
bursts of activity.82 Reduced activation of deeper muscles mented stability (estimated from an EMG-driven model)
is commonly associated with augmented activity of other (Fig. 6-2).1 This observation is consistent with the pro-
muscles,83,84 although the pattern of activation is highly posal that the nervous system adapts to acute pain with a
variable between individuals.1 Within this variation, there strategy for protection and implies that some order can
58 PART II  Advances in Theory and Practice

Vasti EMG 1

EMG
Hz Hz

(mV)
5
8.7 6.5
A
Discharge rate
B

Discharge
rate (Hz)

1 mV
C Derecruitment
10 ms
20 D
New recruitment
0
Vasti EMG 2

EMG
(mV)
3
9.5 7.1
E
Discharge rate
F

Discharge
rate (Hz)
20 New recruitment
G
0 500 ms

$ %
-8° 15°
39°
44°

No pain
Pain

& '
FIGURE 6-3  ■  Redistribution of muscle activity in acute pain. (A) During acute pain activity of motor units is redistributed within and
between muscles. (B) Fine-wire electromyography (EMG) recordings are shown during contractions performed at identical force
before (left) and during (right) pain for two recording sites in the vasti muscles. The time of discharge of individual motor units is
displayed below the raw EMG recordings. The template for each unit is shown. Pain led to redistribution of activity of the motor
units. Units A and E discharged at a slower rate during pain. Units B and C stopped discharging during pain and units F and G,
which were not active prior to pain, began to discharge only during pain. These changes indicate that the participant maintained
the force output of the muscle, by using a different population of motor units (i.e. redistribution of activity within a muscle). 
(C) Knee extension task. (D) The direction of force used by the participants to match the force during contractions with and without
pain differed between trials. During pain, participants generated force more medially or laterally than in the pain-free trials. For
colour version see Plate 4. (A, B Redrawn from data from Tucker et al.;26 C, D redrawn from data from Tucker et al.64)

be found amongst the variation that is characteristic of muscle stress using ultrasound elastography techniques
the motor adaptation present in people with spinal pain. indicates that unloading of a painful tissue is not always
In other regions of the body there is substantial evi- achieved, and depends on the task (unloading of painful
dence for modified or redistributed muscle activity. There tissues is more likely in more complex tasks that involve
are too many examples to summarize here. Some typical a greater number of body segments91) and appears to
examples include changes such as delayed reaction time differ between body regions.91
of ankle evertor muscles in ankle sprain,88 delayed activa- Why do different individuals adopt different strate-
tion of gluteus medius during stair-stepping in patello- gies? The answer to this question has not been resolved,
femoral pain,89 delayed activation of subscapularis during but it may relate to different functional histories, experi-
arm movement in shoulder pain,90 and reduced activity ences with pain, or habitual postures/movement patterns.
of the extensor carpi radialis brevis associated with grip- The adopted patterns of activity are likely to relate to the
ping in patients with lateral epicondylagia (Heales et al. clinical subgroups that have been identified by several
2014, unpublished data). groups.5,24 Recent work3 shows that some people use the
Each of the examples presented above is thought to same muscle synergies during multijoint planar reaching
change the loading on the painful tissues, although there tasks in non-painful and painful conditions, which is con-
is limited direct evidence of mechanical factors to test this sistent with the observation that some people perform a
hypothesis. Recent work with direct measurement of particular task in a more stereotyped manner than
 6  Interaction Between Pain and Sensorimotor Control 59

Start Mid End

Cranial 40

30

Control 20

10

Caudal 0 mV
Medial Lateral

30

20
Low back pain

10

$ %
0 mV
FIGURE 6-4  ■  Reduced redistribution of muscle activation in low back pain. Although healthy individuals redistribute muscle activity
to maintain the motor output in the presence of fatigue, this is not observed in people with low back pain. (A) A 13 × 5 grid of
electromyography electrodes was placed over the lumbar erector spinae in a group of healthy controls and people with chronic low
back pain to assess the spatial distribution of erector spinae activity and change in the distribution during performance of a repeti-
tive lifting task for ~200 second. (B) Representative topographical maps of the root mean square EMG amplitude from the right
lumbar erector spinae muscle for a person with low back pain and a control. EMG maps are shown for the start, mid and end of a
repetitive lifting task. Areas of blue correspond to low EMG amplitude and dark red to high EMG amplitude. Note the shift (redis-
tribution) of activity in the caudal direction as the task progresses but for the control subject only. For colour version see Plate 5.
(Reprinted with permission from Falla et al.17)

others.65 Those individuals with less variable motor pro- Fig. 6-6), increased injury risk (e.g. compromised balance
grammes seem to be those more prone to develop pain underpinning greater falls risk secondary to increased
as they overuse the same strategy rather than taking trunk stiffness93), or decreased load sharing (e.g. reduced
advantage of the redundancy of the motor system. movement variation during function in neck-shoulder
pain;48 Fig. 6-6). A recent study also demonstrated delayed
activation of neck muscles in people with chronic neck
Sensorimotor Adaptations Provide a Short-
pain in response to rapid, unanticipated full-body pertur-
Term Solution, but have Potential Long-
bations (resembling slipping or tripping), suggesting that
Term Consequences
the cervical spine may be vulnerable to further strain/
What is the outcome of the adaptation in sensorimotor injury under such conditions due to inadequate muscle
control? As indicated above, adapted motor behaviour is support.98
presumed to enhance protection of the injured/painful Persistence of the motor adaptation could also under-
tissue,15 although the manner in which this is achieved pin reduced ‘confidence’ regarding the injured part, thus
differs between conditions and between individuals.1 A promoting disuse or modified use of the body part. That
major issue is that although the adaptation has potential is, the adapted motor behaviour could interact with psy-
benefits in the short term (either to change load and chosocial issues and feed into the fear–avoidance cycle.28
protect the injured/potentially injured tissue, or to meet For example, patients with low back pain may reduce
the requirement of the nervous system to take action92) their velocity of movement as a protective-guarding
there are potential long-term consequences. This could behaviour against excessive force and loading, and ensuing
arise for a number of reasons (see below, Fig. 6-6). pain. A recent study confirmed an association between
Sensorimotor adaptation could contribute to further the angular velocity of trunk movement and psychologi-
tissue damage as a result of actual changes to loading of cal features including fear of movement, pain catastroph-
the lesioned tissues or to loading of other tissues of the izing and anxiety which supports this notion.99
same or related body parts. This could arise if the adapta- The redistribution of activity between muscles could
tion to protect the painful part leads to; increased load also lead to problems if the adapted solution leads to
(e.g. increased muscle activity in people with back pain disuse of specific muscles that provide a unique contribu-
increases load on the spine during lifting,94 and greater tion to joint control. One key example is that, although
co-activation of the neck muscles during neck62,95 and enhanced activation of larger, more superficial muscles of
upper limb96 tasks may increase compressive loading on the neck and back is common in the presence of pain and
the cervical spine) (Fig. 6-6), reduced movement for may enhance protection, these muscles generally lack
shock absorption (e.g. delayed spinal motion in back pain segmental attachments to the spine and have a limited
leads to greater perturbation from arm movement;97 capacity to fine-tune control of intersegmental motion.100
60 PART II  Advances in Theory and Practice

12
12 (0°)

9 (270°) 3 (90°)

9 3

Baseline
Control
$ % 6 Pain

BIO ANC BME BLA

BIA TLA TLO DME

PEC DAN DPO LAT

&

DAN DPO DAN DPO

' (
FIGURE 6-5  ■  Changes in muscle activity vary between individuals when challenged by pain, with no few consistent changes across
participants. (A) Pain-free volunteers (n=8) performed multijoint reaching in the horizontal plane using a manipulandum, with the
starting point at the centre of the circle. The subject had to reach the 12 targets depicted in A with each reaching movement lasting
1 second followed by a 5 second rest period at the target position before returning to the centre point over 1 second. Subjects
performed the task at baseline, and following the injection of isotonic (control) and hypertonic (painful) saline. Saline was injected
into the right anterior deltoid (DAN) muscle. (B) Representative example of endpoint trajectories recorded from one subject during
the baseline (blue), control (magenta), and painful (red) conditions. Note that pain did not affect the kinematics of this controlled
task. (C) Directional tuning of the EMG envelope peak value recorded from 12 muscles during the baseline (blue), the control
(magenta), and pain (red) conditions. The ‘shrinking’ of the pain curves of the DAN muscle was due to a consistent decrease of the
EMG activity of this muscle across subjects. Other muscles also change their activity, however the direction of change was different
across subjects, demonstrating the variability in subject response. For example, the activity of the posterior deltoid (DPO), increased
during pain in three subjects while it decreased in five subjects, so that on average it was unchanged. (D) Representative data from
a single subject showing a decrease in DAN activity with a simultaneous increase in DPO activity during pain. (E) In contrast, rep-
resentative data from another subject shows that decreased DAN activity occurred together with a decrease in DPO activity during
pain. ANC, Anconeus; BIA, Brachialis; BIO, Brachioradialis; BLA, Lateral head of the biceps brachii; BME, Medial head of the biceps
brachii; DME, Medial deltoid; LAT, Latissimus dorsi; PEC, Pectoralis major; TLA, Lateral head of the triceps brachii; TLO, Long head
of the triceps brachii. For colour version see Plate 6. (Reprinted with permission from Muceli et al.3)
 6  Interaction Between Pain and Sensorimotor Control 61

Preparatory Resultant
motion motion

Sh

Sh

L-P
L-P

100 ms

Onset LP Onset Sh
$ % motion motion '

–8

–7

–6
Resultant motion

–5

–4

Performance
–3

–2

–1

0
r = 0.34
1
–2 0 2 4 6 8 10 12 Variability
& Preparatory motion (
FIGURE 6-6  ■  Potential mechanisms for long-term consequences of motor adaptation with pain and injury. (A–C) Absence of move-
ment to prepare the spine for the perturbation from the reactive forces induced by arm movement leads to exaggerated disturbance
to the spine. (A) Shoulder (Sh) and lumbopelvic (LP) motion were measured with motion sensors. (B) Spine movement in the direc-
tion opposite to the reactive forces (preparatory motion) is initiated prior to the movement of the arm. Resultant motion is the
motion resulting from the reactive moments. (C) Individuals with less preparatory motion are more likely to have a large resultant
motion. If the adaptation with pain and injury reduces movement this would reduce the potential for motion to dampen imposed
forces. (D) Increased co-contraction to protect the spine would have the negative consequence of increased compressive load on
the spine, potentially accelerating tissue changes. (E) Both too little and too much variability of movement have negative conse-
quences for the quality of performance. If variation is too low, this will compromise sharing of load between structures and com-
promise potential to learn and change. (A–C Redrawn from data from Mok et al.93)

Redistribution of activity to these muscles, at the expense changes in joint/muscle mobility [relative flexibility,105
of the deeper muscles that provide this control could be muscle length changes,106 consolidated swelling, joint
problematic in the long term.15 Exaggerated interseg- trauma, osteophytes, etc.]). Thirdly, dysfunction23 or
mental motion may be linked to tissue load and pain, as absence of sensory information107 may preclude resolu-
evidenced by larger intersegmental translation during tion of adaptation. Fourthly, in some cases it may not be
trunk motion in spondylolisthesis100 and increased inter- possible or optimal to return to the pre-injury sensorimo-
segmental rotation at the time of pain provocation in a tor control, as a modified solution may be required to
weight-lifting effort.12 compensate for the injured tissues (e.g. modified knee
Why is sensorimotor adaptation maintained beyond muscle control following complete anterior cruciate liga-
when it is necessary? There are several possible explana- ment rupture108). Finally, lack of resolution of the adapta-
tions. Firstly, although nociceptive stimulation and pain tion may be underpinned by the more complex issues
is a motivator to adapt, recovery from pain might not related to the physiology of persistent pain. Pain is a non-
motivate a return to the initial strategy. Secondly, it may linear system (that is, pain experienced by an individual
not be possible to return to the initial sensorimotor is not linearly related to the nociceptive input from the
control strategy. This could be because adaptation to periphery) and the experience of pain does not linearly
body structures precludes recovery (e.g. changes in relate to the threat to the tissues. This may be because
muscle capacity [muscle fibre changes in neck and back of sensitization37 and/or modified cognitive emotional
muscles,101–103 changes in muscle fatigability104], or mechanisms.109 As a result, the adaptation to pain may be
62 PART II  Advances in Theory and Practice

greater than what is required, the adaptation may persist fibrosis of the intervertebral disc,116 and tendon and this
for longer than is required (i.e. the time for tissue healing could be altered by injury and/or pain.
may have passed and the requirement for protection is There is evidence of modification of the sensory
no longer present) or the adaptation may be completely integration at higher centres, which may mediate inac-
inappropriate (i.e. the nervous system may perceive the curate interpretation of sensory input or reduce respon-
need to protect the tissues in a manner that is not relevant siveness to sensory information.23 In terms of the latter,
for the injury or in the absence of injury). In each case a the nervous system can reduce the reliance on a par-
different clinical strategy may be required to resolve the ticular source of sensory information (sensory reweight-
adaptation, and this may not be possible or desirable (if ing). For instance, although vibration of the back muscles
some degree of maintenance of the adaptation is required induces the perception of muscle stretch in pain-free
for compensation) in all individuals. The key message is individuals and leads to initiation of a postural adjust-
that although the adaptation may be necessary in the ment if applied in standing, in people with back pain
short term, in the long term it may become part of the this is substantially reduced despite the fact that injury
problem. to all muscle spindles is unlikely.23 There is also con-
siderable emerging evidence for reorganization of
sensory representations in the primary sensory cortex
Mechanisms for Sensorimotor Changes
(e.g. shift of the representation of the back region in
in Musculoskeletal Conditions
people with low back pain,30 and smudging of cortical
The diverse array of sensorimotor changes in musculo- representations of independent fingers in focal dystonia
skeletal conditions could be mediated by an equally associated with difficulty to move the fingers indepen-
diverse array of mechanisms. Potential mechanisms can dently117), distortion of the body schema,118 and modified
be broadly defined as primarily motor or sensory, or cortical integration.119
related to the cognitive/emotional aspects of pain. The Reduced, enhanced or distorted afferent input or inac-
following sections outline some of the most established curate integration of sensory information will also affect
mechanisms. the planning and organization of motor behaviours at
higher centres. Inaccurate sensory input or representa-
Sensory System Mechanisms.  Absent, reduced or tion of the body and/or environment has the potential to
inaccurate sensory input will compromise sensorimotor distort any process that depends on the interpretation of
control. Any compromise to normal afferent information position or movement of the body. This could have the
regarding position or movement of the body will affect potential to affect planning and control of any class of
the potential for accurate control.38 Function of the motor activity including voluntary movements, postural
sensory system can be compromised at multiple points adjustments, and motor learning processes. Although
along its path from the receptor to higher supraspinal there is some evidence that acute pain interferes with
sensory functions. The most obvious source of sensory motor learning,120 if performance of the training task is
dysfunction is direct trauma to the sensory receptors or controlled interference with learning is less apparent.121
the tissues in which they are located.38,40 Complete or Recent evidence indicates limited interference with
partial rupture of a ligament, intervertebral disc, or other learning, but compromised retention of learning.122 In
structure not only compromises the mechanical contribu- persistent pain states, with accompanying distorted body
tion to control, but also removes or compromises afferent schema and sensory integration, there is likely to be
input.39 Injury, inflammation and oedema may also com- greater interference with learning.
promise the responsiveness of receptors. In the presence In summary, many of the distorted motor behaviours
of tissue damage, afferent discharge from mechanorecep- identified in musculoskeletal conditions could be medi-
tors can induce pain (e.g. muscle mechanoreceptor exci- ated, at least in part, by dysfunction on the sensory side
tation is painful in the presence of eccentric muscle of the sensorimotor equation. Although injury to the
damage).110 Plasticity in spinal cord circuits underpinning receptors may not be amenable to rehabilitation, the uti-
central sensitization,37 such as the modification of func- lization and integration of sensory information, distor-
tion of the wide-dynamic range cells that converge input tion of the body schema and compensation with alternative
from multiple afferent sources, might also modify the sources of feedback may be modifiable.
utility of information provided by sensory afferents.
Further, muscle spindles receive sympathetic innerva- Motor System Mechanisms.  Like the sensory system,
tion,111 increased sympathetic drive could modulate the sensorimotor changes can be mediated by changes at any
discharge of these receptors either through an action level of the motor system from the spinal cord to the
exerted on the receptors themselves or on their primary motor cortex and beyond. Most research has focused on
afferent neurons.112 the spinal cord and primary motor cortex as these are the
Abnormal sensory input can affect motor function at most accessible to non-invasive investigation. In the
a spinal level. Effects include modification of reflex mod- spinal cord there is substantial evidence of reflex inhibi-
ulation of muscle activation, such as the stretch reflex, tion (which involves an important sensory component)
which may be augmented by greater sensitivity of the following injury to joint structures such as the joint
muscle spindles in the presence of inflammatory media- capsule and ligaments.115 Reflex inhibition involves
tors,113 or compromised in the presence of muscle damage. reduced excitation of motoneurons (primarily to extensor
Muscle activation is also modulated by afferent activity muscles) that is mediated by afferent input at a single
from receptors in the skin,114 ligaments,115 annulus level of the spinal cord.115 There can be concomitant
 6  Interaction Between Pain and Sensorimotor Control 63

excitation of flexor muscle motoneuron pools.115 The Considerable current work has been focused not on
source of afferent input is unclear, but occurs in the the anatomical sites of dysfunction, but the potential
absence of nociceptive input.41 Reflex inhibition appears role of changes in motor planning. This has been
counterintuitive – it reduces the activity of the muscles inferred from motor behaviours. It has been assumed
that could protect the joint – but is consistently observed that the change in motor behaviour to one that protects
for limb joint lesions and can explain reduced excitability the painful region, is not a simple consequence of a
of inputs to multifidus after intervertebral disc lesion123 change in ‘excitability’ or ‘representation’, but a pur-
and facet joint infusion.116 Reflex inhibition may serve to poseful modification of the planning of behaviour to
reduce joint load, although this occurs in a manner that meet a new goal (i.e. protection).15 The basic premise
interferes with function (e.g. ‘giving way’ of the knee with is that the central regions involved in planning and
effusion). initiation of motor behaviours (premotor, frontal,
Although early theories of adaptation to pain pre- somatosensory areas, limbic system) modify the coor-
dicted uniform inhibition32 or excitation31 of a painful dination of muscle to achieve this new goal. Changes
muscle at a spinal or brainstem level, nociceptive affer- in activation of these areas have been reported in brain
ents have both excitatory and inhibitory effects on moto- imaging studies during pain.137 Modification of the
neurons in animals.124 In humans, the discharge rate of pattern of muscle activity initiated in advance of a
motoneurons within a single muscle can simultaneously movement52 is consistent with this proposal. Further-
increase and decrease leading to redistribution of activ- more, when people with either neck or low back pain
ity26 and this observation is corroborated by recent evi- perform rapid arm movements, the activation of the
dence of differential effects on excitability of motoneurons deep muscles adopts a direction-specific response, which
identified using novel experimental methods.125 contrasts the response observed in healthy individuals.52,81
As stated earlier, changes in the muscle, the effector This indicates the change in activation is not simply a
organ of the motor system, are common in many muscu- delay that could be explained by factors such as decreased
loskeletal conditions. These changes (e.g. atrophy,72,126 motoneuron excitability, but rather, consistent with the
fatty infiltration,127,128 decreased endurance,129 changes in change in the strategy used by the central nervous
muscle fibre type proportion101,103) might be secondary to system to control the spine.
disuse as a result of general physical inactivity (e.g. avoid- Changes in movement variability also appear to
ance of activity secondary to fear28), reflex inhibition,41 or reflect the objective to adapt control to protect – during
reduced (gravitational) load.130 Recent work has high- pain, variability initially increases which concurs with
lighted alternative mechanisms such as a potential role of a search for a new solution, and then decreases as a
pro-inflammatory cytokines.101 Tumor necrosis factor is new solution is identified.48,65 Further work is required
expressed after disc lesion and plays a role in regulation to clarify the processes involved in the changed behav-
of muscle fibres131 and could explain changes in muscle iour. If this process aims to find a new solution, it is
fibre distribution after injury.101 not surprising that this could be affected by cognitive
Using transcranial magnetic stimulation, the repre- emotional aspects of pain such as catastrophization and
sentations of specific muscles at the motor cortex have kinesiophobia, both of which would be expected to
been found to be modified in people with persistent up-regulate the adaptation to further enhance protection
low back (e.g. convergence of cortical representations (see below).
of long and short back muscles,132 posterolateral shift In summary, motor processes are adapted at multiple
of representation of transversus abdominis;53 Fig. 6-7) levels of the nervous system and these changes could be
and elbow pain (loss of the multiple peaks of excit- both complementary and opposing. What is observed in
ability in the cortical representation of wrist extensor a patient will be a complex interplay of these processes
muscles in lateral epicondylagia.133 There is some evi- and there is potential for clinical interventions that target
dence that cortical changes are related to behaviour. different components of the nervous system (e.g. tech-
For instance, shift of the cortical representation of niques to change excitability at the spinal cord, or motor
transversus abdominis is correlated with delayed activa- learning to change control at higher centres) to have
tion of the muscle in an arm movement task.53 Although relevance for recovery.
difficult to test or confirm, the posterolateral shift
might be secondary to expansion of representation of Interaction with Psychosocial Factors.  Although it
other trunk muscles involved in a protective response. is well recognized that musculoskeletal conditions
Consistent with this argument, the excitability of inputs have biological, psychological and social elements,138 to
to the more superficial oblique abdominal muscles is varying degrees, these are often considered in isolation.
increased in acute pain.134 The ‘smudged’ cortical rep- As stated above, there is enormous potential for interac-
resentation of the extensor muscles is consistent with tion between psychosocial features and the biological
the loss of differential control of these muscles in mechanisms that underpin sensorimotor changes. From
back pain,73 and could be interpreted as a strategy to one perspective, psychosocial features may amplify the
simplify the protection of the back. Other studies of motor adaptation, which may lead to both greater muscle
excitability of the corticospinal path (which is affected activity or altered movement for protection (e.g. relation-
by excitability at the cortex and spinal cord) show ship between increased erector spinae muscle activity and
increases and decreases depending on the muscle123,135,136 kinesiophobia at the end range of trunk flexion61 and the
and the effects at the cortex and spinal cord may be association between reduced angular velocity of trunk
opposite.123,135 movement and kinesiophobia, pain catastrophizing and
64 PART II  Advances in Theory and Practice

Motor cortex
(M1)

Medulla

Corticospinal
Vertex tract
(Cz) $ TMS over scalp grid
Spinal cord

' MEPs superimposed

over scalp sites % Abdominal muscle
EMG recordings

& MEP recorded at each site

( Motor cortical map

) Relationship between cortical map
5
4 and onset in arm movement task
Healthy
4
LBP
3 3
CoG-lateral (cm)

1 2

Cz 1 2 3 4 5 1

r = 0.57 p <0.001
0
-100 -50 0 50 100
Relative onset of TrA (ms)
FIGURE 6-7  ■  Changes in motor cortex organization in low back pain. (A) Transcranial magnetic stimulation (TMS) was applied
according to a grid over the motor cortex to stimulate the corticospinal pathway. (B) Electromyography was recorded from the
transversus abdominis (TrA) muscle. (C) Motor evoked potentials (MEP) were recorded from stimuli applied at each point on the
grid. (D) The amplitude of MEPs is larger when stimulation is applied to the cortical region with neural input to the muscle.
(E) The gradient from low (blue) to high (light green) MEP amplitude is shown relative to the vertex (Cz). White/blue dots indicate
the centre of the region with input to TrA in healthy participants, and the grey/orange indicates that for people with a history of
LBP. The centre is positioned further posterior and lateral in the LBP group, providing evidence of reorganization of the motor cortex.
(F) The degree of reorganization was correlated with the delay of the onset of activation of TrA EMG during an arm movement task.
For colour version see Plate 7.

anxiety99) and more profound avoidance of activity and CONCLUSIONS

participation.28 From a different perspective, cognitive
emotional aspects of pain drive central sensitization, It is clear from the current state of the literature that
which underpins changes in excitability of sensory path- there is diversity in the manner in which the senso-
ways, nociceptive and otherwise,37 and this may modulate rimotor system is modified in pain and this is under-
many of the sensory mechanisms for adapted sensorimo- pinned by mechanisms that involve multiple regions
tor control. of the nervous system. Although it is unquestionable
 6  Interaction Between Pain and Sensorimotor Control 65

that sensorimotor control is affected, the key challenge 19. Bernstein N. The Co-Ordination and Regulation of Movements.
facing clinical intervention is to decide how sensorimo- Oxford: Pergamon Press; 1967.
20. Hamill J, van Emmerik RE, Heiderscheit BC, et al. A dynamical
tor changes relate to an individual patient’s presentation, systems approach to lower extremity running injuries. Clin
which aspects of sensorimotor control require manage- Biomech 1999;14:297–308.
ment, and how this might be best achieved for the 21. Moseley GL, Hodges PW. Are the changes in postural control
patient. associated with low back pain caused by pain interference? Clin J
Pain 2005;21:323–9.
22. Wu HG, Miyamoto YR, Gonzalez Castro LN, et al. Temporal
Acknowledgements structure of motor variability is dynamically regulated and predicts
motor learning ability. Nature Neurosci 2014;17:312–21.
PH is supported by a Senior Principal Research Fellow- 23. Brumagne S, Cordo P, Verschueren S. Proprioceptive weighting
ship from the National Health and Medical Research changes in persons with low back pain and elderly persons during
upright standing. Neurosci Lett 2004;366:63–6.
Council (NHMRC) of Australia. 24. Van Dillen LR, Sahrmann SA, Norton BJ, et al. Movement system
impairment-based categories for low back pain: stage 1 validation.
J Orthopaed Sports Phys Ther 2003;33:126–42.
25. Karayannis NV, Jull GA, Hodges PW. Physiotherapy movement
REFERENCES based classification approaches to low back pain: comparison of
1. Hodges PW, Coppieters MW, MacDonald D, et al. New insight subgroups through review and developer/expert survey. BMC
into motor adaptation to pain revealed by a combination of model- Musculoskelet Disord 2012;13:24.
ling and empirical approaches. Eur J Pain 2013;17:1138–46. 26. Tucker K, Butler J, Graven-Nielsen T, et al. Motor unit recruit-
2. Hodges PW, Moseley GL, Gabrielsson A, et al. Experimental ment strategies are altered during deep-tissue pain. J Neurosci
muscle pain changes feedforward postural responses of the trunk 2009;29:10820–6.
muscles. Exp Brain Res 2003;151:262–71. 27. Falla D, Arendt-Nielsen L, Farina D. The pain-induced change
3. Muceli S, Falla D, Farina D. Reorganization of muscle synergies in relative activation of upper trapezius muscle regions is indepen-
during multidirectional reaching in the horizontal plane dent of the site of noxious stimulation. Clin Neurophysiol
with experimental muscle pain. J Neurophysiol 2014;111(8): 2009;120:150–7.
1615–30. 28. Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in
4. Van Dillen LR, Sahrmann SA, Norton BJ, et al. Reliability of chronic musculoskeletal pain: a state of the art. Pain 2000;85:
physical examination items used for classification of patients with 317–32.
low back pain. Phys Ther 1998;78:979–88. 29. Garn SN, Newton RA. Kinesthetic awareness in subjects with
5. O’Sullivan P. Diagnosis and classification of chronic low back pain multiple ankle sprains. Phys Ther 1988;68:1667–71.
disorders: maladaptive movement and motor control impairments 30. Flor H, Braun C, Elbert T, et al. Extensive reorganization of
as underlying mechanism. Man Ther 2005;10:242–55. primary somatosensory cortex in chronic back pain patients. Neu-
6. Shumway-Cooke A, Woollacott MH. Motor Control. Baltimore: rosci Lett 1997;224:5–8.
Williams and Wilkins; 1995. 31. Roland M. A critical review of the evidence for a pain-spasm-pain
7. Massion J. Postural changes accompanying voluntary movements. cycle in spinal disorders. Clin Biomech 1986;1:102–9.
Normal and pathological aspects. Human Neurobiol 1984;2: 32. Lund JP, Donga R, Widmer CG, et al. The pain-adaptation
261–7. model: a discussion of the relationship between chronic musculo-
8. Hodges PW, Richardson CA. Feedforward contraction of trans- skeletal pain and motor activity. Can J Physiol Pharmacol
versus abdominis is not influenced by the direction of arm move- 1991;69:683–94.
ment. Exp Brain Res 1997;114:362–70. 33. Murray GM, Peck CC. Orofacial pain and jaw muscle activity: a
9. Hodges PW, Cresswell AG, Thorstensson A. Preparatory trunk new model. J Orofac Pain 2007;21:263–78.
motion accompanies rapid upper limb movement. Exp Brain Res 34. Dye SF. The knee as a biologic transmission with an envelope of
1999;124:69–79. function: a theory. Clin Orthopaed Rel Res 1996;10–18.
10. Hodges P, Cholewicki J. Functional control of the spine. In: 35. Ito S, Ivancic PC, Panjabi MM, et al. Soft tissue injury threshold
Vleeming A, Mooney V, Stoeckarteditors R, editors. Movement, during simulated whiplash: a biomechanical investigation. Spine
Stability and Lumbopelvic Pain. Edinburgh: Elsevier; 2007. 2004;29:979–87.
11. Saunders SW, Schache A, Rath D, et al. Changes in three dimen- 36. D’Ambrosia P, King K, Davidson B, et al. Pro-inflammatory cyto-
sional lumbo-pelvic kinematics and trunk muscle activity with kines expression increases following low- and high-magnitude
speed and mode of locomotion. Clin Biomech 2005;20:784–93. cyclic loading of lumbar ligaments. Eur Spine J 2010;19:1330–9.
12. Cholewicki J, McGill SM. Mechanical stability of the in vivo 37. Woolf CJ. Central sensitization: implications for the diagnosis and
lumbar spine: implications for injury and chronic low back pain. treatment of pain. Pain 2011;152:S2–15.
Clin Biomech 1996;11:1–15. 38. Panjabi M. A hypothesis of chronic back pain: ligament subfailure
13. Gurfinkel V, Kots Y, Paltsev E, et al. The compensation of respira- injuries lead to muscle control dysfunction. Eur Spine J
tory disturbances of erect posture of man as an example of the 2006;15:668–76.
organisation of interarticular interaction. In: Gelfard I, Gurfinkel 39. Johansson H, Sjolander P, Sojka P. A sensory role for the cruciate
V, Formin S, et al., editors. Models of the Structural Functional ligaments. Clin Orthopaed Rel Res 1991;268:161–78.
Organisation of Certain Biological Systems. Cambridge, Mass: 40. Dolan P, Adams MA. Time-dependent mechanisms that impair
MIT Press; 1971. p. 382–95. muscle protection of the spine. In: Hodges PW, Cholewicki J, van
14. Hodges P, Gurfinkel VS, Brumagne S, et al. Coexistence of stabil- Dieeneditors J, editors. Spinal Control: The Rehabilitation of
ity and mobility in postural control: evidence from postural com- Back Pain. Edinburgh: Churchill Livingstone; 2013.
pensation for respiration. Exp Brain Res 2002;144:293–302. 41. Stokes M, Young A. The contribution of reflex inhibition to
15. Hodges PW, Tucker K. Moving differently in pain: a new theory arthrogenous muscle weakness. Clin Sci 1984;67:7–14.
to explain the adaptation to pain. Pain 2011;152:S90–8. 42. Van Tiggelen D, Cowan S, Coorevits P, et al. Delayed vastus
16. Panjabi MM. The stabilizing system of the spine. Part I. Function, medialis obliquus to vastus lateralis onset timing contributes to
dysfunction, adaptation, and enhancement. J Spinal Disord the development of patellofemoral pain in previously healthy men:
1992;5:383–9. a prospective study. Am J Sports Med 2009;37:1099–105.
17. Falla D, Gizzi L, Tschapek M, et al. Reduced task-induced varia- 43. Roy SH, DeLuca CJ, Snyder-Mackler L, et al. Fatigue, recovery,
tions in the distribution of activity across back muscle regions in and low back pain in varsity rowers. Med Sci Sports Exerc
individuals with low back pain. Pain 2014;155(5):944–53. 1990;22:463–9.
18. Smith M, Coppieters MW, Hodges PW. Effect of experimentally 44. Vogt L, Pfeifer K, Portscher M, et al. Influences of nonspecific
induced low back pain on postural sway with breathing. Exp Brain low back pain on three-dimensional lumbar spine kinematics in
Res 2005;166:109–17. locomotion. Spine 2001;26:1910–19.
66 PART II  Advances in Theory and Practice

45. Hodges PW, Heijnen I, Gandevia SC. Reduced postural activity 69. Madeleine P, Leclerc F, Arendt-Nielsen L, et al. Experimental
of the diaphragm in humans when respiratory demand is increased. muscle pain changes the spatial distribution of upper trapezius
J Physiol 2001;537:999–1008. muscle activity during sustained contraction. Clin Neurophysiol
46. Smith M, Coppieters M, Hodges PW. Postural response of the 2006;117:2436–45.
pelvic floor and abdominal muscles in women with and without 70. Dideriksen JL, Gizzi L, Petzke F, et al. Deterministic accessory
incontinence. Neurourol Urodyn 2007;26:377–85. spinal movement in functional tasks characterizes individuals with
47. Scholtes SA, Gombatto SP, Van Dillen LR. Differences in lum- low back pain. Clin Neurophysiol 2013;125:1663–8.
bopelvic motion between people with and people without low 71. Ferreira P, Ferreira M, Hodges P. Changes recruitment of the
back pain during two lower limb movement tests. Clin Biomech abdominal muscles in people with low back pain: ultrasound mea-
2009;24:7–12. surement of muscle activity. Spine 2004;29:2560–6.
48. Madeleine P, Mathiassen SE, Arendt-Nielsen L. Changes in the 72. Hides JA, Stokes MJ, Saide M, et al. Evidence of lumbar multifi-
degree of motor variability associated with experimental and dus muscle wasting ipsilateral to symptoms in patients with acute/
chronic neck-shoulder pain during a standardised repetitive arm subacute low back pain. Spine 1994;19:165–77.
movement. Exp Brain Res 2008;185:689–98. 73. MacDonald D, Moseley GL, Hodges PW. Why do some patients
49. McCabe CS, Haigh RC, Halligan PW, et al. Simulating sensory- keep hurting their back? Evidence of ongoing back muscle dys-
motor incongruence in healthy volunteers: implications for a cor- function during remission from recurrent back pain. Pain
tical model of pain. Rheumatol 2005;44:509–16. 2009;142:183–8.
50. Brumagne S, Cordo P, Lysens R, et al. The role of paraspinal 74. Falla DL, Jull GA, Hodges PW. Patients with neck pain demon-
muscle spindles in lumbosacral position sense in individuals with strate reduced electromyographic activity of the deep cervical
and without low back pain. Spine 2000;25:989–94. flexor muscles during performance of the craniocervical flexion
51. Luomajoki H, Moseley GL. Tactile acuity and lumbopelvic motor test. Spine 2004;29:2108–14.
control in patients with back pain and healthy controls. Br J Sports 75. Schomacher J, Farina D, Lindstroem R, et  al. Chronic trauma-
Med 2011;45:437–40. induced neck pain impairs the neural control of the deep
52. Hodges PW, Richardson CA. Inefficient muscular stabilisation semispinalis cervicis muscle. Clin Neurophysiol 2012;123:
of the lumbar spine associated with low back pain: a motor 1403–8.
control evaluation of transversus abdominis. Spine 1996;21: 76. Hodges P, Kaigle Holm A, Holm S, et al. Intervertebral stiffness
2640–50. of the spine is increased by evoked contraction of transversus
53. Tsao H, Galea MP, Hodges PW. Reorganization of the motor abdominis and the diaphragm: in vivo porcine studies. Spine
cortex is associated with postural control deficits in recurrent low 2003;28:2594–601.
back pain. Brain 2008;131:2161–71. 77. Anderson JS, Hsu AW, Vasavada AN. Morphology, architecture,
54. Wand BM, O’Connell NE. Chronic non-specific low back pain and biomechanics of human cervical multifidus. Spine 2005;30:
– sub-groups or a single mechanism? BMC Musculoskel Disord E86–91.
2008;9:11. 78. Ward SR, Kim CW, Eng CM, et al. Architectural analysis and
55. Smart KM, Blake C, Staines A, et al. Mechanisms-based classifica- intraoperative measurements demonstrate the unique design of
tions of musculoskeletal pain: part 3 of 3: symptoms and signs of the multifidus muscle for lumbar spine stability. J Bone Joint Surg
nociceptive pain in patients with low back (+/- leg) pain. Man Am 2009;91:176–85.
Ther 2012;17:352–7. 79. Boyd-Clark LC, Briggs CA, Galea MP. Comparative histochemi-
56. Gracely RH, Lynch SA, Bennett GJ. Painful neuropathy: altered cal composition of muscle fibres in a pre- and a postvertebral
central processing maintained dynamically by peripheral input. muscle of the cervical spine. J Anat 2001;199:709–16.
Pain 1992;51:175–94. 80. Kaigle AM, Holm SH, Hansson TH. 1997 Volvo Award winner
57. Picavet HS, Vlaeyen JW, Schouten JS. Pain catastrophizing and in biomechanical studies. Kinematic behaviour of the porcine
kinesiophobia: predictors of chronic low back pain. Am J Epide- lumbar spine: a chronic lesion model. Spine 1997;22:2796–806.
miol 2002;156:1028–34. 81. Falla D, Jull G, Hodges PW. Feedforward activity of the cervical
58. Sterling M, Jull G, Vicenzino B, et al. Physical and psychological flexor muscles during voluntary arm movements is delayed in
factors predict outcome following whiplash injury. Pain 2005; chronic neck pain. Exp Brain Res 2004;157:43–8.
114:141–8. 82. Saunders S, Coppieters M, Hodges P. Reduced tonic activity of
59. Nadler SF, Malanga GA, DePrince M, et al. The relationship the deep trunk muscle during locomotion in people with low back
between lower extremity injury, low back pain, and hip muscle pain. In: Proceeedings of World Congress of Low Back and Pelvic
strength in male and female collegiate athletes. Clin J Sport Med Pain. Melbourne, Australia; 2004.
2000;10:89–97. 83. Ng JK, Richardson CA, Parnianpour M, et al. EMG activity of
60. Clarke RW, Harris J. The organization of motor responses to trunk muscles and torque output during isometric axial rotation
noxious stimuli. Brain Res Brain Res Rev 2004;46:163–72. exertion: a comparison between back pain patients and matched
61. Watson PJ, Booker CK. Evidence for the role of psychological controls. J Orthop Res 2002;20:112–21.
factors in abnormal paraspinal activity in patients with chronic low 84. van Dieen JH, Selen LP, Cholewicki J. Trunk muscle activation in
back pain. J Musculo Pain 1997;5:41–56. low-back pain patients, an analysis of the literature. J Electro-
62. Lindstrom R, Schomacher J, Farina D, et al. Association between myogr Kinesiol 2003;13:333–51.
neck muscle coactivation, pain, and strength in women with neck 85. Jull G, Kristjansson E, Dall’Alba P. Impairment in the cervical
pain. Man Ther 2011;16:80–6. flexors: a comparison of whiplash and insidious onset neck pain
63. Hubley-Kozey C, Deluzio K, Dunbar M. Muscle co-activation patients. Man Ther 2004;9:89–94.
patterns during walking in those with severe knee osteoarthritis. 86. Arendt-Nielsen L, Graven-Nielsen T, Svarrer H, et  al. The
Clin Biomech 2008;23:71–80. influence of low back pain on muscle activity and coordination
64. Tucker KJ, Hodges PW. Changes in motor unit recruitment strat- during gait: a clinical and experimental study. Pain 1996;64:
egy during pain alters force direction. Eur J Pain 2010;14:932–8. 231–40.
65. Moseley GL, Hodges PW. Reduced variability of postural strategy 87. O’Sullivan PB, Beales DJ, Beetham JA, et al. Altered motor
prevents normalisation of motor changes induced by back pain – a control strategies in subjects with sacroiliac joint pain during the
risk factor for chronic trouble? Behav Neurosci 2006;120:474–6. active straight-leg-raise test. Spine 2002;27:E1–8.
66. Bergin MJ, Tucker KJ, Vicenzino B, et al. Does movement vari- 88. Lofvenberg R, Karrholm J, Sundelin G, et al. Prolonged reaction
ability increase or decrease when a simple wrist task is performed time in patients with chronic lateral instability of the ankle. Am J
during acute wrist extensor muscle pain? Eur J Appl Physiol Sports Med 1995;23:414–17.
2014;114:385–93. 89. Cowan SM, Crossley KM, Bennell KL. Altered hip and trunk
67. Hug F, Hodges PW, Salomoni SE, et al. Insight into motor adap- muscle function in individuals with patellofemoral pain. Brit J
tation to pain from between-leg compensation. Eur J Appl Physiol Sports Med 2009;43:584–8.
2014;114(5):1057–65. 90. Hess SA, Richardson C, Darnell R, et al. Timing of rotator cuff
68. Svensson P, Arendt-Nielsen L, Houe L. Sensory-motor interac- activation during shoulder external rotation in throwers with and
tions of human experimental unilateral jaw muscle pain: a quanti- without symptoms of pain. J Orthop Sports Phys Ther 2005;35:
tative analysis. Pain 1995;64:241–9. 812–20.
 6  Interaction Between Pain and Sensorimotor Control 67

91. Hug F, Hodges PW, Tucker KJ. Task dependency of motor 115. Ekholm J, Eklund G, Skoglund S. On the reflex effects from the
adaptations to an acute noxious stimulation. J Neurophysiol knee joint of the cat. Acta Physiol Scand 1960;50:167–74.
2014;111:2298–306. 116. Indahl A, Kaigle AM, Reikeras O, et al. Interaction between the
92. Moseley GL. Trunk muscle control and back pain: Chicken, egg, porcine lumbar intervertebral disc, zygapophysial joints, and para-
neither or both? In: Hodges PW, Cholewicki J, van Dieeneditors spinal muscles. Spine 1997;22:2834–40.
J, editors. Spinal Control: The Rehabilitation of Back Pain. Edin- 117. Byl NN, Merzenich MM, Cheung S, et al. A primate model for
burgh: Elsevier; 2013. studying focal dystonia and repetitive strain injury: effects on the
93. Mok NW, Brauer SG, Hodges PW. Failure to use movement in primary somatosensory cortex. Phys Ther 1997;77:269–84.
postural strategies leads to increased spinal displacement in low 118. Bray H, Moseley GL. Disrupted working body schema of the
back pain. Spine 2007;32:E537–43. trunk in people with back pain. Br J Sports Med 2011;45:
94. Marras WS, Davis KG, Ferguson SA, et al. Spine loading charac- 168–73.
teristics of patients with low back pain compared with asymptom- 119. Schabrun SM, Jones E, Kloster J, et al. Temporal association
atic individuals. Spine 2001;26:2566–74. between changes in primary sensory cortex and corticomotor
95. Fernandez-de-las-Penas C, Falla D, Arendt-Nielsen L, et al. Cer- output during muscle pain. Neurosci 2013;235:159–64.
vical muscle co-activation in isometric contractions is enhanced in 120. Boudreau S, Romaniello A, Wang K, et al. The effects of intra-
chronic tension-type headache patients. Cephalalgia 2008;28: oral pain on motor cortex neuroplasticity associated with
744–51. short-term novel tongue-protrusion training in humans. Pain
96. Johnston V, Jull G, Darnell R, et al. Alterations in cervical muscle 2007;132:169–78.
activity in functional and stressful tasks in female office workers 121. Ingham D, Tucker KJ, Tsao H, et al. The effect of pain on
with neck pain. Eur J Appl Physiol 2008;103:253–64. training-induced plasticity of the corticomotor system. Eur J Pain
97. Mok N, Brauer S, Hodges P. Changes in lumbar movement in 2011;15:1028–34.
people with low back pain are related to compromised balance. 122. Bouffard J, Bouyer LJ, Roy JS, et al. Tonic pain experienced
Spine 2011;36:E45–52. during locomotor training impairs retention despite normal per-
98. Boudreau SA, Falla D. Chronic neck pain alters muscle activation formance during acquisition. J Neurosci 2014;34(28):9190–5.
patterns to sudden movements. Exp Brain Res 2014;232: 123. Hodges PW, Galea MP, Holm S, et al. Corticomotor excitability
2011–20. of back muscles is affected by intervertebral disc lesion in pigs.
99. Vaisy M, Gizzi L, Petzke F, et al. Estimation of lumbar spine Eur J Neurosci 2009;29:1490–500.
functional movement in low back pain. In: Proceedings of Schmer- 124. Kniffki KD, Schomburg ED, Steffens H. Synaptic effects
zkongress. 2013. from chemically activated fine muscle afferents upon alpha-
100. Crisco JJ, Panjabi MM. The intersegmental and multisegmental motoneurones in decerebrate and spinal cats. Brain Res 1981;206:
muscles of the lumbar spine: a biomechanical model comparing 361–70.
lateral stabilising potential. Spine 1991;7:793–9. 125. Hodges PW, Tucker K, Garland SJ, et al. Non-uniform effects of
101. Hodges PW, James G, Blomster L, et al. Can pro-inflammatory nociceptive input to motorneurons during experimental pain. In:
cytokine gene expression explain multifidus muscle fibre changes Proceedings of International Motoneuron Meeting. Sydney, Aus-
after an intervertebral disc lesion? Spine 2014;39(13):1010–17. tralia; 2012.
102. Mannion AF. Fibre type characteristics and function of the human 126. Jull G, Amiri M, Bullock-Saxton J, et al. Cervical musculoskeletal
paraspinal muscles: normal values and changes in association with impairment in frequent intermittent headache. Part 1: subjects
low back pain. J Electromyogr Kinesiol 1999;9:363–77. with single headaches. Cephalalgia 2007;27:793–802.
103. Uhlig Y, Weber BR, Grob D, et al. Fibre composition and fibre 127. Alaranta H, Tallroth K, Soukka A, et al. Fat content of lumbar
transformations in neck muscles of patients with dysfunction of extensor muscles in low back disability: a radiographic and clinical
the cervical spine. J Orthop Res 1995;13:240–9. comparison. J Spinal Disord 1993;6:137–40.
104. Falla D, Jull G, Rainoldi A, et al. Neck flexor muscle fatigue is 128. Elliott J, Jull G, Noteboom JT, et al. Fatty infiltration in the cervi-
side specific in patients with unilateral neck pain. Eur J Pain cal extensor muscles in persistent whiplash-associated disorders: a
2004;8:71–7. magnetic resonance imaging analysis. Spine 2006;31:E847–55.
105. Van Dillen LR, McDonnell MK, Fleming DA, et al. Effect of knee 129. Biering-Sørensen F. Physical measurements as risk indicators for
and hip position on hip extension range of motion in individuals low-back trouble over a one year period. Spine 1984;9:106–19.
with and without low back pain. J Orthop Sports Phys Ther 130. Hides JA, Belavy DL, Stanton W, et al. Magnetic resonance
2000;30:307–16. imaging assessment of trunk muscles during prolonged bed rest.
106. Janda V. Muscles, central nervous motor regulation and back Spine 2007;32:1687–92.
problems. In: Korreditor IM, editor. The Neurobiologic Mecha- 131. Li YP, Schwartz RJ. TNF-alpha regulates early differentiation of
nisms in Manipulative Therapy. New York: Plenium Press; 1978. C2C12 myoblasts in an autocrine fashion. FASEB J 2001;15:
p. 27–41. 1413–15.
107. Courtney C, Rine RM, Kroll P. Central somatosensory changes 132. Tsao H, Danneels LA, Hodges PW. ISSLS prize winner: smudg-
and altered muscle synergies in subjects with anterior cruciate ing the motor brain in young adults with recurrent low back pain.
ligament deficiency. Gait Posture 2005;22:69–74. Spine 2011;36:1721–7.
108. Bryant AL, Newton RU, Steele J. Successful feed-forward strate- 133. Schabrun SM, Hodges PW, Vicenzino B, et al. Novel adaptations
gies following ACL injury and reconstruction. J Electromyogr in motor cortical maps: The relationship to persistent elbow pain.
Kinesiol 2009;19:988–97. Med Sci Sports Exerc 2014;[Epub ahead of print].
109. Moseley GL. Reconceptualising pain according to its underlying 134. Tsao H, Tucker KJ, Hodges PW. Changes in excitability of cor-
biology. Phys Ther Rev 2007;12:169–78. ticomotor inputs to the trunk muscles during experimentally-
110. Weerakkody NS, Whitehead NP, Canny BJ, et al. Large-fibre induced acute low back pain. Neurosci 2011;181:127–33.
mechanoreceptors contribute to muscle soreness after eccentric 135. Martin PG, Weerakkody N, Gandevia SC, et al. Group III and
exercise. J Pain 2001;2:209–19. IV muscle afferents differentially affect the motor cortex and
111. Barker D, Saito M. Autonomic innervation of receptors and motoneurones in humans. J Physiol 2008;586:1277–89.
muscle fibres in cat skeletal muscle. Proc Royal Soc Lond Series 136. Le Pera D, Graven-Nielsen T, Valeriani M, et al. Inhibition of
B 1981;212:317–32. motor system excitability at cortical and spinal level by tonic
112. Passatore M, Roatta S. Influence of sympathetic nervous system muscle pain. Clin Neurophysiol 2001;112:1633–41.
on sensorimotor function: whiplash associated disorders (WAD) 137. Fomberstein K, Qadri S, Ramani R. Functional MRI and pain.
as a model. Eur J Appl Physiol 2006;98:423–49. Curr Opin Anaesthesiol 2013;[Epub ahead of print].
113. Pedersen J, Sjolander P, Wenngren BI, et al. Increased intramus- 138. Waddell G. The Back Pain Revolution. Edinburgh: Churchill
cular concentration of bradykinin increases the static fusimotor Livingstone; 1998.
drive to muscle spindles in neck muscles of the cat. Pain
1997;70:83–91.
114. McNulty PA, Turker KS, Macefield VG. Evidence for strong
synaptic coupling between single tactile afferents and motoneu-
rones supplying the human hand. J Physiol 1999;518:883–93.
 CHAPTER 7 

Neuromuscular
Adaptations to Exercise
Ross Pollock  • Stephen Harridge

INTRODUCTION Neural Control of Muscle Contraction

At the level of voluntary control, the smallest functional
Performing regular exercise is the single most effective unit that can be activated is the motor unit (MU). A MU
method of maintaining health. It also results in a is a single α-motoneuron and all the muscle fibres that it
myriad of adaptations in the cardiovascular, respiratory innervates. When a contraction is initiated in the motor
and neuromuscular systems that can improve physical cortex of the brain a depolarizing electrical current
performance. The focus of this chapter is on the (action potential) is transmitted along the axon of the
adaptations that occur in the neuromuscular system as motoneuron and its branches, and at the neuromuscular
a result of exercise. While it is beyond the scope of junction a neurotransmitter (acetylcholine) is released
this chapter to provide a detailed description of muscle resulting in the propagation of the action potential along
structure and function, we give a short introduction the muscle fibre. This depolarization spreads into the
to provide context for discussions of exercise-induced muscle fibre through invaginations in the muscle mem-
adaptations. brane (T-tubules) which causes the sarcoplasmic reticu-
lum to open ryanodine-binding channels allowing the
diffusion of calcium (Ca2+) into the cytoplasm. Ca2+ binds
Skeletal Muscle to troponin, a regulatory protein coupled to tropomyosin
Movement is ultimately facilitated by the action of our on the actin filament. The result of Ca2+ binding is a con-
skeletal muscles which are responsible for converting the formational change of the tropomyosin molecule causing
chemical energy stored in the bonds of adenosine tri- binding sites on actin to be revealed, allowing cross-
phosphate (ATP) into mechanical work and, like all bridges to bind to actin and exert force. The control of
machines, into heat. All of our muscles, depending on voluntary force levels is determined by two basic mecha-
size, are made up of thousands and in some cases hun- nisms: (a) the recruitment/de-recruitment of motor units
dreds of thousands of elongated cells, known as muscle and (b) the rate of action potential firing by each motor
fibres which are wrapped in a connective tissue sheath unit to regulate Ca2+ concentration within each cell.
(epimysium) comprising the protein collagen. Structur-
ally, each muscle is divided into smaller units called ‘fas-
cicles’, which are groups or bundles of fibres surrounded
Muscle Function
by a layer of thick connective tissue (perimysium), while Understanding the relationship between muscle force/
each fibre is surrounded by a fine layer of connective power and velocity (Fig. 7-1A) helps put into context the
tissue (endomysium). A single muscle fibre consists of a functional adaptations that can occur as a result of exer-
number of myofibrils lying in parallel with the long axis cise training. The strength of a muscle is defined as the
of the muscle. Each myofibril contains myofilaments force (or torque) generated about a joint during a
consisting primarily of the contractile proteins actin and maximum isometric contraction. Power is the rate at
myosin. The myofibril is made up of a number of sarco- which a muscle does mechanical work and is determined
meres that lie in series and repeat along the length of the by the product of the force of a contraction and velocity
myofibril demarcated by Z-lines. Myosin and actin fila- of shortening (concentric contraction). Any bodily action
ments are arranged such that the two filaments interdigi- that involves movement therefore requires the genera-
tate and overlap, with muscle contracting and shortening tion of power, with no power being generated during an
through the interaction of myosin cross-bridges cyclically isometric contraction where no movement occurs. The
attaching, rotating and detaching from the actin filament. maximal velocity of shortening is a point when force is
This process is powered by the hydrolysis of ATP as it zero (which does not occur in natural movements as there
breaks down to ADP (adenosine diphosphate), with the is always some loading on the muscle) representing the
removal of the inorganic phosphate (Pi) bond being asso- maximal rate of cross-bridge turnover. Finally, Figure
ciated with the ‘power stroke’ of the cross-bridge as it 7-1A depicts the situation where a muscle is active,
rotates and acts on actin causing force generation and but rather than shortening is being forcibly lengthened
movement. (eccentric contraction). This stretching of muscle results
68
 7  Neuromuscular Adaptations to Exercise 69

Lengthening Shortening
Eccentric

Force/Power
Isometric

Concentric

0 I IIa IIx
$ Velocity % Velocity
FIGURE 7-1  ■  (A) Schematic representation of the relationship between force (solid line)/power (dashed line) and velocity for muscle
shortening (concentric), lengthening (eccentric) and static (isometric) contractions. (B) The force and power–velocity relationships
for slow (type I) and the two types of fast (type IIa and IIx) fibres.

in the performance of negative work where it acts as a

brake. Here the cross-bridges have their elastic elements
stretched and the muscle is able to bear higher forces
than it can during isometric or shortening contractions.

Muscle Fibre Types

Muscle fibres are not homogeneous entities and can be
broadly classified into two main groups based on their
contractile speed; type I (slow) or type II (fast) (Fig.
7-1B). Compared to type II fibres, type I fibres exhibit
lower levels of isometric force production per unit area,
demonstrate a longer time to contract and relax from a
single electrical impulse (a twitch), have lower maximal
speeds of shortening, but are more resistant to fatigue.
This aspect is made possible by the fact that they possess
more mitochondria (the organelles responsible for the
generation of ATP through aerobic metabolism) and FIGURE 7-2  ■  Muscle biopsy sample taken from vastus lateralis,
sectioned and processed using myosin ATPase histochemistry
have a higher potential for aerobic metabolism. They following preincubation at pH4.5. Type I (dark), type IIa (light).
contain the slowest cycling cross-bridges (containing Fibres with a more intermediate stain are likely to contain
myosin heavy chain isoform-I, MHC-I). Type II fibres MHC-IIx isoforms, either alone or more commonly co-expressing
can be further subdivided into type IIa and IIx (formally with MHC-IIA.
known as IIb and sometimes IId).1 Type IIa fibres (con-
taining MHC-IIa), have a high contractile speed and are
moderately fatigue-resistant. These fibres are sometimes mechanically or metabolically, will result in specific and
termed ‘fast-oxidative’ fibres. Type IIx fibres, the fastest different adaptations that can improve performance. The
to contract (contain MHC-IIa), exhibit little fatigue magnitude of the adaptation is dependent on the type,
resistance and possess few mitochondria. These fibres intensity, frequency and duration of exercise. In addition
have a higher potential for generating ATP through to these factors there is emerging evidence that as well as
anaerobic (glycolytic) pathways. Each muscle comprises an initial level of fitness, there are genetic influences
a mixture of fibre types (Fig. 7-2), but with a distribution which determine the body’s responsiveness (responders
favouring type I fibres in postural muscles such as the and non-responders) to given training intervention.3
soleus and type II fibres dominating muscles such as the The mode of exercise performed is an important factor
triceps brachii of the arm.2 It is this heterogeneity in in determining the type and magnitude of adaptation. For
muscle composition that allows us to be able to generate example, if endurance training (high-repetition low-load
explosive power when needed in some situations and yet contractions) is undertaken there will be specific changes
have some resistance to fatigue in others. in muscle which targets aerobic metabolism and improved
fatigue resistance. By contrast, high-resistance strength
Adaptation to Exercise: training (low repetition with high-load contractions)
causes muscle to adapt by increasing myofibrillar protein
The Overload Principle synthesis, such that muscle size, strength and power all
Improvement and adaptation to exercise rely on the over- may increase. Even within the context of either strength
load principle. Overloading the muscular system, whether or endurance training it is important to consider the
70 PART II  Advances in Theory and Practice

specific type of exercise being performed. The principle

of specificity dictates that in regard to targeting particular
adaptations ‘specific exercise elicits specific adaptations
creating specific training effects’.4 For example, the most
effective way to increase and improve endurance running a

Training progess
performance is through running not cycling or swim-
ming training, even though each mode elicits general
adaptations in muscle and cardiorespiratory fitness.
While it is acknowledged that exercise represents both b
a continuum of types and intensities, for clarity in regard
to describing the means by which adaptation occurs, we
will consider two types that represent the two ends of the c
exercise spectrum. These are the adaptations that occur
due to high-resistance strength training and those due to
endurance training.
0 2 4 6 8 End
Time (weeks)
ADAPTATIONS TO HIGH-RESISTANCE FIGURE 7-3  ■  Time course of adaptation to resistance training.
a, Strength improvements; b, neural adaptations; and c,
STRENGTH TRAINING hypertrophy.

Progressive resistance training refers to any type of train-

ing which, through muscular contraction, aims to increase Neural Adaptations
the strength, power and size of skeletal muscle. These
improvements in general rely on the overload principle Initial studies investigating neural adaptations to resis-
in which strength is improved and muscle growth stimu- tance training suggested that increased central drive con-
lated by working a muscle near to its maximal force- tributed to strength gains as evidenced by increased
generating capacity. While it is not the purpose of this electromyographic activity of muscles measured from
chapter to provide practical details of the myriad of train- surface electrodes placed over the muscle belly. Such
ing regimens used, a typical programme might involve adaptations have been confirmed in studies investigating
lifting and lowering a weight 6–12 times (repetitions), the V-wave and H-reflex that are evoked by submaximal
with this being repeated 3–4 times (sets) and using loads and supramaximal electrical stimulation of a nerve (e.g.
which are equivalent to approximately 70–80% of the tibial nerve exciting the soleus) giving an estimate of the
maximum weight that can be lifted once (1-RM). For excitability of the motoneuron pool and transmission
optimal improvements in strength the intensity (how efficiency of Ia afferent synapses (presynaptic inhibition).
much weight is lifted) should be progressively increased It was found that 14 weeks of resistance training increased
over the course of the training programme so as to main- the amplitude of the V-wave and H-reflex, indicating an
tain a level of overload. enhanced neural drive in the corticospinal pathways
Muscle is particularly sensitive to mechanical signals and increased excitability of the α-motoneuron.7 Taken
with overload resulting in strength and mass gains. together these findings indicate that there is an enhanced
However, the reverse is also true with limb immobiliza- drive from the higher centres of the brain after resistance
tion, bed-rest and exposure to a microgravity environ- training, which are partly responsible for the improve-
ment where unloading results in significant losses in ments in strength observed. There may also be an
muscle mass and function. The specificity of high- increased MU synchronization (several MUs firing at
resistance strength training is highlighted by the fact that similar times),8 a decrease in the force threshold at which
gains in the amount of weight that can be lifted are mark- MUs are recruited,9 an increase in MU firing rates10 and
edly greater than the increase in force produced during a decrease in the level of co-activation of antagonist
a maximum voluntary isometric contraction of the same muscles11 after training. The latter is likely to be medi-
muscle when measured in the laboratory, which in turn ated by inhibitory effects on agonist inhibitory interneu-
is greater than the gain in muscle mass.5 At first it appears rons, excitation of Golgi tendon interneurons or directly
reasonable to assume that increases in the amount of from central drive from the motor pathways.12
weight lifted and isometric strength would be due to
increases in the size (hypertrophy) of the muscle.
However, it is widely acknowledged that improvements,
Muscular Adaptations
particularly in the initial phases, are primarily due to Although the initial gains in strength are primarily related
adaptations in the central nervous system. Typical resis- to neural mechanisms it is well known that skeletal muscle
tance training programmes last between 8–20 weeks with will ultimately adapt to mechanical overload by increas-
increases in strength occurring as early as 2 weeks, with ing its size. As is explained below, resistance training
muscle hypertrophy only becoming apparent after 6–8 triggers various signalling mechanisms that initiate the
weeks of training.6 The relative time course of neural creation of new proteins and enlargement of muscle
adaptations and hypertrophy to increased muscle strength fibre/cell size. This is the prime, if not sole, means by
is summarized in Figure 7-3. which a muscle as a whole hypertrophies, with little
 7  Neuromuscular Adaptations to Exercise 71

evidence to show an increase in the number of muscle elevated protein breakdown.18 However, in a fed state
fibres (hyperplasia) occurring.13 protein synthesis is greater than breakdown which,
When measured at the whole muscle level with high- coupled with the shorter time course of protein break-
resolution magnetic resonance imaging, increases in the down (<24 hours),18 results in a net gain in protein. The
anatomical cross-section area of the quadriceps average accumulated effect of this process over multiple exercise
about 10% after 12–14 weeks of training.14 In addition, bouts results in a net gain in protein and therefore muscle
changes in muscle architecture can also be observed. growth.
Ultrasound imaging has shown changes in the angle of It is apparent from the findings discussed above that
fibre pennation, which reflects the angle at which fibres adaptations to muscle are dependent on nutrient avail-
are aligned in regard to their insertion to aponeuroses. ability. By altering the availability of certain nutrients it
This affects force output by determining physiological is possible to modulate the immediate protein breakdown
cross-section area (where the cross-section area is deter- and synthesis response post exercise (Fig. 7-4). Resistance
mined perpendicular to the line of pull of muscle fibres) training and amino acid ingestion can both increase
and by altering the line of pull of muscle fibres. protein synthesis with an even greater effect present
At the cellular level, hypertrophy can be seen in all when both are combined.20 The consumption of protein
fibre types, although type II fibres appear to have a post exercise also promotes protein synthesis while simul-
greater propensity for hypertrophy than type I.14 The taneously suppressing breakdown. The suppression of
patterns of activity during resistance training and prefer- protein breakdown post exercise in the fed state is further
ential effect on the fast twitch fibres might suggest the enhanced by the associated increase in insulin levels,21
possibility of a slow-to-fast transformation in fibre phe- highlighting the importance of adequate nutrition to
notype. However, while there is little evidence of change maximize the benefits of resistance training.
in relative proportions of the two fibre types, there is What is the mechanism by which muscle protein syn-
good evidence to show that there is in fact a decrease in thesis is regulated? Muscle anabolism is regulated inside
the number of type IIx fibres accompanied by an increase the muscle cell by the Akt/mTOR signalling pathway22
in type IIa fibres.15 That said, a selective hypertrophy of as depicted in Figure 7.5. It is also referred to as the
type II relative to type I fibres will alter the contractile canonical insulin-like growth factor 1 (IGF-1) pathway,
protein profile of the muscle as a whole, as relatively where at the top activation is triggered by the binding of
more of the muscle would be occupied by the fast MHC-II IGF-1 to a receptor which activates a cascade of steps
isoforms. This is functionally important as evidence from regulating the initiation, elongation and termination of
human single-fibre studies suggests that as well as having proteins in the synthetic process. A detailed review of this
a high speed of shortening, fast fibres are inherently pathway is beyond the scope of this chapter; suffice to say
stronger (greater force per unit area or ‘specific force’). that IGF-1 is not actually essential for this process.23
In other words, a given enlargement of a fast twitch fibre Indeed, activation of mTOR is initiated through the
should have a proportionately greater effect on strength amino acid, leucine, independent of other signals, explain-
and power than the same growth of a slow twitch fibre. ing how muscle protein synthesis can be increased as a
result of feeding. While it is tempting to view feeding as
the way to increase muscle protein synthesis without
Muscle Protein Synthesis
exercise, it is known that the gains are transient and that
It is clear that muscle is sensitive to the loads placed on the muscle becomes resistant (‘full’) to further increases
it during training. Muscle is a dynamic system with pro- in muscle protein synthesis with additional feeding.24
teins being synthesized and degraded. For a muscle to Interestingly, there has been a ‘scaling down’ in the nutri-
grow this balance between synthesis and degradation tional requirements needed to initiate protein synthesis.
needs to be altered by either increasing the rate at which Initially, it was observed that feeding of a mixed meal
protein is synthesized, decreasing the rate at which it is would stimulate protein synthesis. Subsequently it was
degraded or a combination of both. Using tracer tech- suggested that ingestion of protein alone followed by just
niques, where labelled amino acids (such as [1-13C] essential amino acids and finally then just the amino acid
leucine) are infused into volunteers and their rate of leucine would be sufficient to initiate protein synthesis.
incorporation into muscle determined, it has been pos- More recently, it has now been shown that one specific
sible to measure objectively protein synthesis in response metabolite of leucine, β-hydroxyl-β-methylbutyrate, is
to exercise and feeding. Determining the rate of protein sufficient to activate the anabolic pathway.25
breakdown is more challenging and requires the mea-
surement of a tracer in blood across a limb. To summarize Satellite Cells
a number of studies, the following is known about human
muscle protein turnover. Muscle protein synthesis is The growth and repair of all skeletal muscle is inextrica-
~0.04% per hour in the fasted state. Muscle, particularly bly linked to the action of a group of muscle stem cells
myofibrillar, protein synthesis is stimulated by both exer- known as ‘satellite cells’. Muscle is a post-mitotic tissue,
cise and feeding. Following resistance training muscle meaning that muscle fibres have exited the cell cycle and
protein synthesis increases twofold to fivefold post exer- are no longer capable of further division. Thus, for repair
cise.16,17 Increases in protein synthesis occur 1–2 hours they rely on their resident stem cells. These specialized
post exercise; however, when in the fed state they can cells are located in a niche between the basal lamina and
remain elevated for 48–72 hours.18,19 This increase in the sarcolemma of a muscle fibre. When satellite cells are
protein synthesis post exercise is also accompanied by an activated by damage and/or sufficient exercise, these cells
72 PART II  Advances in Theory and Practice

Normal
Protein gain
Protein loss

% Change in MPB and MPS

Meal Meal Meal Meal

Post Training
% Change in MPB and MPS

Exercise bout
+ meal Meal Meal Meal
Time
FIGURE 7-4  ■  Schematic of muscle protein synthesis (MPS; solid line) and muscle protein breakdown (MPB; dashed line) in the normal
state and after performing a bout of exercise. Highlighted areas indicate either a net gain in muscle protein or net loss of muscle
protein. Note the greater increase in muscle protein synthesis in the fed state post exercise.

Signalling in Muscle Protein Homeostasis

Myostatin
IGF1-R

Activin
PTEN

SMAD2,3 AKT

RANK
elF4B
Initiation elF4e
FOXO NF I
mTOR
Elongation EEF2 4EBP-1
Nucleus
GSK3
Termination RPS6 P70s6K MURF-1 MAFBx

Ubiquitinization
Folding

Protein synthesis Protein breakdown

FIGURE 7-5  ■  The Akt/mTOR signalling pathway showing the intracellular regulation of muscle anabolism and catabolism.
 7  Neuromuscular Adaptations to Exercise 73

proliferate, differentiate and fuse to an existing myofibre, GH is secreted by the anterior pituitary gland where it
forming new contractile proteins and repair damage. The acts on the liver to stimulate the synthesis of IGF-1. As
effect of resistance training on satellite cells is indicated can be seen from the Figure 7.5 IGF-1 acts as an initiator
by an increase in their number within 4 days of training.26 molecule of this anabolic cascade. However, rather than
When resistance training is continued over a prolonged circulating levels of IGF-1, it seems that IGF-1 produced
period satellite cell numbers may increase by ~30% and locally by muscle for autocrine and paracrine actions is
remain elevated even if training is stopped.27 the most critical for muscle hypertrophy. In rodent
In addition to acting as a means by which muscles can studies, both localized infusion and genetically induced
repair themselves following damage, another important overexpression of IGF-1 result in hypertrophy.36,37 IGF-1
role of satellite cells is the donation of their nuclei to act is a 70-amino-acid peptide and its gene comprises five
as post-mitotic nuclei in the growing muscle fibre. Muscle exons and two promoter regions. Alternative splicing of
fibres are large cells with multiple nuclei, each of which pre-mRNA results in the creation of E peptides (e.g.
is responsible for the maintenance of a certain volume of mechano growth factor, MGF) that may have different
cytoplasm within the muscle fibre. In order for hypertro- and specialized functions in muscle repair and adapta-
phy to occur, the myonuclear domain (the volume of tion.38 In humans, circulating IGF-1 can be increased
cytoplasm that a nucleus can ‘manage’, i.e. the DNA to with administration of recombinant growth hormone
protein ratio) must be maintained within a certain limit.28 (rhGH). rhGH is an effective clinical treatment for both
In human muscle the ‘ceiling’ of the myonuclear domain GH-deficient adults and children, which led to its use as
has been estimated to be ~2000 µm2 in cross section.29 a potential doping agent in sport. However, laboratory
The theory is that if the myonuclear domain is below this trials have not shown convincing effects on muscle
value then increased rates of transcription can result in protein synthesis or growth over that induced by exercise
hypertrophy without the need for additional nuclei. training alone,39 and the roles of both GH and IGF-1 in
However, as this ceiling value is approached, an increase muscle growth in adults remain unclear.
in the number of nuclei is required.30
Myostatin
Hormonal Influences A final factor to consider in this section is the growth
The milieu surrounding and influencing a muscle in factor, myostatin (or growth differentiation factor 8).
response to resistance training is intricate and in addition This growth factor secreted by muscle works differently
to mechanical and nutritional factors, a hormonally to testosterone or IGF-1, in that it acts to suppress muscle
complex environment is created. Here we give a brief growth. It was discovered in 1997 through analysis of
description of a few of those implicated in the hypertro- samples obtained from Belgium Blue cattle that demon-
phic process. strated a highly hypertrophied (double-muscled) pheno-
type.40 A mutation in the myostatin gene was discovered
and causal effects of myostatin were shown in genetically
Testosterone
modified mice which had the myostatin gene experimen-
Testosterone is secreted from the Leydig cells of the tally knocked out and were characterized by a highly
testes in males. It is responsible for the increased muscu- hypertrophied phenotype.41 A case report of a child
larity seen in males at puberty and forms the basis of the exhibiting a highly hypertrophied phenotype related to a
anabolic steroids used by some athletes and body builders mutation in the myostatin gene42 provided evidence in
to increase muscle mass. Despite many years of hearsay humans of its role in the regulation of muscle mass.
about the purported effects of anabolic steroids, the first Myostatin works as a negative regulator of muscle mass
randomized controlled trial showing the efficacy of phar- and it is thus not surprising that resistance training has
macological doses of testosterone was not published until been shown to result in its down-regulation43 (i.e. the
the mid-nineties.31 Testosterone has subsequently been brake on growth inhibition is being taken off). Myostatin
shown to increase muscle fibre size, satellite cell and works through the Smad signalling pathway, but its inter-
myonuclear number in a dose-dependent manner.32 Con- action with the anabolic Akt/mTOR pathway can be seen
versely, when testosterone production is pharmacologi- in Figure 7.5.
cally blocked there is an inhibition of the acute These are only three of the factors that may influence
exercise-induced increase in testosterone and an attenu- muscle. We have described studies where muscle growth
ation in the exercise-induced hypertrophic response.33 is facilitated by pharmacological administration of GH or
Working through the androgen receptors within the cell testosterone and indeed impaired by use of a pharmaco-
the exact mechanisms of its action are not fully clear. The logical inhibitor of testosterone, but on a final note it
effects of testosterone may be related to its role in satel- is worth discussing the recent study by West and
lite cell entry into the cell cycle and differentiation or its co-workers.44 Subjects undertook strength training of the
influence on the IGF-1 system.34,35 elbow flexor muscles, but used prior leg exercise to insti-
gate physiologically elevated levels of GH, IGFI and tes-
tosterone, thereby creating a physiologically induced
Growth Hormone/Insulin-Like
hormonally enhanced environment. Interestingly, while
Growth Factor 1
these were elevated threefold to tenfold above the resting
The second hormonal system relevant to the regulation condition, the elbow flexors showed no greater increase
of muscle mass is the growth hormone (GH)/IGF-1 axis. in muscle mass or strength compared to training in the
74 PART II  Advances in Theory and Practice

resting normal hormonal environment. This suggested is a transcription factor named peroxisome proliferator-
that exercise-induced elevations of these hormones within activated receptor gamma co-activator 1α (PGC-1α).47
the normal physiological range do not enhance muscle Within 2 hours of a single bout of endurance exercise
anabolism, adding weight to the argument that local the PGC-1α gene transcription is elevated tenfold,48 with
factors regulating muscle protein synthesis are the most the resulting increase in expression initiating mitochon-
important in a non-pharmacological context. drial biogenesis. A rapid increase in mitochondrial pro-
teins occurs prior to increased expression of PGC-1α
suggesting that activation of PGC-1α mediates the initial
ENDURANCE TRAINING phase of mitochondrial biogenesis while the delayed
increase in PGC-1α protein may sustain and enhance
In contrast to resistance training, which is focused on it.49 This initial phase is likely to be mediated by the
increasing muscle mass strength and power, endurance movement of PGC-1α from the cytosol into the nucleus
training is targeted at increasing muscle fatigue resistance of the cell via the activity of a number of enzymes such
for exercise of longer durations. Fatigue can be defined as AMPK, CamK and p38 MAPK which are up-regulated
as ‘a loss in the capacity for developing force and/or as a result of endurance exercise. Upon entering the
velocity of a muscle, resulting from muscular activity nucleus PGC-1α co-activates transcription factors
under load and which is reversible by rest’.45 Performance including nuclear respiratory factor and mitochondrial
in endurance activities is reliant on the body’s ability to transcription factor A that regulate the expression of
generate ATP at a sufficient rate through aerobic respira- mitochondrial proteins resulting in mitochondrial
tion, a process which requires interaction of the neuro- biogenesis.50
muscular, cardiovascular and respiratory systems. While
adaptations in the cardiovascular system are particularly
important, the focus here will be on the local adaptations
Angiogenesis
that occur in skeletal muscle. Ultimately, endurance In regard to oxygen delivery, it is the network of capil-
training improves the oxidative capacity and metabolic laries that run adjacent to muscle fibres which is respon-
efficiency of skeletal muscle. It does this through adapta- sible for allowing the diffusive exchange of gases,
tions in oxygen utilization (mitochondrial biogenesis), substrates and metabolites between the circulation and
oxygen delivery (angiogenesis) and local substrate the working muscle fibres. As with the adaptations in
availability. mitochondria, it is well known that endurance exercise
results in the growth of new capillaries, a process known
as ‘angiogenesis’, with an increase of ~20% being found
Mitochondrial Adaptations after as little as 8 weeks of training in both type I and II
In regard to oxygen utilization, mitochondria are organ- fibres.51 A number of factors contribute to exercise-
elles responsible for the generation of the majority of induced angiogenesis, of which the most important is the
the cell’s supply of ATP through aerobic respiration and regulatory protein vascular endothelial growth factor
thus have been termed ‘the power house’ of the cell. (VEGF) which has a strong effect on endothelial cell
Numerous studies have shown that endurance training division.52 A single bout of endurance exercise elevates
can increase the volume and number of mitochondria VEGF mRNA content in the working muscle,53 while
with the magnitude of these changes relating to the fre- repeated bouts of exercise lead to a greater expression of
quency and intensity of training.46 The advantage of an VEGF protein54 and subsequent capillary formation.
increased number and size of mitochondria is that the Exercise-induced increases in VEGF are stimulated by a
proportion of pyruvate formed during glycolysis passing number of events which include increased shear stress as
into the mitochondria for oxidative phosphorylation is a result of increased blood flow,55 elevated AMPK and
increased with less used for the production of lactate and local tissue hypoxia elevating the transcription factor
its by-products (e.g. H+). Lactate accumulation in the HIF-1-alpha. While the total cardiac output is increased
circulation is interpreted as the point where aerobic following endurance training, through a left ventricular
metabolism is no longer able to supply the metabolic hypertrophy-mediated increase in stroke volume, at the
demands of the working muscles. After training, the local tissue level increase in capillary density serves to
blood lactate–workload relationship is shifted to the right increase the mean transit time for a given arterial blood
such that the exercise intensity at which lactate begins flow, facilitating diffusion and thus oxygen delivery and
to accumulate (the lactate threshold) is increased. In CO2 removal.
other words, the exercise intensity, which can be sus-
tained through reliance primarily on aerobic metabolism,
is higher. While it has been known for many years that
Substrate Utilization
these adaptations in oxygen delivery and utilization The primary fuel sources used during submaximal exer-
occur, the mechanisms driving these changes have not cise are carbohydrate (predominantly muscle glycogen)
been so well understood. and fats (both local lipid deposits and circulating fatty
Mitochondria are interesting and unique organelles acids). The oxidation of protein contributes minor
in that they comprise both nuclear and mitochondrial amounts to fuel utilization and only becomes significant
DNA requiring complex mechanisms to construct and in times of energy crisis. One of the key adaptations to
remodel them. One of the key regulators identified in endurance training is that for a given level of submaximal
the encoding of both nuclear and mitochondrial proteins exercise the contribution of fatty acid oxidation to the
 7  Neuromuscular Adaptations to Exercise 75

total energy requirement increases with a marked increase the excitability of the H-reflex pathway63 suggesting the
in the muscle’s ability to utilize intramuscular triglycer- recruitment threshold of the motoneuron to Ia afferent
ides as the primary fuel source.56 Training results in fibres input has been lowered, while the difference in thresholds
storing both more glycogen, in the form of granules, and between motoneurons has decreased (i.e increased
a greater number of intramuscular lipid droplets in recruitment gain).64,65 It is likely that these responses
contact with the mitochondria.57 Improved fatty acid oxi- reflect adaptations that improve fatigue resistance thereby
dation is beneficial to endurance athletes as it helps con- enhancing endurance performance. Indeed the specificity
serve or ‘spare’ muscle glycogen stores, which are more of adaptations to a particular activity (e.g. cycling versus
important during exercise of a higher intensity. Circulat- running) can, in part, be explained by the different pat-
ing blood glucose acts as another important fuel source terns of motor unit activation that are required by the
during exercise, and is taken up into muscle through same muscles undertaking different activities.
action of glucose transporter 4 with evidence that the
content of this protein is increased as a result of endur-
ance training. SUMMARY
Muscle is highly malleable tissue adapting to changes in
Can We Switch Muscle Fibre Types? both the mechanical and metabolic signals that result
As discussed earlier, muscle fibres can be classified on the from exercise (Table 7-1). On the one hand resistance
basis of a number of different parameters (twitch time, training induces a number of adaptations not only in
myosin isoform composition, ATPase activity, fatigability skeletal muscle, but also the neural network that result in
and their metabolic properties). Usually, fibre types are gains in strength, power and muscle size. This type of
discussed in relation to their ATPase activity/MHC exercise results in increases in myofibrillar muscle protein
isoform content. On this basis a number of studies have synthesis and activation of the satellite cells to facilitate
tried to establish the effect of endurance training on the a hypertrophic adaptation of muscle to the loads placed
relative proportions of type I and type II fibres. While it upon them. In contrast, rather than increasing the
has long been recognized that high-level endurance ath- strength of muscular contractions, endurance training
letes have a greater proportion of type I than type II exerts its influence by improving the aerobic capacity of
fibres58 than non-athletes, with the opposite being true muscle fibres. The main factors that allow this are the
of sprint athletes, this cross-sectional approach does not increased capillary network to facilitate local oxygen
provide clear evidence that this is a result of endurance delivery and an increase in the size and number of mito-
training. Indeed, it is known from studies of monozygotic chondria to facilitate oxygen utilization enabling a greater
and dizygotic twins that there is a large genetic compo-
nent in establishing muscle phenotype.59 It could be that
people with a higher percentage of these slow twitch
TABLE 7-1  Summary of the Broad Changes
fibres preferentially participate in endurance activities
that are Associated with the
because they are more naturally talented in this regard
Two Extremes of Training:
and find it easier. In general, it is assumed that there is
High Resistance Compared
little change in fibre type with endurance training
to Endurance Training
although there will be a transformation from type IIx to
type IIa, as indeed there is for power and strength train- Resistance Endurance
ing.60 The evidence for a type II to type I fibre-type Training Training
transformation has come from animal studies which have Functional adaptations:
employed long-term chronic low-frequency electrical Strength and power ↑ ↔
stimulation regimens rather than voluntary exercise.61 Fatigue resistance ↔ ↑
However, the adaptations that result in an increased Muscular adaptations:
potential for increased aerobic metabolism can occur Muscle size ↑ ↔
readily in all fibre types and do not require a switching Fibre switching IIx→IIa IIx→IIa→I(?)
of the molecular motor (i.e. the myosin cross-bridge). Muscle protein ↑ Myofibrillar ↑ Mitochondrial
Thus the classification of muscle becomes more blurred synthesis fraction fraction
following endurance training, with fibres still maintain- Mitochondria ↔ ↑
ing their given myosin isoform content, but markedly volume/oxidative
changing their metabolic properties and ability to resist enzyme activity
fatigue. Capillary network ↔/↓ ↑
Neural adaptations:
Central drive ↑ ↔
Neural Adaptations MU synchronization ↑ ↔
As with resistance training, endurance training results in MU recruitment ↓ ↓
threshold
adaptations to the neural system. In contrast to resistance
MU firing rate ↑ ↓
training MU discharge rate decreases10 while a slower
Antagonist ↓ ↔
rate of decline in MU conduction velocity during sus- co-activation
tained contractions is found after endurance training.62
In addition, endurance training has been found to increase MU, Motor unit.
76 PART II  Advances in Theory and Practice

ATP production through aerobic metabolism. All of 24. Cuthbertson D, Smith K, Babraj J, et al. Anabolic signalling deficits
these changes require a complex interaction of signalling underlie amino acid resistance of wasting, ageing muscle. FASEB J
2005;19:422–4.
events, our understanding of which has been aided by the 25. Wilkinson DJ, Hossain T, Hill DS, et al. Effects of leucine and its
rapid advances there have been in recent years in muscle metabolite β-hydroxy-β-methylbutyrate on human skeletal muscle
molecular and cell biology. protein metabolism. J Physiol 2013;591:2911–23.
26. Crameri RM, Langberg H, Magnusson P, et al. Changes in satellite
cells in human skeletal muscle after a single bout of high intensity
REFERENCES exercise. J Physiol 2004;558:333–40.
1. Schiaffino S, Reggiani C. Fibre types in mammalian skeletal 27. Kadi F, Schjerling P, Andersen LL, et al. The effects of heavy
muscles. Physiol Rev 2011;91:1447–531. resistance training and detraining on satellite cells in human skel-
2. Harridge SDR, Bottinelli R, Canepari M, et al. Whole-muscle and etal muscles. J Physiol 2004;558:1005–12.
single-fibre contractile properties and myosin heavy chain isoforms 28. Kadi F, Eriksson A, Holmner S, et al. Cellular adaptation of the
in humans. Pflugers Arch J Physiol 1996;432:913–20. trapezius muscle in strength-trained athletes. Histochem Cell Biol
3. Bouchard C, Rankinen T. Individual differences in response to 1999;111:189–95.
regular physical activity. Med Sci Sports Exerc 2001;33:S446–51. 29. Petrella JK, Kim J, Cross JM, et al. Efficacy of myonuclear addition
4. McArdle W, Katch F, Katch V. Exercise Physiology: Energy, Nutri- may explain differential myofiber growth among resistance-trained
tion, and Human Performance. 8th ed. Philidelphia: Lippincott, young and older men and women. Am J Endocrinol Metab
Williams & Wilkins; 2014. 2006;291:E937–46.
5. Jones DA, Rutherford OM, Parker DF. Physiological changes in 30. Kadi F, Charifi N, Denis C, et al. The behaviour of satellite cells
skeletal muscle as a result of strength training. Exp Physiol 1989; in response to exercise: what have we learned from human studies?
74:233–56. Pflugers Arch 2005;451:319–27.
6. Sale D. Neural adaptations to resistance training. Med Sci Sports 31. Bhasin S, Storer TW, Berman N, et al. The effects of supraphysi-
Exerc 1988;20:S135–45. ologic doses of testosterone on muscle size and strength in normal
7. Aagaard P, Simonsen E, Andersen J, et al. Neural adaptation to men. N Engl J Med 1996;335:1–7.
resistance training: changes in evoked V-wave and H-reflex 32. Sinha-Hikim I, Roth SM, Lee MI, et al. Testosterone-induced
responses. J Appl Physiol 2002;92:2309–18. muscle hypertrophy is associated with an increase in satellite cell
8. Pucci AR, Griffin L, Cafarelli E. Maximal motor unit firing rates number in healthy, young men. Am J Physiol Endocrinol Metab
during isometric resistance training in men. Exp Physiol 2006;91: 2003;285:E197–205.
171–8. 33. Kvorning T, Andersen M, Brixen K, et al. Suppression of endog-
9. Van Cutsem M, Duchateau J, Hainaut K. Changes in single motor enous testosterone production attenuates the response to strength
unit behaviour contribute to the increase in contraction speed after training: a randomized, placebo-controlled, and blinded interven-
dynamic training in humans. J Physiol 1998;513:295–305. tion study. Am J Physiol Endocrinol Metab 2006;291:1325–32.
10. Vila-Chã C, Falla D, Farina D. Motor unit behaviour during sub- 34. Goldspink G. Loss of muscle strength during ageing studied at the
maximal contractions following six weeks of either endurance or gene level. Rejuvenation Res 2007;10:397–405.
strength training. J Appl Physiol 2010;109:1455–66. 35. Sinha-Hikim I, Cornford M, Gaytan H, et al. Effects of testoster-
11. Häkkinen K, Alen M, Kraemer WJ, et al. Neuromuscular adapta- one supplementation on skeletal muscle fibre hypertrophy and sat-
tions during concurrent strength and endurance training versus ellite cells in community-dwelling older men. J Clin Endocrinol
strength training. Eur J Appl Physiol Appl Physiol 2003;89: Metab 2006;91:3024–33.
42–52. 36. Musarò A, McCullagh K, Paul A, et al. Localized Igf-1 transgene
12. Carolan B, Cafarelli E. Adaptations in coactivation after isometric expression sustains hypertrophy and regeneration in senescent skel-
resistance training. J Appl Physiol 1992;73:911–17. etal muscle. Nat Genet 2001;27:195–200.
13. McCall GE, Byrnes WC, Dickinson A, et al. Muscle fibre hyper- 37. Adams G, McCue S. Localized infusion of IGF-I results in skeletal
trophy, hyperplasia, and capillary density in college men after resis- muscle hypertrophy in rats. J Appl Physiol 1998;84:1716–22.
tance training. J Appl Physiol 2004;81:2004–12. 38. Velloso CP, Harridge SDR. Insulin-like growth factor-I E peptides:
14. Aagaard P, Andersen J, Dyhre-Poulsen P, et al. A mechanism for implications for ageing skeletal muscle. Scand J Med Sci Sports
increased contractile strength of human pennate muscle in response 2010;20:20–7.
to strength training: changes in muscle architecture. J Physiol 39. Yarasheski K. Growth hormone effects on metabolism, body com-
2001;534:613–23. position, muscle mass, and strength. Exerc Sport Sci Rev 1994;22:
15. Andersen J, Aagaard P. Myosin heavy chain IIX overshoot in human 285–312.
skeletal muscle. Muscle Nerve 2000;23:1095–104. 40. Grobet L, Martin L, Poncelet D, et al. A deletion in the bovine
16. Burd N, West DWD, Staples AW, et al. Low-load high volume myostatin gene causes the double-muscled phenotype in cattle. Nat
resistance exercise stimulates muscle protein synthesis more than Genet 1997;17:71–4.
high-load low volume resistance exercise in young men. PLoS 41. McPherron A, Lawler A, Lee S. Regulation of skeletal muscle mass
ONE 2010;5:e12033. in mice by a new TGF-beta superfamily member. Nature 1997;387:
17. Phillips SM, Tipton KD, Ferrando AA, et al. Resistance training 83–90.
reduces the acute exercise-induced increase in muscle protein turn- 42. Schuelke M, Wagner K, Stolz L, et al. Myostatin mutation associ-
over. Am J Physiol 1999;276:E118–24. ated with gross muscle hypertrophy in a child. N Engl J Med
18. Phillips SM, Tipton KD, Aarsland A, et al. Mixed muscle protein 2004;350:1–30.
synthesis and breakdown after resistance exercise in humans. Am J 43. Roth SM, Martel GF, Ferrell RE, et al. Myostatin gene expression
Physiol 1997;273:E99–107. is reduced in humans with heavy-resistance strength training: a
19. Kumar V, Selby A, Rankin D, et al. Age-related differences in the brief communication. Exp Biol Med 2003;228:706–9.
dose-response relationship of muscle protein synthesis to resistance 44. West DWD, Burd NA, Tang JE, et al. Elevations in ostensibly
exercise in young and old men. J Physiol 2009;587:211–17. anabolic hormones with resistance exercise enhance neither
20. Tipton KD, Ferrando AA, Phillips SM, et al. Postexercise net training-induced muscle hypertrophy nor strength of the elbow
protein synthesis in human muscle from orally administered amino flexors. J Appl Physiol 2010;108:60–7.
acids. Am J Physiol Physiol 1999;276:E628–34. 45. NHLBI Workshop Summary. NHLBI Workshop summary. Respi-
21. Hawley JA, Burke LM, Phillips SM, et al. Nutritional modulation ratory muscle fatigue. Report of the Respiratory Muscle Fatigue
of training-induced skeletal muscle adaptations. J Appl Physiol Workshop Group. Am Rev Respir Dis 1990;142:474–80.
2011;110:834–45. 46. Hickson RC. Skeletal muscle cytochrome c and myoglobin, endur-
22. Rommel C, Bodine SC, Clarke BA, et al. Mediation of IGF-1-in- ance, and frequency of training skeletal muscle cytochrome c and
duced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and myoglobin, endurance, and frequency of training. J Appl Physiol
PI(3)K/Akt/GSK3 pathways. Nat Cell Biol 2001;3:1009–13. 1981;51:746–9.
23. Fernández AM, Dupont J, Farrar RP, et al. Muscle-specific inacti- 47. Lin J, Wu H, Tarr P, et al. Transcriptional co-activator PGC-1 a
vation of the IGF-I receptor induces compensatory hyperplasia in drives the formation of slow-twitch muscle fibres. Nature
skeletal muscle. J Clin Invest 2002;109:347–55. 2002;418:797–801.
 7  Neuromuscular Adaptations to Exercise 77

48. Pilegaard H, Saltin B, Neufer PD. Exercise induces transient tran- mitochondrial ultrastructure, substrate use, and mitochondrial
scriptional activation of the PGC-1 gene in human skeletal muscle. enzyme activity. Am J Physiol Regul Integr Comp Physiol
J Physiol 2003;546:851–8. 2007;292:R1271–8.
49. Wright DC, Han D-H, Garcia-Roves PM, et al. Exercise-induced 58. Ricoy J, Encinas A, Cabello A, et al. Histochemical study of the
mitochondrial biogenesis begins before the increase in muscle vastus lateralis muscle fibre types of athletes. J Physiol Biochem
PGC-1a expression. J Biol Chem 2007;282:194–9. 1998;54:41–7.
50. Holloszy JO. Regulation by exercise of skeletal muscle content of 59. Komi P, Viitasalo J, Havu M, et al. Skeletal muscle fibres and
mitochondria and GLUT4. J Physiol Pharmacol 2008;59(Suppl. muscle enzyme activities in monozygous and dizygous twins of both
7):5–18. sexes. Acta Physiol Scand 1977;100:385–92.
51. Ingjer F. Effects of endurance training on muscle fibre ATP-ase 60. Andersen P, Henriksson J. Training induced changes in the sub-
activity, capillary supply and mitochondrial content in man. groups of human type II skeletal muscle fibres. Acta Physiol Scand
J Physiol 1979;294:419–32. 1977;99:123–5.
52. Bloor C. Angiogenesis during exercise and training. Angiogenesis 61. Pette D, Vrbova G. Adaptation of mammalian skeletal muscle fibers
2005;8:263–71. to chronic electrical stimulation. Rev Physiol Biochem 1992;
53. Richardson RS, Wagner H, Mudaliar SRD, et al. Human VEGF 120:115–202.
gene expression in skeletal muscle: effect of acute normoxic and 62. Vila-Chã C, Falla D, Correia MV, et al. Adjustments in motor unit
hypoxic exercise. Am J Physiol – Hear Circ Physiol 1999;277: properties during fatiguing contractions after training. Med Sci
H2247–52. Sports Exerc 2012;44:616–24.
54. Gustafsson T, Knutsson A, Puntschart A, et al. Increased expression 63. Vila-Chã C, Falla D, Correia MV, et al. Changes in H reflex and
of vascular endothelial growth factor in human skeletal muscle in V wave following short-term endurance and strength training.
response to short-term one-legged exercise training. Pflugers Arch J Appl Physiol 2012;112:54–63.
2002;444:752–9. 64. Kernell D, Hultborn H. Synaptic effects on recruitment gain: a
55. Brown M, Hudlicka O. Modulation of physiological angiogenesis mechanism of importance for the input-output relations of moto-
in skeletal muscle by mechanical forces: involvment of VEGF and neurone pools? Brain Res 1990;507:176–9.
metalloproteinases. Angiogenesis 2003;6:1–14. 65. Maffiuletti N, Martin A, Babault N, et al. Electrical and mechanical
56. Martin W 3rd. Effect of endurance training on fatty acid metabo- H(max)-to-M(max) ratio in power- and endurance-trained athletes.
lism during whole body exercise. Med Sci Sport Exerc 1997; J Appl Physiol 2001;90:3–9.
29:635–9.
57. Tarnopolsky MA, Rennie CD, Robertshaw HA, et al. Influence of
endurance exercise training and sex on intramyocellular lipid and
 CHAPTER 8 

The Peripheral Nervous System and

its Compromise in Entrapment
Neuropathies
Annina Schmid

and physiology of the peripheral nervous system with

INTRODUCTION a focus on its compromise following entrapment neu-
ropathies. Common clinical signs and symptoms are put
The nervous system is an intricate network of intercon- in context with potential underlying mechanisms.
nected systems of neuronal and non-neuronal cells that
relay messages between the periphery, spinal cord and
brain. This chapter will focus on the peripheral nervous
system (including the sensory ganglia) which contains
ANATOMY AND PHYSIOLOGY
motor, sensory and sympathetic neurons that travel in Peripheral Neurons
close proximity within the same nerve trunk. Peripheral
neurons are the largest cells of the body, spanning up to The main functional component of peripheral neurons
100 cm (e.g. motor neurons of the sciatic nerve). This consists of the axon and dendrites as well as their cell
extraordinary length not only permits communication body (e.g. in the dorsal root ganglion for sensory neurons).
between the periphery and the central nervous system, Another integral part of neurons is Schwann cells that
but it also means that neurons need specific anatomical can be myelinating or non-myelinating (see section on
and physiological properties to cater for their length. Schwann cells and myelin). Neurons can broadly be
Given the extensive length of peripheral nerves and their divided into three main groups based on anatomical and
unique anatomy and physiology, it is not surprising that functional criteria (Fig. 8-1): thick myelinated fibres
nerve injuries cause symptoms and signs that are distinct transmitting signals to and from muscles (e.g. Aα fibres)
from other musculoskeletal conditions. Typically, these and conducting sensations such as touch and propriocep-
include a mix of gain and loss of function such as motor tion (Aβ fibres);1 thinly myelinated fibres (Aδ fibres)
(e.g. weakness) and sympathetic signs (e.g. impaired transmitting nociceptive signals evoked by stimuli such
sweating), as well as sensory symptoms and signs such as as cold and pin prick;2 and small-diameter unmyelinated
numbness, paraesthesia, dysaesthesia, allodynia, hyperal- nerve fibres (C fibres) subserving nociception evoked by
gesia and neuropathic pain (for taxonomy see IASP1) in heat or mechanical stimuli as well as innocuous tempera-
the innervation territory of the affected nerve. Nerve ture changes (e.g. warm detection) and itch.3 As such, C
injuries can also lead to increased sensitivity of the nerve fibres are not purely nociceptive. In fact, it has recently
itself.2 In contrast to pain of other origins, symptoms been suggested that C fibres may also mediate pleasant
related to nerve injury are more severe and are associated touch sensations elicited by brushing of the skin.10 Fur-
with higher depression, anxiety and poorer quality of thermore, postganglionic sympathetic neurons are also
life.3,4 small-diameter unmyelinated axons belonging to the C
The most common condition affecting the peripheral fibre category.
nervous system is entrapment neuropathy. For instance, Whereas motor fibres are efferent and send signals
the prevalence of lumbar radiculopathy in the general from the central nervous system to target tissue (e.g.
population is ~2.2%,4 whereas carpal tunnel syndrome muscles), sensory afferent fibres convey information from
(CTS) occurs in ~3.7% of people.5 Systemic diseases such the periphery to the central nervous system. The non-
as obesity or diabetes can, however, elevate the lifetime nociceptive sensory afferents originate from receptors in
risk of developing entrapment neuropathies to up to peripheral tissues (e.g. Meissner and Ruffini corpuscles,
85%.6 Despite their high prevalence, the exact patho- Merkel cells, muscle spindles). In contrast, the receptor
physiology underlying entrapment neuropathies remains organs of nociceptors are free nerve endings. These
elusive,7 but significant advances in neuroscience research endings form an intricate network of fine axonal branches
have been made in the past decade. A better understand- which contain an abundance of membrane proteins (ion
ing of the pathophysiology may help to improve diagnos- channels) that respond to different chemical, mechanical
tic reasoning and facilitate the design of more effective and thermal stimuli and agents in the surrounding tissue.
management options. Whereas the readers are directed Nociceptors can not only be subdivided according to
to specialized texts for a comprehensive overview of the their fibre diameter and myelination, but a more recent
anatomy and physiology of the peripheral nervous and more functional differentiation distinguishes their
system,8,9 this chapter summarizes the normal anatomy sensitivity to the type (modality) of stimulus (e.g.
78
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 79

mechanosensitive, heat sensitive or chemosensitive) and The distinct patterns of responsiveness of sensory
their response characteristics (e.g. low or high threshold) neurons to different stimuli have led to the development
according to the type of ion channels present in their free of quantitative sensory testing, in which the functions of
nerve endings. Using this functional approach, four main these different fibre domains are examined (see Chapter
groups of C-nociceptors can be distinguished (Table 20).13 Clinicians are reminded that a standard bedside
8-1):11 C-polymodal fibres (activated by mechanical, neurological examination (reflex, muscle and light touch
thermal and chemical stimuli;1 C fibres that are activated testing) is limited to the function of large-diameter motor
by specific modalities (e.g. mechanonociceptors, heat and sensory neurons, and does not provide any informa-
nociceptors, etc.);2 low-threshold C fibres which mediate tion on the functional or structural integrity of small
pleasant touch;3 and silent (sleeping) nociceptors.4 The myelinated or unmyelinated neurons, which represent
latter are not normally activated by thermal or mechani- the majority of neurons within a peripheral nerve.
cal stimuli, but become sensitized after exposure to
inflammatory stimuli (for a review see Michaelis et al.12).
Schwann Cells and Myelin
Whereas both myelinated and unmyelinated axons are
associated with Schwann cells, only the Schwann cells of
the myelinated fibres produce an insulating layer of lipids
and proteins, the so-called myelin sheaths. In the periph-
eral nervous system, one Schwann cell produces the
myelin sheath for only a short axon segment whereas
oligodendrocytes can produce myelin sheaths for up to
30 axons in the central nervous system.14 A thick myelin-
ated sensory neuron of the human femoral nerve contains
up to 500 Schwann cells.14 The Schwann cells and the
axons maintain close contact in regions called paranodes
(Fig. 8-2), which are adjacent to the nodes of Ranvier.
Nodes of Ranvier are the gaps between myelin sheaths.
These are around 1 µm in length and expose the axon
membranes to the extracellular space. A thick myelinated
human femoral neuron contains around 300–500 nodes
of Ranvier.14 These nodes comprise a high density of
voltage-gated sodium channels, whereas potassium chan-
nels are localized to the juxtaparanodes (the region adja-
cent to the paranodes) beneath the myelin.16 Together
with the myelin sheath (the internodes), this specific ion
channel architecture allows saltatory action potential
FIGURE 8-1  ■  Cross-section through a healthy peripheral nerve conduction in myelinated axons, which explains the
trunk. Electron microscope image of a normal sciatic nerve of a
rat taken at 8000× magnification demonstrates the different
higher conduction velocities of Aα and Aβ fibres (thick
structures present within a peripheral nerve trunk. These include myelinated, ~70–120 m/s) followed by Aδ fibres (thinly
the perineurium, which surrounds a fascicle, the endoneurium, myelinated, ~6–25 m/s) and C fibres (unmyelinated,
large-diameter myelinated neurons (LDM), small-diameter ~1 m/s).17 The distinct myelination and resulting differ-
myelinated neurons (SDM) and unmyelinated neurons (UM), ence in conduction velocity of the two nociceptor fibre
which form Remak bundles. Several Schwann cell nuclei of both
myelinating and non-myelinating Schwann cells as well as cap- types is suggested to account for the rapid, acute and
illaries are present in this field. (Image courtesy of A/Prof Mar- sharp (Aδ) versus delayed, diffuse and dull pain evoked
garita Calvo, Pontificia Universidad Católica de Chile.) by noxious stimuli (C fibres).18

TABLE 8-1  Cutaneous Sensory Fibre Types

Fibre Myelination Fibre Diameter Fibre Type Modality %
Aβ Thick myelinated Large Slowly adapting mechanoreceptor Touch 12
Rapidly adapting mechanoreceptor Touch 10
Aδ Thinly myelinated Smaller Low-threshold D-hair mechanoreceptors Touch 6
Mechanonociceptors Nociception 12
C Unmyelinated Very small C-polymodal Nociception 30
C-mechanonociceptor, C-mechanoheat nociceptor; Nociception 20
C-mechanocold nociceptor; C-heat nociceptor
C-low threshold Pleasant touch ~5
Silent Nociception ~5

The table details the differentiation of cutaneous sensory nerve fibres according to their myelination properties and fibre diameters.
Furthermore, the different subtypes and their sensory modalities are outlined. The percentage reflects cutaneous fibre distribution.
(Adapted from Smith and Lewin.11)
80 PART II  Advances in Theory and Practice

Paranodal loops

Internode Juxtaparanode Paranode Node Paranode Juxtaparanode Internode

VGSC Potassium
channels

FIGURE 8-2  ■  Nodal architecture. The image depicts an axon and its myelin sheath, which have a close interaction in the paranodal
region (paranodal loops). The gap between the myelin sheath is called node of Ranvier and contains an abundance of voltage-gated
sodium channels (VGSC). In contrast, potassium channels are localized beneath the myelin sheath at the juxtaparanodes. (Figure
adjusted from Poliak and Peles15 with permission.)

Neural Connective Tissue nervi nervorum also arise from perivascular neural plexi
and Its Innervation that surround the major blood vessels that supply the
nerve trunks.24 Nervi nervorum run longitudinally as well
The peripheral nervous system not only contains axons as spirally along the epineurium and perineurium and are
and associated Schwann cells, but also a substantial also present in the endoneurium. Nervi nervorum consist
amount of connective tissue, which has an important of both myelinated and unmyelinated fibres and some of
protective function. There are three distinct connective them end as free nerve endings,24 which suggests a poten-
tissue sheaths (Fig. 8-3). The endoneurium surrounds tial role as nociceptors. This proposal is further strength-
single axons and is in close contact with Schwann cells. ened by the expression of calcitonin gene-related peptide
The perineurium surrounds each nerve fascicle (bundle (CGRP), peripherin or substance P in some nervi nervo-
of axons) and consists of several layers of flat perineurial rum.25,26 These neuropeptides have been implicated with
cells (epithelial-like cells) with tight junctions (see section nociceptors and neurogenic inflammation (see section on
on neural blood circulation and blood–nerve interface).20 neurogenic inflammation).27
The perineurium has an important mechanical and
physiological protective function for the nerve fascicles.21 Neural Blood Circulation
The epineurium is the outermost layer and surrounds all
fascicles of a peripheral nerve trunk. Its thickness not
and Blood–Nerve Interface
only varies between individuals, but also along the nerve Similar to other cells, neurons are highly dependent on
trunk. Generally, the epineurial tissue is thickest where a an adequate energy supply for metabolic processes such
nerve passes close to a joint and thinnest in intervening as protein synthesis (e.g. neurotransmitters). Whereas
regions.22 The epineurium is loosely attached to its sur- neuron cell bodies have the greatest metabolic demand,
rounding nerve bed but relatively fixed in regions where peripheral nerve trunks also use energy for active pro-
branches depart to innervate muscle tissue.21 At the sub- cesses including axonal transport or ion pumps to restore
arachnoidal angle of the dorsal root ganglia, the connec- membrane potentials following action potential genera-
tive tissues of the peripheral nerve trunk merge with the tion. In order to meet the required energy supply, the
meninges of the central nervous system. Whereas the nervous system possesses an intricate blood circulation
epineurium is continuous with the dura mater, the peri- system, the vasa nervorum. The blood supply to the
neurium splits to form the arachnoid layers and the root peripheral nervous system stems from radicular vessels
sheaths (comparable to the pia mater).20 that branch off blood vessels that commonly run in paral-
Peripheral nerves also contain a small amount of lel with the major peripheral nerves (e.g. the tibial nerve
adipose tissue. This is especially apparent in the sciatic together with the tibial artery and vein). The intrinsic
nerve, whereas the nerves of the upper extremity rarely neural blood circulation consists of longitudinally orien-
contain significant amounts of fat.23 It has therefore been tated epineural vessels that descend into the perineurium
suggested that the main function of intraneural fat is and ultimately pierce into the endoneurium where a
protection from excessive pressure.23 dense capillary network can be found (Fig. 8-3). This
The neural connective tissue is innervated by so-called network is characterized by extensive anastomoses that
nervi nervorum.24 In the periphery, these run together assure a continuous blood supply. In line with the
with the nerve trunk, whereas spinal nerves, dorsal root increased metabolic demand, the capillary density and
ganglia and nerve roots are innervated by axons that blood flow in dorsal root ganglia is greater than
project directly to the dorsal root ganglia. Some of the in peripheral nerve trunks.28 To maintain adequate
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 81

microcirculation of a nerve, a specific pressure gradient endoneurial space and blood vessels, it has been sug-
is required.29 This gradient is characterized by the gested that the term blood–nerve interface rather than
highest pressure in the arteries followed by the capillar- blood–nerve barrier is appropriate.20 Since the blood–
ies, the nerve fascicles, the veins and the lowest pressure nerve interface is relatively impermeable and there is a
in the space surrounding the nerve.29 slight positive pressure in the endoneurial space, the
In contrast to the epineurium, the endoneurial space regulated exchange of vital molecules (e.g. to maintain
does not contain a lymphatic system.30 Therefore, axons, pH, hydrostatic pressure and ion concentrations) depends
Schwann cells and other resident cells within the endo- on the presence of pumps and transporters in the blood–
neurium are dependent on a protective interface that nerve interface.31 Another mechanism that contributes
preserves them from potentially harmful plasma materi- to the maintenance of the specialized microenvironment
als. This is achieved by tight junctions of the epithelium of peripheral nerves is the turnover of endoneurial fluid
of endoneurial blood vessels and layers of perineurial by a proximal to distal fluid flow whose speed is estimated
cells,20 that provide a diffusion barrier to larger molecules to be ~3  mm per hour.32
and restrict smaller molecules from entering the endo- In contrast to the relatively impermeable blood–nerve
neurial space. As this structure not only restricts, but interface in the distal nerve trunks, the endoneurial
also regulates, the exchange of molecules between the vessels of nerve roots, dorsal root ganglia as well as

Artery

Epineurium
Radicular vessel
Endoneurium

Perineurium

Unmyelinated Schwann
axons cell

Blood
vessels

Fascicle

Capillaries
Schwann
cell soma

Node of
Ranvier

Myelinated Myelin
axon sheath
FIGURE 8-3  ■  Neural blood circulation and connective tissue of a peripheral nerve trunk. The image shows the anatomical orientation
of the endoneurium which surrounds single axons and their Schwann cells, the perineurium that surrounds fascicles as well as the
epineurium that surrounds all fascicles of the nerve trunk. The peripheral nerve trunk receives its blood supply from radicular vessels
that branch off major extraneural arteries. The intraneural vessels form an intricate network of longitudinal epineural and perineural
vessels that also pierce into the endoneurium. Note the many anastomoses that assure continuous blood supply. (Figure adjusted
from19 with permission.)
82 PART II  Advances in Theory and Practice

sympathetic and cranial ganglia have a fenestrated endo- Central Nervous System
thelium, which allows relatively free passage of mole-
cules.33 Furthermore, the perineurium is thinner at the The peripheral nervous system is well connected with the
subarachnoidal angle and the intercellular junctions of central nervous system. Even though we anatomically
the nerve root sheaths are not as dense as those of the differentiate these two systems, they form a functional
perineurium in the peripheral nerve trunk.34 As such, entity that cannot be separated. Due to the focus of this
these structures are not well protected from potentially chapter on the peripheral nervous system, readers are
harmful plasma extravasates. referred to other texts detailing the anatomy and physiol-
ogy of the central nervous system.8,9
Axonal Transport
In addition to the intricate blood supply, axonal transport PATHOPHYSIOLOGY OF
is another system that is essential for the functioning and ENTRAPMENT NEUROPATHIES
health of neurons. It serves the transportation of cargoes
such as proteins that are produced in the neuronal cell Whereas the exact aetiology of entrapment neuropathies
bodies but are needed in the axons and synaptic termi- remains elusive and is most likely multifactorial, there
nals. This transport system can be divided into antero- is an established link with increased extraneural pres-
grade and retrograde transport. Anterograde transport sures.38,39 These pressures may lead to ischaemia with
assures the provision of structural components and new resulting functional changes. Structural compromise of
organelles such as synaptic boutons or ion channels neural components may ensue in some patients. Presum-
towards the proximal and distal regions of neurons. ably, the relative contribution of functional and structural
Retrograde transport brings organelles and ligands from changes to the pathophysiology of entrapment neuropa-
the synapses or peripheral nerve endings to the neuron’s thies is a matter of disease severity or progression. This
cell body.21 Membranous organelles (e.g. receptors, neu- part of the chapter summarizes the available evidence on
rotransmitters, mitochondria) are usually transported by the impact of entrapment neuropathies on the previously
fast axonal transport (~400  mm/day) whereas cytoskeletal outlined anatomical and physiological aspects of the
proteins and peptides (e.g. CGRP) are transported by peripheral nervous system. Rather than discussing the
slow axonal transport (~0.2–2.5  mm/day).35 The trans- changes triggered by acute and severe experimental nerve
port of these cargoes occurs along longitudinally orien- injuries (which may be distinct from entrapment neu-
tated, hollow microtubules, which serve as rails for the ropathies), focus will be placed on the growing evidence
transport within axons.21 Within these microtubules, from animal models of chronic mild nerve compression
specific molecular motors (kinesin and dynein families) and patients with entrapment neuropathies.
bind to the cargoes and transport them along the axons
and dendrites.21 These motors use energy (e.g. ATP),
which makes axonal transport an active process. This is
Entrapment Neuropathies and Ischaemia
why the previously used term ‘axonal flow’ has been Entrapment neuropathies are thought to lead to changes
replaced with ‘transport’, which implies a more active in intraneural blood flow by reversal of the pressure gra-
process. dient necessary to assure adequate blood supply. Animal
models demonstrate that extraneural pressures as low as
20–30 mmHg disrupt intraneural venous circulation and
The Immune Cells of the Nervous System pressures of 40–50 mmHg suppress arteriolar and capil-
The immune system operates to defend an organism lary blood flow.40 In patients with entrapment neuropa-
against foreign proteins such as infectious microbes,36 but thies, extraneural pressure is elevated. In CTS for
it also plays an important role in the clearance of the instance, the mean pressure in the carpal tunnel is over
body’s own tissue debris. Circulating immune cells in the 30 mmHg in neutral wrist positions38,41 and rises up to
blood freely enter most tissues of the body. The blood– 250 mmHg in end-range wrist positions.38,42 In patients
nerve interface, however, limits trafficking of immune with lumbar disc herniations, comparably high pressures
cells into the nervous system. Nevertheless, a small of over 50 mmHg were measured around the affected
number of resident immune cells can be found within the nerve roots with some patients exhibiting pressures as
peripheral nervous system and its connective tissues. high as 250 mmHg.39 Such elevated pressures – especially
These cells include mast cells, macrophages, dendritic if present for prolonged periods of time – will be suffi-
cells and lymphocytes, which assume a surveillance func- cient to reverse the normal pressure gradient,29 causing
tion within the peripheral nerve. The complement obstruction of venous return with subsequent intraneural
system, which consists of around 30 different plasma pro- circulatory slowing and oedema formation.
teins, is also a major component of the immune system Transient ischaemia is a common finding in patients
that once activated induces destruction of pathogens and with entrapment neuropathies. It not only explains the
facilitates inflammation.37 In addition to immune cells, classic position-dependent paraesthesia, but can also con-
some cells such as Schwann cells and satellite glial cells tribute to the reproduction of symptoms during provoca-
in the dorsal root ganglia can acquire an immune modu- tive manoeuvres such as Phalen’s or reverse Phalen’s test
latory function. Within the central nervous system, peri- for CTS or Spurling’s test for cervical radiculopathy. The
vascular cells and glial cells (astrocytes and microglia) are typical exacerbation of symptoms at night that resolves
immune-competent. upon gentle movement can also be attributed to
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 83

ischaemia. The physiological nocturnal decrease of blood Entrapment Neuropathies

pressure and related drop in intraneural blood flow43 can Cause Demyelination
reverse the pressure gradient, which induces ischaemia
with subsequent changes in metabolic activity and ectopic Focal demyelination is considered a hallmark of nerve
firing. Venous distension itself may also contribute to the entrapments.54 It is thought to be responsible for the
pain experience by activating venous afferents.44 characteristic slowing of nerve conduction,61 although
In mild entrapment neuropathies, ischaemia may be ischaemia alone is also capable of inducing conduction
present in the absence of structural changes. This is block.62,63 Demyelination is a typical downstream effect
apparent by the immediate relief of symptoms after of prolonged ischaemia that leads to Schwann cell dys-
surgery in some patients.45 Prolonged or repetitive com- function,64 but it can also be attributed to mechanical
pression and ischaemia can, however, initiate downstream deformation65 or a cytotoxic environment due to pro-
effects including demyelination (see section entitled cesses such as inflammation (see section on the role of
entrapment neuropathies cause demyelination) or a com- the immune system in entrapment neuropathies). Histo-
promise of the blood–nerve interface.46,47 This may lead logical data from animal models of mild nerve
to an influx of inflammatory cells (see section on the role compression66–68 and from patients with entrapment
of the immune system in entrapment neuropathies) and neuropathies69–71 confirm focal demyelination and remy-
plasma macromolecules, which elevates the osmolality of elination with intra-fascicular fibrosis and connective
endoneurial fluid with subsequent oedema formation. A tissue thickening. Similar histological findings have,
decrease in endoneurial fluid flow due to mechanical however, also been identified in asymptomatic individuals
compression and the absence of a lymphatic system may at common entrapment sites.72,73 This suggests that such
further challenge the evacuation of intraneural oedema.48 focal histological changes alone do not necessarily lead
Clinically, the presence of oedema in entrapment neu- to symptoms.
ropathies is apparent by an enlargement of the com- In addition to focal demyelination, there is recent evi-
pressed nerves49,50 as well as by increases in signal intensity dence that myelin changes extend beyond the lesion site.
on specialized magnetic resonance sequences.51–53 This is supported by demyelination of the tibial nerve
If prolonged, oedema can eventually lead to intraneu- following focal mild nerve compression of the sciatic
ral and extraneural fibrotic changes affecting the connec- nerve in rats67 as well as by the presence of elongated
tive as well as adipose tissues.54 Neural fibrosis has been nodes of Ranvier in skin biopsies taken over 9 cm beyond
found both in radiculopathies55 as well as entrapments of the compression site in patients with CTS (Fig. 8-4).74 As
peripheral nerve trunks (e.g. cubital and carpal tunnel mentioned above, nodes of Ranvier have a specific con-
syndrome).56,57 It can be speculated that extraneural figuration of ion channels. After severe experimental
fibrotic changes may underlie the impaired gliding ability nerve injury, the gene expression of electrosensitive,
of compressed nerves in relation to their surrounding mechanosensitive and chemosensitive channels changes
tissues such as is found in patients with CTS.58–60 However, in the cell bodies of sensory neurons.75,76 Since ion chan-
such biomechanical changes are unlikely to be the only nels are more easily inserted into the membrane at
mechanism underlying signs of increased nerve sensitiv- demyelinated sites and the neuronal cell body, modifica-
ity during neurodynamic testing (e.g. provocation of tions of ion channel configuration are prevalent at
symptoms, change in symptoms by moving joints at some these sites.77–80 Changes can include both down- and
distance from the symptomatic area [structural differen- up-regulation of certain channels as well as expression of
tiation], and potentially reduced range of motion). Rather, novel channels. These ion channel changes have been
a plethora of neurophysiological changes leading to implicated in spontaneous ectopic generation of action
increased neural mechanosensitivity may account for potentials.81,82 Since action potentials are normally only
positive neurodynamic tests in patients with entrapment transmitted but not initiated along the axon or their cell
neuropathies. Some of these neurophysiological changes bodies, these sites are called abnormal impulse generat-
are discussed below. ing sites. There is preliminary evidence that experimental

$ %

FIGURE 8-4  ■  Patients with CTS have elongated nodes of Ranvier. (A) Normal nodal architecture of a dermal myelinated fibre shown
by a distinct band of voltage-gated sodium channels (pNav, blue) located in the middle of the gap between the myelin sheaths
(green, myelin basic protein [MBP]). Paranodes are stained with contactin associated protein (Caspr, red). (B) A dermal myelinated
fibre of a patient with carpal tunnel syndrome demonstrating an elongated node with an increased gap between the myelin sheaths.
Voltage-gated sodium channels are dispersed within the elongated node. For colour version see Plate 8.
84 PART II  Advances in Theory and Practice

mild nerve compression is sufficient to induce a de novo an animal model of mild nerve compression.67 There is a
expression of specific voltage-gated sodium channels in growing body of clinical evidence that small fibres are
the injured neurons.83 We have recently confirmed this affected in patients with entrapment neuropathies. For
in patients with CTS, who demonstrated changes in the instance, most studies using quantitative sensory testing
localization of voltage-gated sodium channels within suggest loss of function of small myelinated and unmy-
elongated nodes in their skin74 (Fig. 8-4). Furthermore, elinated fibres (deficit in cold and warm detection) in
threshold tracking has previously revealed sensory axon both lumbar and cervical radiculopathy as well as
hyperexcitability in patients with CTS.84 This is a special- CTS.74,92–96 Furthermore, several studies find significant
ized neurophysiological technique that provides informa- alterations of sympathetic axon function in patients with
tion on the excitability (hyper or hypo) of axons that are CTS and radiculopathy97–102 and laser-evoked brain
presumably caused by changes in ion channels.85 If con- potentials (mediated by Aδ and C fibres) are reduced in
firmed in other studies, changes to the configuration of patients with CTS.103
ion channels in entrapment neuropathies may not only It has been confirmed that small fibres are not only
underlie the ectopic activity (e.g. paraesthesia, Tinel’s compromised in their function, but also in their struc-
sign, nerve mechanosensitivity upon palpation), but may tural integrity in patients with entrapment neuropa-
also impair normal saltatory impulse conduction, which thies.74,104 This is apparent by a striking loss of epidermal
manifests itself by the characteristic slowing or block of nerve fibres in the skin of patients with CTS (Fig. 8-5).
nerve conduction upon electrodiagnostic testing.61,62 The density of these free nerve endings (exclusively C
and Aδ fibres) can be quantified in skin biopsies using
specific markers for axonal proteins (immunohistochem-
Entrapment Neuropathies Affect Both istry). A loss of small epidermal axons has previously been
implicated with more severe neuropathic pain conditions
Large- and Small-Diameter Nerve Fibres such as diabetes mellitus105 or HIV-associated neuropa-
It is commonly believed that entrapment neuropathies thy,106 but the underlying mechanisms remain elusive.
predominantly affect the large myelinated fibres (e.g. Potentially, ischaemia64 or prolonged exposure to inflam-
demyelination, axon damage)54,86 and that small axons are mation may induce changes in axonal integrity (see
relatively resistant to compression.86 Indeed, numbness section on the role of the immune system in entrapment
to light touch within the innervation territory of the neuropathies).107
affected nerve or nerve root is common and indicative of The impact of the identified loss of small fibres on
Aβ fibre dysfunction. Furthermore, motor axons can be diagnosis and management of entrapment neuropathies
compromised in patients with severe entrapment neu- remains to be further explored. Interestingly though,
ropathies as apparent by muscle atrophy (e.g. thenar preliminary data in patients with symptoms indicative of
atrophy in CTS) or paresis (e.g. foot drop in lumbar CTS but normal neurophysiology suggest that small
radiculopathy). Clinical diagnosis of suspected entrap- axon dysfunction or loss may precede changes in electro-
ment neuropathy therefore largely relies on large fibre diagnostic testing.74,93 These findings suggest that (early)
tests. For instance, the guidelines on the diagnosis of diagnosis of entrapment neuropathies should include
CTS by the American Association of Orthopedic tests for small fibre function. Clinical small fibre tests
Surgeons mention two point discrimination, Semmes- include simple bedside neurological tests (e.g. evaluation
Weinstein monofilaments, vibrometry and texture dis- of pin prick sensitivity, cold and warm detection) as well
criminations as sensory tests to diagnose CTS.87 These as more equipment-intensive examinations such as quan-
tests exclusively evaluate the large myelinated fibres and titative sensory testing, sympathetic reflex testing, laser
no mention is made of tests evaluating small fibre func- or heat-evoked brain potentials or skin biopsies. Further
tion. Similarly, the guidelines for the diagnosis and treat- research is required to evaluate the utility and diagnostic
ment of cervical radiculopathy focus on tests for large performance of small fibre tests in patients with entrap-
fibres (e.g. reflexes, muscle strength, light touch sensa- ment neuropathies.
tion) and only mention one study where pin prick was
tested.88 Electrodiagnostic testing, which exclusively
examines the function of large myelinated sensory and The Role of the Immune System in
motor axons is also commonly used to diagnose and clas-
sify patients with entrapment neuropathies.89 Its correla-
Entrapment Neuropathies
tion with patients’ symptoms and functional deficit is, It is well established that the immune system plays a
however, often poor.90 Furthermore, electrodiagnosis pivotal role in severe peripheral nerve injuries and neu-
and bedside neurological examination are within normal ropathic pain (for reviews see references 108–111). There
limits in a subgroup of patients with symptoms indicative is growing evidence that the immune system also
of entrapment neuropathy.91,92 This suggests that other contributes to signs and symptoms in entrapment neu-
factors apart from large fibre (functional or structural) ropathies. It is well known that experimental exposure of
compromise are at play in patients with entrapment nerve roots to nucleus pulposus material induces a local
neuropathies. immune inflammation within nerve roots.112,113 Similarly,
In contrast to common beliefs that small fibres are experimental mild peripheral nerve compression activates
relatively resistant to compression,86 a predominant com- immune cells locally67,114 (Fig. 8-6A). Influx of blood-
promise of small axons with structural sparing of large borne immune cells is facilitated by a compromise of the
axons (apart from their demyelination) was apparent in protective blood–nerve interface.47 Furthermore, myelin
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 85

$ % &
FIGURE 8-5  ■  Patients with CTS have a loss of small fibres. (A) Cross-section through a healthy skin taken on the lateropalmar aspect
of the second digit. The dermal–epidermal junction is marked with a faint line with the epidermis located on top. Axons are stained
with protein gene product 9.5 (a panaxonal marker, red) and cell nuclei are stained with DAPI (blue). There is an abundancy of nerve
fibres in the subepidermal plexus as well as inside papillae (arrowheads). Many small fibres pierce the dermal–epidermal junction
(arrows). (B) Skin of an age- and gender-matched patient with carpal tunnel syndrome (CTS) demonstrates a clear loss of intraepi-
dermal nerve fibres and a less dense subepidermal plexus. (C) Graph confirms a substantial loss of intraepidermal nerve fibres (per
mm epidermis) in patients with CTS (p < 0.0001, mean and standard deviations). For colour version see Plate 8.

and axon debris contributes to recruitment and activation vessels, which limit the protective function of the blood–
of neutrophils, mast cells and phagocytic macrophages,115 nerve interface at this level. Animal models of radiculopa-
which in turn trigger a complex cascade that leads to thy also demonstrate an activation of glial cells in the
immune cell activation (Fig. 8-7). Upon their activation, dorsal horn of the spinal cord,125–127 whereas such a reac-
immune cells release a plethora of pro-inflammatory tion seems to require more severe injuries to the periph-
mediators (e.g. cytokines, prostaglandins). Immunocom- eral nerve trunk.67,128,129 Prolonged nerve root injuries or
petent cells such as Schwann cells also ingest myelin115 severe peripheral nerve injuries may also activate glial
and subsequently release pro-inflammatory and chemo- cells in the contralateral dorsal horn.126,127,130 Such remote
tactic factors that attract other immune cells.117 Pro- immune inflammation in areas where both injured and
inflammatory mediators lower the firing threshold of non-injured neurons lie in close proximity may increase
both mechanosensitive and nociceptive neurons118–120 and the excitability of intact neurons that originate from sites
can activate silent nociceptors.12 As such, intraneural distant to the actual injury. The resulting hyperexcitabil-
inflammation is another mechanism that can explain ity of intact neurons could explain the clinically observed
evoked (e.g. palpation, provocation tests such as Spurling, extradermatomal and extraterritorial pain and hyperalge-
Phalens’ or neurodynamic tests) and spontaneous pain or sia that are commonly observed in patients with entrap-
paraesthesia in patients with entrapment neuropathies. ment neuropathies.131–133
Together with ischaemia, it may also account for the Apart from inducing neuronal hyperexcitability, pro-
nocturnal exacerbation of symptoms. The presence of an inflammatory cytokines and other substances associated
inflammatory component is supported by the beneficial with activated immune cells (e.g. neurotoxic oxygen radi-
short-term effect of anti-inflammatory medication (non- cals and proteolytic enzymes) can induce mitochondrial
steroidal and steroidal) in patients with radiculopathies or damage. Since mitochondria are vital energy sources for
entrapment neuropathies of peripheral nerve trunks.121,122 neurons and Schwann cells (e.g. for ion pumps, axonal
In addition to intraneural inflammation, mild nerve transport, myelination), their dysfunction and the result-
compression also induces an inflammatory reaction in ing energy shortage leads to demyelination and neuronal
the connective tissue sheaths (Fig. 8-6B). If exposed degeneration.107,134 Whereas the effect of inflammation
to an inflammatory environment, the nervi nervorum on small peripheral axon integrity has not specifically
in the connective tissue increase their mechanosensitiv- been examined, immune cell infiltration of the central
ity.123 It has therefore been postulated that the nervi nervous system such as in multiple sclerosis can induce
nervorum may contribute to heightened nerve sensitivity axonal damage,67 particularly of small-calibre axons.68
or pain (upon palpation, provocative manoeuvres and Further studies are, however, needed to reveal whether
neurodynamic tests) even if nerve conduction (electro- inflammation is a potential explanation for small axon
diagnostic tests and bedside neurological examination) loss in patients with entrapment neuropathies.
is preserved.124
Interestingly, the activation of immune and immune-
competent cells is not restricted to the lesion site, but can
Neurogenic Inflammation
be found in associated dorsal root ganglia after peripheral In peripheral sensory neurons, action potentials normally
nerve compression67 (Fig. 8-8) or nerve root compro- travel towards the central nervous system (orthodromic).
mise.112 Immune cell influx into the dorsal root ganglia is Upon activation and sensitization of nociceptive C fibres,
facilitated by the fenestrated epithelia of local blood however, action potentials can also travel towards the
86 PART II  Advances in Theory and Practice

$ CD68

% CD68 / GFAP

FIGURE 8-6  ■  Experimental mild nerve compression induces a local immune-inflammatory reaction intraneurally as well as in con-
nective tissue. Longitudinal sections through non-operated (left) and mildly compressed (right) sciatic nerves of rats. (A) Top panel
shows the presence of resident CD68+ macrophages in a non-operated nerve (left) and an intraneural activation and recruitment of
macrophages beneath a mild nerve compression (right). (B) The activation and recruitment of CD68+ macrophages (red) within the
epineurium following mild nerve compression (right) compared to a healthy nerve (left). Schwann cells are stained in green with
glial fibrillary acid protein (GFAP). For colour version see Plate 9.

axon branches of the peripheral free nerve endings (anti- within the connective tissue of the peripheral nervous
dromic). These antidromic impulses lead to the release system is another mechanism that may explain height-
of vasoactive and inflammatory mediators in a subgroup ened nerve mechanosensitivity.
of small fibres (peptidergic fibres).135 In humans, these
fibres include mechano-insensitive C-nociceptors but not Experimental Mild Nerve Compression
polymodal C fibres as is the case in animal models.136
Human microdialysis experiments suggest that the main
Impairs Axonal Transport
mediator is the potent vasodilator CGRP whereas the Nerve or nerve root compression can affect both the slow
contribution of substance P (a vasodilator and activator and fast retrograde and anterograde axonal transports
of mast cells) seems minor.137 This phenomenon is called as shown by radioactive labelling of the transported
neurogenic inflammation and if present in the skin of proteins.139–143 In animals, pressures on nerves as low as
patients with entrapment neuropathies, it may be visible 20 mmHg are sufficient to impair axonal transport.141
by a slight reddening, increase in temperature or trophic Even though direct comparison with humans warrants
changes in the corresponding dermatome or peripheral caution, the extraneural pressures observed in patients
nerve territory. Neurogenic inflammation may also be with entrapment neuropathies are well above this critical
present in deeper tissues including the connective tissue experimental threshold.38,39 In addition to mechanical
of the nervous system, where nervi nervorum have been factors, inflammation also impairs axonal transport.144
shown to secrete CGRP.138 Neurogenic inflammation Experimental blockage of axonal transport results in
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 87

Neutrophils

Mast cell

Macrophages T-cells

IL-1, IL-2 and TNF or

TNF, PGE, IL-1, IL-4, IL-5, IL-10
IL-6, IL-12

Schwann cell Axon

NGF, TNF, IL-1,

IL-6, IL-8, PGE, ATP

Intraneural blood vessel

FIGURE 8-7  ■  Activation of immune and inflammatory cells at the site of a peripheral nerve injury. A peripheral nerve lesion leads
to an early activation of mast cells and neutrophils, which release chemicals that activate resident macrophages. The macrophages
phagocytose axonal or myelin debris and secrete pro-inflammatory substances that sensitize axons or attract other immune cells.
A breakdown of the blood–nerve interface by physical damage or substances released by immune cells leads to an additional influx
of blood-borne immune cells. Schwann cells also ingest myelin and subsequently release pro-inflammatory chemicals. Both
Schwann cells and macrophages signal T cells, some of which will also secrete inflammatory chemicals. This complex cascade
leads to a local inflammatory environment that lowers the firing threshold of axons and contributes to neuropathic pain. ATP,
Adenosine triphosphate; IL, Interleukin; NGF, Nerve growth factor; PGE, Prostaglandin; TNF-α, Tumour necrosis factor α. (Figure
adapted from Schmid et al.116 with permission.)

increased nerve mechanosensitivity,145 presumably by the in addition to impaired axonal transport have to be con-
accumulation and insertion of ion channels at the lesion sidered to explain the occurrence of dual nerve disorders.
site. Impaired axonal transport may thus contribute to the Readers are referred to Schmid et al (149)149 for further
heightened neural mechanosensitivity in patients with reading.
entrapment neuropathies.
Axonal transport gained a lot of interest in the context
of the double crush syndrome. This syndrome was first
Central Nervous System Changes
described by Upton and McComas,146 who hypothesized Since the peripheral and central nervous system form
that single axons having been compressed at one site a functional entity, injuries of peripheral nerves inevi-
become especially susceptible to damage at another site. tably initiate central changes, which are beyond the
In a recent Delphi survey, axonal transport was rated as scope of this chapter. Central changes following severe
one of the most plausible mechanisms to explain the nerve injury include, but are not limited to, immu-
occurrence of dual nerve disorders.147 Impaired axonal noinflammatory reactions at the level of the spinal
transport may indeed contribute to the development of cord or higher pain centres,126,127,149,150 central sensitiza-
dual nerve disorders along the same axonal pathway tion151 and changes to cortical representations.152–155
(e.g. tarsal tunnel syndrome and piriformis syndrome). Furthermore, psychosocial factors can be associated
However, the major criticism concerns the proposition with peripheral nerve injuries. The exact nature of
that the peripheral axons and the dorsal nerve roots have central nervous system changes in patients with entrap-
separate axonal transport systems,148 making axonal trans- ment neuropathies remains to be explored. If present,
port unlikely to account for the most common combina- central changes together with changes in the dorsal
tion of dual nerve disorders (cervical radiculopathy and root ganglia may contribute to the frequently observed
CTS). Furthermore, impaired axonal transport cannot spread of symptoms to anatomically unrelated areas
explain dual nerve disorders in two distinct peripheral (e.g. extraterritorial paraesthesia or pain in the ulnar
nerves such as the frequently observed ulnar neuropathy nerve area in CTS or non-dermatomal pain in patients
in the presence of CTS.148 Therefore, other mechanisms with radiculopathies).132,156
88 PART II  Advances in Theory and Practice

FIGURE 8-8  ■  Experimental mild nerve compression induces an immunoinflammatory reaction in dorsal root ganglia. (A) Satellite
glia cells (glial fibrillary acid protein, GFAP) in longitudinal sections of L5 dorsal root ganglia contralateral (top left) and ipsilateral
(top right) to a mild chronic compression of the sciatic nerve in rats (top right). Arrows indicate satellite glia cell proliferation as
apparent by the formation of multilayer rings around sensory neuron cell bodies. (B) Macrophage recruitment is apparent by more
abundant CD68 (macrophage) staining in a L5 dorsal root ganglion on the ipsilateral side of a mild experimental nerve compression
(bottom right).

SUMMARY knowledge of the pathophysiology may facilitate diag-

nostic clinical reasoning, which may improve the
This chapter summarized the anatomy and physiology understanding of the mechanisms at play in individual
of the peripheral nervous system with a focus on patients. Future research will shed light on the diag-
the evidence for its compromise following entrapment nostic performance of tests to differentiate these mecha-
neuropathies. It should be noted that these pathophysi- nisms. In the meantime, clinicians are advised to
ological mechanisms do not follow a defined time incorporate them in their clinical reasoning framework.
course or cascade. Rather, the above outlined mecha- A better understanding of the pathophysiology is a
nisms (and future research will undoubtedly unveil crucial first step in our vision to provide mechanism-
many more) interact in a complex manner (Fig. 8-9). based interventions and to design and implement effec-
In addition, some mechanisms may be absent or neg- tive management strategies, which are beyond the
ligible in some patients and more prominent in others. scope of this chapter.
The complex interaction and heterogeneity of the
pathophysiology not only explains the diverse symptoms Acknowledgement
and signs in patients with the same diagnosis, but
also why examining and treating entrapment neuropa- I would like to dedicate this chapter to Max Zusman, who
thies remains a challenge for clinicians. An enhanced continues to be a great inspiration to so many of us.
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 89

FIGURE 8-9  ■  Schematic representation of the different pathophysiological mechanisms at play in patients with entrapment neuropa-
thies. Mechanical nerve compression and ischaemia lead to many different pathophysiological changes, some of which have been
discussed in this chapter. There is a complex interaction between these mechanisms (e.g. immune cell activation may lead to axonal
degeneration; impaired axonal transport may lead to ion channel changes) and future research will most certainly unveil more
interactions. The presence and predominance of the various mechanisms varies however between patients. This explains the het-
erogeneous clinical presentation of patients, which is represented by the outer circle containing a wide variety of symptoms and
signs present in patients with entrapment neuropathies.

REFERENCES 10. Loken LS, Wessberg J, Morrison I, et al. Coding of pleasant touch
1. Merskey H, Bogduk N, editors. Part III: Pain Terms, A Current by unmyelinated afferents in humans. Nat Neurosci 2009;12(5):
List with Definitions and Notes on Usage. Classification of 547–8.
Chronic Pain. 2nd ed. IASP Task Force on Taxonomy. Seattle: 11. Smith ES, Lewin GR. Nociceptors: a phylogenetic view. J Comp
IASP Press; 1994. p. 209–14. Physiol A Neuroethol Sens Neural Behav Physiol 2009;195(12):
2. Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and 1089–106.
treatment. Man Ther 1999;4(2):63–73. 12. Michaelis M, Habler HJ, Jaenig W. Silent afferents: a separate
3. Attal N, Lanteri-Minet M, Laurent B, et al. The specific disease class of primary afferents? Clin Exp Pharmacol Physiol 1996;23(2):
burden of neuropathic pain: results of a French nationwide survey. 99–105.
Pain 2011;152(12):2836–43. 13. Rolke R, Magerl W, Campbell KA, et al. Quantitative sensory
4. Younes M, Bejia I, Aguir Z, et al. Prevalence and risk factors of testing: a comprehensive protocol for clinical trials. Eur J Pain
disk-related sciatica in an urban population in Tunisia. Joint Bone 2006;10(1):77–88.
Spine 2006;73(5):538–42. 14. Zhu DQ, Zhu Y, Qiao K, et al. Proximally evoked soleus H-reflex
5. Papanicolaou GD, McCabe SJ, Firrell J. The prevalence and char- to S1 nerve root stimulation in sensory neuronopathies (ganglion-
acteristics of nerve compression symptoms in the general popula- opathies). Muscle Nerve 2013;48(5):814–16.
tion. J Hand Surg [Am] 2001;26(3):460–6. 15. Poliak S, Peles E. The local differentiation of myelinated axons at
6. Singh R, Gamble G, Cundy T. Lifetime risk of symptomatic nodes of Ranvier. Nat Rev Neurosci 2003;4(12):968–80.
carpal tunnel syndrome in Type 1 diabetes. Diabet Med 2005; 16. Rasband MN, Trimmer JS. Developmental clustering of ion chan-
22(5):625–30. nels at and near the node of Ranvier. Dev Biol 2001;236(1):
7. Bland JD. Carpal tunnel syndrome. Curr Opin Neurol 2005; 5–16.
18(5):581–5. 17. Julius D, Basbaum AI. Molecular mechanisms of nociception.
8. Kandel ER, Schwartz J, Jessell TM, et al. Principles of Neural Nature 2001;413(6852):203–10.
Science. New York: McGrath-Hill; 2012. 18. Basbaum AI, Jessell TM. Part V. Pain. In: Kandel ER, Schwartz
9. Gould DJ, Fix JD. Neuroanatomy. Philadelphia, Pennsylvania: JH, Jessell TM, editors. Principles of Neuroscience. New York:
Lippincott Wiliams & Wilkins; 2013. McGraw-Hill; 2000. p. 472–91.
90 PART II  Advances in Theory and Practice

19. Ransom R. Organization of the nervous system. In: Boron WF, 47. Yoshii Y, Nishiura Y, Terui N, et  al. The effects of repetitive
Boulapaep EL, editors. A Cellular and Molecular Approach. Saun- compression on nerve conduction and blood flow in
ders; 2009. p. 267–88. the rabbit sciatic nerve. J Hand Surg Eur Vol 2010;35(4):
20. Weerasuriya A, Mizisin AP. The blood-nerve barrier: structure 269–78.
and functional significance. Methods Mol Biol 2011;686:149–73. 48. Mizisin AP, Weerasuriya A. Homeostatic regulation of the endo-
21. Sunderland S. The connective tissues of peripheral nerves. Brain neurial microenvironment during development, aging and in
1965;88(4):841–54. response to trauma, disease and toxic insult. Acta Neuropathol
22. Sunderland S, Bradley KC. The cross-sectional area of peripheral 2011;121(3):291–312.
nerve trunks devoted to nerve fibers. Brain 1949;72(3):428–49. 49. Nakamichi KI, Tachibana S. Enlarged median nerve in idiopathic
23. Sunderland S. The adipose tissue of peripheral nerves. Brain carpal tunnel syndrome. Muscle Nerve 2000;23(11):1713–18.
1945;68:118–22. 50. Yoon JS, Walker FO, Cartwright MS. Ulnar neuropathy with
24. Hromada J. On the nerve supply of the connective tissue of some normal electrodiagnosis and abnormal nerve ultrasound. Arch
peripheral nervous system components. Acta Anat 1963;55: Phys Med Rehabil 2010;91(2):318–20.
343–51. 51. Cudlip SA, Howe FA, Clifton A, et al. Magnetic resonance neu-
25. Lincoln J, Milner P, Appenzeller O, et al. Innervation of normal rography studies of the median nerve before and after carpal
human sural and optic nerves by noradrenaline- and peptide- tunnel decompression. J Neurosurg 2002;96(6):1046–51.
containing nervi vasorum and nervorum: effect of diabetes and 52. Sirvanci M, Kara B, Duran C, et al. Value of perineural edema/
alcoholism. Brain Res 1993;632(1–2):48–56. inflammation detected by fat saturation sequences in lumbar mag-
26. Bove GM, Light AR. Calcitonin gene-related peptide and periph- netic resonance imaging of patients with unilateral sciatica. Acta
erin immunoreactivity in nerve sheaths. Somatosens Mot Res Radiol 2009;50(2):205–11.
1995;12(1):49–57. 53. Lewis AM, Layzer R, Engstrom JW, et al. Magnetic resonance
27. McDonald DM, Bowden JJ, Baluk P, et al. Neurogenic inflamma- neurography in extraspinal sciatica. Arch Neurol 2006;63(10):
tion. A model for studying efferent actions of sensory nerves. Adv 1469–72.
Exp Med Biol 1996;410:453–62. 54. Mackinnon SE. Pathophysiology of nerve compression. Hand
28. McManis PG, Schmelzer JD, Zollman PJ, et al. Blood flow and Clin 2002;18(2):231–41.
autoregulation in somatic and autonomic ganglia. Comparison 55. Ido K, Urushidani H. Fibrous adhesive entrapment of lumbosacral
with sciatic nerve. Brain 1997;120(Pt 3):445–9. nerve roots as a cause of sciatica. Spinal Cord 2001;39(5):269–73.
29. Sunderland S. The nerve lesion in the carpal tunnel syndrome. 56. Abzug JM, Jacoby SM, Osterman AL. Surgical options for recal-
J Neurol Neurosurg Psychiatry 1976;39(7):615–26. citrant carpal tunnel syndrome with perineural fibrosis. Hand (N
30. Sunderland S. Nerves and Nerve Injury. Edinburgh: Churchill Y) 2012;7(1):23–9.
Livingstone; 1978. 57. Chhabra A, Wadhwa V, Thakkar RS, et al. Recurrent ulnar nerve
31. Allt G, Lawrenson JG. The blood-nerve barrier: enzymes, trans- entrapment at the elbow: correlation of surgical findings and
porters and receptors – a comparison with the blood-brain barrier. 3-Tesla magnetic resonance neurography. Can J Plast Surg – J Can
Brain Res Bull 2000;52(1):1–12. de Chir Plast 2013;21(3):186–9.
32. Mellick R, Cavanagh JB. Longitudinal movement of radioiodin- 58. Erel E, Dilley A, Greening J, et al. Longitudinal sliding of the
ated albumin within extravascular spaces of peripheral nerves fol- median nerve in patients with carpal tunnel syndrome. J Hand
lowing three systems of experimental trauma. J Neurol Neurosurg Surg [Br] 2003;28(5):439–43.
Psychiatry 1967;30(5):458–63. 59. Wang Y, Filius A, Zhao C, et al. Altered median nerve deformation
33. Arvidson B. A study of the perineurial diffusion barrier of a and transverse displacement during wrist movement in patients
peripheral ganglion. Acta Neuropathol 1979;46(1–2):139–44. with carpal tunnel syndrome. Acad Radiol 2014;21(4):472–80.
34. McCabe JS, Low FN. The subarachnoid angle: an area of transi- 60. Hough AD, Moore AP, Jones MP. Reduced longitudinal excursion
tion in peripheral nerve. Anat Rec 1969;164(1):15–33. of the median nerve in carpal tunnel syndrome. Arch Phys Med
35. Grafstein B, Forman DS. Intracellular transport in neurons. Rehabil 2007;88(5):569–76.
Physiol Rev 1980;60(4):1167–283. 61. Mallik A, Weir AI. Nerve conduction studies: essentials and pit-
36. Abbas AK, Lichtman AH, Pillai S. Cellular and Molecular Immu- falls in practice. J Neurol Neurosurg Psychiatry 2005;76(Suppl.
nology. 6th ed. Philadelphia: Saunders Elsevier; 2007. 2):ii23–31.
37. Janeway C. Janeway’s Immunobiology. In: Murphy K, Travers P, 62. Kiernan MC, Mogyoros I, Burke D. Conduction block in carpal
Walport M, editors. 7th ed. New York: Garland Science, Taylor tunnel syndrome. Brain 1999;122(5):933–41.
& Francis Group; 2008. 63. Cappelen-Smith C, Lin CS, Burke D. Activity-dependent hyper-
38. Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal polarization and impulse conduction in motor axons in patients
tunnel syndrome. A study of carpal canal pressures. J Bone Joint with carpal tunnel syndrome. Brain 2003;126(4):1001–8.
Surg Am 1981;63(3):380–3. 64. Nukada H, Powell HC, Myers RR. Spatial distribution of nerve
39. Takahashi K, Shima I, Porter RW. Nerve root pressure in lumbar injury after occlusion of individual major vessels in rat sciatic
disc herniation. Spine 1999;24(19):2003–6. nerves. J Neuropathol Exp Neurol 1993;52(5):452–9.
40. Rydevik B, Lundborg G, Bagge U. Effects of graded compression 65. Lin MY, Frieboes LS, Forootan M, et al. Biophysical stimulation
on intraneural blood blow. An in vivo study on rabbit tibial nerve. induces demyelination via an integrin-dependent mechanism. Ann
J Hand Surg 1981;6(1):3–12. Neurol 2012;72(1):112–23.
41. Coppieters MW, Schmid AB, Kubler PA, et al. Description, reli- 66. O’Brien JP, Mackinnon SE, MacLean AR, et al. A model of
ability and validity of a novel method to measure carpal tunnel chronic nerve compression in the rat. Ann Plast Surg 1987;
pressure in patients with carpal tunnel syndrome. Man Ther 19(5):430–5.
2012;17(6):589–92. 67. Schmid AB, Coppieters MW, Ruitenberg MJ, et al. Local and
42. Seradge H, Jia YC, Owens W. In vivo measurement of carpal remote immune-mediated inflammation after mild peripheral
tunnel pressure in the functioning hand. J Hand Surg 1995; nerve compression in rats. J Neuropathol Exp Neurol 2013;
20(5):855–9. 72(7):662–80.
43. Low PA, Tuck RR. Effects of changes of blood pressure, respira- 68. Gupta R, Rowshan K, Chao T, et al. Chronic nerve compression
tory acidosis and hypoxia on blood flow in the sciatic nerve of the induces local demyelination and remyelination in a rat model of
rat. J Physiol 1984;347:513–24. carpal tunnel syndrome. Exp Neurol 2004;187(2):500–8.
44. Sumikawa K, Sakai T, Ono T. Peripheral vascular pain. Nippon 69. Foix C, Marie P. Atrophie isolée de l’éminence thénar d’origin
Rinsho 2001;59(9):1733–7. névritique. Rôle du ligament annulaire antérieur du carpe dans la
45. Werner RA, Andary M. Carpal tunnel syndrome: pathophysiology pathogénie de la lésion. Rev Neurol 1913;26:647–8.
and clinical neurophysiology. Clin Neurophysiol 2002;113(9): 70. Neary D. The pathology of ulnar nerve compression in men.
1373–81. Neuropathol Appl Neurobiol 1975;1:69–88.
46. Mackinnon SE, Dellon AL, Hudson AR, et al. Chronic nerve 71. Mackinnon SE, Dellon AL, Hudson AR, et al. Chronic human
compression – an experimental model in the rat. Ann Plast Surg nerve compression–a histological assessment. Neuropathol Appl
1984;13(2):112–20. Neurobiol 1986;12(6):547–65.
 8  The Peripheral Nervous System and its Compromise in Entrapment Neuropathies 91

72. Jefferson D, Eames RA. Subclinical entrapment of the lateral 95. Tampin B, Slater H, Hall T, et al. Quantitative sensory testing
femoral cutaneous nerve: an autopsy study. Muscle Nerve somatosensory profiles in patients with cervical radiculopathy are
1979;2(2):145–54. distinct from those in patients with nonspecific neck-arm pain.
73. Neary D, Ochoa J, Gilliatt RW. Sub-clinical entrapment neuropa- Pain 2012;153(12):2403–14.
thy in man. J Neurol Sci 1975;24(3):283–98. 96. Samuelsson L, Lundin A. Thermal quantitative sensory testing in
74. Schmid AB, Bland JD, Bhat MA, et al. The relationship of nerve lumbar disc herniation. Eur Spine J 2002;11(1):71–5.
fibre pathology to sensory function in entrapment neuropathy. 97. Wilder-Smith EP, Fook-Chong S, Chew SE, et al. Vasomotor
Brain 2014;137(Pt 12):3186–99. dysfunction in carpal tunnel syndrome. Muscle Nerve 2003;
75. Pertin M, Ji RR, Berta T, et al. Upregulation of the voltage-gated 28(5):582–6.
sodium channel beta2 subunit in neuropathic pain models: char- 98. Kiylioglu N. Sympathetic skin response and axon counting in
acterization of expression in injured and non-injured primary carpal tunnel syndrome. J Clin Neurophysiol 2007;24(5):424,
sensory neurons. J Neurosci 2005;25(47):10970–80. author reply.
76. Kim DS, Choi JO, Rim HD, et al. Downregulation of voltage- 99. Kuwabara S, Tamura N, Yamanaka Y, et al. Sympathetic sweat
gated potassium channel alpha gene expression in dorsal root responses and skin vasomotor reflexes in carpal tunnel syndrome.
ganglia following chronic constriction injury of the rat sciatic Clin Neurol Neurosurg 2008;110(7):691–5.
nerve. Brain Res Mol Brain Res 2002;105(1-2):146–52. 100. Kiylioglu N, Akyol A, Guney E, et al. Sympathetic skin response
77. Liu X, Zhou JL, Chung K, et al. Ion channels associated with the in idiopathic and diabetic carpal tunnel syndrome. Clin Neurol
ectopic discharges generated after segmental spinal nerve injury Neurosurg 2005;108(1):1–7.
in the rat. Brain Res 2001;900(1):119–27. 101. Reddeppa S, Bulusu K, Chand PR, et al. The sympathetic skin
78. Jiang YQ, Xing GG, Wang SL, et al. Axonal accumulation of response in carpal tunnel syndrome. Auton Neurosci 2000;
hyperpolarization-activated cyclic nucleotide-gated cation chan- 84(3):119–21.
nels contributes to mechanical allodynia after peripheral nerve 102. Erdem Tilki H, Coskun M, Unal Akdemir N, et al. Axon count
injury in rat. Pain 2008;137(3):495–506. and sympathetic skin responses in lumbosacral radiculopathy.
79. Drummond PD, Drummond ES, Dawson LF, et al. Upregulation J Clin Neurol 2014;10(1):10–16.
of alpha1-adrenoceptors on cutaneous nerve fibres after partial 103. Arendt-Nielsen L, Gregersen H, Toft E, et  al. Involvement
sciatic nerve ligation and in complex regional pain syndrome type of thin afferents in carpal tunnel syndrome: evaluated quan-
II. Pain 2014;155(3):606–16. titatively by argon laser stimulation. Muscle Nerve 1991;14(6):
80. England JD, Gamboni F, Ferguson MA, et al. Sodium channels 508–14.
accumulate at the tips of injured axons. Muscle Nerve 1994;17(6): 104. Ramieri G, Stella M, Calcagni M, et al. An immunohistochemical
593–8. study on cutaneous sensory receptors after chronic median nerve
81. Amir R, Michaelis M, Devor M. Membrane potential oscillations compression in man. Acta Anat 1995;152(3):224–9.
in dorsal root ganglion neurons: role in normal electrogenesis and 105. Casanova-Molla J, Morales M, Planas-Rigol E, et al. Epidermal
neuropathic pain. J Neurosci 1999;19(19):8589–96. Langerhans cells in small fiber neuropathies. Pain 2012;153(5):
82. Chen Y, Devor M. Ectopic mechanosensitivity in injured sensory 982–9.
axons arises from the site of spontaneous electrogenesis. Eur J 106. Martinez V, Fletcher D, Martin F, et al. Small fibre impairment
Pain 1998;2(2):165–78. predicts neuropathic pain in Guillain-Barre syndrome. Pain
83. Frieboes LR, Palispis WA, Gupta R. Nerve compression activates 2010;151(1):53–60.
selective nociceptive pathways and upregulates peripheral sodium 107. Bradl M, Lassmann H. Progressive multiple sclerosis. Semin
channel expression in Schwann cells. J Orthop Res 2010; Immunopathol 2009;31(4):455–65.
28(6):753–61. 108. Watkins LR, Maier SF. Beyond neurons: evidence that immune
84. Han SE, Lin CS, Boland RA, et al. Nerve compression, mem- and glial cells contribute to pathological pain states. Physiol Rev
brane excitability, and symptoms of carpal tunnel syndrome. 2002;82(4):981–1011.
Muscle Nerve 2011;44(3):402–9. 109. Wieseler-Frank J, Maier SF, Watkins LR. Immune-to-brain com-
85. Z’Graggen WJ, Bostock H. Nerve membrane excitability testing. munication dynamically modulates pain: physiological and patho-
Eur J Anaesthesiol Suppl 2008;42:68–72. logical consequences. Brain Behav Immun 2005;19(2):104–11.
86. Dahlin LB, Shyu BC, Danielsen N, et al. Effects of nerve com- 110. Thacker MA, Clark AK, Marchand F, et al. Pathophysiology of
pression or ischaemia on conduction properties of myelinated and peripheral neuropathic pain: immune cells and molecules. Anesth
non-myelinated nerve fibres. An experimental study in the rabbit Analg 2007;105(3):838–47.
common peroneal nerve. Acta Physiol Scand 1989;136(1): 111. Moalem G, Tracey DJ. Immune and inflammatory mechanisms in
97–105. neuropathic pain. Brain Res Rev 2006;51(2):240–64.
87. American Academy of Orthopedic Surgeons (AAOS). Clinical 112. Otoshi K, Kikuchi S, Konno S, et al. The reactions of glial cells
Practice Guideline on the Diagnosis of Carpal Tunnel Syndrome. and endoneurial macrophages in the dorsal root ganglion and
AAOS: Rosemont, IL. 2007. their contribution to pain-related behavior after application of
88. Bono CM, Ghiselli G, Gilbert TJ, et al. An evidence-based clini- nucleus pulposus onto the nerve root in rats. Spine 2010;
cal guideline for the diagnosis and treatment of cervical radicu- 35(3):264–71.
lopathy from degenerative disorders. Spine J 2011;11(1):64–72. 113. Shamji MF, Allen KD, So S, et al. Gait abnormalities and inflam-
89. Werner RA. Electrodiagnostic evaluation of carpal tunnel syn- matory cytokines in an autologous nucleus pulposus model of
drome and ulnar neuropathies. PM & R 2013;5(Suppl. 5):S14–21. radiculopathy. Spine 2009;34(7):648–54.
90. Longstaff L, Milner RH, O’Sullivan S, et al. Carpal tunnel syn- 114. Gupta R, Channual JC. Spatiotemporal pattern of macrophage
drome: the correlation between outcome, symptoms and nerve recruitment after chronic nerve compression injury. J Neu-
conduction study findings. J Hand Surg [Br] 2001;26(5):475–80. rotrauma 2006;23(2):216–26.
91. Koyuncuoglu HR, Kutluhan S, Yesildag A, et al. The value of 115. Hirata K, Kawabuchi M. Myelin phagocytosis by macrophages
ultrasonographic measurement in carpal tunnel syndrome in and nonmacrophages during Wallerian degeneration. Microsc Res
patients with negative electrodiagnostic tests. Eur J Radiol Tech 2002;57(6):541–7.
2005;56(3):365–9. 116. Schmid AB, Nee RJ, Coppieters MW. Reappraising entrapment
92. Witt JC, Hentz JG, Stevens JC. Carpal tunnel syndrome with neuropathies – mechanisms, diagnosis and management. Man
normal nerve conduction studies. Muscle Nerve 2004;29(4): Ther 2013;18(6):449–57.
515–22. 117. Tofaris GK, Patterson PH, Jessen KR, et al. Denervated Schwann
93. Tamburin S, Cacciatori C, Praitano ML, et al. Median nerve cells attract macrophages by secretion of leukemia inhibitory
small- and large-fiber damage in carpal tunnel syndrome: a quan- factor (LIF) and monocyte chemoattractant protein-1 in a process
titative sensory testing study. J Pain 2010;12(2):205–12. regulated by interleukin-6 and LIF. J Neurosci 2002;22(15):
94. Chien A, Eliav E, Sterling M. Whiplash (grade II) and cervical 6696–703.
radiculopathy share a similar sensory presentation: an investiga- 118. Sorkin LS, Xiao WH, Wagner R, et al. Tumour necrosis factor-
tion using quantitative sensory testing. Clin J Pain 2008; alpha induces ectopic activity in nociceptive primary afferent
24(7):595–603. fibres. Neuroscience 1997;81(1):255–62.
92 PART II  Advances in Theory and Practice

119. Grossmann L, Gorodetskaya N, Baron R, et al. Enhancement of prostaglandin E2 in response to noxious stimuli: evidence that
ectopic discharge in regenerating A- and C-fibers by inflammatory nervi nervorum are nociceptors. Neuroscience 1999;92(1):
mediators. J Neurophysiol 2009;101(6):2762–74. 319–25.
120. Takebayashi T, Cavanaugh JM, Cuneyt Ozaktay A, et al. Effect of 139. Kobayashi S, Kokubo Y, Uchida K, et al. Effect of lumbar nerve
nucleus pulposus on the neural activity of dorsal root ganglion. root compression on primary sensory neurons and their central
Spine 2001;26(8):940–5. branches: changes in the nociceptive neuropeptides substance P
121. Marshall S, Tardif G, Ashworth N. Local corticosteroid injection and somatostatin. Spine 2005;30(3):276–82.
for carpal tunnel syndrome. Cochrane Database Syst Rev 2007; 140. Dahlin LB, McLean WG. Effects of graded experimental com-
(2):CD001554. pression on slow and fast axonal transport in rabbit vagus nerve.
122. Benoist M, Boulu P, Hayem G. Epidural steroid injections in the J Neurol Sci 1986;72(1):19–30.
management of low-back pain with radiculopathy: an update of 141. Dahlin LB, Rydevik B, McLean WG, et al. Changes in fast axonal
their efficacy and safety. Eur Spine J 2012;21(2):204–13. transport during experimental nerve compression at low pressures.
123. Bove GM, Ransil BJ, Lin HC, et al. Inflammation induces ectopic Exp Neurol 1984;84(1):29–36.
mechanical sensitivity in axons of nociceptors innervating deep 142. Dahlin LB, Sjostrand J, McLean WG. Graded inhibition of ret-
tissues. J Neurophysiol 2003;90(3):1949–55. rograde axonal transport by compression of rabbit vagus nerve.
124. Asbury AK, Fields HL. Pain due to peripheral nerve damage: an J Neurol Sci 1986;76(2–3):221–30.
hypothesis. Neurology 1984;34(12):1587–90. 143. Ando Y. Experimental study on chronic entrapment neuropathy.
125. Takahata S, Takebayashi T, Terasima Y, et al. Activation of glial Nippon Seikeigeka Gakkai Zasshi 1990;64(7):633–47.
cells in the spinal cord of a model of lumbar radiculopathy. 144. Armstrong BD, Hu Z, Abad C, et al. Induction of neuropeptide
J Orthop Sci 2011;16(3):313–20. gene expression and blockade of retrograde transport in facial
126. Rothman SM, Nicholson KJ, Winkelstein BA. Time-dependent motor neurons following local peripheral nerve inflammation in
mechanics and measures of glial activation and behavioral sensitiv- severe combined immunodeficiency and BALB/C mice. Neurosci-
ity in a rodent model of radiculopathy. J Neurotrauma 2010; ence 2004;129(1):93–9.
27(5):803–14. 145. Dilley A, Bove GM. Disruption of axoplasmic transport induces
127. Rothman SM, Winkelstein BA. Chemical and mechanical nerve mechanical sensitivity in intact rat C-fibre nociceptor axons.
root insults induce differential behavioral sensitivity and glial J Physiol 2008;586(2):593–604.
activation that are enhanced in combination. Brain Res 2007; 146. Upton AR, McComas AJ. The double crush in nerve entrapment
1181:30–43. syndromes. Lancet 1973;2(7825):359–62.
128. Hu P, Bembrick AL, Keay KA, et al. Immune cell involvement in 147. Schmid AB, Coppieters MW. The double crush syndrome
dorsal root ganglia and spinal cord after chronic constriction or revisited – a Delphi study to reveal current expert views on
transection of the rat sciatic nerve. Brain Behav Immun 2007; mechanisms underlying dual nerve disorders. Man Ther 2011;
21(5):599–616. 16(6):557–62.
129. Hu P, McLachlan EM. Macrophage and lymphocyte invasion of 148. Morgan G, Wilbourn AJ. Cervical radiculopathy and coexisting
dorsal root ganglia after peripheral nerve lesions in the rat. Neu- distal entrapment neuropathies: double-crush syndromes? Neu-
roscience 2002;112(1):23–38. rology 1998;50(1):78–83.
130. Koltzenburg M, Wall PD, McMahon SB. Does the right side 149. Mor D, Bembrick AL, Austin PJ, et al. Evidence for cellular injury
know what the left is doing? Trends Neurosci 1999;22(3):122–7. in the midbrain of rats following chronic constriction injury of the
131. Caliandro P, La Torre G, Aprile I, et al. Distribution of paresthe- sciatic nerve. J Chem Neuroanat 2011;41(3):158–69.
sias in carpal tunnel syndrome reflects the degree of nerve damage 150. LeBlanc BW, Zerah ML, Kadasi LM, et al. Minocycline injection
at wrist. Clin Neurophysiol 2006;117(1):228–31. in the ventral posterolateral thalamus reverses microglial reactivity
132. Murphy DR, Hurwitz EL, Gerrard JK, et al. Pain patterns and and thermal hyperalgesia secondary to sciatic neuropathy. Neuro-
descriptions in patients with radicular pain: does the pain neces- sci Lett 2011;498(2):138–42.
sarily follow a specific dermatome? Chiropr Osteopat 2009;17:9. 151. Latremoliere A, Woolf CJ. Central sensitization: a generator of
133. Zanette G, Cacciatori C, Tamburin S. Central sensitization in pain hypersensitivity by central neural plasticity. J Pain 2009;10(9):
carpal tunnel syndrome with extraterritorial spread of sensory 895–926.
symptoms. Pain 2010;148(2):227–36. 152. Druschky K, Kaltenhauser M, Hummel C, et al. Alteration of the
134. Viader A, Golden JP, Baloh RH, et al. Schwann cell mitochondrial somatosensory cortical map in peripheral mononeuropathy due to
metabolism supports long-term axonal survival and peripheral carpal tunnel syndrome. Neuroreport 2000;11(17):3925–30.
nerve function. J Neurosci 2011;31(28):10128–40. 153. Napadow V, Kettner N, Ryan A, et al. Somatosensory cortical
135. Szolcsanyi J. Capsaicin-sensitive sensory nerve terminals with plasticity in carpal tunnel syndrome–a cross-sectional fMRI evalu-
local and systemic efferent functions: facts and scopes of an ation. Neuroimage 2006;31(2):520–30.
unorthodox neuroregulatory mechanism. Prog Brain Res 1996; 154. Napadow V, Kettner N, Liu J, et al. Hypothalamus and amygdala
113:343–59. response to acupuncture stimuli in carpal tunnel syndrome. Pain
136. Schmelz M, Michael K, Weidner C, et al. Which nerve fibers 2007.
mediate the axon reflex flare in human skin? Neuroreport 2000; 155. Tecchio F, Padua L, Aprile I, et al. Carpal tunnel syndrome modi-
11(3):645–8. fies sensory hand cortical somatotopy: a MEG study. Hum Brain
137. Schmelz M, Luz O, Averbeck B, et al. Plasma extravasation and Mapp 2002;17(1):28–36.
neuropeptide release in human skin as measured by intradermal 156. Nora DB, Becker J, Ehlers JA, et al. Clinical features of 1039
microdialysis. Neurosci Lett 1997;230(2):117–20. patients with neurophysiological diagnosis of carpal tunnel syn-
138. Sauer SK, Bove GM, Averbeck B, et al. Rat peripheral nerve drome. Clin Neurol Neurosurg 2004;107(1):64–9.
components release calcitonin gene-related peptide and
 CHAPTER 9 

Functional Anatomy
CHAPTER OUTLINE

Ch 9.1  The Cervical Spine  93 Ch 9.2  Lumbar Spine  101

Gail Forrester-Gale • Ioannis Paneris Michael Adams • Patricia Dolan

CHAPTER 9.1  ■  THE CERVICAL SPINE

Gail Forrester-Gale • Ioannis Paneris

INTRODUCTION as anatomically the A-A joint is specifically designed

for rotation. It has a central pivot joint between the odon-
The following chapter aims to review and highlight toid peg and the osseoligamentous ring formed by the
the key anatomical and biomechanical features of the transverse ligament and anterior arch of the atlas, double
craniocervical region that are relevant to and support convex joints bilaterally and it lacks an intervertebral
clinical practice. disc.1,12,13 In addition to its large range of rotation, in vivo
The occiput, atlas, axis and surrounding soft tissues studies on asymptomatic subjects have shown that the
are collectively referred to as the craniocervical region. A-A joint plays a key role in the initiation of cervical
It is a unique spinal region that exhibits highly specialized rotation.9,14 Cervical rotation has been shown to start at
anatomy and considerable mobility in comparison to the C1–C2 level and to continue sequentially down the
other spinal regions. Of particular note are the atypical, cervical spine with each joint moving only once the pre-
modified vertebrae (the atlas and axis), the absence of ceding joint has completed its range of movement.1,14
intervertebral discs, the presence of an odontoid peg and
the configuration of double convex joints bilaterally at
the C1–C2 articulation.1
CRANIOCERVICAL-COUPLED
The atlas (C1) and axis (C2) together with the occiput MOVEMENTS AND CLINICAL
form a unique triad of articulations referred to as the IMPLICATIONS
occipito–atlantoaxial (O-AA) complex. This complex is
responsible for approximately one-third or 20° of the Alongside movement analysis studies exploring the range
total cervical sagittal plane movements of flexion and and direction of CCS mobility, there is a growing body
extension.2–8 In vivo movement analysis studies report of evidence from in vivo three-dimensional computed
that 4–7° of flexion and 17–21° of extension occur across tomography (3D CT) scan studies demonstrating the
this complex with the majority of this movement occur- coupling of movements occurring in the CCS.15–19
ring specifically at the atlanto-occipital joint (C0-C1).4–8 A recent study by Salem et al. carried out on 20
The atlanto-occipital joint (A-O joint) configuration is
specifically designed to facilitate upper cervical flexion
and extension (retraction and protraction). The lack of Superior articular surface
(for occipital condyle)
intervertebral disc along with the congruous joint sur-
faces, which are long and thin and orientated in a Articular facet for dens
posterior–anterior direction, facilitate the nodding move-
ment of the head on neck.2,5,8
Clinically, in situations where craniocervical spine
(CCS) pain is associated with movements of upper
Atlas (CI)
cervical flexion and extension, the A-O joint should be
a primary consideration in terms of assessment and
treatment.
Axial rotation is the largest range of motion available
across the O-AA complex.1 Studies consistently show that Axis (CII)
the atlanto-axial joint (A-A joint; Fig. 9-1) provides 60% FIGURE 9-1  ■  The atlanto-axial joint. (Adapted from Drake et al.
of the total cervical rotation, which amounts to approxi- Grey’s Anatomy for Students. Edinburgh: Churchill Livingstone;
mately 38–56° to each side.1,5,9–11 This is unsurprising, 2005.)

93
94 PART II  Advances in Theory and Practice

asymptomatic participants used up-to-date imaging tech- axial rotation and lateral flexion across the O-AA
niques (3D CT kinematic analysis) to explore the coupled complex.16,17,37,38 They are strong, collagenous cords
motion patterns of the CCS in maximal axial rotation.1 approximately 1 cm in length, which run from the pos-
This study found that rotation in the CCS was consis- terolateral aspect of the odontoid peg to the medial
tently coupled with contralateral lateral flexion, which is surface of the occipital condyles.15 Due to their posterior
in contrast to the ipsilateral coupling pattern found in the attachment on the odontoid peg, they are wound around
sub-axial cervical spine.20 the process during contralateral axial rotation and become
maximally tightened at 90° cervical rotation. Further
stretch can be added to these ligaments with the addition
SYNOVIAL FOLDS IN THE of upper cervical flexion.16,17,34
CRANIOCERVICAL SPINE
Clinical Anatomy and Biomechanics of
The synovial folds of the CCS are formed by wedge- the Transverse Ligament and Relevance
shaped folds of synovial membrane.21–24 They have an to Clinical Testing
abundant vascular network and are innervated.21,25 The
composition of the synovial folds varies across the cra- Magnetic resonance imaging (MRI) studies on healthy
niocervical region possibly due to the different amounts participants have confirmed findings from cadaveric
of mechanical stress they are subjected to at each level. studies that the transverse ligament is a broad collage-
The synovial folds found at the A-O joint do not project nous band, approximately 2.5 mm thick, which extends
between the joint surfaces and are therefore unlikely to across the atlantal ring directly behind the odontoid peg
be exposed to mechanical stresses. They are composed of and attaches to the medial aspect of each lateral mass of
adipose-type synovial membrane. The synovial folds of the atlas.16,31 It acts like a sling and serves to hold the
the A-A articulation, however, project as far as 5 mm odontoid peg against the anterior arch of the atlas. In this
between the articular surfaces and will therefore be way it restricts forward translation of the atlas in relation
exposed to mechanical stresses. They are formed of a to the axis particularly during movements of cervical
stronger more fibrous type of synovial membrane.21,24,25 flexion.35,39
The synovial folds have been suggested to perform
various functions in the CCS. They have been described Clinical Anatomy and Biomechanics of
as ‘passive space fillers’ serving to fill non-congruent the Tectorial Membrane and Relevance
areas of the joint and thus enhance joint congruity and to Clinical Testing
stability. They may also help to protect or lubricate the
articular surfaces and assist in weight bearing or shock Combined findings from in vitro cadaveric studies and in
absorption.21 Additionally, the CCS synovial folds may vivo MRI scan studies concur that the tectorial mem-
have a proprioceptive role providing mechanosensory brane is a broad fibroelastic band, approximately 5–7.5 cm
information important for sensorimotor control in the in length, 1.5–3 cm in width and 1–1.5 mm thick.37,40
upper cervical spine.25 Recent anatomical and radiological studies have con-
firmed that it originates on the posterior surface of the
C2 body and runs vertically upwards, as a specialized
cranial continuation of the posterior longitudinal liga-
THE ANATOMY OF CRANIOCERVICAL ment, attaching to the basilar grove of the occipital
STABILITY AND CLINICAL bone.35,37 It is adherent to the anterio superior dura
IMPLICATIONS mater that may be of clinical relevance in patients with
whiplash-associated disorder (WAD) or other disorders
CCS stability is provided through a combination of presenting with head, neck or facial pain and altered
mechanical restraint from the ligamentous system response to neurodynamic testing such as passive neck
and sensorimotor control from the neuromuscular flexion.36,40–42 The tectorial membrane becomes taught at
system.26–33 15° of craniocervical flexion; however, anatomical studies
suggest that its primary role is not to limit craniocervical
flexion but to prevent posterior migration of the odon-
Ligamentous System toid peg into the cervical spinal canal.37,40 Due to its high
The chief mechanical restraints of the craniocervical elastin content it is thought that the membrane acts as a
region are generally recognized as the transverse and alar hammock, stretching and tightening over the odontoid
ligaments with other ligaments such as the tectorial peg in craniocervical flexion thus assisting the transverse
membrane, capsular ligaments, ligamentum flavum, A-A ligament in preventing a posterior movement of the
ligaments, ligamentum nuchea, posterior atlanto-occipital odontoid peg into the spinal canal and preventing
membranes and atlanto-axial membranes acting as sec- impingement of the peg onto the spinal cord.36,40
ondary stabilizers (Fig. 9-2).15,17,34–36
Craniocervical Muscles and Their
Clinical Anatomy and Biomechanics Clinical Significance
of the Alar Ligaments
The key muscles acting directly on the CCS are the
There is consensus in the literature that the alar liga- suboccipital muscle (SOM) group posteriorly and the
ments provide the main passive restraints to contralateral craniocervical flexor (CCF) muscle group anteriorly.
 9  Functional Anatomy 95

Superior longitudinal band Jugular foramen

of cruciform ligament
Anterior edge of
foramen magnum
Transverse process of atlas
Alar ligament
Transverse ligament of atlas Ends of membrana tectoria

Anterior capsule of atlanto-axial joint Posterior longitudinal ligament

Inferior longitudinal band
A of cruciform ligament

Temporal bone
petrous part Internal acoustic meatus

Foramen magnum Occipital bone basilar part

posterior border Membrana tectoria
Anterior atlanto-occipital membrane
Apical ligament of dens
Superior longitudinal band
of cruciform ligament
Vertebral artery Dens
First cervical nerve Anterior arch of atlas
Posterior arch of atlas Bursal space in fibrocartilage
Transverse ligament of atlas Remains of intervertebral disc
Inferior longitudinal band
Body of atlas
of cruciform ligament
Ligamentum flavum
Posterior longitudinal ligament
Anterior longitudinal ligament
B
FIGURE 9-2  ■  The craniocervical ligamentous system.

Both groups are composed of short, deep segmental

muscles that largely function to provide segmental control
and support to the craniocervical joints.18,43–46 Both
Rectus
muscle groups have been shown to contain a high density capitis
of muscle receptors, particularly muscle spindles, with anterior
the largest concentration of muscle spindles being found
Longus capitis
in the SOM.18,19,46–48 This would suggest that both these C2
muscle groups are likely to act primarily as sensory recep- Upper part
tors monitoring and controlling the position, direction, C3
amplitude and velocity of craniocervical joint movement C4
Longus
and therefore have an important role in the maintenance colli
Middle part
of dynamic stability in the CCS. In addition, afferent C5
information from the SOM and CCF muscle spindles is C6
integrated with information from the vestibular and Lower part
C7
visual apparatus via the vestibular nuclei and is thus
involved in various postural reflexes in the control of T1
balance.49–51 T2
The CCF muscle group include longus capitis (LCap), T3
rectus capitis anterior (RCA), rectus capitus lateralis
FIGURE 9-3  ■  The craniocervical flexor muscle group. (Adapted
(RCL) and longus colli (Fig. 9-3). The first three muscles from Palastanga et al. Anatomy and Human Movement. Edinburgh:
all have an attachment in the CCS. LCap arises from the Churchill Livingstone; 2006.)
transverse processes of the third to sixth cervical verte-
brae and ascends to insert onto the inferior surface of
the occiput. It is narrow subaxially but broad and thick
in the CCS.3,13,44
96 PART II  Advances in Theory and Practice

The RCA muscle is a short, flat muscle, situated complex. However, studies have shown that both muscles,
immediately behind the upper part of the LCap. It arises in particular the RCPminor, have a high density of muscle
from the anterior surface of the lateral mass of the atlas, spindles suggesting that they have a more important role
and passes obliquely upward and medially to insert on the in CCS proprioception than in movement and may help
inferior surface of the occiput in front of the foramen to stabilize the atlas in relation to the occiput.18,19,47 This
magnum. The RCL is another short, flat muscle, which has been supported by a recent electromyographic study
arises from the upper surface of the transverse process of on RCPminor muscles that demonstrated activity in the
the atlas, and is inserted onto the undersurface of the muscle with the head in a neutral position but signifi-
jugular process of the occiput.3,13,51–53 cantly increased activity with the head in a retracted
Acting as a group, the CCF muscle group provides position.46
support to the cervical lordosis and segmental stability to Anatomical connections between the anterior surfaces
the cervical spine as a whole. RCA and LCap in particular of RCPmajor and RCPminor muscles and the posterior
provide stability to the upper cervical motion segments.54 cervical spinal dura mater through fibrous connective
In addition to their proprioceptive role, they serve to tissue or myodural bridges have been consistently
produce flexion of the upper cervical spine or a nodding reported.56–58 These connections may provide a form of
movement of the head on the neck.55 anchorage for the dura mater but more importantly,
The SOM group includes rectus capitis posterior due to findings of proprioceptive fibres throughout the
major (RCPmajor), rectus capitis posterior minor (RCP- myodural connections, are believed to be involved in
minor), obliqus capitis superior (OCS) and obliqus capitis the monitoring and controlling of dural tension during
inferior (OCI) (Fig. 9-4).13,52,53 flexion and extension movements of the head and neck.46,56
RCPminor is stated to be the only muscle with a direct Additionally, the fibrous bridge may provide propriocep-
attachment to the atlas (C1). It is documented to arise tive information regarding the position of the AO and
from the posterior arch of the atlas (C1) and to insert AA joints to help prevent infolding of the pain-sensitive
onto the occipital bone below the inferior nuchal line dura mater during head and neck movements.46,56 Clini-
lateral to the midline and medial to RCPmajor.20 cally, the myodural bridges between the SOM and the
The RCPmajor muscle is commonly cited to arise cervical spinal dura may be of relevance in relation to
from the spinous process of the axis (C2) and to ascend cervicogenic headache.46,56,59–61
to its insertion on the lateral part of the inferior nuchal The OCS is a small muscle arising from the lateral
line of the occiput.13 However, Scali et al. carried out an mass of the atlas (C1) ascending to attach onto the lateral
anatomical and histological study on 11 cadavers primar- half of the inferior nuchal line on the occiput. It acts at
ily to explore the atlanto-axial interspace.56 They found the A-O joint to extend and side flex the head. The OCI
in all 11 cadavers examined that the RCPmajor muscle muscle is the larger of the two oblique craniocervical
was firmly attached to the spinous process of the atlas muscles. It lies deep to semispinalis capitus, arising from
(C1). It would therefore appear that both RCPmajor and the apex of the spinous process of the axis (C2) and
RCPminor have an attachment onto the atlas (C1). passing laterally and upwards to insert on the posterior
The main actions of RCPmajor and RCPminor are aspect of the transverse process of the atlas (C1). It is
extension, side flexion and rotation of the O-AA joint responsible for rotation of the A-A joint.13 Similarly to
RCPmajor and RCPminor, both OCS and OCI have a
high density of Golgi tendon organs and muscle spindles
indicating that proprioception is likely to be the primary
role of these and indeed all the SOM allowing for accu-
rate positioning of the head on the neck.

MID TO LOW CERVICAL SPINE

Oblique capitis
superior
Although the first, second and seventh vertebrae have
Rectus capitis special features, the rest of the vertebrae of the cervical
posterior minor spine are almost identical with the sixth having only
Rectus capitis minor distinguishing features.62
posterior major
Obliquus capitis The Vertebral Body
inferior
The typical vertebra consists of two parts: the vertebral
body and the vertebral arch. The body of the typical
vertebra is a relatively small and broad mass of trabecular,
spongy bone covered by a layer of cortical bone.63 The
shape of the cervical vertebral body is oval with the trans-
verse diameter being greater than the anteroposterior
FIGURE 9-4  ■  The suboccipital muscle group. (Adapted from diameter and height.63 The cervical intervertebral joints
Middleditch & Oliver. Functional Anatomy of the Spine. Edinburgh: are saddle-shaped and they consist of two concavities
Butterworth Heinnemann; 2005.) facing each other at 90°.64 The opposing surfaces of the
 9  Functional Anatomy 97

vertebral bodies are gently curved in the sagittal plane a contralateral rotation and side flexion pattern seem to
with the anterior part of the vertebra sloping downwards take place on C2.64 The orientation of the superior facets
partially overlapping the anterior surface of the interver- in relation to the transverse plane seems to change gradu-
tebral disc. The superior surface of the vertebral body is ally from posteromedially at C3 to posterolaterally at C7
also curved on the coronal plane forming a concavity of to T1. However this change could be either gradual or
which its sides are the uncinate processes.62 sudden and the level of change of the orientation was not
The uncinate processes are projections that arise from constant, occurring at any level of the lower cervical spine
most of the circumference of the upper margin of the with the most common being the level of C5–C6.70 The
vertebral body of C3 to C7. Although the uncinate pro- shape of the superior articular facets gradually changes
cesses are present in utero, they start to enlarge gradually from almost circular at the level of C3, to oval with an
between the ages of 9 to 14 years reaching their maximum elongated transverse diameter at C7.70
height.63,65 In mature spines the uncinate processes artic- The cervical zygapophyseal joints were found to be
ulate with the superior vertebra at its incisures forming the most common source of pain after whiplash injury.71
the uncovertebral joints or joints of Luschka. The size of This could be due to the mechanical compressional and
the uncinate processes varies slightly from level to level. shear forces applied to the dorsal part of the joints during
Their average height ranges from 3–6.1 mm and the this form of impact.72–74 Further, the absence of articular
anteroposterior length from 5–8.3 mm,66 and they are cartilage, especially at the dorsal part of the joint, could
significantly higher at C4 to C6 compares to C3 and C7 lead to impingement and bone to bone contact and
levels.67 trauma.75 The facet joint capsule consists of bundles of
The uncinate processes and the uncovertebral joints dense, regularly arranged, collagen fibres, containing
limit side flexion of the cervical spine and stabilize the elongated nuclei of fibroblasts and loose connective tissue
intervertebral disc in the coronal plane during axial rota- with areas of adipose-like tissue.76,77 Fibroblasts with
tion.5 The uncovertebral joints play a stabilizing role ovoid and round nuclei are found within the loose con-
primarily in extension and side flexion followed by nective tissue.76 The capsule of the lower cervical spine
torsion.68 The uncinate processes, by forming the saddle is also covered by an average of 22.4% by muscle fibres,
shape of the superior surface of the vertebra, working possibly by the semispinalis and multifidi, suggesting a
together with the zygapophyseal joints dictate the cou- potential path for loading of the facet capsule.78 A number
pling movement of side flexion and ipsilateral rotation of of animal and human cadaveric studies have verified the
the vertebrae of the low cervical spine on an the axis presence of mechanoreceptors and nociceptors in the
perpendicular to the plane of the facet joints.64,69 capsules of the cervical facet joints.76,77,79–81 The dorsal
part of the cervical facet joint is innervated by the dorsal
ramus via its middle branch.41
The Vertebral Arch Intra-articular inclusions, or synovial folds, are present
The vertebral arch consists of the pedicles and the in the majority of the zygapophyseal joints. Because of
laminae. The pedicles are short, projecting posterolater- the location, to the ventral and dorsal parts of the joints,
ally and arising midway between the discal surfaces of the it has been hypothesized that they act as space fillers
vertebral bodies making the superior and inferior verte- protecting the parts of the cartilage that become exposed
bral notches of similar depth. The laminae are longer and during translatory movements by maintaining a film of
thinner and project posteromedially. They have a thinner synovial fluid between themselves and the cartilage. In
superior border compared to the inferior and they are addition, and due to their fibrous consistency, it has also
slightly curved. The junction of the laminar forms the been hypothesized that meniscoids could play a role in
spinous process which is short and bifid and the two mechanical stress distribution.82 Although, an earlier
tubercles being often of unequal size. study has indicated that intra-articular meniscoids are
The junction of the pedicle with the ipsilateral lamina features of cervical spine in the first two decades of life,83
bulges laterally forming the superior and inferior articu- more recent cadaveric studies have confirmed their pres-
lar processes. The articulations between the superior and ence in the majority of facet joints of cervical spines of
inferior processes (facet or zygapophyseal joints) form the advanced age.82,84
articular pillar (lateral mass) on each side. The superior
articular processes are flat, oval-shaped and face supero-
posteriorly. Small morphological differences exist for the
Ligaments
superior articular processes of the C3 which, in addition The main ligaments that are associated with the interver-
to facing superiorly and posteriorly, also face medially to tebral and zygapophyseal joints are the anterior longitu-
about 40°. Also, the superior articular facets of C3 lie dinal ligament, the posterior longitudinal ligament and
slightly inferiorly in relation to their vertebral body com- the ligamentum flavum.
pared to the rest of the typical cervical levels.64 This The anterior longitudinal ligament (ALL) is attached
morphological specificity of the superior processes of the to the anterior surfaces of the vertebral bodies and discs.62
C3 lead to alteration of the biomechanical behaviour at The ALL is comprised of four layers with distinguishable
the C2–C3 level. Indeed, the expected coupling of ipsi- patterns of attachment.85 The fibres of the superficial
lateral rotation and side flexion does not seem to exist at layer of the ALL run longitudinally crossing several seg-
this level. The medial orientation on the facets at this ments and they are attached to the central areas of the
level serves to minimize rotation, thus stabilizing the C2 anterior surfaces of the vertebral bodies. They cover
during rotational movements of the neck.14 On average roughly the middle two-quarters of the anterior vertebral
98 PART II  Advances in Theory and Practice

bodies and, in contrast to the upper cervical levels, at the attention, especially in the mid and low cervical seg-
lower cervical segments the fibres of the ALL are less ments. Despite the fact that in most anatomical texts the
densely packed and the ligament expands laterally. The LN is described as a ligament homologous to the supra-
fibres of the second layer also run longitudinally. At this spinous and interspinous ligaments, the LN is not a liga-
layer the fibres cover one intervertebral disc and attach ment but a structure that consists of a dorsal nuchal raphe
to the anterior surfaces of the inferior and superior ver- and a midline fascial septum.89 The dorsal raphe and the
tebrae but never further than half way up or down that ventral fascial portions of the LN are a single entity and
surface. The fibres of the third layer are similar to the consist of muscular aponeurotic fibres and in the mid-
ones of the second one in orientation, but these fibres are cervical spine; they are derived from the trapezius and
shorter, covering one intervertebral disc and attaching splenius capitis. The aponeurotic fibres decussate at the
just cranial of caudal to the margins of the adjacent ver- midline, forming a triangular body representing the
tebrae. The fibres of the fourth layer are of more alar dorsal raphe which becomes progressively larger caudally
disposition. They arise from the anterior surface of the with a progressive increase in aponeurotic fibres. The
vertebra above, close to its inferior margin, and passing decussate fibres then project ventrally to attach to the
inferiorly and laterally insert to the vertebra below just spinous processes of the C2 to C5 vertebrae forming
inferiorly to its superior margin. The most lateral of these the ventral portion of the LN. At the C6, C7 levels the
fibres reach the summit of the uncinate processes.85 two portions of the LN are not distinguishable and
The posterior longitudinal ligament (PLL) covers the the LN is formed by horizontal aponeurotic fibres of the
entire posterior surface of the vertebral bodies in the trapezius, rhomboideus minor, serratus posterior minor
vertebral canal, attaching to the central posterior surfaces and splenius capitis.90
of the vertebral bodies and has three distinct layers.85 The
superficial layer contains longitudinal fibres that bridge
three to four vertebrae and lateral extensions that extend
inferolaterally from the central band to cross an interver-
The Intervertebral Disc
tebral disc and attach to the base of the pedicle one or The intervertebral disc of the cervical spine shows dis-
two levels below.85 The fibres of the intermediate layer tinct morphological and histological differences to the
are longitudinal, span only one intervertebral disc and rest of the discs of the spinal column. The intervertebral
occupy a narrow area close to the midline of the posterior disc consists of the nucleus pulposus and the annulus
surface of the vertebral body. The deep layer consists of fibrosus as in the rest of the sections of the spine. However,
fibres that cover one intervertebral disc and arise from the nucleus pulposus at birth constitutes no more than
the inferior margin of the cephalad vertebra and extend 25% of the entire disc and quickly changes from gelati-
inferiorly and laterally to the superior margin of the nous to fibrocartilagenous in consistency by the middle
caudal vertebrae. The most lateral fibres extend in an alar of the second decade of life.65
fashion to the posterior end of the base of the uncinate The annulus fibrosus has a crescentic form anteriorly
process.85 In the cervical spine the ALL and the deep with a thick anterior part in the sagittal plane, which
layer of the PPL are continuous, surrounding the entire becomes progressively thinner when traced to the unci-
vertebral body while the superficial layer of the PPL sur- nate processes. The posterior part consists only of a
rounds the dura matter, nerve root and the vertebral thin layer of collagen fibres. The anterior part of the
artery suggesting a dual role for this structure: as a con- annulus is covered by a thin layer of collagen fibres.
ventional ligament; and as a protective membrane for the This is a transitional layer between the deepest layers
soft tissues inside the vertebral canal.86 of the anterior longitudinal ligament and the annulus.
The ligamentum flavum (LF) connects the laminae of The fibres of the transitional layer pass inferiorly and
the adjacent vertebra and extends from the facet joint diverge laterally, whereas more laterally they pass infe-
capsules to the point where the laminae fuse to form the riorly and laterally in a more alar disposition attaching
spines.62 In the low cervical spine the majority of liga- to the edges of the vertebral bodies. The fibres of the
menta flava do not fuse at the midline,87 leaving gaps that annulus fibrosus proper arise laterally from the apex
admit veins connecting the internal and posterior exter- and anterior surface of the uncinate process and the
nal venous plexuses.62 The LF consists of yellow elastic superior part of the inferior disc and run medially to
and collagen fibres that are longitudinal in orientation insert on the inferior surface of the vertebrae above.
connecting the anterior surface and lower margin of the Towards the midline the fibres interweave with the fibres
lamina above to the posterior surface and upper margin coming from the opposite side. Deeper layers of the
of the lamina below. At the cervical spine the LF is thin, annulus progressively originate closer to the midline
broad and long and it limits separation of the laminae in maintaining the interweaving pattern. At its deepest
flexion and assists restoration of the neutral posture after (2–3  mm), the fibres of the annulus are embedded with
flexion.62 The LF becomes thinner in cervical flexion and proteoglycans to form a fibrocartilagenous mass increas-
thicker and shortened in extension protruding in the ingly becoming less laminated, forming the nucleus of
spinal canal to an average of 3.25 mm approximately.88 the disc.85 The posterior part of the annulus is about
At the levels of C6–C7 and C7–T1 the LF is uniquely 1  mm thin and covers a small posteromedial section.
thick in extension, which may predispose to cord Its fibres run vertically between the facing surfaces of
compression. the adjacent vertebral bodies. The rest of the posterior
From the rest of the ligaments of the cervical fibrocartilagenous core to the uncus either side is covered
spine, the ligamentum nuchae (LN) commands the most by periosteofascial tissue.65,85
 9  Functional Anatomy 99

The Intervertebral Foramina 3. Jull G, Sterling M, Falla D, et al. Whiplash, Headache and
Neck Pain. Research-Based Direction for Physical Therapists.
and Spinal Nerves Edinburgh: Churchill Livingstone; 2008.
4. Amiri M, Jull G, Bullock-Saxton J. Measurement of upper cervical
The cervical spinal nerves exit the spinal cord in an flexion and extension with the 3-space fastrak measurement system:
oblique orientation towards their respective neural a repeatability study. J Man Manip Ther 2003;11(4):
foramen.91 The intervertebral foramen is shaped as a 198–203.
5. Panjabi M, Crisco J, Vasavada A, et al. Mechanical properties of the
funnel with its narrowest part medially and its borders human cervical spine as shown by three-dimensional load displace-
are comprised by the pedicles of the superior and inferior ment curves. Spine 2001;26(24):2692–700.
vertebrae, the facet joint posteriorly and the disc and 6. Ordway N, Seymour R, Donelson R, et al. Cervical flexion, exten-
uncovertebral joint anteriorly.91,92 The foramina are also sion, protrusion and retraction: a radiographic segmental analysis.
larger in the upper cervical spine becoming gradually Spine 1999;24(3):240–7.
7. Panjabi M, Dvorak J, Duranceau J, et al. Three-dimensional move-
narrower at lower levels with the narrowest at the C7–T1 ments of the upper cervical spine. Spine 1988;13(7):
level.91 The anatomical cadaveric study of Tanaka et al.92 726–30.
provided significant findings regarding the anatomy of 8. Bogduk N, Mercer S. Biomechanics of the cervical spine. I: normal
the cervical nerve roots that have clinical implications. kinematics. Clin Biomech 2000;15:633–48.
9. Ishii T, Mukai Y, Hosono N, et al. Kinematics of the cervical spine
The spinal nerve is comprised of the ventral and dorsal in rotation in vivo three-dimensional analysis. Spine 2004;29(7):
nerve roots. The ventral nerve root lies caudal to the 139–44.
dorsal root and courses along the caudal border of 10. Iai H, Moriya H, Goto S, et al. Three-dimensional motion analysis
the dorsal nerve root in the intervertebral foramen. The of the upper cervical spine during axial rotation. Spine 1993;
ventral root is approximately two-thirds the size of the 18(16):2388–92.
11. Mimura M, Moriya H, Watanabe T, et al. Three dimensional
dorsal root. motion analysis of the cervical spine with special reference to axial
Further, at the level of C4-C5 intervertebral foramen rotation. Spine 1989;14(11):1135–9.
the majority of the C5 nerve roots are situated caudal or 12. Palastanga N, Field D, Soames R. Anatomy and Human Move-
just anterior to the intervertebral disc. The majority of ment. Structure and Function. 5th ed. Butterworth Heinnemann,
Elsevier; 2006.
the C6 and C7 nerve roots lie cephalad to the interver- 13. Standring S. Gray’s Anatomy. 40th ed. Churchill Livingstone;
tebral disc while the vast majority of the C8 nerve roots 2008.
have no contact with the disc. Furthermore, below the 14. Hino H, Abumi K, Kanayama M, et al. Dynamic motion analysis
level of C5 the nerve rootlets, which comprise the ventral of normal and unstable cervical spines using cineradiography. An
and dorsal nerve roots, pass downwards with increased in vivo study. Spine 1999;24(2):163–8.
15. Crisco J, Panjabi M, Dvorak J. A model of the alar ligaments of the
obliquity reaching their corresponding intervertebral upper cervical spine in axial rotation. J Biomech 1991;24(7):
foramina, with the dorsal rootlets of C5, C6 and C7 607–14.
forming a number of intra-dural connections. The con- 16. Dvorak J, Schneider E, Saldinger P, et al. Biomechanics of the
sequence is that whichever nerve root is going to be craniocervical region; the alar and transverse ligaments. J Orthop
Res 1988;6:452–61.
compressed, the dorsal, the ventral or perhaps both, 17. Dvorak J, Panajabi M. Functional anatomy of the alar ligaments.
depends upon the compressing structure (disc, superior Spine 1987;12(2):183–9.
facet joint or ligamentum flavum) and its anatomical rela- 18. McPartland J, Brodeur R. Rectus capitus posterior minor: a small
tionship to the nerve root. In addition, the course of the but important suboccipital muscle. J Bodyw Mov Ther 1999;
rootlets and the interconnections between the dorsal 3(1):30–5.
19. Boyd Clark L, Briggs C, Galea M. Comparative histochemical
rootlets can explain the spread of clinical signs and symp- composition of muscle fibres in a pre and post-vertebral muscle of
toms in more than one nerve root from disc herniations, the cervical spine. J Anat 2001;199:709–16.
as well as the variation and overlapping sensory symp- 20. Cook C, Hegedus E, Showalter C, et al. Coupling behaviour of the
toms cause by nerve root compression.92 cervical spine: a systematic review of the literature. J Manipulative
Physiol Ther 2006;29(7):570–5.
The spinal nerves at the lower cervical spine have 21. Mercer S, Bogduk N. Intra-articular inclusions of the cervical syno-
significant connective tissue attachments posteriorly to vial joints. Br J Rheumatol 1993;32(8):705–10.
the medial end of the intervertebral foramina, the cap- 22. Friedrich K, Reiter G, Pretterklieber M, et al. Reference data for
sules of the zygapophyseal joints, the periosteum of the in vivo MRI properties of meniscoids in the cervical zygapophyseal
inferior pedicles and anteriorly to the vertebral bodies, joints. Spine 2008;33(21):E778–83.
23. Webb A, Darekar A, Sampson M, et al. Synoival folds of the lateral
the intervertebral discs and the posterior longitudinal atlanto-axial joints: in vivo quantitative assessment using MRI in
ligament.93 All the above structures are innervated by the healthy volunteers. Spine 2009;34(19):E697–702.
sinuvertebral nerve (intervertebral discs, posterior longi- 24. Tang X, Liu L, Yang H, et al. Anatomic study of the synovial folds
tudinal ligament and ventrolateral spinal canal perios- of the O-AA joints. Clin Anat 2007;20(4):376–81.
25. Inami S, Shiga T, Tsujino A, et al. Immunohistochemical demon-
teum) and by the cervical dorsal ramus (zygapophyseal stration of nerve fibres in the synovial folds of the human cervical
joints). The potential of those structures to evoke pain facet joint. J Orthop Res 2001;19:593–6.
could render the findings of the neural tension tests more 26. Goel V, Winterbottom J, Schulte K, et al. Ligamentous laxity
difficult to interpret.93 across C0-C1-C2 complex. Axial torque-rotation characteristics
until failure. Spine 1990;15(10):990–6.
REFERENCES 27. Panjabi M, Dvorak J, Duranceau J, et  al. Three-dimensional move-
ments of the upper cervical spine. Spine 1988;13(7):726–30.
1. Salem W, Lenders C, Mathieu J, et al. In vivo three-dimensional 28. Panjabi M. The stabilising system of the spine. Part I. Function,
kinematics of the cervical spine during maximal axial rotation. Man dysfunction, adaptation and enhancement. J Spinal Disord 1992a;
Ther 2013;18:339–44. 5(4):383–9.
2. Chancey V, Ottaviano D, Myers B, et al. A kinematic and anthro- 29. Panjabi M. The stabilising system of the spine. Part II. Neutral
pometric study of the upper cervical spine and the occipital con- zone and instability hypothesis. J Spinal Disord 1992b;5(4):
dyles. J Biomech 2007;40:1953–9. 390–7.
100 PART II  Advances in Theory and Practice

30. Panjabi M, Abumi K, Duranceau J, et al. Spinal stability and inter- 55. Kelly M, Cardy N, Melvin E, et al. The craniocervical flexion test:
segmental muscle forces: a biomechanical model. Spine an investigation of performance in young asymptomatic subjects.
1989;14:194–200. Man Ther 2013;18:83–6.
31. Panjabi M, Lydon C, Vasavada A, et al. On the understanding of 56. Scali F, Pontell M, Enix D, et al. Histological analysis of the rectus
clinical instability. Spine 1994;19(23):2642–50. capitus posterior major’s myodural bridge. Spine J 2013;13:
32. Panjabi M, Cholewicki J, Nibu K, et al. Critical load of the human 558–63.
cervical spine: an in vitro experimental study. Clin Biomech 57. Hack G, Koritzer R, Walker L. Anatomic relation between the
1998;13:11–17. rectus capitus posterior minor muscle and the dura mater. Spine
33. Brolin K, Halldin P. Development of a finite model of the upper 1995;20:2484–6.
cervical spine in a parameter study of ligament characteristics. 58. Scali F, Marsili E, Pontell M. Anatomical connection between the
Spine 2004;29(4):376–85. rectus capitis posterior major and the dura mater. Spine 2011;
34. Goel V, Winterbottom J, Schulte K, et al. Ligamentous laxity 36:E1612–14.
across C0-C1-C2 complex. Axial torque-rotation characteristics 59. Alix M, Bates D. A proposed etiology of cervicogenic headache: the
until failure. Spine 1990;15(10):990–6. neurophysiological basis and anatomic relationship between the
35. Krakenes J, Kaale B, Nordli H, et al. MR analysis of the transverse dura mater and rectus capitis minor muscle. J Manipulative Physiol
ligament in the late stage of whiplash injury. Acta Radiol 2003; Ther 1999;22:534–9.
44:637–44. 60. Hack G, Hallgren R. Chronic headache relief after section of sub-
36. Krakenes J, Kaale B, Moen G, et al. MR analysis of the tectorial occipital muscle dural connections: a case report. Headache
and posterior antlanto-occipital membranes in the late stage of 2004;44:84–9.
whiplash injury. Neuroradiology 2003;45:585–91. 61. Haldeman S, Dagenais S. Cervicogenic headaches: a critical review.
37. Krakenes J, Kaale B. Magnetic resonance imaging assessment of Spine J 2001;1(1):31–46.
craniovertebral ligaments and membranes after whiplash trauma. 62. Standring S. Standring S, editor. Gray’s Anatomy. The Anatomical
Spine 2006;31(24):2820–6. Basis of Clinical Practice. 39th ed. Oxford: Elsevier, Churchill
38. Dvorak J, Hayek J, Zehnder R. CT-functional diagnostics of the Livingstone; 2005.
rotatory instability of the upper cervical spine: 2. An evaluation on 63. Levangie PK, Norkin CC. Joint Structure and Function. A Com-
healthy adults and patients with suspected instability. Spine prehensive Analysis. 3ed ed. Philadelphia: F. A. Davis Company;
1987;12:726–31. 2001.
39. Dickman C, Mamourian A, Sonntag V, et al. Magnetic resonance 64. Bogduk N, Mercer S. Biomechanics of the cervical spine. I: normal
imaging of the transverse atlantal ligament for the evaluation of kinematics. Clin Biomech (Bristol, Avon) 2000;15(9):633–48.
atlantoaxial instability. J Neurosurg 1991;75:221–7. [Epub 2000/08/18].
40. Tubbs S, Kelly D, Humphrey R, et al. The tectorial membrane: 65. Mercer SR, Jull GA. Morphology of the cervical intervertebral disc:
anatomical, biomechanical and histological analysis. Clin Anat implications for McKenzie’s model of the disc derangement syn-
2007;20:382–6. drome. Man Ther 1996;1(2):76–81.
41. Krakenes J, Kaale B, Rorvik J, et al. MRI assessment of normal 66. Tubbs RS, Rompala OJ, Verma K, et al. Analysis of the uncinate
ligamentous structures in the craniovertebral junction. Neuroradi- processes of the cervical spine: an anatomical study. J Neurosurg
ology 2001;43:1089–97. Spine 2012;16(4):402–7. [Epub 2012/01/24].
42. Kaale B, Krakenes J, Albreksten G, et al. Whiplash associated dis- 67. Ebraheim NA, Lu J, Biyani A, et al. Anatomic considerations for
orders impairment rating: neck disability index score according to uncovertebral involvement in cervical spondylosis. Clin Orthop
severity of MR-findings of ligaments and membranes in the upper Relat Res 1997;334:200–6. [Epub 1997/01/01].
cervical spine. J Neurotrauma 2005;22(4):466–75. 68. Kotani Y, McNulty PS, Abumi K, et al. The role of anteromedial
43. Schomacher J, Falla D. Function and structure of the deep cervical foraminotomy and the uncovertebral joints in the stability of the
extensor muscles in patients with neck pain. Man Ther 2013;18: cervical spine. A biomechanical study. Spine (Phila Pa 1976)
360–6. 1998;23(14):1559–65. [Epub 1998/07/31].
44. Falla D. Unravelling the complexity of muscle impairment in 69. Penning L. Differences in anatomy, motion, development and
chronic neck pain. Man Ther 2004;9(3):125–33. aging of the upper and lower cervical disk segments. Clin Biomech
45. Jull G, Falla D, Treleaven J, et al. A therapeutic exercise approach 1988;3(1):37–47.
for cervical disorders. In: Boyling J, Palastanga N, editors. 70. Pal GP, Routal RV, Saggu SK. The orientation of the articular
Grieves’ Modern Manual Therapy. 3rd ed. Edinburgh: Churchill facets of the zygapophyseal joints at the cervical and upper tho-
Livingstone; 2004. racic region. J Anat 2001;198(Pt 4):431–41. [Epub 2001/
46. Hallgren R, Pierce S, Prokop L, et al. EMG activity of rectus 05/01].
capitus posterior minor muscles associated with voluntary head 71. Barnsley L, Lord SM, Wallis BJ, et al. The prevalence of chronic
retraction. Spine J 2014;14:104–12. cervical zygapophysial joint pain after whiplash. Spine (Phila Pa
47. Boyd Clark L, Briggs C, Galea M. Muscle spindle distribution, 1976) 1995;20(1):20–5, discussion 6. [Epub 1995/01/01].
morphology and density in longus colli and multifidus muscles of 72. Bogduk N, Yoganandan N. Biomechanics of the cervical spine Part
the cervical spine. Spine 2002;27(7):694–701. 3: minor injuries. Clin Biomech (Bristol, Avon) 2001;16(4):267–75.
48. Kettler A, Hartwig E, Schultheib L, et al. Mechanically stimulated [Epub 2001/05/19].
muscle forces strongly stabilise intact and injured upper cervical 73. Stemper BD, Yoganandan N, Pintar FA. Gender dependent cervical
spine specimens. J Biomech 2002;35:339–46. spine segmental kinematics during whiplash. J Biomech 2003;
49. Armstrong B, McNair P, Taylor D. Head and neck position sense. 36(9):1281–9. [Epub 2003/08/02].
Sports Med 2008;38(2):101–17. 74. Stemper BD, Yoganandan N, Pintar FA. Gender- and region-
50. Treleaven J. Sensorimotor disturbances in neck disorders affecting dependent local facet joint kinematics in rear impact: implications
postural stability, head and eye movement control. Man Ther in whiplash injury. Spine (Phila Pa 1976) 2004;29(16):1764–71.
2008;13(1):2–11. [Epub 2004/08/11].
51. Kristjansson, E. The Cervical spine and proprioception. In: Boyling 75. Yoganandan N, Knowles SA, Maiman DJ, et al. Anatomic study of
J, Jull G, editors. Grieve’s Modern Manual Therapy. 3rd ed. the morphology of human cervical facet joint. Spine (Phila Pa 1976)
Churchill Livingstone; 2004. 2003;28(20):2317–23. [Epub 2003/10/16].
52. Middleditch A, Oliver J. Functional Anatomy of the Spine. 76. Kallakuri S, Singh A, Chen C, et  al. Demonstration of substance
2nd ed. Edinburgh: Elsevier Butterworth Heinnemann; 2005. P, calcitonin gene-related peptide, and protein gene product 9.5
53. Taylor J, Twomey L. Functional and applied anatomy of the cervical. containing nerve fibers in human cervical facet joint capsules.
In: Spine IN, Grant R, editors. Physical Therapy of the Cervical and Spine (Phila Pa 1976) 2004;29(11):1182–6. [Epub 2004/05/29].
Thoracic Spine. 3rd ed. New York: Churchill Livingstone; 2002. 77. Kallakuri S, Li Y, Chen C, et al. Innervation of cervical ventral facet
54. O’Leary S, Falla D, Jull G. The relationship between superficial joint capsule: histological evidence. World J Orthop 2012;3(2):10–
muscle activity during the craniocervical flexion test and clinical 14. [Epub 2012/04/04].
features in patients with chronic neck pain. Man Ther 2011; 78. Winkelstein BA, McLendon RE, Barbir A, et al. An anatomical
16:452–5. investigation of the human cervical facet capsule, quantifying
 9  Functional Anatomy 101

muscle insertion area. J Anat 2001;198(Pt 4):455–61. [Epub 87. Lirk P, Kolbitsch C, Putz G, et al. Cervical and high thoracic liga-
2001/05/01]. mentum flavum frequently fails to fuse in the midline. Anesthesiol-
79. Chen C, Lu Y, Kallakuri S, et al. Distribution of A-delta and ogy 2003;99(6):1387–90. [Epub 2003/11/26].
C-fiber receptors in the cervical facet joint capsule and their 88. Jia LS, Shen QA, Chen DY, et al. Dynamic changes of the cervical
response to stretch. J Bone Joint Surg 2006;88(8):1807–16. [Epub ligamental flavum in hyperextension – hyperflexion movement
2006/08/03]. and their measurements. Chin Med J 1990;103(1):66–70. [Epub
80. Fukui S, Ohseto K, Shiotani M, et al. Referred pain distribution of 1990/01/01].
the cervical zygapophyseal joints and cervical dorsal rami. Pain 89. Mercer SR, Bogduk N. Clinical anatomy of ligamentum nuchae.
1996;68(1):79–83. [Epub 1996/11/01]. Clin Anat 2003;16(6):484–93. [Epub 2003/10/21].
81. McLain RF. Mechanoreceptor endings in human cervical facet 90. Johnson GM, Zhang M, Jones DG. The fine connective tissue
joints. Spine 1994;19(5):495–501. [Epub 1994/03/01]. architecture of the human ligamentum nuchae. Spine 2000;25(1):
82. Mercer S, Bogduk N. Intra-articular inclusions of the cervical syno- 5–9. [Epub 2000/01/27].
vial joints. Br J Rheumatol 1993;32(8):705–10. 91. Caridi JM, Pumberger M, Hughes AP. Cervical radiculopathy: a
83. Fletcher G, Haughton VM, Ho KC, et al. Age-related changes in review. HSS J 2011;7(3):265–72. [Epub 2012/10/02].
the cervical facet joints: studies with cryomicrotomy, MR, and CT. 92. Tanaka N, Fujimoto Y, An HS, et al. The anatomic relation among
Am J Roentgenol 1990;154(4):817–20. [Epub 1990/04/01]. the nerve roots, intervertebral foramina, and intervertebral discs of
84. Inami S, Kaneoka K, Hayashi K, et al. Types of synovial fold in the cervical spine. Spine 2000;25(3):286–91. [Epub 2000/03/07].
the cervical facet joint. J Orthop Sci 2000;5(5):475–80. [Epub 93. Moses A, Carman J. Anatomy of the cervical spine: implications for
2001/02/17]. the upper limb tension test. Aust J Physiother 1996;42(1):31–5.
85. Mercer S, Bogduk N. The ligaments and annulus fibrosus of human [Epub 1996/01/01].
adult cervical intervertebral discs. Spine 1999;24(7):619–26, discus-
sion 27–8.
86. Hayashi K, Yabuki T, Kurokawa T, et al. The anterior and the
posterior longitudinal ligaments of the lower cervical spine. J Anat
1977;124(Pt 3):633–6. [Epub 1977/12/01].

CHAPTER 9.2  ■  LUMBAR SPINE

Michael Adams • Patricia Dolan

THE VERTEBRAL COLUMN vertebrae: typically 13° of combined flexion and exten-
sion, 4° of lateral bending to each side, and 1–2° of axial
The lumbar vertebral column provides a semi-rigid axis rotation (Fig. 9-6). Movements are greater in the cervical
for the body, one that enables upright stance and which spine, and less in the thoracic spine, largely because of
provides attachment points for muscles to move the differing proportions in the heights of discs and vertebral
limbs. It also protects the spinal cord within the bony bodies. Vertebral bodies grow in height faster than inter-
vertebral foramina. This segmented column can bend vertebral discs, causing spinal mobility to decrease during
and twist because its rigid vertebrae are separated by the growth period. Further decreases in spinal mobility
deformable intervertebral discs (Fig. 9-5). However, after skeletal maturity are largely attributable to bio-
only small movements are permitted between individual chemical changes in collagen which stiffen spinal tissues.

14
Range of movement (degrees)

12

10
vb T T
np 8
ivd
af
6
B
4
C
R 2

S 0
L1–2 L2–3 L3–4 L4–5 L5–S1
A C Lumbar level
FIGURE 9-5  ■  (A) Lumbar spine in the sagittal plane (anterior on
Flexion Lateral bend
left) showing intervertebral discs (ivd) between the vertebral
Extension Axial rotation
bodies (vb). Bold arrows indicate muscle forces on the spine,
which can be summed to a resultant force (R) with compressive FIGURE 9-6  ■  Ranges of normal movement at each lumbar level.
(C) and shear (S) components. (B) Intervertebral discs have a Note that the combined range of flexion and extension is
soft nucleus pulposus (np) surrounded by a fibrous annulus approximately constant at different lumbar levels. Values for
fibrosus (af). Spinal compression increases the fluid pressure lateral bending and axial rotation are averaged for movements
in the nucleus, and generates tension (T) in the annulus. to the left and right. Data from bilateral radiographs of healthy
(C) Exploded view of annulus, showing its lamellar structure, young men standing upright. (Adapted from: The Biomechanics
with alternating orientation of collagen fibres. of Back Pain, published by Churchill Livingstone.1)
102 PART II  Advances in Theory and Practice

Postnatal development of a thoracic kyphosis, and a Neural Arch

cervical and lumbar lordosis, leads to the familiar S-shape
of the adult spine. These sagittal plane curves play a role The neural arch, which is mostly cortical bone, contains
in shock absorption and energy conservation during loco- more than 50% of the mineral content of a typical ver-
motion, because they increase when the body sinks down tebra. It protects the spinal cord in a ring of bone, while
in mid-stride, and decrease when the body rises at toe-off. its processes act as attachment points for muscles and
Spinal ligaments, discs and (especially) tendons of the ligaments to effect and limit spinal movements, respec-
trunk muscles all resist changes in spinal curvature, tively. The ends of the spinous and transverse processes
storing energy as they are deformed, and releasing it later are cartilaginous during childhood, contributing to
in the gait cycle.1 The effect is similar to the action of enhanced spinal mobility. Conversely they can be sites of
flexing the knees when landing from a jump: stretched bony hypertrophy in old age, when they contribute to
muscles and tendons oppose rapid knee flexion and soften reduced mobility and to kyphosis.
the landing.
Apophyseal Joints
Two plane synovial joints regulate movement between
LUMBAR VERTEBRAE adjacent vertebrae and help to stabilize the spine. The
The Vertebral Body cartilage-covered articular surfaces are oblique in both
the sagittal and transverse planes, and this obliquity varies
This short cylindrical bone lies between adjacent inter- with spinal level (Fig. 9-8). Apophyseal (‘facet’) joints
vertebral discs, and primarily resists compressive forces primarily resist forward shear and axial rotation between
acting down the long axis of the spine (Fig. 9-5). It is vertebrae, but under certain circumstances (see below)
mostly trabecular bone, with a thin shell of cortical bone they resist compression also.
that is perforated on the superior and inferior surfaces
(‘endplates’) in order to facilitate nutrient transport into
the discs.2 Vertebral body trabeculae are predominantly INTERVERTEBRAL DISCS
parallel, or at right angles, to the spine’s long axis (Fig.
9-7), but parasagittal sections show that trabeculae also These pads of fibrocartilage allow small intervertebral
arch in from the pedicles to provide additional support movements, and serve to distribute compressive loading
for the endplates. These curved trabeculae appear to evenly on to the vertebral bodies, even when the spine is
reinforce the inferior endplate more than the superior, flexed or extended.
because the superior endplate is more easily injured.3
The vertebral body has a rich blood supply, and nerves
have been identified within it, including close to the
Nucleus Pulposus
endplates.4 The central amorphous nucleus pulposus (Fig. 9-9A)
comprises a soft gel of water-binding proteoglycan mol-
ecules which is so soft and deformable that it behaves
mechanically like a pressurized fluid (Fig. 9-9B). A loose
network of very fine collagen type II fibrils binds the
nucleus together, and anchors it to adjacent annulus and
endplates.5

Annulus Fibrosus
The nucleus is surrounded by concentric lamellae (layers)
of the annulus fibrosus, which are mostly composed of

Sagittal Transverse

A P L1–2

FIGURE 9-7  ■  Radiograph of a mid-sagittal plane slice of a human

lumbar vertebral body. In the mid-sagittal plane, trabeculae are L5–S1
mostly orientated vertically or horizontally, and the anterior
cortex (on the left) is thicker than the posterior. Note two
common features of elderly vertebrae: a large Schmorl’s node FIGURE 9-8  ■  Orientation of the articular surfaces (shaded) of
adjacent to the upper endplate (black arrow), and large out- lumbar apophyseal joints varies gradually with spinal level,
growths (‘osteophytes’) around the superior and inferior from L1–L2 to L5–S1, both in the sagittal plane and in the trans-
margins of the anterior cortex (white arrow). (Adapted from: The verse (horizontal) plane. (Adapted from: The Biomechanics of Back
Biomechanics of Back Pain, published by Churchill Livingstone.1) Pain, published by Churchill Livingstone.1)
 9  Functional Anatomy 103

A B

P A

3.0

Compressive stress (MPa)

2.5 h

2.0
1.5
1.0
0.5
P A
P 0.0
0 10 20 30
C Distance across disc (mm)
FIGURE 9-9  ■  (A) Photograph of a typical middle-aged intervertebral disc sectioned in the transverse plane (A, anterior; P, posterior).
The dashed line indicates the mid-sagittal diameter. (B) A similar disc sectioned in the mid-sagittal plane. (C) Distribution of com-
pressive stress measured across the mid-sagittal diameter of a similar disc. Note that in the central region of the disc, bounded by
the vertical dashed lines, horizontal and vertical stresses (shown by broken and solid graphs respectively) are very similar. Small
stress concentrations (h) are common in the posterior annulus. (Adapted from: The Biomechanics of Back Pain, published by Churchill
Livingstone.1)

and shearing movements by intervertebral ligaments and

by the neural arch.1

Vertebral Endplates
Central regions of the perforated cortical bone endplate
of the vertebral body are weakly bonded to a thin layer
of hyaline cartilage on the disc side. This cartilage, which
1 2 3 4 5 6 resembles articular cartilage, is more rigid than annulus
and does not normally swell. It serves as a biological filter
FIGURE 9-10  ■  In the annulus fibrosus of intervertebral discs, which restricts movements of large molecules into the
several adjacent lamellae (numbered) are bound together in the disc, and also the expulsion of water from the disc nucleus
radial direction by ‘translamellar bridges’ (arrows) which are
probably made of collagen. Photograph of a sheep disc sec- when it is compressed.2
tioned in a para-sagittal plane. (Reproduced with permission from
Schollum et al.6)
Internal Mechanical Function of
Intervertebral Discs
coarse fibres of collagen type I, embedded in a hydrated Internal disc function has been investigated by pulling
proteoglycan matrix. Collagen fibres within each lamella a miniature pressure transducer along the mid-sagittal
run obliquely from bone to bone, with the fibre orienta- diameter of loaded cadaveric discs.9 These measure-
tion alternating in successive lamellae (Fig. 9-5C). This ments confirm that the nucleus and inner annulus do
arrangement, together with radially directed ‘translamel- indeed behave like a fluid (Fig. 9-9B). However, with
lar bridges’ (Fig. 9-10), which bind adjacent lamellae advancing age, the fluid-like region shrinks, and local-
together, ensures that any cracks developing in the ized concentrations of compressive stress develop in
annulus do not easily spread in a radial direction, so that the annulus.
the tissue is extremely tough.7 Spinal compression creates
a high fluid pressure in the disc nucleus, which is resisted
by a tensile ‘hoop’ stress in the annulus lamellae (Fig.
Blood and Nerve Supply
9-5B). In addition, the annulus is stiff enough to resist Intervertebral discs are the largest avascular structures in
compression in its own right. Collagen fibres in the outer the human body, and consequent nutrient transport
lamellae are strongly anchored to the adjacent vertebrae, problems limit cell density to very low levels, particularly
but in the inner annulus they merely envelop the nucleus. in the adult nucleus.10 Nerves are found within the discs
During flexion movements, the posterior annulus can be of infants, but they retreat in early childhood, and in the
stretched vertically by more than 50%,8 but discs are adult do not normally penetrate more than 1–3 mm into
effectively protected from excessive bending, twisting the peripheral annulus.
104 PART II  Advances in Theory and Practice

INTERVERTEBRAL LIGAMENTS processes, and intertransversarii between the transverse

processes. They are weak but contain a particularly high
Longitudinal Ligaments density of muscle spindles, which probably enables them
to play a major role in proprioception and the subtle
The anterior and posterior longitudinal ligaments bind control of movements and postures.
together adjacent vertebrae, covering the anterior and
posterior surfaces of the disc and vertebral bodies. The Short Polysegmental Back Muscles
anterior ligament is strong, and helps to resist spinal
extension, but the posterior ligament is mechanically These are exemplified by multifidus, a deep medial
weak and probably functions mainly as a ‘nerve net’ to muscle which extends from the lumbar spinous process
sense changes (such as bulging) in the underlying disc. at each level to insert onto the mammillary processes of
lower vertebrae and on to the sacrum and ilium. Because
it has a long lever arm posterior to the centre of rotation
Ligamentum Flavum in the intervertebral discs,12 multifidus is a powerful
The ligamentum flavum, which joins the laminae of adja- extensor of the lumbar spine, and largely determines
cent neural arches, is comprised mainly of elastin, which lumbar lordosis.
allows it to be stretched by up to 80% before failure. This
ligament is pre-stressed in all postures except hyperex- Long Polysegmental Back Muscles
tension, and habitual tension within the ligament acts in
conjunction with pre-stress in the annulus fibrosus to These are typified by the three large back muscles which
provide intrinsic spinal stability in bending. comprise the ‘erector spinae’ group: iliocostalis lies most
lateral and superficial, longissimus is more medial, and
Supraspinous and Interspinous spinalis is most medial and deep (although diminished
in the lumbar spine). They arise from the laminae,
Ligaments transverse processes and ribs at several spinal levels,
These ligaments join adjacent spinous processes, and and insert on to other spinal levels, and to the pelvis.
are mechanically coupled to each other. They provide The erector spinae are powerful extensors of the whole
minimal resistance to small flexion movements, but in full spine and play a major role in the lifting of heavy
flexion they become taut and are the first structures to be weights. All of these strong back muscles have a high
damaged in hyperflexion.11 proportion of large type I (‘endurance’) fibres, which
enable the muscles to maintain spinal posture for long
Iliolumbar Ligaments periods of time.

By joining the transverse processes of lower lumbar ver-

tebrae to the ilia, these ligaments help to stabilize L5 Other Muscles Relevant to
(especially) within the pelvis.
the Lumbar Spine
Four layers of abdominal muscles (transversus abdominis,
rectus abdominis, internal obliques and external obliques)
MUSCLES OF THE LUMBAR SPINE move and stabilize the trunk. More distant muscles such
Anterolateral Muscles as latissimus dorsi and the gluteals also affect the lumbar
spine because they attach to the lumbodorsal fascia, a
Psoas major originates from the anterolateral surfaces of strong collagenous sheet which lies superficial to the back
the lumbar vertebral bodies and passes over the rim of muscles and which can be employed to help extend the
the pelvis to the lesser trochanter. As well as flexing the spine from a flexed position.13
hip, it compresses and stabilizes the upright lumbar spine.
Quadratus lumborum arises from the anterior aspect
of the transverse processes and twelfth rib to insert on to
the ilium. It is essentially a muscle of respiration, but can REFERENCES
also move the lumbar spine into lateral bending. 1. Adams M, Bogduk N, Burton K, et al. The Biomechanics of Back
Pain. 3rd ed. Edinburgh: Churchill Livingstone; 2013.
2. Rodriguez AG, Slichter CK, Acosta FL, et al. Human disc nucleus
Back Muscles properties and vertebral endplate permeability. Spine (Phila Pa
1976) 2011;36(7):512–20. [Epub 2011/01/18]; PubMed PMID:
True ‘back muscles’ are innervated by the posterior 21240044. Pubmed Central PMCID: 3062730.
rami of the spinal nerves, and lie posterior to the 3. Zhao FD, Pollintine P, Hole BD, et al. Vertebral fractures usually
affect the cranial endplate because it is thinner and supported by
transverse processes. They can be classified into three less-dense trabecular bone. Bone 2009;44(2):372–9. PubMed
groups: intersegmental, short polysegmental and long PMID: 19049912. eng.
polysegmental. 4. Fields AJ, Liebenberg EC, Lotz JC. Innervation of pathologies in
the lumbar vertebral end plate and intervertebral disc. Spine J
2013;PubMed PMID: 24139753.
Intersegmental Back Muscles 5. Wade KR, Robertson PA, Broom ND. On how nucleus-endplate
integration is achieved at the fibrillar level in the ovine lumbar disc.
Several small and deep back muscles join adjacent verte- J Anat 2012;221(1):39–46. [Epub 2012/04/27. eng]; PubMed
brae, including the interspinales between the spinous PMID: 22533741.
 9  Functional Anatomy 105

6. Schollum ML, Robertson PA, Broom ND. A microstructural inves- 10. Hastreiter D, Ozuna RM, Spector M. Regional variations in certain
tigation of intervertebral disc lamellar connectivity: detailed analy- cellular characteristics in human lumbar intervertebral discs,
sis of the translamellar bridges. J Anat 2009;214(6):805–16. [Epub including the presence of alpha-smooth muscle actin. J Orthop Res
2009/06/23. eng]; PubMed PMID: 19538627. 2001;19(4):597–604. PubMed PMID: 11518268.
7. Green TP, Adams MA, Dolan P. Tensile properties of the annulus 11. Adams MA, Hutton WC, Stott JR. The resistance to flexion of
fibrosus II. Ultimate tensile strength and fatigue life. Eur Spine J the lumbar intervertebral joint. Spine 1980;5(3):245–53. PubMed
1993;2(4):209–14. PubMed PMID: 20058407. PMID: 0007394664.
8. Adams MA, Hutton WC. Prolapsed intervertebral disc. A 12. Pearcy MJ, Bogduk N. Instantaneous axes of rotation of the lumbar
hyperflexion injury 1981 Volvo Award in Basic Science. Spine intervertebral joints. Spine 1988;13(9):1033–41. PubMed PMID:
1982;7(3):184–91. PubMed PMID: 0007112236. 0003206297.
9. Adams MA, McNally DS, Dolan P. ‘Stress’ distributions inside 13. Dolan P, Mannion AF, Adams MA. Passive tissues help the back
intervertebral discs. The effects of age and degeneration. J Bone muscles to generate extensor moments during lifting. J Biomech
Joint Surg Br 1996;78(6):965–72. PubMed PMID: 0008951017. 1994;27(8):1077–85. PubMed PMID: 0008089162.
 CHAPTER 10 

Tendon and Tendinopathy

CHAPTER OUTLINE

Ch 10.1  Tendon and Tendon Pathology  106 Ch 10.2  Managing Tendinopathies  112
Hazel Screen Jill Cook  •  Ebonie Rio  •  Jeremy Lewis

CHAPTER 10.1  ■  TENDON AND TENDON PATHOLOGY

Hazel Screen

movement in different ways. Tendons such as the flexor

INTRODUCTION AND TENDON and extensor tendons in our hands are subjected to low
FUNCTION stresses and strains, but must modulate muscle contrac-
tion with extreme precision to allow us to perform intri-
Tendons perform the primary role of connecting muscle cate activities such as writing. They must be reasonably
to bone to facilitate motion. At first glance, these passive, inextensible, so muscle contraction is transferred fully
collagen-rich tissues appear to be very simple rope-like and precisely to the fingers, yet must provide a degree of
structures. However, as we delve further into their mech- damping in the system so our movements are not jerky
anobiology, we discover that this view is far too simplistic. but finely controlled.4 This functional role contrasts
Structure and material properties are not universal across heavily with that of a tendon such as the Achilles. The
tendons, but are optimized to enable different types of Achilles must withstand multiples of body weight when
tendons to effectively perform their varied functional we walk or run, and act as part of the locomotory system
roles within the musculoskeletal system.1 As a clinician, to help propel us forward. It must act like a spring,
it may therefore not be appropriate to treat all tendons stretching when it is loaded before recoiling to return
in the same manner, and knowledge of how tendon struc- energy to the system as we push off, thereby improving
ture and function are optimized becomes critical to locomotory efficiency.5 While tendons, such as the Achil-
understanding and treating injuries and diseases effec- les, must be sufficiently stiff to enable efficient force
tively. As our understanding of the differences between transfer to the skeleton, they must also incorporate a
tendons evolves, we can begin looking for opportunities degree of elasticity to enable them to stretch and store
to target treatment modalities towards specific types of energy.6,7
tendon or even types of injury, based on an understanding Tendons such as the Achilles and patellar are termed
of the basic science of these conditions. energy-storing tendons, whereas those in the hand are
In connecting muscle and bone, tendons provide a referred to as positional tendons. While the hand tendons
passive linkage to ensure that active muscle contrac- and Achilles provide examples of extreme functional
tion results in joint movement. Including a tendon in requirements, many tendons require a combination of
the muscle-to-bone connection is vital for a number these properties, and must find an appropriate balance
of reasons. Firstly, muscle is compliant whereas bone between elasticity for energy storage and stiffness for
is very stiff. Tendon provides a graduated change in efficient force transfer. Creating these opposing func-
material characteristics between these extremes, mini- tional requirements necessitates subtle structural and
mizing the development of areas of stress concentration compositional differences between tendons to provide
where failure is likely to occur.2 Secondly, to provide appropriate mechanical behaviour;8 such differences may
active contraction, muscles are often quite bulky, par- also result in differences in the mechanisms of damage or
ticularly when they must generate significant power. injury between these tendons.
The role of the tendon in this instance is to move
the muscle belly away from its point of action.3 This
creates space, but also allows the tendon to work like COMPOSITION AND STRUCTURE
a lever arm, moving the point of action away from
the centre of rotation, thereby reducing the forces It is staggering to appreciate that the tendon extracellular
required for movement, much like a spanner when matrix, as in all biological materials, is made entirely from
manipulating a nut. the tissue’s resident cells. The cellular component only
Beyond these universal functions, specific tendons, constitutes approximately 10% of the dry weight in
aided by their individual material properties, assist mature tendon, with the predominant cell type termed
106
 10  Tendon and Tendinopathy 107

the tenocyte.9 While tenocyte phenotype remains poorly elastin, 2–5% proteoglycans and small amounts of a
understood, it is known that tenocytes are sensitive to the range of other types of collagens12,13 (Fig. 10-1B). While
mechanical loading environment they perceive during these proteins are far less abundant than collagen type I,
tendon use, and control tendon structure, composition they may still play important roles, with elastin known to
and health at least partly in response to these stimuli.10 provide high elasticity and proteoglycans responsible for
Understanding the important chemical and mechanical imbibing water and resisting compressive strains or pro-
stimuli that govern tenocyte metabolism, and harnessing viding lubrication. A range of other glycoproteins have
these to promote healthy matrix production or repair, is been reported in different tendons in varying amounts,
subsequently a key area of interest in tendon basic science but no clear structural roles have been identified for most
research. of these additional proteins to date.
The general structure of tendon extracellular matrix From a materials science perspective, the tendon
(ECM) was first described in the late 1970s in the seminal ECM may be described as a fibre-composite material.
work of Kastelic and co-workers.11 Tendon ECM is typi- Fibre composites are made by combining two distinct
cally 60–90% type I collagen, arranged in a series of materials together, where each material is known as a
hierarchical levels. The smallest structural unit is the phase; the fibre material makes the ‘fibre’ phase, and
nanoscale individual collagen molecule and these cross- the secondary material surrounding them makes another
link together to build collagen fibrils, in the order of phase known as the ‘matrix’ phase. The ‘fibres’ of a
50–500 nm diameter. Collagen fibrils aggregate into fibre composite are strong under tension and reinforce
fibres, then fascicles, and finally the whole tendon, with the material, whereas the surrounding ‘matrix’ is usually
the collagen at each of these hierarchical levels inter- more ductile, holding the ‘fibres’ together and helping
spersed with a proteoglycan-rich matrix (Fig. 10-1A). them to share or distribute the applied loads.14 Fibre-
The highly aligned, hierarchical organization of collagen composite materials are in common use, examples
is responsible for the exceptional tensile strength of include steel-reinforced concrete and carbon fibre. They
tendon. Tendon also contains approximately 0.5–3% provide a number of advantages over single-phase

Interfascicular Tendon
tenocytes
Tenocyte
Fascicle
Fibre

Fibril

Tropocollagen

Crimp
Crimping waveform
Endotendon (inter-fascicular matrix)

1.5 nm 50–500 nm 10–50 µm 50–400 µm 500–2000 µm

A
Other
Proteoglycans glycoproteins
2–5% 0.5–5%
Elastin
0.5–3%

Cells
~10%

Collagen (type I)
70–90%

B
FIGURE 10-1  ■  (A) Schematic depicting the hierarchical structure of tendon, in which collagen units are bound together by either
crosslinks or non-collagenous matrix at multiple hierarchical levels, to make a fibre-composite material with outstanding tensile
strength. (B) Tendon composition varies according to the functional role of the tendon, but the composition of the majority of
tendons is within the ranges outlined in the pie chart.
108 PART II  Advances in Theory and Practice

materials, as they combine the properties of both con-

stituent parts, allowing material to both be light weight MECHANICAL BEHAVIOUR
and strong. They also have good fatigue resistance, as
damage in one area cannot easily propagate through There have been numerous investigations into the
the whole material because the ‘fibres’ of the composite mechanical properties of tendons. Typically a tendon is
are all separate entities. pulled to failure, recording how much force is required
When considering tendon from a materials science to stretch the tissue, and how much it stretches before it
perspective as a fibre composite, the aligned collagen breaks. This is shown graphically in a force-extension
units constitute the ‘fibres’ and the surrounding curve (Fig. 10-2A), and the stiffness can be found from
proteoglycan-rich phase the ‘matrix’. As such, tendon is the slope of the curve, where a steeper curve denotes a
effectively a multilevel fibre-composite material, as there stiffer tendon. While these data are useful, they are not
is a fibre-composite arrangement (collagen units sur- only dependent on the properties of the tendon, but also
rounded by matrix) at every level of its hierarchical struc- the size of the piece of tendon tested (intuitively, it takes
ture. It is easy to get confused with the terminology as, more force to break a thicker sample, simply because it
from a biological perspective, the term fibre is also used is thicker), so data are usually normalized and presented
to describe a single level of the tendon hierarchy. Indeed, as a stress–strain curve, which specifically describes the
to add to the confusion, different terms are also regularly properties of the tissue itself (Fig. 10-2B). The term
used by different research groups to describe each level modulus is then used for the gradient of the curve, so
of the tendon collagen hierarchy, so care must be taken modulus is simply a normalized stiffness measure, taking
when reviewing the literature to be clear to what the text into account dimensions of the test sample.
is referring. In this text, quotation marks around the word The three-stage shape to the tendon stress–strain
fibre denote the more generic materials science use of the curve is typical of the mechanical behaviour of many of
word. our soft tissues, although compared to other tissues such

2.5
Toe Linear
2.0 region region
Force (N)

1.5

1.0
Force
0.5 Stiffness = gradient of curve = —————
Extension

0.0
0.0 0.2 0.4 0.6 0.8 1.0 1.2
A Extension (mm)

35 Ultimate
Tensile
30 Strength
(UTS)
25
Stress (MPa)

20

Stress 15
normalizes for 10
sample Stress
thickness (area) Modulus = gradient of curve = ———
5 Strain
Force
Stress = ——— 0
Area 0 2 4 6 8 10 12
Strain (%)

Strain
Extension
normalizes for Strain = ——————————
sample length Original sample length
B
FIGURE 10-2  ■  (A) Schematic depicting a typical force–extension curve for a tendon pulled apart to failure. The data show how much
force is required to stretch the tendon until it breaks. The gradient of the force–extension curves denotes the stiffness of the sample.
A steeper gradient would denote a stiffer sample, where more force was required to extend the sample. (B) The force–extension
data can be normalized for sample dimensions and shown as a stress–strain curve. The stress–strain characteristics of a material
are thus independent of the test sample size, so the stress–strain curve describes the generic material behaviour. The gradient of
the stress–strain curve is referred to as the modulus.
 10  Tendon and Tendinopathy 109

TABLE 10-1  The mechanical properties of a range of different tendons

Tendon Type Modulus (MPa) Ultimate Tensile Strength (MPa) Authors Ref
Ovine plantaris tendon 1650 ± 290 90 ± 12 Bennett et al. (1986) 17
(energy storing)
Wallaby tail tendon 1662 ± 105 107 ± 19 Bennett et al. (1986) 17
(positional)
Equine superficial digital 614 ± 115 115 ± 24 Thorpe et al. (2011) 18
flexor tendon (energy
storing)
Equine common digital 1012 ± 154 157 ± 34 Thorpe et al. (2011) 18
extensor tendon
(positional)
Rat tail tendon 663 ± 167 47 ± 8.4 Screen et al. (2004) 15
(positional)
Rat Achilles tendon 400 ± 50 40 ± 6 Netti et al. (1996) 19
(energy storing)
Human Achilles tendon 816 ± 218 71 ± 17 Wren et al. (2001) 20
(energy storing)
Human hamstring tendon 362 ± 21 87 ± 13 Butler et al. (1984), 21,22
(energy storing) Schechtman et al.
(2000)

The modulus and ultimate tensile strength are reported in MPa (as described in Fig. 10-2).

as skin, tendon has a high failure stress and modulus 180

(Table 10-1). The low stiffness behaviour we can see 160
within the toe region results from the alignment and
140
organization of collagen in the loading direction, in addi-
tion to straightening of the collagen fibres, which display 120
Stress (MPa)

a periodic crimp pattern in the unstressed state.15,16 With 100

further applied strain, the stiffness of the tendon increases
80
rapidly, in what is commonly referred to as the linear Energy storing
region. With all the collagen straightened and aligned in 60 tendon (equine
SDFT)
the loading direction, the large increase in stiffness in this 40
region reflects the direct loading of the tendon structure. Positional tendon
20
The stress–strain behaviour of the tendon is then reason- (equine CDET)
ably linear until close to failure, at which point material 0
microrupture leads to a steady drop in stiffness, as the 0 5 10 15 20 25
fibres pull apart and the sample fails.2 Strain (%)
Modulus or stiffness values for tendon are generally FIGURE 10-3  ■  Typical stress–strain curves, contrasting the
reported from the linear region, and most tendons prob- mechanical behaviour of the energy-storing equine superior
ably operate within this region during physiological digital extensor tendon (SDFT) and the positional equine
common digital extensor tendon (CDET). The high failure strain
loading. Positional tendons, which experience very small and reduced stiffness of the energy-storing tendon is important
loads in use, are stiffer (high moduli), but probably only to facilitate its energy-storing role.
just encounter sufficient load to operate in the linear
region, whereas energy-storing tendons are more exten-
sible and are often loaded to values close to the absolute arranged like individual springs, and when the tendon is
failure stress of the tissue, explaining their significantly stretched, the springs can stretch to store energy and
high risk of injury23,24 (Fig. 10-3). In order to facilitate recoil very effectively.26 In energy-storing tendons,
these different load requirements and mechanical char- sliding occurs predominantly between fascicles and is
acteristics, the mechanisms by which positional and more elastic in nature, with recent data indicating
energy-storing tendons extend through the linear region that fascicle sliding may be critical for energy-storing
also differ. Tendons with a more positional function function18 (Fig. 10-4). While these data are very recent,
appear to stretch predominantly through sliding between and further work is necessary to fully understand the
collagen fibrils and fibres.25 This sliding is governed by important structural differences between tendon types,
the proteoglycan-rich matrix between these collagen they do highlight the importance of taking a tendon-
units, which creates the more viscoelastic and damped specific, or at least tendon-function-specific, approach to
behaviour required in positional tendons such as the considering an injury. Some data suggest that the specific
digital extensor and flexor tendons of the hand, and high-strain mechanisms in energy-storing tendons (both
possibly the rotator cuff. By contrast, recent data indicate fascicle sliding and helical arrangement) reduce in effi-
that there is very little viscous sliding behaviour between cacy as tendon ages, coinciding with an increased injury
fibres and fibrils in energy-storing tendons such as the risk.27,28 If factors such as reduced fascicle sliding are
Achilles and patella. Instead, the fascicles are helically implicated in increased tendon injury risk, it may be
110 PART II  Advances in Theory and Practice

Energy storing tendons Positional tendons

Fibres

Fascicles

Large  Small 
Fascicles No helix
twisted as present
a spring

Strain applied Strain applied

Fascicle Fascicles
sliding extend

Fibre
Fascicle sliding
spring
stretches
FIGURE 10-4  ■  Energy-storing and positional tendons meet their different mechanical requirements though differences in their struc-
ture and how it responds to applied strain. Energy-storing tendons extend through stretching or unwinding of the helical organization
in their fascicles, so the fascicles act like springs (see the large θ, denoting a larger twist to the resting fibre arrangement). The
fascicles also slide past one another to enable the high strains seen in these tendons. By contrast, positional tendons have little
twist in the resting configuration (small θ) and instead extend through sliding between adjacent collagen fibres within fascicles.

possible to develop more targeted treatments to directly containing increased levels of collagen type III, proteo-
treat these mechanical and structural changes. glycans and water, with increased vasculature but no signs
of inflammation29,31,32 (Fig. 10-5 compares healthy and
tendinopathic tendon sections). However, while these
TENDON INJURIES AND REPAIR findings have led to a strong leaning towards diagnoses
of tendinosis, this perspective has been derived from the
Despite our increased understanding of normal tendon analysis of tendons months after the initiation of the
structure and function, there remains a surprising dearth disease, and provides little insight into the early develop-
of knowledge concerning tendon pathophysiology. This ment of the condition.
lack of knowledge reflects not just the complexities asso- It seems highly likely that tendon pathogenesis will
ciated with tendon diseases, but also the difficulties in involve an interplay between localized overuse matrix
exploring these during the early stages of disease devel- damage, and a cell-mediated response to the loading con-
opment. We do not know if the pain signals alerting a ditions. Various animal models have been adopted to
patient to tendon damage are delayed relative to injury investigate the interplay of these factors in early tendi-
onset, and it is rare to perform any immediate invasive nopathy.34 These generally report that cyclic overuse of
protocol to assess injury post diagnosis. tendon results in disruption of the tendon matrix, and an
There is a suggestion that the processes leading to increase in cell number and a rounding of the cells, along-
sudden tendon rupture are different to those involved in side an up-regulation of various catabolic proteinases.35–38
the development of tendinopathic conditions,29 but it is However, the order in which these processes are initiated
also quite possible that the development of tendinopathy and how they progress to the aetiology reported in
differs between tendon types. Sudden tendon ruptures long-term degenerate tendinopathy remains unknown,
tend to occur in people who have been largely pain-free and significantly more work is necessary if the aetiology
in the lead up to injury, whereas tendinopathic patients of tendinopathy is to be established. Current theories
present with significant, often debilitating pain, but the suggest that the up-regulation of various matrix proteases
condition rarely progresses to rupture.30 Understanding in early tendinopathy may be accompanied by an inflam-
of pain mechanisms is currently very limited and it is matory response, a cellular attempt to turnover and repair
uncertain if the different presentation of these conditions the tendon.39–42 The increase in cell number is addition-
indicates different underlying pathophysiologies, or if ally thought to occur as a result of infiltration of inflam-
the pain associated with tendinopathy simply prevents matory cells to the injured site.41 Such a repair response
additional overuse and damage accumulation in this fits with the concept that tendon pathology is a contin-
condition. For a tendon to rupture it must already be uum in which early-stage reactive tendinopathy may cor-
structurally compromised; however, these injuries have relate with minimal local damage that can be effectively
only ever been viewed post rupture, so the nature of early repaired by the cells, whereas excess overload can imbal-
tendon deterioration and structural compromise remains ance any repair attempts and lead to an inappropriate
unknown. In tendinopathic tendon, classic reports of the cell metabolic response and more significant matrix
condition describe a highly disordered tendon matrix breakdown.43
 10  Tendon and Tendinopathy 111

A 20.00 um B 20.00 um

FIGURE 10-5  ■  Histological sections, viewed with a Nikon Eclipse 80i, from the energy-storing equine superior digital extensor tendon.
Images compare (A) a healthy tendon and (B) a tendinopathic tendon. Note the aligned and ordered matrix in the healthy tendon,
and clearly differentiated interfascicular matrix. By contrast, the tendinopathic sample shows the disordered matrix, rounded cells
and increased cellularity. For colour version see Plate 10. (Photographs taken in Professor Peter Clegg’s laboratory, University of
Liverpool.33)

Fibre-composite theory indicates that tendon damage 6. Alexander RM. Energy-saving mechanisms in walking and running.
will initiate in the non-collagenous matrix components,44 J Exp Biol 1991;160:55–69.
hence the fraying of collagen seen in late-stage chronic 7. Alexander RM. Tendon elasticity and muscle function. Comp
Biochem Physiol A Mol Integr Physiol 2002;133(4):1001–11.
tendinopathy is likely a later phenomenon, quite possibly 8. Batson EL, Paramour RJ, Smith TJ, et  al. Are the material
cell-mediated in nature. Indeed, the turnover of non- properties and matrix composition of equine flexor and extensor
collagenous matrix is substantially faster than that of col- tendons determined by their functions? Equine Vet J 2003;35(3):
lagenous matrix in tendon,45 with some studies indicating 314–18.
9. Elliott DH. Structure and function of mammalian tendon. Biol Rev
that the half-life of tendon collagen is hundreds of years, Camb Philos Soc 1965;40:392–421.
so is barely altered in normal healthy mature tendon.46 10. Banes AJ, Horesovsky G, Larson C, et al. Mechanical load stimu-
Furthermore, the turnover of non-collagenous matrix is lates expression of novel genes in vivo and in vitro in avian flexor
faster in more highly loaded energy-storing tendons, sug- tendon cells. Osteoarthritis Cartilage 1999;7(1):141–53.
gesting it may provide an important mechanism by which 11. Kastelic J, Galeski A, Baer E. The multicomposite structure of
tendon. Connect Tissue Res 1978;6(1):11–23.
tendons can manage and repair injuries before they prop- 12. Kannus P. Structure of the tendon connective tissue. Scand J Med
agate.45 With fascicle sliding currently proposed as a key Sci Sports 2000;10(6):312–20.
mechanism facilitating tendon extension in energy- 13. Woo SL, Debski RE, Zeminski J, et al. Injury and repair of liga-
storing tendons, the non-collagenous matrix between ments and tendons. Annu Rev Biomed Eng 2000;2:83–118.
14. Martin JW. Composite materials. In: Martin JW, editor. Materials
fascicles is an interesting target for further study. for Engineering. ed 3. Woodhead Publishing Ltd; 2006.
With such limited understanding of the initiation and 15. Screen HRC, Lee DA, Bader DL, et al. An investigation into the
development of tendinopathic conditions, it is perhaps effects of the hierarchical structure of tendon fascicles on micro-
unsurprising that so many treatment options for tendon mechanical properties. J Eng Med 2004;218(2):109–19.
conditions have been proposed. However, as we begin to 16. Atkinson TS, Ewers BJ, Haut RC. The tensile and stress relaxation
responses of human patellar tendon varies with specimen cross-
identify the structural and functional differences between sectional area. J Biomech 1999;32(9):907–14.
tendons in health, it becomes less surprising that a one- 17. Bennett MB, Ker RF, Dimery NJ, et al. Mechanical-properties of
size-fits-all approach is ineffective in treating tendinopa- various mammalian tendons. J Zool 1986;209:537–48.
thies.47 All of the intrinsic and extrinsic factors which may 18. Thorpe CT, Udeze CP, Birch HL, et al. Specialization of tendon
mechanical properties results from interfascicular differences. J R
lead to tendinopathy must be considered, with epigenetics Soc Interface 2012;9(76):3108–17.
and ageing also currently of prominent interest in estab- 19. Netti P, DAmore A, Ronca D, et al. Structure-mechanical proper-
lishing disease risk.47 Studies are now focusing on tendon ties relationship of natural tendons and ligaments. J Mater Sci-
overload or fatigue damage development in different Mater M 1996;7(9):525–30.
types of tendon, and how ageing alters matrix structure 20. Wren TA, Yerby SA, Beaupre GS, et al. Mechanical properties of
the human achilles tendon. Clin Biomech (Bristol, Avon) 2001;16(3):
and increases injury risk. Hopefully new opportunities 245–51.
for targeting treatments will soon be forthcoming. 21. Butler DL, Grood ES, Noyes FR, et al. Effects of structure and
strain measurement technique on the material properties of young
human tendons and fascia. J Biomech 1984;17(8):579–96.
REFERENCES 22. Schechtman H, Bader DL. Fatigue damage of human tendons.
1. Ker RF. Mechanics of tendon, from an engineering perspective. Int J Biomech 2002;35(3):347–53.
J Fatigue 2007;29(6):1001–9. 23. Biewener AA. Muscle-tendon stresses and elastic energy storage
2. Woo SL. Mechanical properties of tendons and ligaments. I. Quasi- during locomotion in the horse. Comp Biochem Physiol B Biochem
static and nonlinear viscoelastic properties. Biorheology 1982;19(3): Mol Biol 1998;120(1):73–87.
385–96. 24. Birch HL, Thorpe CT, Rumian AP. Specialisation of extracellular
3. Zajac FE. Muscle and tendon – properties, models, scaling, and matrix for function in tendons and ligaments. Muscles Ligaments
application to biomechanics and motor control. Crit Rev Biomed Tendons J 2013;3(1):12–22.
Eng 1989;17(4):359–411. 25. Cheng VWT, Screen HRC. The micro-structural strain response
4. Lin TW, Cardenas L, Soslowsky LJ. Biomechanics of tendon injury of tendon. J Mater Sci 2007;42(21):8957–65.
and repair. J Biomech 2004;37(6):865–77. 26. Thorpe CT, Klemt C, Riley GP, et al. Helical sub-structures in
5. Wilson AM, McGuigan MP, Su A, et al. Horses damp the spring energy-storing tendons provide a possible mechanism for efficient
in their step. Nature 2001;414(6866):895–9. energy storage and return. Acta Biomater 2013;9(8):7948–56.
112 PART II  Advances in Theory and Practice

27. Thorpe CT, Riley G, Birch HL, et al. Fascicles from energy- 38. Sereysky JB, Andarawis-Puri N, Jepsen KJ, et al. Structural and
storing tendons show an age-specific response to cyclic fatigue mechanical effects of in vivo fatigue damage induction on murine
loading. J R Soc Interface 2014;11(92):20131058. tendon. J Orthop Res 2012;30(6):965–72.
28. Thorpe CT, Udeze CP, Birch HL, et al. Capacity for sliding 39. Legerlotz K, Jones ER, Screen HR, et al. Increased expression of
between tendon fascicles decreases with ageing in injury prone IL-6 family members in tendon pathology. Rheumatology
equine tendons: a possible mechanism for age-related tendinopa- 2012;51(7):1161–5.
thy? Eur Cell Mater 2013;25:48–60. 40. Legerlotz K, Jones GC, Screen HR, et al. Cyclic loading of tendon
29. Riley G. Tendinopathy–from basic science to treatment. Nat Clin fascicles using a novel fatigue loading system increases interleukin-6
Pract Rheumatol 2008;4(2):82–9. expression by tenocytes. Scand J Med Sci Sports 2013;23(1):31–7.
30. Sharma P, Maffulli N. Tendon injury and tendinopathy: healing and 41. Dakin SG, Dudhia J, Smith RK. Science in brief: resolving tendon
repair. J Bone Joint Surg Am 2005;87(1):187–202. inflammation. A new perspective. Equine Vet J Jul 2013;45(4):
31. Jones GC, Corps AN, Pennington CJ, et al. Expression profiling 398–400.
of metalloproteinases and tissue inhibitors of metalloproteinases in 42. Scott A. The fundamental role of inflammation in tendon injury.
normal and degenerate human achilles tendon. Arthritis Rheum Curr Med Res Opin 2013;29(Suppl. 2):3–6.
2006;54(3):832–42. 43. Cook JL, Purdam CR. Is tendon pathology a continuum? A pathol-
32. Khan KM, Cook JL, Kannus P, et al. Time to abandon the ‘tendi- ogy model to explain the clinical presentation of load-induced ten-
nitis’ myth. BMJ 2002;324(7338):626–7. dinopathy. Br J Sports Med 2009;43(6):409–16.
33. Clegg PD, Strassburg S, Smith RK. Cell phenotypic variation in 44. Shepherd JH, Legerlotz K, Demirci T, et al. Functionally distinct
normal and damaged tendon. Int J Exp Pathol 2007;88(4): tendon fascicles exhibit different creep and stress relaxation behav-
227–35. iour. J Eng Med 2013;e-pub ahead of print.
34. Lake SP, Ansorge HL, Soslowsky LJ. Animal models of tendinopa- 45. Thorpe CT, Streeter I, Pinchbeck GL, et al. Aspartic acid racemi-
thy. Disabil Rehabil 2008;30(20–22):1530–41. zation and collagen degradation markers reveal an accumulation of
35. Fung DT, Wang VM, Andarawis-Puri N, et al. Early response to damage in tendon collagen that is enhanced with aging. J Biol
tendon fatigue damage accumulation in a novel in vivo model. Chem 2010;285(21):15674–81.
J Biomech 2010;43(2):274–9. 46. Heinemeier KM, Schjerling P, Heinemeier J, et al. Lack of tissue
36. Sun HB, Andarawis-Puri N, Li Y, et al. Cycle-dependent matrix renewal in human adult Achilles tendon is revealed by nuclear
remodeling gene expression response in fatigue-loaded rat patellar bomb (14)C. FASEB J 2013;27(5):2074–9.
tendons. J Orthop Res 2010;28(10):1380–6. 47. Cook J. Tendinopathy: no longer a ‘one size fits all’ diagnosis. Br
37. Shepherd JH, Screen HR. Fatigue loading of tendon. Int J Exp J Sports Med 2011;45(5):385.
Pathol 2013;94(4):260–70.

CHAPTER 10.2  ■  MANAGING TENDINOPATHIES

Jill Cook  •  Ebonie Rio  •  Jeremy Lewis

INTRODUCTION substantial deficits in the knowledge required to treat

this common musculoskeletal problem exist and manag-
Tendinopathy is the term given to the combination of ing tendinopathies remains a challenge. Chapter 10.1
pain and loss of function originating from tendon. It is highlighted differences in tendons and their function
a common clinical presentation and occurs in upper and and it is clear that clinically a ‘one-size-fits-all’ approach
lower limb tendons. Tendinopathy is typically associated is not appropriate and treatment must be individualized.
with changes in tendon structure, but not all changes A holistic approach that appreciates the individual’s
result in symptoms and a loss of function. This is con- aspirations, and a consideration of other relevant factors
fusing for patients and clinicians, and as such, clinical such as; age, previous injuries, co-morbidities, hormonal
examination currently remains the cornerstone of assess- status and lifestyle factors (e.g. smoking) need to be
ment. Changes in tendon-loading behaviour typically factored in to treatment planning.8
precede the onset of symptomatic tendinopathy and load
management currently underpins the treatment for
tendinopathies. TENDON PATHOLOGY
Prevalence of tendinopathy generally increases with
age; ageing tissue and cumulative load increase suscepti- Tendon structure is complex and the process that leads
bility.1 Lateral epicondylopathy has a reported prevalence to tendon pathology is controversial. Chapter 10.1 has
of 1.3% in the general population,2 but may be as high comprehensively covered normal tendon and tendon
as 40% in tennis players,3 and it is most common in the pathology; however, additional clinical and imaging
fourth and fifth decades.2,4 An episode of lateral epicon- factors need to be considered. Firstly, as described in
dylopathy may be prolonged and associated with episodes Chapter 10.1, tendon pathology may not be uniform
of recurrence.2 Patellar tendinopathy is common in sports and there may be discrete regions of pathology within
that involve jumping (energy storage and release) and a tendon that are surrounded by normal tendon. Sec-
quick changes in direction, such as occur in basketball. It ondly, there are pathological variations between different
is more common in younger populations, with prevalence tendons, for example, patellar tendinopathy tends to
rates reported as high as 40% in jumping athletes.5,6 develop well-defined areas of pathology, whereas the
Tendinopathy can be persistent and recalcitrant to Achilles may demonstrate quite diffuse pathology.
treatment and symptoms may continue for more than Thirdly, and as mentioned, pathological changes
15 years.7 Although ongoing research has resulted in a observed within tendons do not always correlate with
better understanding of tendinopathy management, symptoms.
 10  Tendon and Tendinopathy 113

Pure tendinopathy (within the body of the tendon) capacity to repair tendon. There is also the challenge of
occurs most commonly in the mid-Achilles tendon region. translating knowledge from large quadrapedal animal
Tensile overload is the key driver of tendon pathology, models such as equine tendon to bipedal humans.
and energy storage (rapid tendon lengthening) and release There are several hypothetical models to describe the
loads are particularly stressful for tendon.9 The use of a transition from normal tendon to pathology. The models
tendon like a spring (stretch and release) occurs in many can be divided into: (a) the cell models, where the cell is
vocational and athletic activities to reduce the metabolic the first response to overload; and (b) collagen-tearing
demand of high-speed movement. This is exemplified in models, where the initial injury occurs in the ECM. The
the Achilles during activities involving sprinting and cell model was first proposed by Leadbetter19 and devel-
jumping. Normally, tendon structure can sustain these oped further in the continuum model.20 The continuum
loads, and Chapter 10.1 describes the sliding between model proposes that the cells detect overload and respond
helically arranged fascicles during energy storage. by increased proteoglycan production that progressively
Most other tendons develop pathology at the complex separates and then disrupts the collagen matrix, leaving
bone–tendon junction, excess tensile, compressive or potential for vessel ingrowth. Tendon pain has not been
shear loads (and combinations) can induce pathology. fully integrated into this pathology model but is likely to
The bone–tendon junction is designed to transition occur in the early reactive phase or in a reactive on
mechanical load between the more flexible tendon and degenerative presentation where the remaining normal
stiffer bone. This complex structure is called the enthesis part of the tendon that is loadbearing is overloaded as the
organ10 where compression of the tendon against the area of the pathology fails to absorb and transfer load.
bone proximal to the insertion protects the insertion and Conversely, the collagen-tearing models propose a
improves the mechanical advantage of the tendon.11 The variable response after collagen tearing, including inflam-
compression is ameliorated by fibrocartilage within the mation,21 pain, failed healing22 and degeneration. Pain is
tendon and on the bone, and bursae are typically present integrated into these models, however the link to common
between the tendon and bone.12 clinical presentation is not always obvious, and the cause
Excessive compressive load at the insertion causes of pain in tendons throughout the various stages of
change within the enthesis organ, increasing pathology pathology has not yet been identified.
in the tendon and possible inflammation in the bursa. It Definitive evidence of an inflammatory process, in the
is a clinical homily that symptomatic bursitis is part of traditional sense, is lacking at any stage of tendon pathol-
compressive insertional tendinopathy and should be ogy. There has been recent interest in inflammation
managed as a tendinopathy and not as an isolated bursitis. having a role in tendon pathology23 and the literature and
For example, trochanteric and subacromial bursal injec- evidence in this complicated area remains uncertain and
tions should not be seen as a standalone treatment but incomplete. One area of confusion is semantics, particu-
should be considered as part of the staged management larly the definition of inflammation, and the presence of
of gluteal and rotator cuff tendinopathy.13,14 what substances, cells or processes indicate inflammation.
Tendons where compressive loads have a role in ten- It is important to note that tendon pain is not consistent
dinopathy include the Achilles insertion, hamstring with a triphasic inflammatory process, so clinicians should
origin, gluteal medius and minimus, tibialis posterior, consider avoiding therapies such as absolute rest, ice and
peroneals and adductor tendons. In the upper limb the anti-inflammatory medications as definitive treatments
rotator cuff tendons are susceptible to compressive ten- for tendinopathy.
dinopathy. It is important to note that the site of com- It is important to emphasize that current understand-
pression can be immediately before the insertion or quite ing of the structural, cellular and chemical changes that
distant from it, as is the case with the peroneal tendon occur in pain-free and painful tendons is poor. Most
and tibialis posterior. During extremes of shoulder move- importantly, how pathology and pain are linked is not
ment, compression may occur within the structurally clear.
independent parallel fascicles of the rotator cuff tendons.15
The compression proximal to the tendon insertion is not
true of all tendons; patellar and elbow tendinopathy do
Source of Tendon Pain
not have an obvious compressive site. The tip of the Pain is the primary reason people with tendinopathy
patella16 and the fat pad17 have been proposed as potential present to clinicians. This is true for the young athlete
compressive structures in the patellar tendon, but their experiencing tendinopathy for the first time or for
involvement is not confirmed. someone with a long history of tendon symptoms. Both
seek resolution of pain but we currently know little about
the origin of the pain, and if it differs in these clinical
Pathoaetiology examples and in different tendons.
The transition from structurally normal tendon to struc- Pain is an output from the central nervous system
turally degenerative tendon is well described in animal (CNS), which may or may not be associated with a
models, with a cell-initiated process that affects the physiological nociceptive input caused by tissue disrup-
ECM.18 Uncertainty exists if this process is identical in tion. Persistent symptoms often indicate that there are
humans and remains the subject of ongoing debate due changes within the CNS which are contributing to a
in part to the differences between small animal and chronic pain state. The clinical features of tendinopathy
human tendons. Small animals have different anatomical include tenderness to palpation (primary hyperalgesia),
architecture, different metabolic rates and different well-localized pain, impaired function but no spreading
114 PART II  Advances in Theory and Practice

of pain (secondary hyperalgesia) regardless of the length never experience symptoms, even in the presence of
of time of symptoms and variable evidence of local tendon pathology. This reinforces the fact that tendon
and more distant sensory change. This indicates that injury and tendon pain are a result of a complex interac-
physiological (tissue protecting) and pathophysiological tion of intrinsic and extrinsic factors, as well as bio­
(functional changes within the nervous system) pain are psychosocial factors. The experience of pain is unique for
present in tendinopathy. each individual and is based around the context of the
The evidence for local nociceptive input is strong as experience, alterations to sensory integration and motor
tendon pain typically has a transient on/off nature closely changes.38
linked with loading. It appears that tendon pain serves to
protect the injured tendon. However, many features of
tendon pain, such as its tendency for chronicity and the ASSESSMENT
fact that pain during rehabilitation is sometimes encour-
aged24 and may not be deleterious,25 demonstrate that it A thorough history is mandatory when assessing someone
is more complex than local tissue damage. To add to this with tendinopathy. The priority is to identify recent
complexity, there may be differences in upper and lower tendon overload and current aggravating activities.
limb tendons, as well as between energy storage and Changes in loading may be very subtle, especially in ath-
positional tendons. letes where a simple change in running shoe may bring
Furthermore, the source of pain in tendons cannot on Achilles tendon symptoms. Similarly, a change in
currently be seen on tendon imaging, as there is an incon- working height, speed of activity, weight or resistance of
sistent relationship between pain and pathological equipment may provoke rotator cuff and lateral elbow
changes identified on imaging. Tendons demonstrating tendinopathy. It is important to identify previous epi-
little tissue disruption on imaging may still be associated sodes of tendon pain, their cause, what treatments were
with pain.26 Neither ECM change27 nor neovasculariza- received and the response to treatment.
tion28,29 has been consistently linked to pain. Similarly, Assessment should enquire about pain and pain behav-
severe pathology that progresses to tendon rupture may iour. Tendon pain commonly is reported as being
never have caused symptoms.30 Lastly recovery, defined maximal 24 hours after the aggravating activity. However,
by improvement in the experience of pain and return to each tendon has its own classic pain behaviour, for
activity, also correlates poorly with imaging.31 example Achilles tendinopathy will be associated with
The source of local nociception may include changes morning stiffness and pain, patellar and hamstring ten-
in tendon biochemistry, the tendon cell or nerve. Early- dinopathy with pain on sitting. In the upper limb, pain
stage tendinopathy may have profound biochemical and associated with lateral epicondylopathy commonly
cell changes but little neural ingrowth; conversely, increases with wrist extension and the rotator cuff (espe-
degenerative tendons may have areas of acellularity and cially the supraspinatus and infraspinatus) is typically
less biochemical involvement but an increase in the painful in shoulder external rotation (often with shoulder
nerve supply.32 Furthermore, the nerve supply is not elevation). Due to difficulties in achieving a definitive
uniform throughout tendon, and in fact there appear diagnosis, other causes of pain in these regions need to
to be few neural structures within tendon even when be considered.
it is pathological.33 Most of the nerve supply appears Questioning is required pertaining to risk factors that
to be peritendinous so it is possible that pathology may may heighten the tendon’s response to load, or contribute
occur within the tendon, without the CNS receiving to a low baseline capacity of the tendon, making it more
any nociceptive input, potentially explaining asymptom- vulnerable to loading. Factors such as gender, age, obesity
atic tendinopathy. and systemic conditions (such as diabetes and meno-
There is some evidence for CNS modulation in ten- pause) may also influence the response to treatment.
dinopathy; multiple studies have demonstrated altera- These conditions may sometimes be undiagnosed and in
tions in sensory response, both at the site of tendon pain many cases require referral for investigation. Lifestyle
and at other body sites.34,35 Changes to brain and spinal factors such as smoking behaviour need to be identified.
cord excitability and cortical reorganization may occur The level of the clinical examination will be deter-
with tendon pain.36 This may explain the poor correlation mined by the responses gained in the interview, as the
between local tendon imaging changes and symptoms.37 history will indicate tendon irritability and capacity.
Modulation of neural activity may occur at the spinal Someone who is older and generally inactive presenting
cord and cortical levels; input (nociception) may be either with substantial pain when the tendon is first loaded, will
up-regulated or down-regulated to produce variable not be examined to the same level or in the same way as
outputs (motor/muscle activation and pain). Ongoing a younger athlete with mild pain, experienced after
research into the contribution from, and the changes to, extreme activity. Clinical reasoning skills will determine
the CNS in tendon pain are required. the appropriate level of examination for the individual
patient.
What Causes Tendon to Become Painful? Key features of physical examination include deter-
mining the area of pain. Typically, tendon pain should
Unusual or unaccustomed load on tendon is associated be localized and require no more than two fingers
with onset of pain, but why change in load results in pain to demonstrate the area. Bursal involvement in some
or where the pain is coming from remains unknown. tendinopathies, such as in rotator cuff and gluteus
However, many people place high loads on tendons and medius tendinopathies, may have a more extensive pain
 10  Tendon and Tendinopathy 115

distribution. However, extensive pain distribution that between exercise sessions should be considered, and the
does not change with increasing load should trigger 24-hour pain response following loading will guide pro-
suspicion for an alternative or coexisting condition. gression. Three to four days between sessions may ini-
Examination may reveal muscle wasting in the affected tially be important when introducing increases in speed,
muscle–tendon unit and this may extend to regions above especially in substantially deconditioned tendon.
and below the affected tendon. In the lower limb, it is Endurance and compression loads should be included
necessary to assess how the person absorbs and transfers as tolerated but usually not in the initial stages of man-
load in both single leg and bilateral activities. In the agement as they can be provocative. Eccentric loading is
upper limb it is important to determine how load is trans- inherent in all these stages, but the authors do not use it
ferred from the lower limb to the upper limb, especially as an isolated treatment.
in explosive activities such as pitching in baseball and Lifestyle management is a critical component of
serving in tennis. Local tendon assessment involves tendon rehabilitation, as many people with tendon pain
graded loading of the involved tendon and examination are unable to exercise effectively. Excess weight, insulin
is complete when sufficient information about tendon resistance or diabetes, high cholesterol, poor diet and
pain and capacity has been obtained. Although com- smoking can all affect the recovery of a tendon and treat-
monly used clinically, tendon palpation may not be infor- ment should include discussion and education of these
mative39 and more research is needed. important issues.
Imaging is frequently used as a diagnostic tool in ten- Treatments such as massage of the muscle, electro-
dinopathy, and will demonstrate the extent of the pathol- therapy and taping or bracing may be considered as
ogy and determine if there are any associated structural adjuncts to a load-based rehabilitation, but they should
abnormalities such as peritendinopathy or bursal thicken- not be the main focus of management. Frictions over the
ing. Its application in clinical reasoning currently remains tendon, heavy stretching and excessive loading will all be
limited due to the poor relationship between structural detrimental to a tendon, especially in the early stages of
pathology and pain. Recent advances in ultrasound rehabilitation.
imaging such as ultrasound tissue characterization that There is no quick-fix solution and adequate time and
can produce relative quantities of four echotypes that care must be given to restore the tendon to the optimal
have been correlated with tendon pathology may improve level.
the utility of imaging in clinical diagnosis.40 Ruling the
tendon in or out as the source of symptoms should still
be primarily based on the patient’s history and clinical CONCLUSION
examination.
Tendinopathy is a common yet complex musculoskeletal
problem. Assessment requires a thorough history to
MANAGEMENT OF TENDINOPATHY ascertain the loading and individual factors that contrib-
uted to symptoms and a detailed physical evaluation to
The management of tendinopathy is primarily deter- guide load-based rehabilitation. Patient education is an
mined by the clinical presentation, the risk factor profile essential component of tendon rehabilitation.
of the individual and an appreciation of, but limited reli- The presence of tendon pain 24 hours after loading
ance on, any imaging findings. Tendon rehabilitation should guide rehabilitation as opposed to pain on palpa-
should always be specific to the person and their func- tion or pain during exercise. The role of the CNS in the
tional level. modulation of tendon pain is gaining increasing interest
Patient education and appropriate loading strategies and assessment of the contribution of the CNS may be
are essential in successful management. Patient education an important consideration.
should include explanation that while excessive load is the Rehabilitation must be graded, commencing with
likely initiating factor it is also load that will reduce pain isometric loads to reduce tendon pain, followed by pro-
and improve function. Therapeutic load must be admin- gression through strength, power and sports- and activity-
istered carefully and in a graduated and controlled specific function. However, the progression needs to be
fashion. Education must reinforce that treating a tendi- adjusted to reflect the goals of the specific individual and
nopathy demands the same respect as fracture healing. the capacity of the tendon.
No-one would consider serving in tennis with a broken
humerus, or running on a fractured tibia. Equally, tendon REFERENCES
rehabilitation must be given time and be carefully 1. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of achilles
planned. tendon rupture and tendinopathy in male former elite athletes. Clin
The key to rehabilitation is a graduated exercise- J Sport Med 2005;15(3):133–5.
2. Hamilton PG. The prevalence of humeral epicondylitis: a survey
loading programme. Initially consider isometric contrac- in general practice. J R Coll Gen Pract 1986;36(291):464–5.
tions as this type of muscle contraction may reduce 3. Gruchow HW, Pelletier D. An epidemiologic study of tennis elbow.
tendon pain. This may be followed by muscle strengthen- Incidence, recurrence, and effectiveness of prevention strategies.
ing involving heavy slow-resistance training (considering Am J Sports Med 1979;7(4):234–8. [Epub 1979/07/01].
all relevant muscles within the kinetic chain).41 The next 4. Shiri R, Viikari-Juntura E, Varonen H, et al. Prevalence and deter-
minants of lateral and medial epicondylitis: a population study. Am
stage involves increasing load on the tendon by incre- J Epidemiol 2006;164(11):1065–74.
mentally introducing speed and finally energy storage 5. Ferretti A. Epidemiology of jumper’s knee. Sports Med 1986;3(4):
loads. When designing a rehabilitation programme, time 289–95.
116 PART II  Advances in Theory and Practice

6. Lian O, Engebretsen L, Bahr R. Prevalence of jumper’s knee patients with Achilles tendinopathy: a randomized controlled study.
among elite athletes from different sports: a cross-sectional study. Am J Sports Med 2007;35(6):897–906.
Am J Sports Med 2005;33(4):561–7. 26. Malliaras P, Cook J. Patellar tendons with normal imaging and pain:
7. Kettunen J, Kvist M, Alanen E, et al. Long-term prognosis for change in imaging and pain status over a volleyball season. Clin J
jumper’s knee in male athletes. Am J Sports Med 2002;30(5): Sport Med 2006;16(5):388–91.
689–92. 27. Cook JL, Khan KM, Harcourt PR, et al. Patellar tendon ultraso-
8. Holmes GB, Lin J. Etiologic factors associated with symptomatic nography in asymptomatic active athletes reveals hypoechoic
achilles tendinopathy. Foot Ankle Int 2006;27(11):952–9. [Epub regions: a study of 320 tendons. Victorian Institute of Sport Tendon
2006/12/06]. Study Group. Clin J Sport Med 1998;8(2):73–7.
9. Soslowsky LJ, Thomopoulos S, Esmail A, et al. Rotator cuff tendi- 28. Lewis JS, Raza SA, Pilcher J, et al. The prevalence of neovascularity
nosis in an animal model: role of extrinsic and overuse factors. Ann in patients clinically diagnosed with rotator cuff tendinopathy.
Biomed Eng 2002;30(8):1057–63. BMC Musculoskelet Disord 2009;10(1):163.
10. Benjamin M, Moriggl B, Brenner E, et al. The ‘enthesis organ’ 29. Wilde B, Havill A, Priestley L, et al. The efficacy of sclerosing
Concept. Why enthesopathies may not present as focal insertional injections in the treatment of painful tendinopathy. Phys Ther Rev
disorders. Arthritis Rheum 2004;50(10):3306–13. 2011;16(4):244–60.
11. Cook J, Purdam C. Is compressive load a factor in the development 30. Kannus P, Jozsa L. Histopathological changes preceding spontane-
of tendinopathy? Br J Sports Med 2012;46(3):163–8. ous rupture of a tendon. A controlled study of 891 patients. J Bone
12. Rufai A, Ralphs J, Benjamin M. Structure and histopathology of Joint Surg Am 1991;73(10):1507–25.
the insertional region of the human Achilles tendon. J Orthop Res 31. de Vos RJ, Weir A, Tol JL, et al. No effects of PRP on ultrasono-
1995;13(4):585–93. graphic tendon structure and neovascularisation in chronic midpor-
13. Lewis JS. Subacromial impingement syndrome: a musculoskeletal tion Achilles tendinopathy. Br J Sports Med 2011;387–92.
condition or a clinical illusion? Phys Ther Rev 2011;16(5): 32. Rio E, Moseley L, Purdam C, et al. The pain of tendinopathy:
388–98. physiological or pathophysiological? Sports Med 2013;1–15.
14. Fearon AM, Scarvell JM, Neeman T, et al. Greater trochanteric 33. Bjur D, Alfredson HK, Forsgren S. The innervation pattern of the
pain syndrome: defining the clinical syndrome. Br J Sports Med human Achilles tendon: studies of the normal and tendinosis
2013;47(10):649–53. [Epub 2012/09/18]. tendon with markers for general and sensory innervation. Cell
15. Lewis JS. Rotator cuff tendinopathy. Br J Sports Med 2009; Tissue Res 2005;320(1):201–6.
43(4):236–41. [Epub 2008/09/20]. 34. Slater H, Gibson W, Graven-Nielsen T. Sensory responses to
16. Johnson DP. Arthroscopic surgery for patellar tendinitis: a new mechanically and chemically induced tendon pain in healthy sub-
technique. Arthroscopy 1998;14(Suppl. 1):S44. jects. Eur J Pain 2011;15(2):146–52.
17. Culvenor A, Cook JL, Warden SJ, et al. Infrapatellar fat pad size, 35. van Wilgen CP, Konopka KH, Keizer D, et al. Do patients with
but not patellar alignment, is associated with patellar tendinopathy. chronic patellar tendinopathy have an altered somatosensory
Scand J Med Sci Sports 2011;21(6):e405–11. profile? – A Quantitative Sensory Testing (QST) study. Scand J
18. Scott A, Cook JL, Hart DA, et al. Tenocyte responses to mechani- Med Sci Sports 2013;23(2):149–55.
cal loading in vivo: a role for local insulin-like growth factor 1 36. Ngomo S, Mercier C, Roy J-S. Cortical mapping of the infraspi-
signaling in early tendinosis in rats. Arthritis Rheum 2007;56(3): natus muscle in healthy individuals. BMC Neurosci 2013;14(1):52.
871–81. 37. Lewis JS. Rotator cuff tendinopathy/subacromial impingement
19. Leadbetter WB. Cell-matrix response in tendon injury. Clin Sports syndrome: is it time for a new method of assessment? Br J Sports
Med 1992;11(3):533–78. Med 2009;43(4):259–64. [Epub 2008/10/08].
20. Cook J, Purdam C. Is tendon pathology a continuum? Br J Sports 38. Coombes BK, Bisset L, Vicenzino B. A new integrative model of
Med 2009;43(6):409–16. lateral epicondylalgia. Br J Sports Med 2009;43(4):252–8.
21. Abate M, Silbernagel KG, Siljeholm C, et al. Pathogenesis of ten- 39. Cook J, Khan K, Kiss S, et al. Reproducibility and clinical utility
dinopathies: inflammation or degeneration? Arthritis Res Ther of tendon palpation to detect patellar tendinopathy in young bas-
2009;11(3):235. ketball players. Br J Sports Med 2001;35:65–9.
22. Fu S, Rolf C, Cheuk Y, et al. Deciphering the pathogenesis of 40. van Schie H, de Vos R, de Jonge S, et al. Ultrasonographic tissue
tendinopathy: a three-stage process. Sports Med Arthrosc Rehabil characterisation of human Achilles tendons: quantification of
Ther Technol 2010;2(1):30. tendon structure through a novel non-invasive approach. Br J
23. Rees JD, Stride M, Scott A. Tendons – time to revisit inflammation. Sports Med 2010;44(16):1153–9.
Br J Sports Med 2014;48(21):1553–7. 41. Kongsgaard M, Kovanen V, Aagaard P, et al. Corticosteroid injec-
24. Alfredson H, Pietila T, Jonsson P, et al. Heavy-load eccentric calf tions, eccentric decline squat training and heavy slow resistance
muscle training for the treatment of chronic Achilles tendinosis. training in patellar tendinopathy. Scand J Med Sci Sports
Am J Sports Med 1998;26(3):360–6. 2009;19(6):790–802.
25. Silbernagel KG, Thomee R, Eriksson BI, et al. Continued sports
activity, using a pain-monitoring model, during rehabilitation in
 CHAPTER 11 

Lifestyle and
Musculoskeletal Health
Elizabeth Dean  •  Anne Söderlund

of maximizing health and preventing, reversing

INTRODUCTION as well as managing chronic lifestyle-related
conditions.
Musculoskeletal conditions are non-communicable dis- 4. Lifestyle behaviour change, a non-pharmacologic
orders (NCDs) that are the most common conditions intervention, is the basis for promoting patients’
treated by physiotherapists.1 They also remain the most overall health as well as maximizing conventional
common causes of physical disability and pain globally.2,3 physiotherapy outcomes.
Health-related quality of life associated with musculosk- 5. Physiotherapists are the leading established health
eletal conditions including back pain has been reported professionals who primarily exploit non-
to be comparable to that in individuals with chronic con- pharmacologic interventions.
ditions such as complicated diabetes and terminal cancer.4 Based on these lines of support, physiotherapists have a
This chapter synthesizes the evidence supporting the professional responsibility to implement health-based
associations between patients’ lifestyle practices such as physiotherapy consistent with the established definition
smoking, diet and exercise that underlie modifiable of health promotion (Box 11-2), and serve as a resource
NCDs. It describes how these practices affect musculo- and model for other health professionals. Given the
skeletal health with special attention to back pain. Lastly, escalating epidemic of NCDs worldwide8–10 in conjunc-
this chapter addresses how musculoskeletal disability tion with that of disability from musculoskeletal condi-
may impact lifestyle-related health behaviours such as; tions, the majority of patients seen by physiotherapists
smoking, nutrition, activity, sleep quality, and anxiety and likely have one or more risk factors for lifestyle-related
stress, further compromising back pain. conditions.
Health-based physiotherapy practice refers to maxi- Extending the content of this chapter, Chapter 37
mizing a person’s overall health through healthy living to describes the clinical implications of lifestyle behaviours
help address the presenting complaint as well as maxi- on musculoskeletal health. It describes basic assessment
mize long-term health and well-being.1 By so doing, the and outcome evaluation tools, and evidence-based strat-
physiotherapist may reduce the patient’s risk factors for egies and interventions that may be integrated into
lifestyle-related conditions and their severity.5 physiotherapy practice, with a view to minimizing the
To assess the status of health-based practice within the patient’s musculoskeletal complaints and maximizing
profession and develop a global strategic plan, two phys- health overall.
iotherapy summits on global health have been convened.
The goal of the first summit in 2007 was to examine the
findings of global health surveillance initiatives and syn-
NON-COMMUNICABLE DISEASES AND
thesize the findings with respect to implications for con- EVIDENCE-INFORMED ORTHOPAEDIC
temporary physiotherapy practice.1 The second summit PHYSIOTHERAPY
in 2011 developed a global action plan for integrating
health promotion as a clinical competency into entry- The findings of a United Nations high-level meeting on
level physiotherapy education, research and practice.5 NCDs were reported recently in a special issue of The
The evidence supporting these initiatives and also Lancet.12–14 This publication re-iterated multiple World
underpinning this chapter includes: Health Reports concerning the urgency around prevent-
1. Physiotherapists have adopted the International ing and, in some cases, reversing ischaemic heart disease,
Classification of Functioning, Disability and Health smoking-related conditions, hypertension, stroke, type 2
(ICF) globally,6 which is holistic and person- diabetes mellitus and cancer. The report concluded that
centred, and predicated on the World Health Orga- there needs to be a concerted effort on the part of health
nization’s global definition of health7 (Fig. 11-1 and professionals to address these largely preventable condi-
Box 11-1). tions clinically, as well as those involved in health services
2. Physiotherapists espouse best, evidence-based delivery and health policy. These initiatives are consistent
practice. with long-standing recommendations from the World
3. Healthy living (e.g. not smoking, healthy diet, Health Organization.12 To do its part in addressing
healthy weight, minimal periods of prolonged NCDs, the World Confederation for Physical Therapy
sitting, regular physical activity, optimal sleep and has published several position statements related to
manageable stress) is the best evidence-based means health promotion, particularly physical activity.
117
118 PART II  Advances in Theory and Practic

Health condition
prevalence of smoking, weight gain, inactivity, and
depressive symptoms and stress, compared with people
(disorder or disease) without such conditions.19 Lifestyle-related health prac-
tices (beyond ergonomic practices) can impact musculo-
skeletal health status, specifically, positive health practices
Body functions may prevent back pain; and unhealthy practices may con-
Activity Participation tribute to back pain, worsen it or impair treatment
and structures
response. Experiencing chronic back pain may have vari-
(impairments) (limitations) (restrictions) able effects in patients. Patients who smoke may smoke
more, patients may eat un-nutritious foods for comfort,
and they may sit longer and be less physically active in
Contextual factors general, have poorer sleep, and experience more anxiety
and stress. On the other hand, back pain may be an incen-
tive for the patient to improve one or more adverse
Environmental Personal lifestyle-related health behaviours under the guidance of
factors factors the physiotherapist, with the added benefit of improving
health overall. Various factors contribute to back pain,
FIGURE 11-1  ■  The International Classification of Functioning, thus the physiotherapist through systematic assessment
Disability and Health. (World Health Organization, 2001).6 can examine the degree to which lifestyle-related health
practices impact a patient’s back pain and how these may
need to be addressed with or without conventional phys-
BOX 11-1  Definition of Health iotherapy interventions.
Evidence supporting such relationships with respect
World Health Organization Definition of Health (1948) to shoulder conditions may have implications for
spinal conditions. Associations have been reported, for
‘Health is a state of complete physical, mental and social
wellbeing and not merely the absence of disease or infirmity’ example, between smoking, body mass and type 2 diabe-
tes mellitus and shoulder pain.20,21 Further, lifestyle-
SOURCE:
World Health Organization. Definition of health. Available at: related co-morbidity negatively impacts pre-operative
www.who.int/about/definition/en/print.html. Accessed 1/20/2014.7 pain and general health status reported by patients with
rotator cuff tears.22 Research is needed to elucidate these
associations in relation to medical and surgical manage-
BOX 11-2  Definition of Health Promotion ment of orthopaedic conditions such as back pain.
Finally, sex differences have been reported with respect
Health as Conceptualized in The Ottawa Charter for Health to the presentation of low back pain and its manage-
Promotion (1986) ment.23 Women are particularly affected by low back pain
and have a worse prognosis than men. Although women
Health is ‘a resource for everyday life, not the objective of
have been reported to adhere to healthy living practices
living; it is a positive concept emphasising social and physical
resources as well as physical and mental capacity’. more than men, they may benefit from greater attention
to lifestyle practices to help mitigate their signs and
‘Health promotion is the process of enabling people to increase symptoms. Men appear to be more active than women,
control over, and to improve, their health.’ yet men’s health disadvantage is related to smoking and
being overweight.24 Given the relationship between back
SOURCE: The Ottawa Charter for Health Promotion. First International pain and impaired bone health, the role of lifestyle and
Conference on Health Promotion, Ottawa, 21 November 1986. Available its impact on bone health in both women and men war-
at: http://www.who.int/healthpromotion/conferences/previous/ottawa/en/.
Accessed 1/14/2014.11 rants greater attention.25

The relationship between lifestyle behaviours and SMOKING AND MUSCULOSKELETAL

NCDs is unequivocal. Table 11-1 summarizes the evi-
dence linking lifestyle practices with six leading NCDs.
HEALTH
Although ischaemic heart disease can manifest as or con- Deleterious Effects of Smoking
tribute to back pain, several risk factors for back pain are
those for heart disease (e.g. smoking, obesity, sedentary Smoking is deleterious to the musculoskeletal system.26–28
lifestyle and stress) as well as other lifestyle-related condi- Best documented are the effects of long-term smoking
tions.15,16 Physiotherapists should play a major role in on bone thinning and fracture. The underlying mecha-
health education (i.e. smoking cessation; healthy nutri- nism has been related to altered bone metabolism and
tion; weight control; increasing physical activity; improv- reduced blood flow given nicotine is a powerful vasocon-
ing sleep hygiene; and reduction of anxiety, depression strictor. Further, bone loss can be accelerated in people
and stress). who have been exposed chronically to second-hand
Musculoskeletal health and back pain, its resolution smoke during their growing years. The onset of meno-
and likelihood of recurrence, may be improved with pause is accelerated in female smokers, and in turn,
lifestyle-related health changes.17,18 People with chronic increased age-related bone loss. Risk of fracture increases
conditions including chronic back pain have a greater the longer a person smokes and smoking delays healing
 11  Lifestyle and Musculoskeletal Health 119

TABLE 11-1  Lifestyle-Related Conditions and Their Modifiable Risk Factors

Cardiovascular (Ischaemic Heart Type 2
Disease and Hypertension) and Chronic Obstructive Diabetes
Risk Factor Peripheral Vascular Disease Lung Disease Stroke Mellitus Cancer Osteoporosis
Smoking X X X X X* X
Physical inactivity X X X X X
Obesity X X X X X
Nutrition X X X X X X
High blood pressure X X X
Dietary fat†/blood lipids X X X X
Elevated glucose levels X X X X
Alcohol‡ X ? X X X

*An increased risk of all-cause cancer. Smoking is not only related to cancer of the nose, mouth, airways, and lungs; smoking increases
the risk of all-cause cancer.
†
Partially saturated, saturated, and trans fats are the most injurious to health.
‡
Alcohol can be protective in moderate quantities, red wine in particular.
Sources:
Goldstein LB, Bushnell CD, Adams RJ, et al. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from
the American Heart Association/American Stroke Association. Stroke 2011;42(2):517–84. doi: 10.1161/STR.0b013e3181fcb238. Epub
2010 Dec 2.
Canadian Heart and Stroke Foundation. Available from: http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.2796497/k.BF8B/Home.htm.
Accessed 1/14/2014.
Harvard School of Public Health.Your Disease Risk Initiative. Available from: http://www.yourdiseaserisk.wustl.edu/YDRDefault.aspx
?ScreenControl=YDRGeneral&ScreenName=YDRAbout. Accessed 1/14/2014.

and increases complications both of fractures and trauma anti-inflammatory responses.32 Quitting smoking can
related to a back condition. Smoking is often associated lower the rate of bone loss and fractures, but may take
with drinking coffee and alcohol. Both long-term high several years to be reduced to the rate of non-smokers.33
caffeine and alcohol consumption have been implicated The benefits of smoking cessation on bone health have
in bone density loss. been documented with respect to improved outcomes
Smoking contributes to the onset of or aggravates the after orthopaedic surgery including faster wound healing,
progression of back pain and arthritis.26 Smokers have reduced complications and reduced hospital stay.34
been reported to have a lower pain threshold (women’s
lower than men’s) and experience more intense pain (dose
dependent) in relation to musculoskeletal conditions as NUTRITION AND MUSCULOSKELETAL
well as other conditions, than former smokers and non- HEALTH
smokers.29,30 Both smoking early in life and over many
years increase the probability of experiencing frequent The relationship between musculoskeletal health and
pain over one’s life. nutrition has been best documented in relation to mal-
The extent to which exercise as well as smoking ces- nutrition in children, athletic performance and in relation
sation can restore bone density and overall bone health to age-related musculoskeletal changes, particularly those
in smokers remains unknown. Compelling findings from related to hormonal changes in the life cycles of women
animal studies suggest that prolonged exercise may offset (menstruation, pregnancy and menopause).35
the damaging effects of smoking on lung function and Commensurate with globalization, the consequences
this effect may be mediated through exercise-induced of the Western diet are now being realized with the
anti-oxidant production.31 It appears that the oxidant- prevalence of NCDs in high-income countries, and
induced injury associated with smoking may have a increasingly in middle- and low-income countries.8 Criti-
reversible component. Research is warranted to establish cism has been lodged against the promoters of estab-
whether such an effect can be observed in other organ lished food pyramids given their apparent role in
systems. contributing to the prevalence of NCDs. The role of
lobby groups in the development of nutritional guide-
lines has been a matter of contention in the United
Beneficial Effects of Quitting Smoking States.36 Plant-based nutritional regimens including the
Individuals who have never smoked are likely to experi- Mediterranean diet have the highest level of evidence
ence less back pain over the course of their lives.26 The supporting their health-protective anti-inflammatory
multisystem benefits of quitting smoking are substantial benefits37,38 and health outcomes overall.
and these benefits can be powerful incentives for people In contemporary society, people may eat for comfort
to quit smoking when they are ready to do so. and emotional support rather than biological needs.39
Smoking cessation improves musculoskeletal health Typically, comfort foods tend to be high in fat, sugar and
primarily by maintaining bone density and maximizing salt, and lack nutrition. Living with a chronic condition
vascular perfusion of tissue for its nutrition, healing and may contribute to such eating patterns and may nega-
repair, and augmenting systemic and local immune and tively impact recovery from injury or illness.
120 PART II  Advances in Theory and Practic

Bone Mineralization study of over 2000 Chinese men reported that pressure
pain threshold was reduced in those individuals with
Bone health begins in childhood and depends on bal- greater abdominal girths and who were less active than
anced nutrition, regular physical activity throughout those with healthy girths.52 Guneli and colleagues53
life and not smoking. In Western countries lifestyle observed that lean people are less susceptible, and obese
practices including smoking, poor nutritional choices people are more susceptible, to pain based on the activa-
and inactivity are common, and contribute to reduced tion of circulating ghrelin. They hypothesized that
bone density and mass, and osteoporosis. Low bone ghrelin, a hormone directly related to body mass index
mineral density is not only a red flag for osteoporosis, and obesity, is involved in the obesity–pain relationship.
but a risk factor for cardiovascular disease which has
implications for the prescription of exercise for back
problems and monitoring during prescribed therapeutic
Immunity and Immune Response
exercise.40 Musculoskeletal complaints are hallmarked by soft tissue
A key index of bone health with respect to mass and trauma and local inflammation which trigger an anti-
density is calcium balance.41 Western lifestyle practices inflammatory response. The quality of this response
contribute to calcium negative balance. Interestingly, largely depends on a person’s health status, in particular
guidelines for maintaining calcium balance, most fre- nutritional status. Biomarkers for CSLGI can be elevated
quently focus on calcium loading, e.g. supplementation, in people with localized inflammation.54 Conversely, the
rather than striving for optimal calcium balance by reduc- role of CSLGI in local inflammation and pain in response
ing calcium loss. Although a requisite amount of calcium to tissue injury is less clear.
is required for healthy physiological function, the deple-
tion of calcium through sedentary living, caffeine and
alcohol consumption, smoking and possibly animal
Obesity
protein consumption has been well documented.42,43 The causes of and contributors to the obesity epidemic
are multifactorial. Food choices that are calorie dense
versus nutrient dense are principal contributors. Typical
Body Composition Western diets remain high in animal protein, refined
Body composition and mass impact bone musculoskeletal grains, sugar, fat and salt content, and low in terms of
health directly and indirectly. High body mass impairs servings of vegetables, fruit and whole grains. The com-
the constituents of bone that are most important for bination of low activity and the Western diet is a deadly
bone strength and fracture protection.44 Although coun- one contributing to the current lifestyle-related condi-
terintuitive, bone loading due to excess body mass is tions including overweight/obesity.55,56 Overweight/
not necessarily protective against fractures. With respect obesity impacts every organ system, directly or indi-
to an indirect effect on musculoskeletal health, increased rectly.57 With respect to the musculoskeletal system,
mass limits a person’s capacity to be active (biomechani- obesity increases the risk of hyperuricemia and gout,58
cally and energetically). Inactivity can be further com- osteoarthritis of the hips and knees59 and back pain.60,61
pounded by obesity-related conditions such as ischaemic In addition, obesity is related to immobility62 which
heart disease, hypertension and type 2 diabetes mellitus. further contributes to musculoskeletal disability and
Chronic pain and obesity have been associated. Lifestyle delayed therapeutic response and recovery.
behaviour change is recommended as a primary interven- Weight loss has been proposed as a means of offsetting
tion to lose weight, thereby improving a patient’s function back pain in people who are obese.63 Further studies are
and quality of life.45 If surgery is indicated, people who needed to elucidate the relationship between body mass
are obese have increased likelihood of poor post-operative and spine health. Although the association of body mass
outcomes compared with people of healthy weight.46 and the need for total joint replacement has been argued
to be related to inactivity associated with pain limitations
Chronic Systemic Low-Grade from degenerative processes of joints, this supposition
does not appear to be supported. Body weight appears to
Inflammation increase after total joint replacement surgery from pre-
Comparable to other chronic lifestyle-related conditions, operative levels or remain unchanged.64
obesity is associated with chronic systemic low-grade Finally, being overweight or obese is more likely to be
inflammation (CSLGI).47–49 CSLGI is a physiological associated with one or more lifestyle-related risk factors,
stress reaction to pathological insults often associated for one or more lifestyle-related conditions.65 Managing
with chronic lifestyle-related conditions.50 The CSLGI the physiotherapy musculoskeletal needs of patients who
that is associated with obesity may be mitigated with are obese requires detailed multisystem and behavioural
physical activity.51 Whether such low-grade inflammation assessment and monitoring and targeted treatment pre-
predisposes people who are obese to pain and disability scription. Management needs to be informed by the mul-
warrants elucidation. tisystem assessment findings as well as the assessment
of the patient’s musculoskeletal complaint. It is possible
that addressing the lifestyle-related risk factors could
Pain Threshold yield the best long-term physiotherapy musculoskeletal
The relationship between obesity and pain threshold is outcome and minimize recurrence of the presenting
an area of both clinical and research interest. A recent complaint.
 11  Lifestyle and Musculoskeletal Health 121

to this evidence, standing offices and treadmill worksta-

INACTIVITY/ACTIVITY AND tions are being promoted to break-up periods of pro-
MUSCULOSKELETAL HEALTH longed sitting during the work day.78
Current guidelines for physical activity are 150 minutes
The relationship between activity and musculoskeletal of moderately intense activity per week.79 The effect size
health can be viewed in two ways. Firstly, a sedentary of this relatively low level of exercise is substantial. Such
lifestyle is deleterious to musculoskeletal health,66 in levels of activity are consistent with positive health,
addition to being an independent risk factor for NCDs60 reduced morbidity and improved response to health care
including cardiometabolic syndrome.67–69 Joint surfaces management, particularly as people age.4,80 Not only is
may degenerate due to reduced synovial fluid production ‘tolerable’ activity now recommended in standards of
that protects joint surfaces.70 Secondly, this risk factor practice for even acute back pain,81 but it may also reduce
persists even in individuals who are exercising routinely pain-related anxiety and depression particularly if the
based on recommended guidelines but have patterns of pain becomes chronic.82
prolonged periods of inactivity during the day. Like those with other chronic conditions, people
with chronic back pain walk less and are generally less
physically active than people without such conditions.
Deleterious Effects of Inactivity McDonough and co-workers recently reported that
The Western lifestyle tends to be sedentary, i.e. charac- people with low back pain can increase their walking
terized by prolonged periods of inactivity, even in those daily over 8 weeks, in a pedometer-driven walking
individuals who participate in structured exercise regu- programme.83 The programme was reported to be
larly (participate in moderately intense physical activity safe, able to reduce disability and pain, and increase
three to five times a week, for 20 to 40 minutes). Pro- function.
longed periods of inactivity are an independent risk factor
for cardiometabolic disease71,72 and back problems.73
Inactivity has been associated with the prevalence of back SLEEP AND MUSCULOSKELETAL
complaints, with many of the risk factors of back pain HEALTH
being those of cardiovascular disease.74 This association
has important implications for the management of back Regular sleep is biologically necessary for physiological
pain in terms of prescribing healthy living practices to restoration. Most adults require an average of 8 to 10
minimize back complaints and their recurrence, as well hours of sleep a night for optimal health and well-being
as maximizing the outcomes of traditional physiotherapy with periods of intermittent rapid eye movement (REM),
for back complaints. In addition, people with cardiovas- yet they report often falling short of this.84 Young people
cular risk or manifestations of the signs and symptoms of tend to report having substantially fewer hours of sleep
cardiovascular disease warrant related assessment and compared with older people who are more likely to com-
monitoring during exercise. plain of poor-quality sleep (unable to fall asleep, or unable
A sedentary lifestyle along with smoking and unhealthy to fall back to sleep if awakened during the night).85 The
weight contributes to premature ageing. The mechanism impact of sleep deprivation on health is substantial,
has been associated with shortening of teleomere length.75 affecting a person physically, psychologically and cogni-
Teleomere length is further compromised with oxidative tively. For children, poor sleep impacts physical and
stress and inflammation associated with unhealthy life- social development. Inadequate or disturbed and irregu-
styles leading to NCDs.50,75 lar sleep such as in shift workers is associated with illness
Because of the hazards of sedentary living, researchers and injury.86
have focused not only on volume of physical activity, but
also have been interested in quantifying sedentary activ-
ity. Tudor-Locke and colleagues recently quantified daily
Deleterious Effects of Sleep Deprivation
inactivity based on a step-defined sedentary lifestyle Insomnia and sleep deprivation are common in Western
index: <5000 steps/day.76 The use of such a marker could society.87 Sleep deprivation can exist independently of the
be useful in the musculoskeletal assessment of people complaint the patient presents to the physiotherapist, or
with disabilities such as back pain, and as an outcome can be a consequence of that complaint. Recent studies
evaluation tool. have reported that at least 50% of patients with low back
pain report symptoms of insomnia.88,89 Insomnia is associ-
Beneficial Effects of Regular ated with fatigue, cognitive impairment, mood distur-
bance, anxiety and depression90 leading to functional
Physical Activity impairments and accidents.87
Regular physical activity is unequivocally associated with People with pain have been reported to sleep less well,
positive health status and outcomes of multisystem func- and when they sleep better, they report less pain.86 Insom-
tion including musculoskeletal health.77 That regular nia can adversely affect an individual’s experience of pain
physical activity throughout the day is protective of mus- through decreasing pain threshold and tolerance.91,92
culoskeletal health is well established and is highly rec- Hyperalgesia associated with sleep deprivation93 has been
ommended for protection against bone impairment reported in people in the absence of a health condition.
secondary to chronic conditions and potentially medica- Affective pain ratings and health anxiety have been
tions to manage them (e.g. corticosteroids). In response reported to be the best predictors of insomnia severity,
122 PART II  Advances in Theory and Practic

amounting to 30% of the total variance, even when pain with such challenges include those who are anxious or
intensity is controlled.94 exhibit depressive symptoms as well as those with patho-
Tissue injury related to the stress of sleep deprivation logical conditions such as clinical depression, schizophre-
has been proposed to be mediated by impaired immune nia and psychosis. These individuals tend to smoke more,
response and potentially free radical production.95 REM eat less well, are less active, and may consume more
sleep deprivation, specifically, has been associated with an alcohol and use recreational drugs more than those
increase in free radical induced damage in blood shown without mental health conditions.104,105
by increased plasma malondialdehyde levels. Animal Chronic health issues such as chronic pain are well
studies have shown an increase in plasma malondialde- known to affect mental health, i.e. they can contribute to
hyde level as the duration of sleep deprivation increased.96 anxiety, depression and stress.106 Depression influences
Increased malondialdehyde can be attributed to an the course of low back pain.107 Six weeks after shoulder
increase in free radical formation and damage, as the pain onset, for example, assessment of concurrent depres-
duration of REM sleep deprivation increases. Regular sive symptoms has been advised, in order for these to be
REM sleep therefore is essential to minimize free radical identified and addressed, thereby potentially augmenting
formation and consequent tissue irritation. therapeutic outcome and recovery.
Finally, people who are chronically sleep deprived
have poorer immunity than those who are rested,95 thus
they tend to have higher infection rates. Healing may be
Beneficial Effects of Mental Hygiene
impaired due to CSLGI, an index of an impaired immune Mental hygiene refers to the promotion and preservation
response which is independently associated with poor of mental health. Mental hygiene may not necessarily
sleep, a risk factor for heart disease and stroke.97 prevent musculoskeletal problems, but good mental
health may improve a person’s self-efficacy, resilience and
resources to manage their problems and associated mus-
Beneficial Effects of Optimal Sleep culoskeletal disability. Of particular relevance to the
When a person has optimal sleep, both cognitive and physiotherapist is the role of physical exercise in preserv-
physical function are improved, and overall constitution- ing and improving depressive symptoms. People who are
ality is stronger. Importantly, the person is restored physi- inactive report poorer emotional and mental health com-
cally so has the capacity to physically exert him- or herself. pared with active people, thus inactivity can compound
He or she has a greater capacity for healing and repair, the mental health consequences of chronic conditions
and greater resistance to infection due to stronger immu- such as back pain. Structured exercise on the other hand
nity. When pathological factors are ruled out, optimal can improve emotional and mental health, thereby offset-
sleep is best achieved through regular sleep hygiene habits ting impaired mental health associated with chronic con-
and regularity of sleep, place and conditions.84,98 ditions.108 Strategies such as cognitive behaviour therapy
Sleep alone may improve physical and functional per- may have a role in the management of such disability, and
formance. A striking example is that of figure skater, can be adapted to the physiotherapy context.
Sarah Hughes. Following a long plateau of unchanged
performance, Sarah increased her sleep by two hours a
night based on the work of Maas,99,100 whereupon she CONCLUSION
achieved Olympic gold in 2002. This observation has
implications for physiotherapists whose priority is also Patients with musculoskeletal conditions including back
maximal functional capacity in their patients. pain typically complain of discomfort/pain, loss of func-
tional capacity, and reduced capacity to perform daily
activities, all of which can interfere with their health-
MENTAL HEALTH AND related quality of life. This chapter describes how
MUSCULOSKELETAL HEALTH lifestyle-related health behaviours (beyond ergonomic
and biomechanical corrections) may cause or contribute
The relationship between musculoskeletal health and to these complaints, their severity and frequency. This
mental health is bidirectional. People with mental health chapter introduced physiotherapists to the evidence sup-
challenges may be more susceptible to physical health porting that musculoskeletal health is influenced by life-
issues including musculoskeletal problems,101 and people style factors including smoking; nutrition; overweight
with musculoskeletal problems often experience anxiety and obesity; inactivity; sleep deprivation; and anxiety,
and depression,102 which can reduce pain threshold, depression and stress. It also describes how musculo­
further increasing disability.103 skeletal ill health, in turn, can increase negative health
behaviours such as smoking, sub-optimal nutrition,
obesity, inactivity, poor sleep, and anxiety, depression and
Deleterious Effects of Mental Ill Health stress.
The literature related to the relationship between mus- Beyond the scope of this chapter are important issues
culoskeletal health and mental health largely focuses on such as alcohol and drug abuse. Given their detriment to
the adverse health and lifestyles of people with mental health and interference with a patient’s capacity to follow
health challenges, which may secondarily affect the mus- treatment recommendations, these behaviours warrant
culoskeletal system, e.g. smoking, inactivity and poor being assessed and followed, even when these are being
nutritional options and choices, and inactivity. People managed primarily by other health professionals.
 11  Lifestyle and Musculoskeletal Health 123

18. Notarnicola A, Fischetti F, Maccagnano G, et al. Daily pilates

REFERENCES exercise or inactivity for patients with low back pain: a clinical
1. Dean E, Al-Obaidi S, De Andrade AD, et al. The first physical prospective observational study. Eur J Phys Rehabil Med
therapy summit on global health: implications and recommenda- 2014;28(6):372–9.
tions for the 21st century. Physiother Theory Pract 2011;27(8): 19. Huan HC, Chang HJ, Lin KC, et al. A closer examination of the
531–47. interaction among risk factors for low back pain. Am J Health
2. Mody GM, Brooks PM. Improving musculoskeletal health: Promot 2013;Forthcoming.
global issues. Best Pract Res Clin Rheumatol 2012;26(2): 20. Rechardt M, Shiri R, Karppinen J, et al. Lifestyle and metabolic
237–49. factors in relation to shoulder pain and rotator cuff tendinitis: a
3. Vos T, Flaxman AD, Naghavi M, et al. Years lived with disability population-based study. BMC Musculoskelet Disord 2010;11(1):
(YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: 165.
a systematic analysis for the Global Burden of Disease Study 2010. 21. Viikari-Juntura E, Shiri R, Solovieva S, et al. Risk factors of ath-
Lancet 2012;380(9859):2163–96. erosclerosis and shoulder pain – is there an association? A system-
4. Taylor W. Musculoskeletal pain in the adult New Zealand atic review. Eur J Pain 2008;12(4):412–26.
population: prevalence and impact. N Z Med J 2005;118(1221): 22. Tashjian RZ, Henn RF, Kang L, et al. The effect of comorbidity
U1629. on self-assessed function in patients with a chronic rotator cuff
5. Dean E, Dornelas de Andrade A, O’Donoghue G, et al. The tear. J Bone Joint Surg Am 2004;86-A(2):355–62.
second physical therapy summit on global health: developing 23. Chenot J, Becker A, Leonhardt C, et al. Sex differences in presen-
an action plan to promote health in daily practice and tation, course, and management of low back pain in primary care.
reduce the burden of non-communicable diseases. Physiother Clin J Pain 2008;24(7):578–84.
Theory Pract 2013;Ahead of print. Available from: <http:// 24. Ross CE, Bird CE. Sex stratification and health lifestyle: conse-
www.unboundmedicine.com/medline/citation/24252072/The quences for men’s and women’s perceived health. J Health Soc
_Second_Physical_Therapy_Summit_on_Global_Health:_devel Behav 1994;35(2):161–78.
oping_an_action_plan_to_promote_health_in_daily_practice_ 25. Briggs AM, Straker LM, Wark JD. Bone health and back pain:
and_reduce_the_burden_of_non_communicable_diseases>. what do we know and where should we go? Osteoporosis Int
6. International Classification of Functioning, Disability and 2009;20(2):209–19.
Health 2001 [Internet]. Geneva, Switzerland: World Health 26. Abate M, Vanni D, Pantalone A, et al. Cigarette smoking and
Organization; 2001 Available from: <http://rehabmalaysia.org/ musculoskeletal disorders. Muscles Ligaments Tendons J 2013;
wp-content/uploads/2011/12/4-International-Classification-of- 3(2):63–9.
Functioning-Disability-and-Health.pdf>; [cited 2014 Jan 20.]. 27. A clinical practice guideline for treating tobacco use and depen-
7. WHO. Definition of Health 1948 [Internet]. Geneva, Switzer- dence: 2008 Update. A US public health service report. Am J Prev
land: World Health Organization; 2003 Available from: <http:// Med 2008;35(2):158–76.
www.who.int/about/definition/en/print.html>; [cited 2014 Jan 28. Ending the tobacco epidemic | HHS.gov [Internet]. Washington,
20.]. D.C.: US Department of Health and Human Services Available
8. WHO. Priority noncommunicable diseases and conditions from: <http://www.hhs.gov/ash/initiatives/tobacco/>; [cited 2014
[Internet]. Geneva, Switzerland: World Health Organization; Jan 20.].
Available from: <http://www.wpro.who.int/health_research/docu 29. Pisinger C, Aadahl M, Toft U, et al. The association between
ments/dhs_hr_health_in_asia_and_the_pacific_13_chapter active and passive smoking and frequent pain in a general popula-
_8_priority_noncommunicable_diseases_and_disorders.pdf>; tion. Eur J Pain 2011;15(1):77–83.
[cited 2014 Jan 20]. 30. Pulvers K, Hood A, Limas EF, et al. Female smokers show lower
9. Bloom DE, Cafiero ET, Jané-Llopis E, et al. The Global Eco- pain tolerance in a physical distress task. Addict Behav 2012;
nomic Burden of Noncommunicable Diseases [Internet]. Geneva, 37(10):1167–70.
Switzerland: World Economic Forum; 2011 Sept Available from: 31. Al-Obaidi S, Mathew TC, Dean E. Exercise may offset nicotine-
<h t t p : / / w w w 3 . w e f o r u m . o r g / d o c s / W E F _ H a r v a r d _ H E _ induced injury in lung tissue: a preliminary histological study
GlobalEconomicBurdenNonCommunicableDiseases_2011.pdf>; based on a rat model. Exp Lung Res 2012;38(4):211–21.
[cited 2014 Jan 20.]. 32. CDC – fact sheet – health effects of cigarette smoking – smoking
10. Final draft of the global NCD action plan 2013–2020 [Internet]. & tobacco use [Internet]. Atlanta, GA: Centers for Disease
Geneva, Switzerland: World Health Organization; 2013 Available Control and Prevention; 2013 Available from: <http://
from: <http://ncdalliance.org/sites/default/files/rfiles/WHO%20 www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/
Global%20NCD%20Action%20Plan%202013-2020.pdf>; [cited effects_cig_smoking/>; [updated 2013 Dec 17; cited 2014 Jan 20.].
2014 Jan 20.]. 33. Smoking and bone health [Internet]. Bethesda, MD: NIH Osteo-
11. The Ottawa Charter for Health Promotion. First International porosis and Related Bone Diseases National Resource Center;
Conference on Health Promotion, Ottawa, 21 November 1986 2012 Available from: <http://www.niams.nih.gov/Health_Info/
[Internet]. World Health Organization; 2014 Available from: Bone/Osteoporosis/Conditions_Behaviors/bone_smoking.asp>;
<http://www.who.int/healthpromotion/conferences/previous/ [cited 2014 Jan 20.].
ottawa/en/>; [cited 2014 Feb 22]. 34. Lindström D, Azodi OS, Wladis A, et al. Effects of a perioperative
12. Beaglehole R, Yach D. Globalisation and the prevention and smoking cessation intervention on postoperative complications.
control of non-communicable disease: the neglected chronic dis- Ann Surg 2008;248(5):739–45.
eases of adults. Lancet 2003;362(9387):903–8. 35. Morgan SL. Nutrition and bone: it is more than calcium and
13. Beaglehole R, Bonita R, Alleyne G, et al. UN high-level meeting vitamin D. Womens Health 2009;5(6):727–37.
on non-communicable diseases: addressing four questions. Lancet 36. Nestle M. Food lobbies, the food pyramid, and U.S. nutrition
2011;378(9789):449–55. policy. Int J Health Serv 1993;23(3):483–96.
14. Research: UN summit on non-communicable diseases [Internet]. 37. Pitsavos C, Panagiotakos DB, Chrysohoou C, et al. The effect of
GHD-NET Available from: <http://www.ghd-net.org/negoti the combination of Mediterranean diet and leisure time physical
ations/un-summit-non-communicable-diseases/research>; [cited activity on the risk of developing acute coronary syndromes, in
2014 Jan 20.]. hypertensive subjects. J Hum Hypertens 2002;16(7):517–24.
15. Kauppila LI. Atherosclerosis and disc degeneration/low-back 38. Polidori MC. Antioxidant micronutrients in the prevention of
pain: a systematic review. Eur J Vasc Endovasc Surg 2009;37(6): age-related diseases. J Postgrad Med 2003;49(3):229–35.
661–70. 39. Cleobury L, Tapper K. Reasons for eating ‘unhealthy’ snacks in
16. Zhu K, Devine A, Dick IM, et al. Association of back pain fre- overweight and obese males and females. J Hum Nutr Diet
quency with mortality, coronary heart events, mobility, and quality 2013;doi:10.1111/jhn.12169.
of life in elderly women. Spine 2007;32(18):2012–18. 40. Broussard DL, Magnus JH. Coronary heart disease risk and bone
17. Yildirim Y, Gunay S, Karadibak D. Identifying factors associated mineral density among U.S. women and men. J Womens Health
with low back pain among employees working at a package 2008;17(3):479–90.
producing industry. J Back Musculoskelet Rehabil 2014;27(1): 41. Peacock M. Calcium metabolism in health and disease. Clin J Am
25–32. Soc Nephrol 2010;5(Suppl. 1):S23–30.
124 PART II  Advances in Theory and Practic

42. Calvez J, Poupin N, Chesneau C, et al. Protein intake, calcium 65. Schuit AJ, van Loon AJ, Tijhuis M, et al. Clustering of lifestyle
balance and health consequences. Eur J Clin Nutr 2012;66(3): risk factors in a general adult population. Prev Med 2002;35(3):
281–95. 219–24.
43. Ward EM. Osteoporosis diet dangers: foods to avoid [In­ 66. Whedon GD. Disuse osteoporosis: physiological aspects. Calcif
ternet]. Web MD; 2008 Available from: <http://www.webmd Tissue Int 1984;36(Suppl. 1):S146–50.
.com/osteoporosis/living-with-osteoporosis-7/diet-dangers>; [cit- 67. Henson J, Yates T, Biddle SJ, et al. Associations of objectively
ed 2014 Jan 20.]. measured sedentary behaviour and physical activity with markers
44. Madeira E, Mafort TT, Madeira M, et al. Lean mass as a predictor of cardiometabolic health. Diabetologia 2013;56(5):1012–20.
of bone density and microarchitecture in adult obese individuals 68. Stamatakis E, Hamer M, Mishra GD. Early adulthood television
with metabolic syndrome. Bone 2014;59:89–92. viewing and cardiometabolic risk profiles in early middle age:
45. Arranz L, Rafecas M, Alegre C. Effects of obesity on function and results from a population, prospective cohort study. Diabetologia
quality of life in chronic pain conditions. Curr Rheumatol Rep 2012;55(2):311–20.
2014;16(1):390. 69. Thorp AA, Healy GN, Owen N, et al. Deleterious associations of
46. Liljensoe A, Lauersen JO, Soballe K, et al. Overweight preopera- sitting time and television viewing time with cardiometabolic risk
tively impairs clinical outcome after knee arthroplasty: a cohort biomarkers: Australian Diabetes, Obesity and Lifestyle (AusDiab)
study of 197 patients 3–5 years after surgery. Acta Orthop 2013; study 2004–2005. Diabetes Care 2010;33(2):327–34.
84(4):392–7. 70. Hootman JM, Macera CA, Ham SA, et al. Physical activity levels
47. Hulsmans M, Geeraert B, De Keyzer D, et  al. Interleukin-1 among the general US adult population and in adults with and
receptor-associated kinase-3 is a key inhibitor of inflammation without arthritis. Arthritis Rheum 2003;49(1):129–35.
in obesity and metabolic syndrome. PLoS ONE 2012;7(1): 71. Celis-Morales CA, Perez-Bravo F, Ibanez L, et al. Objective vs.
e30414. self-reported physical activity and sedentary time: effects of mea-
48. Issa RI, Griffin TM. Pathobiology of obesity and osteoarthritis: surement method on relationships with risk biomarkers. PLoS
integrating biomechanics and inflammation. Pathobiol Aging Age ONE 2012;7(5):e36345.
Relat Dis 2012;2(2012):17470. 72. Gennuso KP, Gangnon RE, Matthews CE, et al. Sedentary behav-
49. Stienstra R, Duval C, Muller M, et al. PPARs, obesity, and inflam- ior, physical activity, and markers of health in older adults. Med
mation. PPAR Res 2007;95974. Sci Sports Exerc 2013;45(8):1493–500.
50. Dean E, Gormsen Hansen R. Prescribing optimal nutrition and 73. Socio-demographic and lifestyle correlates of obesity: technical
physical activity as ‘first-line’ interventions for best practice man- report on the secondary analyses using the 2000–2001 Canadian
agement of chronic low-grade inflammation associated with Community Health Survey. Canadian Population Health Initia-
osteoarthritis: evidence synthesis. Arthritis 2012;560634. tive [Internet]. Ottawa, ON: Canadian Institute for Health Infor-
51. Wärnberg J, Cunningham K, Romeo J, et al. Physical activity, mation; 2005 Available from: <https://secure.cihi.ca/estore/
exercise and low-grade systemic inflammation. Proc Nutr Soc productFamily.htm?pf=PFC538&lang=en&media=0>; [cited
2010;69(03):400–6. 2014 Jan 20.].
52. Zhang Y, Zhang S, Gao Y, et al. Factors associated with the pres- 74. Smuck M, Kao M, Brar N, et al. Does physical activity influence
sure pain threshold in healthy Chinese men. Pain Med the relationship between low back pain and obesity? Spine J
2013;14(9):1291–300. 2014;14(2):209–16.
53. Guneli E, Gumustekin M, Ates M. Possible involvement of 75. Cherkas LF, Hunkin JL, Kato BS, et al. The association between
ghrelin on pain threshold in obesity. Med Hypotheses 2010;74(3): physical activity in leisure time and leukocyte telomere length.
452–4. Arch Intern Med 2008;168(2):154–8.
54. Shiri R, Viikari-Juntura E, Varonen H, et al. Prevalence and deter- 76. Tudor-Locke C, Craig CL, Thyfault JP, et al. A step-defined sed-
minants of lateral and medial epicondylitis: a population study. Am entary lifestyle index. Appl Physiol Nutr Metab 2013;38(2):
J Epidemiol 2006;164(11):1065–74. 100–14.
55. WHO. Physical inactivity a leading cause of disease and disability, 77. Vuori I. Exercise and physical health: musculoskeletal health and
warns WHO [Internet]. World Health Organization; 2002 Avail- functional capabilities. Res Q Exerc Sport 1995;66(4):276–85.
able from: <http://www.who.int/mediacentre/news/releases/ 78. Tudor-Locke C, Schuna JM, Frensham LJ, et al. Changing the
release23/en/index.html>; [updated 2014; cited 2014 Jan 20.]. way we work: elevating energy expenditure with workstation alter-
56. Obesity: preventing and managing the global epidemic. Report of natives. Int J Obes 2014;38(6):755–65.
a WHO consultation. World Health Organ Tech Rep Ser 2000; 79. 2008 physical activity guidelines for Americans [Internet]. Wash-
894:i–xii, 1–253. ington, D.C.: US Department of Health and Human Services;
57. Kushner RF. Road Maps for Clinical Practice: Case Studies in 2013 Available from: <http://www.health.gov/paguidelines/
Disease Prevention and Health Promotion-Assessment and Man- guidelines/default.aspx#toc>; [updated 2013 Nov 3; cited 2014 Jan
agement of Adult Obesity: A Primer for Physicians [Internet]. 20.].
Atlanta, GA: American Medical Association; 2003 Available from: 80. Warburton DE, Nicol CW, Bredin SS. Prescribing exercise as
<www.yaleruddcenter.org/resources/upload/docs/what/bias/ preventive therapy. CMAJ 2006;174(7):961–74.
AMAprimerforobesitycommunication.pdf>; [cited 2014 Jan 20.]. 81. Delitto A, George SZ, Van Dillen LR, et al. Low back pain: clini-
58. DeMarco MA, Maynard JW, Huizinga MM, et al. Obesity and cal practice guidelines linked to the International Classification of
younger age at gout onset in a community-based cohort. Arthritis Functioning. J Orthop Sports Phys Ther 2012;42(4):A1–57.
Care Res (Hoboken) 2011;63(8):1108–14. 82. Coombes JS, Law J, Lancashire B, et al. ‘Exercise is medicine’:
59. Mezhov V, Ciccutini FM, Hanna FS, et al. Does obesity affect curbing the burden of chronic disease and physical inactivity. Asia
knee cartilage? A systematic review of magnetic resonance imaging Pac J Public Health 2013;Forthcoming.
data. Obes Rev 2014;15(2):143–57. 83. McDonough SM, Tully MA, Boyd A, et al. Pedometer-
60. Paulis WD, Silva S, Koes BW, et al. Overweight and obesity are driven walking for chronic low back pain: a feasibility randomized
associated with musculoskeletal complaints as early as childhood: controlled trial. Clin J Pain 2013;29(11):972–81.
a systematic review. Obes Rev 2014;15(1):52–67. 84. Coren S. Sleep health and its assessment and management in
61. Seaman DR. Body mass index and musculoskeletal pain: is there physical therapy practice: the evidence. Physiother Theory Pract
a connection? Chiropr Man Therap 2013;21(1):15. 2009;25(5–6):442–52.
62. Bierma-Zeinstra SM, Koes BW. Risk factors and prognostic 85. Ohayon MM, Carskadon MA, Guilleminault C, et al. Meta-
factors of hip and knee osteoarthritis. Nat Clin Pract Rheumatol analysis of quantitative sleep parameters from childhood to old
2007;3(2):78–85. age in healthy individuals: developing normative sleep values
63. Woolner J, Dean E. Status of weight reduction as an inter- across the human lifespan. Sleep 2004;27(7):1255–73.
vention in physical therapy management of low back pain: 86. Shift work & sleep [Internet]. Arlington, VA: National Sleep
systematic review and implications. Eur J Physiother 2013;15(2): Foundation; 2013 Available from: <http://www.sleepfoundation
46–55. .org/article/sleep-topics/shift-work-and-sleep>; [cited 2014 Feb
64. Kandil A, Novicoff W, Browne J. Obesity and total joint arthro- 12.].
plasty: do patients lose weight following surgery? Phys Sportsmed 87. Morin CM, Benca R. Chronic insomnia. Lancet 2012;379(9821):
2013;41(2):34–7. 1129–41.
 11  Lifestyle and Musculoskeletal Health 125

88. van de Water AT, Eadie J, Hurley DA. Investigation of sleep 100. Maas JB, FeldmanHall O, Boyles K. Power sleep and peak per-
disturbance in chronic low back pain: an age- and gender-matched formance [Internet]. Health and Fitness; March 2003 Available
case-control study over a 7-night period. Man Ther 2011;16(6): from: <http://www.usfsa.org/Content/parentsarticles/Health%20
550–6. Fitness_March03.pdf>; [cited 2014 Feb 12.].
89. O’Donoghue GM, Fox N, Heneghan C, et al. Objective and sub- 101. Interventions to improve cardiovascular risk factors in people
jective assessment of sleep in chronic low back pain patients com- with serious mental illness – executive summary | AHRQ Effec-
pared with healthy age and gender matched controls: a pilot study. tive Health Care Program [Internet]. Rockville, MD: Agency for
BMC Musculoskelet Disord 2009;10:122. Healthcare Research and Quality; 2013 Apr 22 Available
90. Neckelmann D, Mykletun A, Dahl AA. Chronic insomnia as a risk from: <http://effectivehealthcare.ahrq.gov/index.cfm/search-for
factor for developing anxiety and depression. Sleep 2007;30(7): -guides-reviews-and-reports/?productid=1464&pageaction=displ
873–80. ayproduct>; [cited 2014 Feb 12.].
91. Haack M, Scott-Sutherland J, Santangelo G, et al. Pain sensitivity 102. Lloyd C, Waghorn G, McHugh C. Musculoskeletal disorders and
and modulation in primary insomnia. Eur J Pain 2012;16(4): comorbid depression: implications for practice. Aust Occup Ther
522–33. J 2008;55(1):23–9.
92. Kundermann B, Krieg JC, Schreiber W, et al. The effect of sleep 103. Marazziti D, Castrogiovanni P, Rossi A, et al. Pain threshold is
deprivation on pain. Pain Res Manag 2004;9(1):25–32. reduced in depression. Int J Neuropsychopharmacol 1998;1(1):
93. Schuh-Hofer S, Wodarski R, Pfau DB, et al. One night of total 45–8.
sleep deprivation promotes a state of generalized hyperalgesia: a 104. Centers for Disease Control and Prevention. Prevalence of dis-
surrogate pain model to study the relationship of insomnia and abilities and associated health conditions among adults – United
pain. Pain 2013;154(9):1613–21. States, 1999. JAMA 2001;285(12):1571–2.
94. Tang NK, Wright KJ, Salkovskis PM. Prevalence and correlates 105. Galletly CA, Foley DL, Waterreus A, et al. Cardiometabolic risk
of clinical insomnia co-occurring with chronic back pain. J Sleep factors in people with psychotic disorders: the second Australian
Res 2007;16(1):85–95. national survey of psychosis. Aust N Z J Psychiatry 2012;46(8):
95. Ackermann K, Revell VL, Lao O, et al. Diurnal rhythms in blood 753–61.
cell populations and the effect of acute sleep deprivation in healthy 106. Krishnan KRR, France RD, Pelton S, et al. Chronic pain and
young men. Sleep 2012;35(7):933–40. depression. II: symptoms of anxiety in chronic low back pain
96. Thamaraiselvi K, Mathangi DC, Subhashini AS. Effect of increase patients and their relationship to subtypes of depression. Pain
in duration of REM sleep deprivation on lipid peroxidation. Int J 1985;22(3):289–94.
Biol Med Res 2012;3(2):1754–9. 107. Melloh M, Elfering A, Käser A, et al. Depression impacts the
97. Simpson N, Dinges DF. Sleep and inflammation. Nutr Rev course of recovery in patients with acute low-back pain. Behav
2007;65(12 Pt 2):S244–52. Med 2013;39(3):80–9.
98. Coren S. Sleep Thieves. New York, NY: Free Press; 1996. 108. Eriksson S, Gard G. Physical exercise and depression. Phys Ther
99. Maas JB. Power Sleep. New York, NY: Harper Collins Publishers Rev 2011;16(4):261–8.
Inc.; 1999.
 CHAPTER 12 

Ageing and the

Musculoskeletal System
Christopher McCarthy  •  Aubrey Monie  •  Kevin Singer

This chapter is divided into two sections. Section one oxidative stress fits well with one of the long-standing
describes some of the physiological mechanisms of theories of ageing that suggests that free radicals could
ageing, to introduce the reader to the changes we face be mediators of ageing.5
when dealing with the ageing musculoskeletal system.
The second section details the more specific changes
ageing brings to the axial spine.
Ageing Joints
Oxidative damage from the chronic production of endog-
enous reactive oxygen species and free radicals has been
AGEING OF THE MUSCULOSKELETAL associated with ageing in various human tissues and has
SYSTEM long been thought to play a central role in the ageing
process.5 Increased production of reactive oxygen species
Ageing is the declining ability to respond to stress and leads to oxidative stress, a condition within cells where
by virtue of the increasing homoeostatic imbalance and the amount of reactive oxygen species exceeds the anti-
incidence of pathology, death remains the ultimate con- oxidant capacity of the cell. Human articular chondro-
sequence of ageing.1 There are a number of theories cytes can actively produce reactive oxygen species and
regarding ageing, with a quick reference list displayed in have been found to increase directly with age.5,6
Table 12-1. For a more detailed overview of this area Some of the changes observed in ageing joints and
please consider the excellent review by Weinert and their contribution to the development of osteoarthritis
Timiras published in 2003.2 are detailed in Table 12-2.
Numerous hypotheses regarding the diminishing
function of cells with time exist. Mechanisms that have
been proposed to be life- and/or function-limiting for
Ageing Muscles
cells include cumulative oxidative damage to proteins, In both young and aged skeletal muscle, it has been
accumulation of mutations and genomic instability, gly- shown that oxidative stress increases in response to
cation of proteins and telomere (the protective region unloading (lack of activity/immobilization) and may have
of the chromosome) dysfunction.1 Ageing of tissues is an important role in mediating muscle atrophy.8 Decline
accompanied by increases in genome rearrangements and of muscle mass is primarily due to type II fibre atrophy
mutations, which may cause cell senescence and/or apop- and loss of muscle fibre numbers. Increased variability in
tosis (programmed cell death). Cell senescence refers to fibre size, accumulation of scattered and angulated fibres
the temporal decrements in the ability of cells to repli- and expansion of extracellular matrix are characteristic to
cate, repair and maintain tissue, and is induced by both muscle atrophy.8,9 The rate of muscle loss has been esti-
cell-intrinsic and cell-extrinsic mechanisms.1 mated to range from 1–2% per year past the age of 50,
The cellular senescence theory of ageing (1965) 25% in persons under the age of 70 and 40% of those
describes a process where there is a limit to the number older than 80 years are sarcopenic.10 Significant loss of
of cell divisions normal human cells can undergo in myofibrils results in an increased negative nitrogen
culture. This ‘limit in replicative capacity’ occurs after a balance which exacerbates reductions in strength and
characteristic number of cell divisions and results in ter- endurance.11
minally arrested cells with altered physiology.2 Classical With advancing age, muscles display ‘hybrid’ muscle
descriptions of cell senescence most often refer to the loss fibre characteristics. Ageing muscle demonstrates selec-
of the ability of mitotic cells to further divide in culture tive loss of fast motoneurons, leading to ‘orphan’ fast
after a period of 30–40 population doublings. However, twitch muscle fibres that are adopted by the relatively
cell senescence appears to be much more complex than more abundant slow motor units. These fibres partially
simple cell-cycle arrest occurring after a finite number of convert to slow twitch fibres, ending with a hybrid phe-
cell divisions. More recently, attention has been drawn to notype showing the characteristics of both fast and slow
other forms of cell senescence sometimes referred to as fibres.11 When, fast type II muscle fibres are incorporated
‘extrinsic’ or ‘stress-induced’ senescence as opposed to into slow motor units (and eventually turned into a hybrid
the intrinsic senescence resulting from replication.3,4 fibre), there are irregularities in the size distribution of
Stress-induced senescence can occur from diverse stimuli motor units. This, in turn, affects motor accuracy, espe-
including oxidative damage, activated oncogenes and cially with low force movements, as the recruitment
chronic inflammation.4 Stress-induced senescence due to order does not adjust well to the previously small motor
126
 12  Ageing and the Musculoskeletal System 127

TABLE 12-1  Theories of Ageing

Biological Level/Theory Description
Evolutionary
Mutation accumulation Mutations that affect health at older ages are not selected against
Disposable soma Somatic cells are maintained only to ensure continued reproductive success; after
reproduction, soma becomes disposable
Antagonistic pleiotropy Genes beneficial at younger age become deleterious at older ages

Molecular
Gene regulation Ageing is caused by changes in the expression of genes regulating both development and
ageing
Codon restriction Fidelity/accuracy of mRNA translation is impaired due to inability to decode codons in mRNA
Error catastrophe Decline in fidelity of gene expression with ageing results in increased fraction of abnormal
proteins
Somatic mutation Molecular damage accumulates, primarily to DNA/genetic material
Dysdifferentiation Gradual accumulation of random molecular damage impairs regulation of gene expression

Cellular
Cellular senescence- Phenotypes of ageing are caused by an increase in frequency of senescent cells. Senescence
Telomere theory may result from telomere loss (replicative senescence) or cell stress (cellular senescence)
Free radical Oxidative metabolism produces highly reactive free radicals that subsequently damage lipids,
protein and DNA
Wear-and-tear Accumulation of normal injury
Apoptosis Programmed cell death from genetic events or genome crisis

System
Neuroendocrine Alterations in neuroendocrine control of homoeostasis results in ageing-related physiological
changes
Immunologic Decline of immune function with ageing results in decreased incidence of infectious diseases
but increased incidence of autoimmunity
Rate-of-living Assumes a fixed amount of metabolic potential for every living organism (live fast, die young)

From the review by Weinert and Timiras 2003.2

TABLE 12-2  Ageing and Its Contribution to Osteoarthritis

Ageing Change Contribution to Osteoarthritis
Accumulation of cells exhibiting the senescent secretory Increased cytokine and MMP production stimulates matrix
phenotype degradation
Oxidative stress/damage Increased susceptibility to cell death and reduced matrix
synthesis
Decreased levels of growth factors and decreased growth Reduced matrix synthesis and repair
factor responsiveness
Increased AGE formation Brittle tissue with increased fatigue failure
Reduced aggrecan size and cartilage hydration and Reduced resiliency and tensile strength
increased collagen cleavage
Increased matrix calcification Altered mechanical properties and potential activation of
inflammatory signalling

MMP, Matrix metalloproteinases; AGE, Advanced glycation end-products.

From Shane and Loeser (2010).7

units having grown bigger and stronger, and is one of the proprioceptive) fibres in peripheral nerves.11 In addition
main reasons that motor and locomotor skills deteriorate to reductions in the number of fast myelinated fibres,
with age.12 within the nerve the speed of signal conduction within
the axon also reduces with age.13 Neuromuscular junc-
tions have been shown to demonstrate age-related reduc-
Ageing Nervous System tions in size and speed of conduction, thereby reducing
In the central nervous system there are age-related reduc- the efficiency of efferent transmission to the muscles.10
tions in the total number of brain cells and fibres and the These widespread physiological changes have been shown
organization of fibres within the brain’s white matter in to result in poorer performance on cognitive and motor
addition to the reduction to the large diameter (A-beta tests.14,15
128 PART II  Advances in Theory and Practice

Ageing, Falling and Pain absence of large-scale, long time-lapse epidemiological

surveys to discern patterns and to test predictions. Post-
Rates of falls among community-living, generally healthy mortem surveys and large radiological population-based
elderly people (age ≥65) are of the order of (0.3–1.6 studies21,22,23 agree that spinal degenerative and age
per person annually), with about 5% of these resulting changes have an extremely high prevalence in adult
in a fracture or hospitalization. Fall rates rise steadily populations. Of late, subtle differences in disc degen-
with age and are about doubled for persons aged >75 eration patterns are being realized as genomic sequenc-
years. Persons living in long-term care institutions have ing emerges as an investigatory tool.24 In the current
much higher fall rates (0.6–3.6 annually). Falls among era of Western society, osteoporosis is acutely studied
those in institutions also tend to result in more serious given the cost and morbidity associated with the de-
complications; with 10–25% of such falls resulting in clining bone mineral health of the axial skeleton and
fracture or laceration. It is often reported that older its attendant fracture risk. This trend is not surprising,
adults experience greater prevalence of pain, greater as over the last 100 years developed societies have
pain intensity and pain at more sites than younger evolved from physically demanding occupations to be-
adults.15,16 coming increasingly urbanized and inactive. The call
It has long been thought that the increase in the preva- to add physical activity to counter the epidemic of
lence of pain among older adults is partly due to the poor lifestyle choices (i.e. inactivity, smoking, poor
progressive musculoskeletal degeneration that accompa- nutrition) has become urgent given the projected cost
nies ageing. Another explanation for increased pain in and negative health outcomes for society.25
older populations has been that ageing is associated with Our biology uses both ageing and degeneration strate-
greater sensitivity to painful stimuli that results from gies to constrain the musculoskeletal system against
changes in the structure and function of the nociceptive further injury or damage. In the case of the spine, which
system.17 serves the principal objectives of mobility, stability and
protection of neural elements, overload or dynamic
Ageing and the Beneficial loading strains can induce a spectrum of either local or
regional trauma and degenerative changes. Consequently,
Effects of Movement this chapter draws upon literature that represents both
It is thought that mechanical forces are important regula- age-related and degeneration models, and their outcomes
tors of several biological functions, with mechanical for the axial skeleton.
signals having been shown to mediate the development Normal physiological strains are well accommodated
of a variety of tissues (e.g. skeletal muscle, bone, carti- by each functional mobile segment, which comprises an
lage).18,19 Mechanical signals can affect diverse cellular intervertebral disc (IVD) with an anulus fibrosus and
processes including cell growth, differentiation, cellular nucleus pulposus, and the vertebral end-plates (VEP).
migration, gene expression, protein synthesis and apop- Paired synovial zygapophysial joints link both vertebrae
tosis.18,19 Given the potential importance that mechanical posteriorly and articulate closely to regulate both load
signalling functions have in maintaining cellular homoeo- and movement of the segment. Applied moments from
stasis, it is likely that changes in mechanotransduction muscle actions and axial compressive loads may be
may also play a role in the pathophysiology of disease.19 coupled with shear, bending (rotations) and torsion about
Recent data strongly support this, as it is recognized that the long axis of the spine, which are in turn moderated
many aspects of sarcopenia may be related to alteration by the unique geometry of the segment’s zygapophysial
in cellular mechanotransduction.19 The ability of cells and ligamentous anatomy (Fig. 12-1). Inertial strains
involved in the musculoskeletal system to sense, process from dynamic loading, even several times body weight,
and respond to mechanical stimuli deteriorates with age may also be tolerated by the spine given its unique capac-
and that these changes may be involved in the aetiology ity to attenuate energy.26 The regional response to
of ageing-associated disease.20 Encouragingly, movement loading is reflected in different patterns of injury or
quantity, quality, locality and intensity are relatively mod- degeneration.
ifiable influences and are certainly influences within the Vertebral bone adapts to loading by the cyclic remod-
scope of the manual therapists. The influence of mecha- elling which is optimal by the third decade of life and
notransduction on tissue health and the symptoms of declines variously thereafter.27 Loss of trabecular con-
ageing are exciting areas for future research, particularly nectivity, endocortical bone trabeculation and intra-
for those of us involved in the provision and prescription cortical porosity are the late stages of remodelling. VEP
of therapeutic movement. collapse occurs due to trabecular bone fragility, with ver-
tebral body fracture the clinical end-point in some cases.
IVD degeneration is considered a normal process of
THE AGEING SPINE ageing, but may be precipitated by multiple factors
including genetic, anatomical, mechanical (occupational,
Most individuals achieve old age with some evidence overload, torsion, vibration), cell-mediated molecular
of degenerative or pathological changes in spinal joints, cascades, trauma, infection and toxins as major influences
which reflect the interactions between: genetics, oc­ to disc health28–30 (Fig. 12-2).
cupation, lifestyle, nutrition, trauma and destiny. Most Osteoarthritis of the spine develops as a consequence
published reviews on the health of the spine are seen of the natural ageing process coupled with attrition, and
through the prism of clinical perspectives, with an is associated with a degenerative cascade that may involve
 12  Ageing and the Musculoskeletal System 129

#, OA VEPs34 or through vessels that communicate directly

AOJ
with the outer annular layers. Consequently, disruption
T to either system occurring through normal ageing, surgi-
DD cal intervention, spinal deformity or trauma can disrupt
and lengthen the pathways of nutritional support to the
#, OA disc and is presumed to contribute to subsequent disc
CTJ
Torsion degeneration. The consequence of either ageing or injury
to the functional mobile segment may be degeneration
# DD of its elements with initial progressive increase in strain
tolerance beyond the normal, which may progress to
increased segmental mobility. One mechanical response
L to such changes, particularly affecting the stability and
TLJ #, OA function of the IVD, is spondylosis, initiated through
osteogenic stimulation in the junctional region between
the VEP periphery and the annulus, resulting in the
Shear DD early formation of osteophytes.35 Experimentally induced
osteoarthrosis of the paired zygapophysial joints has been
associated with anular rim lesions of the IVD.36 The
Rotation posterior paired costotransverse and costovertebral zyg-
#, OA
LSJ apophysial joints are true synovial joints invested with
hyaline articular cartilage, a capsule and synovium. These
joints contribute stability of the respective segment(s)
and facilitate respiratory excursions of the thorax and
regional mobility within the vertebral column, respec-
tively. Each may respond to overload with degenerative
FIGURE 12-1  ■  The regional patterns of injury and degeneration
in the spine. AOJ, Atlanto-occipital joint; CTJ, Cervicothoracic
patterns of synovial joints characterized by mechanical
joint; DD, Disc degeneration/Disc disease?; L, Lumbar; LSJ, changes of the articular cartilage. Subchondral bone scle-
Lumbosacral joint; OA, Osteoarthritis; T, Thoracic; TLJ, Thoraco­ rosis, fissuring and detachment of the cartilage, and mar-
lumbar joint;. #, these sites along the column are disposed to ginal joint osteophytosis may follow changes in the IVD,
trauma and fracture. particularly a loss of vertical height which in turn alters
the mechanical alignment of the respective superior and

anical • Struc
inferior articular processes of the posterior joints. Bumper
h fibrocartilage formations at the joint margin are associ-
ec tu ated with evidence of articular cartilage degeneration and
M che
mical N
fissuring, ossification of the ligamentum flavum, and
reactive hyperplasia at the posterior joint margins. A
o ut
ra

Bi
s•

further consequence of degenerative changes leading to

l•

altered morphology of the IVD and vertebral bodies is

rit

em
Gene

och istry the response by the spinal ligaments. With progressive

Bi
ion

Age
Toxins

deformation of the segment, ligaments may demonstrate

buckling and, in response to exaggerated segmental
DISC motion strains, subsequent hypertrophic changes may
Immun

disease contribute to stenotic change within the vertebral and

intervertebral canals.37 Ossification within the ligamen-
e

tum flavum may occur as a consequence of degeneration

tiv

of the articular triad, although this tends to predominate

e
c

in the region of the lower thoracic and upper lumbar

e

Ne f
urog c In segments.38
eni Patterns of spinal degeneration and age changes
become evident when merged onto a common model of
the axial skeleton; the mobile cervical and lumbar seg-
FIGURE 12-2  ■  The influences on the intervertebral disc associ- ments, and their respective stiffer transitional junctions
ated with ageing. display different trends. The general pattern is for spinal
motion to decline in all directions with age, and this
the discrete elements or an entire functional mobile feature is illustrated with the combined movement exam-
segment, individually or regionally.31,32 ination assessment for the lumbar spine (Fig. 12-3).
The IVD is essentially aneural apart from the periph- Where segmental mobility is greatest degeneration of the
eral superficial outer third, although with injury to the disc and facet joints dominate. In the case of the bony
disc, vascular ingrowth associated with repair may con- thorax, focal changes are seen at the respective costo­
tribute vasomotor nerves.33 The disc is also avascular, vertebral joint articulations of the first and last ribs, a
apart from the peripheral annulus, with a reliance upon consequence of transferring large torques from the mus-
nutritional substances transported via diffusion across the culature of the neck and trunk, respectively. When one
130 PART II  Advances in Theory and Practice

Flexion Flexion
50 50

FwLSF 40 FwRSF FwLSF 40 FwRSF

30 30

20 20

10 20s 10
30s
LSF 0 RSF 40s LSF 0 RSF
50s
60s

EwLSF EwRSF EwLSF EwRSF

A Extension B Extension
FIGURE 12-3  ■  The decline in range of motion in all planes, observed when using the combined movement examination of the lumbar
spine. F, flexion; FwRSF, flexion with right side flexion; RSF, right side flexion; EwRSF, extension with right side flexion; E, extension;
EwLSF, extension with left side flexion; LSF, left side flexion; FwLSF, flexion with left side flexion; For colour version see Plate 11.

considers the complete vertebral column as a multiseg- highest prevalence of disc degeneration is in the mid-
mented curved rod, with physiological inflexions that cervical, mid-thoracic and mid-lumbar discs as these
cross the neutral axis line, the literature presents evidence regions show a marked degree of reactive changes of the
of different responses to stress accumulations at points of vertebral bodies with marginal osteophyte formation
both maximum and minimum change in curve. The seg- (Fig. 12-4). Early post-mortem studies by von Lushka45
ments adjacent to the transitional junctions, having less demonstrated a large proportion of cervical discs with
relative motion, are designed more for stability and rep- fissures and clefts. This was considered to be a normal
resent locations where axial compressive load is greater, characteristic of the region, with complete transverse
the change in spinal curvature is least and where arthrosis clefts extending across and into the region of the unco-
of these synovial joints is found. In contrast, where the vertebral joints found in the middle of healthy cervical
curvature away from the neutral axis line is maximum, as discs on coronal section.46 From similar post-mortem
in the middle region of the lordosis and kyphosis, respec- reviews of the thoracic spine, the most severely affected
tively, and where bending, torsion and shear stresses are discs are located predominantly within the middle seg-
relatively higher, the trend is for greater disc degenera- ments, peaking between T6–T7, with a greater incidence
tion (see Fig. 12-1). in males.47 Given the tendency to axial plane segmental
The major degenerative conditions reviewed in this motion in the mid-thoracic spine, reported in the classic
chapter include osteoporosis and anomalies of spinal cur- paper by Gregersen and Lucas,48 such degenerative
vature, and changes that arise secondary to trauma. changes may relate to the large rotation strains imposed
Inflammatory disease of the spine is excluded from this upon these segments. Investigations by Farfan et al.49
discussion; the interested reader is directed to the com- into the effects of torsion on lumbar IVDs concluded that
pilation by Klippel and Dieppe39 for a comprehensive relatively small rotation strains >2° per segment induced
review. Degenerative conditions that principally have a potential injury in the anulus fibrosus. The pattern of
spinal manifestation may involve all elements of the func- age-related decline in anterior disc height in men typifies
tional mobile segment, either singularly as in the case of the disc ageing process associated with senile kyphosis
early IVD degeneration, or across the joint complex, whereby the cumulative effects of axial loading and tor-
exemplified by late zygapophysial joint arthrosis coinci- sional stresses result in degeneration of the anterior
dent with IVD degeneration.40,41 anulus and osteophytosis.21 In females, however, loading
through the anterior aspect of the kyphotic curve is more
likely to produce progressive change of the vertebral
Disc Degeneration
bodies, causing the wedge deformity commonly associ-
Literature describing the incidence of disc degeneration ated with spinal osteoporosis.50 Mechanically, the middle
throughout the vertebral column concentrates predomi- vertebral segments are predisposed to greater axial com-
nantly on the lumbar and cervical regions of the spine.42 pressive and bending moments, due to their position
From post-mortem studies, discs with altered vascularity within the apex of the thoracic kyphosis.51
during the second decade of life show precursor changes
to early degeneration.43 The pathway of age-related Osteophytosis
degeneration change has been described as compromised
nutrition, loss of viable cells, cell senescence, post- Osteophyte formation and its associated IVD degenera-
translational modification of matrix proteins, accumula- tion has been recognized as an attempt to distribute force
tion of degraded matrix molecules, a reduction in pH more uniformly across the VEPs to achieve stress reduc-
levels that may impede cell function and ultimately induce tion on the segment.52 Where thoracolumbar disc degen-
cell death, and finally fatigue failure of the matrix.44 The eration is present, marginal osteophyte formation of the
 12  Ageing and the Musculoskeletal System 131

occurs with gait, acts as a ‘pump’ to assist diffusion of

nutrients within the vascular vertebral body across the
VEP and into/away from the disc. Abrupt or fatigue axial
loading of the spine may cause localized failure of the
VEP resulting in either a frank sharply demarcated ver-
tebral intra-osseous prolapse, often termed a Schmorl’s
node, or marked irregularity of the end-plate. The repair
process for both lesions often results in bony sclerosis
which can significantly impair the normal nutrient
exchange to the IVD by reducing the effectiveness of this
diffusion pathway. Schmorl’s nodes have been reported
to occur during the late teens,55 with lesions as frequent
in the young as in the older individual.21 Cadaveric studies
of lumbar spines have indicated that Schmorl’s nodes
develop at an early age and can exhibit advanced degen-
erative changes.35 Schmorl’s nodes are found most com-
monly in males and are considered to be related to a
genetic disposition, strenuous occupations21 or sports
involving dynamic and violent axial loading as might
occur with a heavy landing in flexion.55 Most authors
agree that the inferior end-plate is more susceptible to
infraction53,56 which implies that the VEP fails under
compression (Fig. 12-5).

Zygapophysial and Costovertebral

Joint Degeneration
There appear to be specific sites within the spine where
preferential degeneration of the synovial joints occur.
The upper and lower segments of the thoracic region
show a tendency for zygapophysial and costovertebral
joint degeneration.57,58,59 Similar trends for osteophytic
FIGURE 12-4  ■  Macroscopic view of the L2–L3 (top) and T10–T11 remodelling of the zygapophysial joints of the lumbo­
(bottom) discs sectioned in the horizontal plane of two elderly sacral junction have been reported.60,61 This may be due
cases to highlight disc herniation and advanced degeneration. to the design of these elements that provide stability and
The T10–T11 section depicts a central disc prolapse deforming
the anterior dural sac. At L2–L3, age-related changes are dem- protection in contrast to the adjacent mobile segments
onstrated in the form of the large right-sided anterolateral which show a correspondingly higher frequency of disc
osteophyte and advanced disintegration of the nucleus. A disease62 (see Fig. 12-1). The development of osteophytes
central fissure is evident through the posterior anulus. and eventual bony fusion of costovertebral and costo-
transverse joints in aged vertebral columns was also noted
by Schmorl and Junghans21 in their extensive survey of
vertebral body is frequently seen.22,35 This pattern of spinal pathology. The cervicothoracic junction and tho-
excess bone formation, commonly referred to as spondy- racolumbar junction represent transitional areas between
losis deformans, is seen in approximately 60% of women mobile and relatively immobile regions of the spine. At
and 80% of men.21 The degree of intervertebral space the cervicothoracic junction, Boyle et al.63,64 found
narrowing and subsequent tilting of the vertebral bodies, evident IVD and VEP changes, along with osteophytic
resulting from disc degeneration, often determines the formation that were more pronounced in the mobile seg-
extent and the type of marginal osteophytes.53 In summary, ments immediately above the transition. The upper tho-
the segments that appear susceptible to osteophytes racic region and thoracic cage acted to impede
are often the most mobile regions with the higher levels intersegmental motion and thus safeguard these levels
of disc degeneration, or where local stress may be from marked degeneration.64 At the thoracolumbar junc-
accumulated. tion, Malmivaara et al.53 demonstrated that particular
pathologies tended to be concentrated at each segment.
The T10–T11 segment was characterized by disc degen-
Vertebral End-Plate Lesions
eration, vertebral body osteophytosis and Schmorl’s
and Schmorl’s Nodes
nodes; the T11–T12 segment tended to show both ante-
The vertebral end-plate is a membrane of tissue compris- rior and posterior degeneration, involving zygapophysial
ing hyaline cartilage and a 0.5-mm-thin trabecular layer and costovertebral joints, while the T12–L1 joint was
at the discovertebral junction.54 Its role is to mediate axial characterized primarily by posterior joint degeneration.
compressive load applied to the IVD and permit transfer A comparison of zygapophysial joint orientation with
of this energy within the subchondral and cancellous degenerative findings suggested that the posterior ele-
bone of the vertebral body. Physiological axial loading, as ments play a significant role in resisting torsional loads.
132 PART II  Advances in Theory and Practice

A C D

FIGURE 12-5  ■  (A) Intravertebral protrusions, or Schmorl’s nodes, are depicted from several views to highlight their location and
extent. They may project cranially and/or caudally through the vertebral end-plate (arrows). End-plate irregularities are typically in
the lower thoracic spine, as represented by the inferior end-plate of T11 (arrow). (B) A depression on the superior end-plate of a
2-mm-thick bone section from T11 with slight sclerosing of the end-plate compared with the regular thin inferior end-plate. (C) A
central Schmorl’s node at T12 in a 100-mm-thick horizontal histological section shows disc material surrounded by sclerotic bony
margins. (D) Multiple Schmorl’s nodes are shown at the thoracolumbar junction, all approximately in the same location and affect-
ing the inferior vertebral end-plate, a characteristic of Scheuermann’s disease. c, Spinal cord; d, Disc; ep, End-plate; pll, Posterior
longitudinal ligament; sn, Schmorl’s nodes. (Adapted from Singer 2000.47)

Asymmetry in the zygapophysial joint orientation tended it may be induced through disordered metabolism and is
to result in degenerative changes occurring mostly on the accelerated following menopause in women.68 A gender
sagittal facing facet,53 an observation originally made by difference in bone fragility emerges due to the dynamic
Farfan et al.49 at the lumbosacral junction. change in relationship between the mechanics of load
transfer and the margins of safety. Males accumulate
more periosteal bone than females, with a corresponding
Degenerative Spinal Curvature Anomalies
increase in vertebral cross-sectional area which confers a
Idiopathic scoliosis involves a lateral curvature of the relatively higher load-bearing capability such that reduc-
spine that is introduced through a disturbance in the tions in bone strength are less dramatic than seen in
longitudinal growth of the spine. It may occur early in women. During ageing, this ratio is disturbed and frac-
the growth of the child and particularly during the early ture risk increases as the stress on bone begins to approxi-
adolescent years.65 Four main curve patterns have been mate its strength. Twenty per cent of postmenopausal
identified: thoracic, lumbar, thoracolumbar and double women have a stress-to-strength ratio imbalance, whereas
major curves. Each of these curvature patterns has its only 2–3% of men are at risk of fracture due to the
own characteristics and predictable end-point.65 It is well greater preservation of bone strength.69 The epidemiol-
accepted that the severity of the scoliosis can continue to ogy of osteoporosis is well known whereby the risk factors
progress through the life span.66,67 Disc degeneration is of age, gender and racial contributors to bone loss and
known to develop due to the often extreme compression corresponding fracture risk increase exponentially with
and ipsilateral tension strains experienced within wedged age. For the thoracic spine, one in four women over the
scoliotic IVDs. A cascade of degenerative changes occur age of 60 years will show at least one vertebral body
in advanced scoliosis due to the attempt to stabilize fracture on radiographic examination, while the inci-
against the increasingly asymmetric mechanical loads dence increases to 100% in women over 80 years of age;70
induced by this deformity (Fig. 12-6). for men, there is a decade offset before osteopenia and
osteoporosis develops.71 The mid-thoracic segments are
the most vulnerable to osteoporotic collapse or progres-
Osteoporosis and Osteoporotic Fracture
sive wedge deformity due to the mechanical disadvantage
Osteoporosis is an endocrine disease characterized by of these segments situated within the apex of the thoracic
decreased bone mass and micro-architectural deteriora- kyphosis.47 The second peak for thoracic osteoporotic
tion of bone, which may lead to bone fragility and sub- fracture is at the thoracolumbar junction where more
sequently to an increased rate of fracture. Although rapid loading of the thoracic spine can induce a hinging
resorption of bone follows the normal process of ageing, of the stiffened thorax on the upper lumbar spine. These
 12  Ageing and the Musculoskeletal System 133

–200 –100 0 100 200

B C

FIGURE 12-6  ■  An elderly macerated spinal column depicting severe kyphoscoliosis and marked osteophytic fusion across several
segments within the region of the thoracolumbar transition, depicted from the (A) posterior and (B) anterior aspect. Note the remark-
able osseous degeneration and remodelling. (C) A surface contour image of a marked scoliosis in an elderly woman, showing the
typical rib hump appearance and asymmetry of the thoracic cage.

more dynamic loads may be sufficient to cause marked the human spine, including those degenerative processes
wedge compression fractures. Degenerative change to that are secondary to metabolic disease, spinal deformity
the IVD is not common in osteoporosis, suggesting or trauma. Ageing of the spine is not merely a chrono-
a sparing of the IVD despite the vertebral body logical process, as remodelling and repair follow such
deformation. insults as trauma, disease, deformity or surgery and
reflects a biological strategy to stabilize against further
Intervertebral Disc Prolapse segment damage from imposed loads.73 While ageing is
an unavoidable certainty, skeletal loading remains a criti-
Clinically, the regions susceptible to prolapse of the cal requirement for optimal function. Loading the mus-
intervertebral disc and the resulting disc degeneration culoskeletal system throughout its dynamic range, over
typically are those with higher levels of mobility within the lifespan, is crucial for sustaining not just musculo­
the mid to lower cervical region and lower lumbar seg- skeletal health but health in general.
ments.42 What is not often appreciated is the high fre-
quency of macroscopic discal prolapse within the thoracic
region47 (see Fig. 12-4) with the T11–T12 level most REFERENCES
commonly involved. This trend may be due to the rela- 1. Carrington JL. Ageing bone and cartilage: cross-cutting issues.
tively greater disc height and volume at this region, Biochem Biophys Res Commun 2005;328(3):700–8.
2. Weinert BT, Timiras PS. Invited review: theories of ageing. J Appl
coupled with localization of torsional forces that can Physiol (1985) 2003;95(4):1706–16.
occur immediately above the level of thoracolumbar 3. DelCarlo M, Loeser RF. Chondrocyte cell death mediated by reac-
junction transition. Markolf72 proposed that the eleventh tive oxygen species-dependent activation of PKC-betaI. Am J
and twelfth thoracic vertebrae represented a site of struc- Physiol Cell Physiol 2006;290(3):C802–11.
tural weakness for stresses in the vertebral column, due 4. Loeser RF. Ageing and osteoarthritis: the role of chondrocyte
senescence and ageing changes in the cartilage matrix. Osteoarthri-
to the reduced constraint of the ribcage and the change tis Cartilage 2009;17(8):971–9.
in zygapophysial joint morphology that facilitated rota- 5. Loeser RF. The effects of ageing on the development of osteo­
tion above the transitional levels and impeded it below. arthritis. HSS J 2012;8(1):18–19.
The implication of disc prolapse is mechanical decom- 6. Loeser RF. Age-related changes in the musculoskeletal system and
the development of osteoarthritis. Clin Geriatr Med 2010;26(3):
pression of the nucleus, fissuring of the annulus and the 371–86.
cascade of changes that follow this injury.44 7. Shane AA, Loeser RF. Why is osteoarthritis an age-related disease?
Best Pract Res Clin Rheumatol 2010;24(1):15–26.
8. Seene T, Kaasik P, Riso EM. Review on ageing, unloading and
Summary reloading: changes in skeletal muscle quantity and quality. Arch
Gerontol Geriatr 2012;54(2):374–80.
The human spine contributes a large proportion of the 9. Seene T, Kaasik P. Role of exercise therapy in prevention of decline
musculoskeletal presentations seen in manual therapy in ageing muscle function: glucocorticoid myopathy and unloading.
practice. This chapter has reviewed the effect of age on J Ageing Res 2012;2012:172492.
134 PART II  Advances in Theory and Practice

10. Kaya RD, Nakazawa M, Hoffman RL, et al. Interrelationship 37. Weinstein P, Ehni G, Wilson C. Clinical features of lumbar spon-
between muscle strength, motor units, and ageing. Exp Gerontol dylosis and stenosis. In: Weinstein PREG, Wilson CB, editors.
2013;48(9):920–5. Lumbar Spondylosis, Diagnosis, Management and Surgical Treat-
11. Jokl P. The biology of ageing muscle: quantitative versus qualitative ment. Chicago: Year Book; 1977.
findings of performance capacity and age. In: Nelson C, Dwyer AP, 38. Maigne JY, Ayral X, Guerin-Surville H. Frequency and size of
editors. The Ageing Musculoskeletal System. Toronto: The Col- ossifications in the caudal attachments of the ligamentum flavum
lamore Press; 1984. p. 49–58. of the thoracic spine. Role of rotatory strains in their development.
12. Hausdorff JM, Levy BR, Wei JY. The power of ageism on physical An anatomic study of 121 spines. Surg Radiol Anat: SRA
function of older persons: reversibility of age-related gait changes. 1992;14(2):119–24. [Epub 1992/01/01].
J Am Geriatr Soc 1999;47(11):1346–9. 39. Klippel JH, Dieppe PA. Rheumatology. London: Mosby; 2008.
13. Mittal KR, Logmani FH. Age-related reduction in 8th cervical 40. Oegema TR Jr, Bradford DS. The inter-relationship of facet joint
ventral nerve root myelinated fiber diameters and numbers in man. osteoarthritis and degenerative disc disease. Br J Rheumatol
J Gerontol 1987;42(1):8–10. 1991;30(Suppl. 1):16–20.
14. Hausdorff JM, Edelberg HK, Cudkowicz ME, et al. The relation- 41. Fujiwara A, Lim TH, An HS, et  al. The effect of disc degen-
ship between gait changes and falls. J Am Geriatr Soc 1997;45(11): eration and facet joint osteoarthritis on the segmental flexibility
1406. of the lumbar spine. Spine 2000;25(23):3036–44. [Epub 2001/
15. Rubenstein LZ. Falls in older people: epidemiology, risk factors and 01/06].
strategies for prevention. Age Ageing 2006;35(Suppl. 2):ii37–41. 42. Kramer J. Intervertebral disk diseases. Causes, Diagnosis, Treat-
16. Rubenstein LZ, Josephson KR. The epidemiology of falls and ment and Prophylaxis. Stuttgart: Georg Thieme Verlag; 1990.
syncope. Clin Geriatr Med 2002;18(2):141–58. 43. Boos N, Weissbach S, Rohrbach H, et al. Classification of age-
17. Cruz-Almeida Y, Black ML, Christou EA, et al. Site-specific dif- related changes in lumbar intervertebral discs: 2002 Volvo Award
ferences in the association between plantar tactile perception and in Basic Science. Spine 2002;27(23):2631–44. [Epub 2002/12/04].
mobility function in older adults. Front Ageing Neurosci 2014;6:68. 44. Buckwalter JA. Ageing and degeneration of the human interverte-
18. Duncan RL, Turner CH. Mechanotransduction and the functional bral disc. Spine 1995;20(11):1307–14. [Epub 1995/06/01].
response of bone to mechanical strain. Calcif Tissue Int 1995;57(5): 45. von Luschka H. Die Halbbgelenke des Menschlichen Körpers.
344–58. Berlin: Druck und Verlag von Georg Reimer; 1858.
19. Shwartz Y, Blitz E, Zelzer E. One load to rule them all: mechanical 46. Tenhave H, Eulderink F. Degenerative changes in the cervical-
control of the musculoskeletal system in development and ageing. spine and their relationship to its mobility. J Pathol 1980;132(2):
Differentiation 2013;86(3):104–11. 133–59.
20. Isermann P, Lammerding J. Nuclear mechanics and mechanotrans- 47. Singer KP. Pathology of the thoracic spine. In: Giles LGF,
duction in health and disease. Curr Biol 2013;23(24):R1113–21. Singer KP, editors. Clinical Anatomy and Management of Thoracic
21. Schmorl G, Junghanns H. The Human Spine in Health and Spine Pain. Oxford: Butterworth Heinemann; 2000. p. 63–82.
Disease. New York Grune and Stratton; 1971. 48. Gregersen GG, Lucas DB. An in vivo study of the axial rotation of
22. Lawrence JS. Rheumatism in Populations. London: William the human thoracolumbar spine. J Bone Joint Surg Am 1967;49(2):
Heinemann Medical Books; 1977. 247–62. [Epub 1967/03/01].
23. Prescher A. Anatomy and pathology of the ageing spine. Eur J 49. Farfan HF, Cossette JW, Robertson GH, et al. The effects of
Radiol 1998;27(3):181–95. torsion on the lumbar intervertebral joints: the role of torsion in
24. Colombier P, Clouet J, Hamel O, et al. The lumbar intervertebral the production of disc degeneration. J Bone Joint Surg 1970;52(3):
disc: from embryonic development to degeneration. Joint Bone 468–97. [Epub 1970/04/01].
Spine 2014;81(2):125–9. [Epub 2013/08/13]. 50. Goh S, Price RI, Leedman PJ, et al. The relative influence of ver-
25. Trost SG, Blair SN, Khan KM. Physical inactivity remains the tebral body and intervertebral disc shape on thoracic kyphosis. Clin
greatest public health problem of the 21st century: evidence, Biomech 1999;14(7):439–48. [Epub 1999/10/16].
improved methods and solutions using the ‘7 investments that 51. Singer K, Edmondston S, Day R, et al. Prediction of thoracic and
work’ as a framework. Br J Sports Med 2014;48(3):169–70. lumbar vertebral body compressive strength – correlations with
26. Adams MA, Bogduk N, Burton K, et al. The Biomechanics of Back bone-mineral density and vertebral region. Bone 1995;17(2):
Pain. Edinburgh: Churchill Livingstone; 2013. 167–74.
27. Tobias JH, Gould V, Brunton L, et al. Physical activity and bone: 52. Nathan H. Osteophytes of the vertebral column – An anatomical
may the force be with you. Front Endocrinol 2014;5:20. [Epub study of their development according to age, race, and sex with
2014/03/14]. considerations as to their etiology and significance. J Bone Joint
28. Battie MC, Videman T, Kaprio J, et al. The twin spine study: Surg 1962;44(2):243–68.
contributions to a changing view of disc degeneration. Spine J 53. Malmivaara A, Videman T, Kuosma E, et al. Facet joint orientation,
2009;9(1):47–59. [Epub 2008/12/30]. facet and costovertebral joint osteoarthrosis, disc degeneration,
29. Gopal D, Ho AL, Shah A, et al. Molecular basis of intervertebral vertebral body osteophytosis, and Schmorl’s nodes in the thoraco-
disc degeneration. Adv Exp Med Biol 2012;760:114–33. [Epub lumbar junctional region of cadaveric spines. Spine 1987;12(5):458–
2013/01/03]. 63. [Epub 1987/06/01].
30. Neidlinger-Wilke C, Galbusera F, Pratsinis H, et al. Mechanical 54. Grignon B, Grignon Y, Mainard D, et al. The structure of the
loading of the intervertebral disc: from the macroscopic to the cel- cartilaginous end-plates in elder people. Surg Radiol Anat
lular level. Eur Spine J 2014;23(Suppl. 3):S333–43. 2000;22(1):13–19. [Epub 2000/06/23].
31. Laplante BL, DePalma MJ. Spine osteoarthritis. PM & R 2012;4 55. Fisk JW, Baigent ML, Hill PD. Scheuermann’s disease. Clinical and
(Suppl. 5):S28–36. [Epub 2012/06/01]. radiological survey of 17 and 18 year olds. Am J Phys Med 1984;
32. Vo N, Niedernhofer LJ, Nasto LA, et al. An overview of underlying 63(1):18–30. [Epub 1984/02/01].
causes and animal models for the study of age-related degenerative 56. Yasuma T, Saito S, Kihara K. Schmorls nodes – correlation of X-ray
disorders of the spine and synovial joints. J Orthop Res 2013;31(6): and histological-findings in postmortem specimens. Acta Pathol
831–7. Jpn 1988;38(6):723–33.
33. Palmgren T, Gronblad M, Virri J, et al. An immunohistochemical 57. Shore LR. On osteo-arthritis in the dorsal intervertebral joints – A
study of nerve structures in the anulus fibrosus of human normal study in morbid anatomy. Br J Surg 1935;22(88):833–49.
lumbar intervertebral discs. Spine 1999;24(20):2075–9. 58. Shore LR. Some examples of disease of the vertebral column found
34. Dolan P, Luo J, Pollintine P, et al. Intervertebral disc decompres- in skeletons of ancient Egypt – A contribution to palaeopathology.
sion following endplate damage implications for disc degeneration Br J Surg 1935;24(94):256–62.
depend on spinal level and age. Spine 2013;38(17):1473–81. 59. Nathan H, Robin GC, Weinberg H, et al. Costovertebral joints
35. Vernon-Roberts B, Pirie CJ. Degenerative changes in interverte- anatomical-clinical observations in arthritis. Arthritis Rheum 1964;
bral disks of lumbar spine and their sequelae. Rheumatol Rehabil 7(3):228–40.
1977;16(1):13–21. 60. Cihak R. Variations of lumbosacral joints and their morphogenesis.
36. Osti OL, Vernonroberts B, Moore R, et al. Annular tears and disk Acta Univ Carol [Med] (Praha) 1970;16(1):145–65.
degeneration in the lumbar spine – a postmortem study of 135 61. Resnick D. Degenerative diseases of the vertebral column. Radiol-
disks. J Bone Joint Surg Br 1992;74(5):678–82. ogy 1985;156(1):3–14.
 12  Ageing and the Musculoskeletal System 135

62. Resnick D, Niwayama G. Diffuse idiopathic skeletal hyperostosis 68. Kanis JA. Textbook of Osteoporosis. Oxford: Blackwell Science;
(DISH): ankylosing hyperostosis of Forestier and Rotes-Querol. In: 1996.
Resnick D, editor. Diagnosis of Bone and Joint Disorders. Phila- 69. Seeman E. During ageing, men lose less bone than women because
delphia: Saunders; 1995. p. 1463–508. they gain more periosteal bone, not because they resorb less end-
63. Boyle JJW, Singer KP, Milne N. Pathoanatomy of the interverte- osteal bone. Calcif Tissue Int 2001;69(4):205–8.
bral discs at the cervicothoracic junction. Man Ther 1998;3:72–7. 70. Melton JL. Epidemiology of fractures. In: Melton LRJ, editor.
64. Boyle JWW, Milne N, Singer KP. Clinical anatomy of the cervico- Osteoporosis: Etiology, Diagnosis, and Management. Philadelphia:
thoracic junction. In: Singer LGK, editor. Clinical Anatomy and Lippincott-Raven; 1995. p. 225–47.
Management of Cervical Spine Pain. Oxford: Butterworth Heine- 71. Seeman E. The dilemma of osteoporosis in men. Am J Med
mann; 1998. p. 40–52. 1995;98:S76–88.
65. Weinstein SL. Adolescent idiopathic scoliosis: prevalence and 72. Markolf KL. Deformation of the thoracolumbar intervertebral
natural history. In: Weinstein S, editor. The Pediatric Spine. New joints in response to external loads: a biomechanical study using
York: Raven; 1994. p. 463–78. autopsy material. J Bone Joint Surg Am 1972;54(3):511–33. [Epub
66. Ascani E, Bartolozzi P, Logroscino CA, et al. Natural history of 1972/04/01].
untreated idiopathic scoliosis after skeletal maturity. Spine 73. Kirkaldy-Willis WH, Farfan HF. Instability of the lumbar spine.
1986;11(8):784–9. [Epub 1986/10/01]. Clin Orthop Relat Res 1982;165:110–23. [Epub 1982/05/01].
67. Gillespy T 3rd, Gillespy T Jr, Revak CS. Progressive senile scolio-
sis: seven cases of increasing spinal curves in elderly patients. Skel-
etal Radiol 1985;13(4):280–6. [Epub 1985/01/01].
 S E C TION 2.2

ADVANCES IN
MEASUREMENT METHODS

Physiotherapists have always been diligent in their understanding of the representation of pain in the brain
attempts to quantify methods of assessment, measure­ is discussed and interactions between musculoskeletal
ment and patient outcomes in the area of musculo­ therapies and central pain processing are considered.
skeletal pain, both in the clinical environment as well This technology has advanced the knowledge of central
as in research. In recent times, significant technological nociceptive processes but its use comes with some caveats
advances have been made in many areas, including that will be discussed. Also discussed is investigation of
those that measure central nervous system functioning, the brain’s functioning and interconnections using the
imaging of various musculoskeletal structures, quantify­ technology of transcranial magnetic stimulation (TMS).
ing movement and muscle function, as well as being Electromyography (EMG) has been used for a long
able to effectively measure the effects of physiotherapy time in physiotherapy research, but significant advances
treatment and patient outcomes. This section will bring in the use, acquisition, analysis and interpretation of
together new developments in these areas and their EMG data have been made and these, along with
implications for musculoskeletal physiotherapy practice their clinical implications, are presented in this section.
and future research. However, EMG cannot provide information about the
The state of the art in the measurement of the me­ load on various structures during movement and the
chanics of human movement is presented with a focus use of computational modelling, the only viable pos­
on data provided by optoelectronic stereophotogram­ sibility for estimating the forces inside the human body
metric systems, magnetic and inertial measurement is therefore also presented. The section then moves
units, and force platforms. Imaging techniques are then to the evaluation of the sensory and nociceptive systems
explored. New developments in ultrasound imaging are using quantitative sensory testing. Although physio­
outlined including both real-time ultrasound imaging as therapists have used sensory tests in simple forms for
a safe and relatively inexpensive means of examining many years, the now greater understanding of nocicep­
various structures including muscle, nerves and tendons, tive processing and neuropathic pain demands more
as well as rehabilitative ultrasound imaging used by rigorous assessment techniques like detailed quantitative
physiotherapists for assessment and biofeedback pur­ sensory testing.
poses. New research findings of changes in musculo­ The final chapter in this section, but by far not the
skeletal tissues that both conventional and more advanced least important, will discuss the current state of play
MRI imaging provide are then discussed. Here technol­ regarding patient-centred outcome measures and their
ogy is progressing at a rapid pace and providing in­ importance in being able to determine change in a
formation about tissue morphology that has not been patient’s health status. This forms the basis for important
possible previously. The use of fMRI to gain an increased evaluation of physiotherapy interventions.

136
 CHAPTER 13 

Movement Analysis
Aurelio Cappozzo • Andrea Cereatti • Valentina Camomilla •
Claudia Mazzà • Giuseppe Vannozzi

corresponding joint axis. Consequently, muscle activity

INTRODUCTION about a joint is described through the couple (Fig. 13-1B)
and power supplied by each of those motors.
Quantitative movement analysis, through measurement In summary, the mechanics of a joint during move-
(see also Chapters 15 and 17) and computational model- ment is described using the time histories of three angles,
ling (see Chapter 19), provides information on functions three couples and three powers. If, at a given joint, one
of the locomotor sub-systems and on the overall strategy rotation angle prevails the other two to the extent that
of motor activity. These outcomes contribute to the these are either irrelevant to the analysis or their estimate
understanding of the key factors that affect internal is unreliable, then that joint may be represented with a
loading and thus injury, tissue degeneration or regenera- cylindrical (one degree of freedom) hinge (Fig. 13-1A).
tion, as well as motor control and its adaptation, energy The above-illustrated model neglects the linear dis-
consumption and fatigue. Quantitative subject-specific placements that occur between adjacent bones in some
analysis can be effectively used in prevention, early joints. This is acceptable on the grounds that the ampli-
diagnosis (e.g. monitoring of functional status in the tude of these displacements is too small to be accurately
elderly, specific workers or athletes), intervention (e.g. estimated with the experimental methodologies dealt
prognosis, therapeutic programming, workplace optimi- with herein and illustrated below. This limitation may be
zation, physical training) and for quantifying outcomes. overcome using three-dimensional videofluoroscopy or
Advanced movement analysis technology may be used dynamic magnetic resonance imaging that are cumber-
for the implementation of real-time biofeedback (virtual some techniques and grant relatively small measurement
reality) both in rehabilitation and training (institutional- volumes, allowing the analysis of one joint at a time,
ized or not). normally during movements on the spot.1,2
In this chapter, which aims to provide the reader with While analysing a motor task, relevant events are
a picture of the state of the art in the measurement of the detected and their time of occurrence marked (event
mechanics of human movement, the attention will be markers) on the time axis of the graphs reporting the time
focused on data provided by optoelectronic stereophoto- history of the mechanical variables of interest. This is
grammetric systems, magnetic and inertial measurement done, for instance, to identify cycles or phases within the
units and force platforms. observed task that help data interpretability and compari-
son. Typical examples are events such as initial contact
(or heel strike) and final contact (or toe-off) of each foot
A MECHANICAL MODEL OF THE during walking, which define the gait cycle and the
MUSCULOSKELETAL SYSTEM stance, swing and double-support phases. These events
are detected either using ad hoc sensors (mostly on–off
A thorough understanding of the way in which an indi- pressure sensors or accelerometers mounted under and
vidual moves is typically obtained through a mechanical on the foot, respectively), or they are extracted from the
model of the portion of the musculoskeletal system time histories of estimated mechanical variables.
(MSS) under analysis, which would represent a trade-off
between tractability and accuracy of the end results (Fig.
13-1). Normally, this model is made of links, which rep- MOTION CAPTURE
resent the bony segments, connected through spherical
hinges (three degrees of freedom) located in points The basic information for the analysis of human move-
approximating the joint centres of rotation. An anatomi- ment, in terms of joint mechanics, dwells in the data that
cal set of axes (anatomical frame) is associated to each allow for the reconstruction in-silico (through computer
link (Fig. 13-1A). For each joint, out of the six axes processing) of each bone of interest. These data include
associated with the two bones involved, three axes are bone morphology and position and orientation relative
chosen as joint axes. Normally these axes, which are not to a laboratory-embedded Cartesian set of axes (global
necessarily orthogonal, are the mediolateral axis of the frame), in each sampled instant of time during the execu-
proximal bone and the anteroposterior and longitudinal tion of the analysed motor act. The combination of posi-
axes of the distal bone (Fig. 13-1B). The rotation angles tion and orientation of a set of axes is referred to as pose.
about these axes are used to describe joint kinematics. After having associated a bone-embedded frame to
Each of these rotations is assumed to be controlled by a each bone (Fig. 13-2A), the reconstruction is achieved in
muscle-equivalent rotational motor acting about the the six phases depicted in Fig. 13-2B–G.3
137
138 PART II  Advances in Theory and Practice

substituted with virtual markers. A virtual marker cor-

yp yf responds to a point assumed to be in common between
Chy two adjacent bones (Fig. 13-3B,C): if the pose of one
zp
bony segment is successfully reconstructed, the position
zp
time history of the virtual marker, which belongs to this
Chz Chx segment, can be obtained and used to reconstruct the
yf xp pose of the second body segment as if it were a physical
xf marker.5 The reconstructed positions in the global frame
of the markers and a mathematical estimator are used to
yt construct a local set of axes (or technical frame) and
zf determine its pose relative to the global frame. The tech-
Cky nical frame is not rigidly associated with the bone because
xf
yt reconstructed marker positions are affected by inaccura-
cies due to experimental errors6 and because the markers
zf move with respect to the underlying bone, due to soft
Ckz xt tissue deformation and sliding (soft tissue artefact7,8).
zt Ckx After the data are processed so as to minimize the propa-
gation of the above errors, the technical frame is taken
xt as an estimate of the bone-embedded frame (Fig. 13-3).
Having carried out the above-illustrated procedures,
the pose of the estimated bone-embedded frame, relative
to the global frame, of each bone of interest in each
sampled instant of time is available (Fig. 13-2E).
A B Markers may be located on a body segment without
FIGURE 13-1  ■  Musculoskeletal mechanical model of pelvis and any reference to the anatomy, thus, normally, their local
lower limb. (A) Anatomical frames of femur and tibia. (B) Hip position is not repeatable, both intra- and inter-subjects.
joint axes made of the mediolateral axis of the pelvis (zp), As a consequence, the obtained bone-embedded frame
anteroposterior axis of the femur (xf), and longitudinal axis of might result in an equally not repeatable relationship
the femur (yf); knee joint axes made of the mediolateral axis of
the femur (zf), anteroposterior axis of the tibia (xt), and longitu- with the morphology of the bone. This repeatability
dinal axis of the tibia (yt); the couples of the three muscle- issue calls for the execution of another procedure referred
equivalent motors acting at the hip and at the knee (Chx, Chy, Chz to as anatomical calibration (Fig. 13-2B–D).3,9 The
and Ckx, Cky, Ckz, respectively). digital model of the bone of interest may be defined at
different levels of resolution, which depend on the
number of points used to describe the bone external
The kinematic quantities required to drive the MSS surface. The minimum number of these points is three,
model described above are normally recorded either as imposed by the possibility of constructing the ana-
using optoelectronic stereophotogrammetry (video tomical frame of the bone involved, which is essential
systems) or magnetic and inertial measurement units. for proceeding in the analysis. A larger number of points
may allow a more realistic rendering of the bone in-silico
representation. The bone digital model is hence con-
Stereophotogrammetry structed with reference to a morphology frame that
Optoelectronic stereophotogrammetry is, to date, the depends on the methodology used. Consequently, the
most widely used and accurate solution for measuring pose of that frame in the bone-embedded frame must
skeletal kinematics. It is made of a number of video also be acquired to allow further registration between
cameras, connected to a computer, the fields of view of the two frames (Fig. 13-2B–D). This is done by record-
which intersect defining the measurement volume. This ing the position of selected points (either anatomical
system provides the position (Cartesian coordinates) of landmarks or markers) both in the morphology frame
markers, either emitting or retro-reflecting light, relative and in the bone-embedded frame.
to a global frame. This is done through mathematical A high-resolution digital model of the bone may be
operators that receive the two-dimensional coordinates acquired using medical imaging (e.g. magnetic reso-
of the marker images, measured on the image plane of at nance), but this is rarely possible. An alternative approach
least two cameras at any given instant of time, and param- is the estimate of the model using subject-specific partial
eters that describe the location in space and optical fea- information and population statistical information.
tures of the cameras. These parameters are obtained Subject-specific information may be as minimal as the
through the calibration of the stereophotogrammetric position of palpable anatomical landmarks (e.g. with ref-
system. erence to the femur: greater trochanter, medial and
Three or more non-aligned physical markers (marker lateral epicondyles) determined using stereophotogram-
cluster) are attached to the skin above the bone of inter- metry. To these points, internal anatomical landmarks
est, either directly or through a plaque or a wand,4 com- may be added when non-invasively identifiable. A typical
plying with the technical requirements illustrated in example in this respect is the centre of the femoral head
Figure 13-3. In the intent to minimize the number of that can be assumed to coincide with the centre of rota-
physical markers to be tracked, some of them may be tion of the femur relative to the pelvic bone. As such,
 13  Movement Analysis 139

yf
yf

BF BF

AF zf AF
zf
ym ym xf
xf

MF xm MF xm
zm zm
A B C D

yf

BF BF

zf AF

yg yg xf yg

GF xg GF xg GF xg
zg zg zg
E F G
FIGURE 13-2  ■  In-silico reconstruction of a bone during movement. (A) An arbitrary bone-embedded frame (BF) is defined. Time
invariant parameters are determined during an anatomical calibration procedure. (B) A digital model of the bone is acquired in a
morphology frame (MF). (C) Morphological features and/or anatomical landmarks of the bone are identified and an anatomical frame
of the bone (AF) is constructed using them. (D) A mathematical operator that would allow the placement of the AF relative to the
BF (registration operator) is determined. In each sampled instant of time during movement the following motion capture procedures
are carried out: (E) the pose of the BF in the global frame (GF) is reconstructed during movement using a motion capture technol-
ogy; (F) given the pose of the BF, the pose of the AF is determined using the registration operator and then the latter frame is
associated to the MSS mechanical model depicted in Figure 13-1; (G) the bone digital model given in the AF can eventually be
represented in-silico as observed from the GF using a chosen rendering approach.

this point is identifiable through an ad hoc experiment Whatever the method used to measure the morphol-
during which a hip circumduction is reconstructed using ogy, the position of an adequate number of anatomical
stereophotogrammetry.10 Although with a lower accu- landmarks must be made available to allow the construc-
racy, the position of this anatomical landmark in the tion of a bone anatomical frame (Fig. 13-2C). This must
pelvic anatomical frame can also be determined using be achievable with the maximum possible repeatability,
predictive equations.9 Another and more sophisticated because the value of the variables used to describe joint
way of gathering partial bone morphological information mechanics strongly depends on position and orientation
is through two planar X-rays of the bone. This method of the set of axes used.9 For the same reason relevant,
is made applicable by X-ray imaging technology per- standardized, definitions must be adopted.
formed at a low dose and with an expanded dynamic One of the axes of an anatomical frame is sometimes
range that allows for whole-body scanning.11 determined using a functional approach,12 similar to the
140 PART II  Advances in Theory and Practice

AF AF

TF = BF TF = BF TF = BF

A B C
FIGURE 13-3  ■  Marker set-up. (A) A minimum of three markers is attached to the segment skin in positions where the soft tissue
artefact is minimal, in order that each marker is visible to at least two cameras in any given instant of time, and so as to maximize
the relative distance between markers. A number of markers greater than three may be beneficial to the reduction of experimental
error propagation to the end results. (B) Some time virtual markers are used:4,5,9 the illustrated example refers to the hip joint centre
of rotation determined in the pelvic anatomical frame (AF), using either a functional approach or a prediction model, and associated
to the femur. (C) With reference to upper and lower limbs, due to their morphology, markers are at a short distance from the body
segment longitudinal axis; this means that internal–external rotations of the segment cause small linear displacements of the marker
and, because of this, are prone to large relative errors, which propagate to the orientation about that axis. In the attempt to minimize
this effect, markers are sometime mounted on wands as shown in this figure. BF, Bone-embedded frame; MF, Morphology frame.

one previously described and used for the determination the three-dimensional orientation of the technical frame
of the hip joint centre of rotation. This may be done relative to a global frame is provided. Although, as with
when the bone ends with a joint that has a dominant the skin markers, the MIMU is subject to soft tissue ar-
rotational degree of freedom for which a mean axis of tefacts, the technical frame is usually assumed to coincide
rotation may be defined with sufficient accuracy using with a bone-embedded frame (Fig. 13-2E ). No literature
stereophotogrammetry (normally the flexion–extension is as yet available dealing with the compensation of this
axis). Other examples are the elbow, the knee and the artefact while using MIMUs.
ankle. Given this axis, at least an additional anatomical As opposed to stereophotogrammetry, MIMUs do not
landmark is required to construct the anatomical frame. supply reliable positional information. Thus, the MSS
In order to construct the MSS model, the centres of model is driven only by the orientation of the body seg-
the relevant joints must be identified. Normally, the loca- ments and is unable to displace in space. This means that
tion of these points is determined using their geometrical this motion capture technology is effectively applicable
relationship with respect to the available anatomical land- only for joint kinematics (that is, for relative rotational
marks (e.g. for the knee, the mid-point between the motion) and not for joint kinetics studies. In fact, nor-
lateral and medial femoral epicondyles; for the ankle, the mally the inertial forces due to linear accelerations, nec-
mid-point between the lateral and medial malleoli), or essary for the estimate of kinetic quantities, cannot be
using a functional approach as with the hip joint. determined. However, this is made possible when the
instantaneous position of at least one point of the MSS
Magnetic and Inertial model is known. This is the case, for instance, when that
point is stationary, as when the base of support is fixed.
Measurement Units Regarding the anatomical calibration, a straightfor-
Miniature magnetic and inertial measurement units ward (but rarely sufficiently accurate) solution is to man-
(MIMU), embedding a microprocessor and often endowed ually align the MIMU case, with observationally detected
with wireless communication technology, are an in­ anatomical planes and axes of the underlying bony
creasingly popular alternative to stereophotogrammetry segment, thus aligning technical and anatomical frames.
for three-dimensional human movement analysis.13,14 A An alternative solution for anatomical frame identifica-
MIMU comprises a three-axes linear accelerometer and tion is based on a functional approach.15–17 A subject is
angular rate sensors, and a three-axes magnetometer. The asked to perform a joint movement about an anatomical
physical quantities provided by each sensor are measured axis. The orientation of this axis coincides with the direc-
with respect to the axis of a unit-embedded technical tion of the mean angular velocity vector measured by the
frame generally aligned with the edges of the unit case. MIMU attached to the body segment of interest. A
Through algorithms able to fuse the redundant informa- second axis of the anatomical frame can be defined using
tion available and compensate for sensor noise and drift, the acceleration vector measured by the MIMU during a
 13  Movement Analysis 141

known resting posture (the gravitational acceleration), in mass moments of inertia, are referred to as the segment’s
which the MIMU acts as an inclinometer. The anatomi- inertial parameters) may be estimated using either data
cal frame of the body segment under analysis can also be provided by medical imaging technologies,19 with the
identified using a specifically designed calibration device obvious utilizability limits, or through predictive math-
consisting of a rod carrying two mobile pointers perpen- ematical20 or geometrical models21 that use easy to make
dicular to it.18 The rod carries a MIMU that provides the anthropometric measurements.
orientation relative to the technical frame of the line The reaction resultant load is measured using dyna-
joining the tips of the pointers. Using this device the mometers. These provide six signals: three force and
orientation of lines passing through palpable anatomical three couple components relative to a technical frame
landmarks and, therefore, an anatomical frame can be embedded in the dynamometer. A typical example of
determined (Fig. 13-2D). If a digital model of the bone dynamometer used in human movement analysis is the
involved in the analysis is available, then this may be so-named force-plate, used to measure the resultant reac-
reconstructed in-silico following the same procedure tion load exchanged between feet and floor (Fig. 13-4A).
described for stereophotogrammetry (Fig. 13-2G). When analysing locomotor acts or stationary postures,
An important limitation of MIMUs is that, for a reli- the trajectory of the centre of pressure, defined in Figure
able use of the magnetic sensor outputs, the Earth’s 13-4B, is also used in a stand-alone fashion for motor
magnetic field must be uniform. This occurs rarely due function assessment.
to the common presence of ferromagnetic materials in,
or in the vicinity of, the measurement volume. Thus,
under average indoor conditions, when the measure­ment
volume exceeds a cubic metre, great care must be taken
JOINT MECHANICS
not to put at risk the reliability of the results. Better Joint Kinematics
results can be expected when the measurements are
performed outdoors. After the pose of the anatomical frames of two adjacent
bones has been estimated, in a given instant of time
during movement, the three angles that describe their
MEASURE OF EXTERNAL FORCES relative orientation can be determined. These angles
measure the three rotations that the distal anatomical
External forces represent the interaction of the human frame must undergo to move from an orientation aligned
body, or portion of it, with the planet Earth and, through with that of the proximal anatomical frame to its current
contact, with other bodies. These are the gravitational orientation. By convention,22 these rotations are assumed
forces and the reaction forces, respectively. The former to occur sequentially, first around the mediolateral axis
forces may be represented by a resultant force vector of the proximal bone, then about the anteroposterior
(weight), acting downward along the gravity line and and finally about the longitudinal axis of the distal bone
applied to the centre of gravity, which for all practical (Fig. 13-1B). Given this definition, for most joints,
purposes coincides with the centre of mass, of the body the resulting angles may be termed flexion–extension,
segment or ensemble of body segments under analysis. abduction–adduction and internal–external rotation,
The reaction forces act through a surface of contact and respectively (Fig. 13-5A). Given their definition, these
are distributed over it. Their resultant may be repre- angles strongly depend on the orientation of the axes
sented using a force vector passing through an arbitrarily used. In particular, it is important to be aware of the
chosen point and a couple vector (resultant load). fact that, when one angle prevails in amplitude, even a
The subject-specific mass and position of the centre slight misorientation of the axes involved causes large
of mass of a single body segment (that, together with the relative errors on the smaller angles (this effect is named

Cy Y Y
Y'

Cy
Fy Fy
Fz Cx X X
Fz
Cz Fx
Z Z CoP Fx X'
Z'

A B
FIGURE 13-4  ■  Force-plate. (A) The force-plate embedded system of axes (technical frame, TF: X, Y, Z), the three scalar components
of the reaction resultant force, and the three scalar components of the reaction resultant couple relative to the force-plate TF (i.e.
output of the measuring instrument) are represented. (B) The resultant reaction force and couple components are represented rela-
tive to a force-plate TF (X’, Y’, Z’) the origin of which is located in the centre of pressure (CoP). This is the pierce point on the force-
plate surface of the resultant of the distributed reaction force component orthogonal to the surface. When using this representation
of the reaction resultant load, only the component of the couple along the vertical axis is different from zero.
142 PART II  Advances in Theory and Practice

Medio-lateral axis (zp) Antero-posterior axis (xf) Vertical axis (yf)

40 20 20

10 10
Angle (deg)

20

Ad

Int
Flex

0 0
0

Ext
Ab
–10 –10
Extn

–20 –20 –20

0 50 100 0 50 100 0 50 100
A

1.0 0.5 0.5

Ad

Int
Couple (Nm/kg)

0.5 0 0
Flex

Ext
Ab
0 –0.5 –0.5
Extn

–0.5 –1.0 –1.0

0 50 100 0 50 100 0 50 100
B

1.0 0.5 0.5

Power (W/kg)

0.5
0 0
0

–0.5 –0.5 –0.5

0 50 100 0 50 100 0 50 100
Stance Swing Stance Swing Stance Swing
Time (% of cycle) Time (% of cycle) Time (% of cycle)
C
FIGURE 13-5  ■  Example of joint mechanics quantitative description. The hip mechanics during level walking of a male adult able-
bodied volunteer is taken as a paradigmatic case: (A) kinematics; (B) muscle-equivalent couples (normalized with respect to body
mass); and (C) muscle-equivalent powers (normalized with respect to body mass). Stance and swing phases are indicated. zp:
mediolateral axis of the pelvis; xf and yf: anteroposterior axis and longitudinal axes of the femur, respectively (see Fig. 13-1B). Ab,
Abduction; Ad, Adduction; Extn, Extension; Flex, Flexion; Ext, External; Int, Internal.

cross-talk). As a consequence, results, for instance, rela- acquiring kinematic data through stereophotogrammetry
tive to abduction–adduction and internal–external rota- or MIMUs, must be determined and measured forces and
tion of the knee during walking or running must be couples represented in the latter frame (Fig. 13-5B,C).
taken with great caution. When these circumstances The most critical stages of the above-mentioned esti-
occur, it may be advisable to modify the MSS model mation procedure are, depending on the experimental
and substitute the spherical hinge involved with a cylin- data source, the single or double differentiation or inte-
drical hinge that accounts only for the largest rotation gration of noisy data and, of course, the discrepancy of
(Fig. 13-1A). the MSS model of the locomotor system from reality. In
the latter respect, the accuracy with which the joint
centres are located in the relevant anatomical frames and
Joint Kinetics the assumption that they will not move with respect to
If, in a given instant of time during movement, the pose them have the greatest impact on the end results.24
of the anatomical frame in the global frame of the under-
lying bone and the inertial parameters are known for each
body segment involved in the analysis, and the resultant FUTURE DEVELOPMENTS
reaction loads have been obtained, then the couples and
related powers of the muscle-equivalent motors embed- The potential of quantitative movement analysis in pro-
ded in the MSS model can be estimated.23 The relevant fessional decision-making and intervention practice, as
mathematical procedure is based on Newton’s equations illustrated in the Introduction to this chapter, is fully
of motion applied to the locomotor system MSS model recognized. Nevertheless, several issues currently limit its
(solution of the inverse dynamics problem) and entails full application. Firstly, the experimental and analytical
the estimate of linear and angular velocities and accelera- protocols used in most movement analysis laboratories
tions. Of course, all vector quantities must be represented were introduced some 30 years ago and do not exploit
in the same global frame. This, for instance, means that the full potential of current technologies. They provide
the relative pose of the technical frame of a dynamome- results with precision and accuracy that are insufficient
ter, such as a force-plate, and the global frame used when to answer many of the questions posed by scientists
 13  Movement Analysis 143

and professionals. Nevertheless, these remain virtually anatomical landmark misplacement and its effects on joint kinemat-
the only protocols implemented in marketed software ics. Gait Posture 2005;21(2):226–37.
10. Camomilla V, Cereatti A, Vannozzi G, et al. An optimized protocol
packages. Secondly, presently available computational for hip joint centre determination using the functional method.
models of the neuromusculoskeletal system encounter J Biomech 2006;39(6):1096–106.
difficulties in incorporating the characteristics of a spe- 11. McKenna C, Wade R, Faria R, et al. EOS 2D/3D X-ray imaging
cific subject. Finally, as mentioned in the previous sec- system: a systematic review and economic evaluation. Health
Technol Asses 2012;16(14):1–188.
tions, the metrics to be used when assessing motor 12. Ehrig RM, Taylor WR, Duda GN, et al. A survey of formal
function calls for refinement. methods for determining functional joint axes. J Biomech 2007;
Overcoming the above-mentioned limitations requires 40(10):2150–7.
the creation of new techniques and knowledge through 13. Aminian K. Monitoring human movement with body-fixed sensors
the fusion of contributions from past and ongoing and its clinical application. In: Begg R, Palaniswami M, editors.
Computational Intelligence for Movement Sciences. Hershey, PA:
research, development programmes, as well as fostering Idea Group Pub; 2006. p. 101–38.
novel conceptual approaches. 14. Luinge HJ, Veltink PH. Measuring orientation of human body
segments using miniature gyroscopes and accelerometers. Med Biol
REFERENCES Eng Comput 2005;43(2):273–82.
15. Cutti AG, Ferrari A, Garofalo P, et al. ‘Outwalk’: a protocol for
1. Borotikara BS, Sipprell WH III, Wiblea EE, et al. A methodology
clinical gait analysis based on inertial and magnetic sensors. Med
to accurately quantify patellofemoral cartilage contact kinematics
Biol Eng Comput 2010;48(1):17–25.
by combining 3D image shape registration and cine-PC MRI veloc-
16. O’Donovan KJ, Kamnik R, O’Keeffe DT, et al. An inertial and
ity data. J Biomech 2007;45(6):1117–22.
magnetic sensor based technique for joint angle measurement.
2. Zhu Z, Li G. An automatic 2D-3D image matching method for
J Biomech 2007;40(12):2604–11.
reproducing spatial knee joint positions using single or dual fluo-
17. Luinge HJ, Veltink PH, Baten CTM. Ambulatory measurement of
roscopic images. Comput Method Biomec 2012;15(11):1245–56.
arm orientation. J Biomech 2007;40(1):78–85.
3. Cappozzo A, Della Croce U, Leardini A, et al. Human movement
18. Picerno P, Cereatti A, Cappozzo A. Joint kinematics estimate using
analysis using stereophotogrammetry. Part 1: theoretical back-
wearable inertial and magnetic sensing modules. Gait Posture
ground. Gait Posture 2005;21(2):186–96.
2008;28(4):588–95.
4. Davis RB, Ounpuu S, Tyburski D, et al. A gait analysis data
19. Mungiole M, Martin PE. Estimating segment inertial properties:
collection and reduction technique. Human Mov Sci 1991;
comparison of magnetic resonance imaging with existing methods.
10(5):575–87.
J Biomech 1990;23(10):1039–46.
5. Kadaba MP, Ramakrishnan HK, Wootten ME. Measurement of
20. de Leva P. Adjustments to Zatsiorsky-Seluyanov’s segment inertia
lower extremity kinematics during level walking. J Orthop Res
parameters. J Biomech 1996;29(9):1223–30.
1990;8(3):383–92.
21. Yeadon MR. The simulation of aerial movement – ii. a mathemati-
6. Chiari L, Della Croce U, Leardini A, et al. Human movement
cal inertia model of the human body. J Biomech 1990;23(1):
analysis using stereophotogrammetry. Part 2: instrumental errors.
67–74.
Gait Posture 2005;21(2):197–211.
22. Grood ES, Suntay WJ. A joint coordinate system for the clinical
7. Leardini A, Chiari L, Della Croce U, et al. Human movement
description of three-dimensional motions: application to the knee.
analysis using stereophotogrammetry. Part 3. Soft tissue artifact
J Biomech Eng-T ASME 1983;105(2):136–44.
assessment and compensation. Gait Posture 2005;21(2):212–25.
23. Zatsiorsky VM. Kinetics of Human Motion. Champaign, IL:
8. Peters A, Galna B, Sangeux M, et al. Quantification of soft tissue
Human Kinetics; 2002.
artifact in lower limb human motion analysis: a systematic review.
24. Riemer R, Hsiao-Wecksler ET, Zhang X. Uncertainties in inverse
Gait Posture 2010;31(1):1–8.
dynamics solutions: a comprehensive analysis and an application to
9. Della Croce U, Leardini A, Chiari L, et al. Human movement
gait. Gait Posture 2008;27(4):578–88.
analysis using stereophotogrammetry. Part 4: assessment of
 CHAPTER 14 

New Developments in Ultrasound

Imaging in Physiotherapy
Practice and Research
Alan Hough  •  Maria Stokes

INTRODUCTION For details on technical aspects, see Kremkau.5

An extended field of view for imaging large muscles or
Real-time ultrasound imaging (USI) is a safe, portable, length of fibres/tissues can be achieved in various ways.
objective and relatively inexpensive means of examining A wide transducer (large footprint) can be used but these
muscle, nerves, tendons and structures (e.g. the bladder) are not available for all types of scanner. A stand-off pad
in research and clinical settings. The term rehabilitative of gel can be placed between the skin and transducer to
ultrasound imaging (RUSI) was introduced in 2006 to increase the field of view. A recent advance in technology
define use by physiotherapists for assessment and bio- is panoramic ultrasound, which extends the view by
feedback purposes.1 Other uses of USI in physiotherapy, building up a composite scan as the operator moves the
such as tissue motion techniques and imaging nerves, fit transducer over the area of interest.9 This is similar to
logically with and extend the boundaries of RUSI, but the way compound scanners (now obsolete) are used to
they are also used by physiologists and sports scientists enable a cross-sectional area view of large muscles to be
so it would not be appropriate to restrict such uses to the measured (e.g. quadriceps);10 panoramic scanning is now
term RUSI. achieved using much more compact equipment.
Physiotherapists also use diagnostic USI of musculo-
skeletal injuries but this requires different skills and train-
ing.2 This chapter focuses on non-diagnostic USI and the ASSESSMENT OF MUSCLE
reader is directed to other sources for diagnostic USI.3–5
Distinction between the two USI applications is impor- MORPHOMETRY AND MORPHOLOGY
tant, as there are implications for practice, including (ARCHITECTURE)
observing professional boundaries.6 Training pathways
and guidelines for musculoskeletal diagnostic imaging are Morphology is the evaluation of muscle structure (archi-
well established7 and are open to physiotherapists (http:// tecture) and morphometry is the measurement of mor-
www.bmus.org), whereas training for RUSI is in its phological features, such as muscle thickness (depth),
infancy. This chapter gives a brief overview of existing cross-sectional area, volume and fibre length and penna-
uses of RUSI and emerging applications. tion angles. More dynamic imaging involves assessing
changes in these features during contraction and the
impact on associated structures (e.g. the bladder), and
tissue movement and deformation (using high-frame rate
TYPES OF ULTRASOUND IMAGING AND USI and elastography).
TECHNICAL CONSIDERATIONS The most common measure of muscle size is its thick-
ness, as it can be made more rapidly and reliably measured
There are several modes of ultrasound imaging used in than cross-sectional area. The relatively small size of
health care (not all available on each machine), as out- transducers means that whole-muscle cross-section can
lined in Table 14-1. only be imaged in very few muscles (e.g. multifidus).6
When imaging muscle, depending on its depth, fre- Much of the RUSI literature has focused on lumbar
quencies of between 5.0 and 7.5 MHz are often used.6 multifidus11 and the anterolateral abdominal muscles
For peripheral nerves, linear transducers with frequen- (transversus abdominis [TrA], external and internal
cies between 7.5 and 15 MHz or higher are preferable.8 oblique)12 due to their role in stabilizing the lumbar
Resolution is lost with lower frequencies. As a general spine.13 Other muscles include: facial, cervical (semispi-
guide: nalis capitis, deep posterior group), trapezius, rectus
• The deeper the structure, the lower the frequency. abdominis and inter-recti distance, hip flexors (psoas) and
• The more superficial the structure the higher the abductor (gluteus medius and minimus) muscles, pelvic
frequency. floor muscles, quadriceps, posterior and anterior tibial
144
 14  New Developments in Ultrasound Imaging in Physiotherapy Practice and Research 145

TABLE 14-1  Types of Ultrasound Imaging

Mode Description and Application
A-Mode (amplitude mode) Shows amplitude of ultrasound echoes over time. Available on specialized systems used in
ophthalmology
B-Mode (brightness mode) A plane is scanned through the body and presented as a two-dimensional anatomical
greyscale image. Most common mode utilized in rehabilitative and musculoskeletal
ultrasound (Fig. 14-1A; see also Figs 14-2 to 14-4)
M-Mode (motion Mode) Displays depth displacement of tissue (vertical axis) over time (horizontal axis). Typically used
to show motion of cardiac structures, but has been used to indicate abdominal muscle
activity (see Fig. 14-1B)
Colour Doppler Colour-coded velocity information superimposed on a B-mode image. Typically used to
visualize blood velocity and flow characteristics (see Fig. 14-1C)
Pulsed-wave (PW) Doppler Doppler information sampled from a small selected region (sample volume) and displayed
usually as velocity (vertical axis) over time (horizontal axis). Used to quantify blood velocity
and flow characteristics (see Fig. 14-1D)
Tissue Doppler Basic colour or PW Doppler modes with parameters adjusted to measure tissue velocity,
displacement and strain. Typically used in cardiac muscle applications
Power Doppler Colour-coded blood flow intensity information superimposed on a B-mode image. Greater
sensitivity to slow flow that can provide an index of relative tissue perfusion and
neovascularity. Potential applications in rheumatology and tendinopathies
3D and 4D modes Multiple B-mode images can be captured and reconstructed to produce 3D volume images.
Advanced 3D transducers provide a rapid electronic sweep of the ultrasound beam over the
region of interest that allows 3D reconstruction and display in real-time, where it is known as
4D ultrasound. Most extensive applications to date have been in obstetrics, but has wide
potential application

3D, Three-dimensional; 4D, Four-dimensional.

A B

C D

FIGURE 14-1  ■  Types of image display. (A) B-mode scan of anterior thigh showing quadriceps (rectus femoris, RF and vastus inter-
medius, VI) above the femur (F). (B) B-/M-mode scan of lateral abdominal muscles during a contraction, showing thickening of
transversus abdominis (TrA). The upper image is B-mode, whereas the lower timeline trace is M-mode. (C) Colour Doppler and
(D) pulsed-wave (spectral) Doppler of the brachial artery. For colour version see Plate 12.
146 PART II  Advances in Theory and Practice

muscles.6 The effects of ageing10 and exercise pro- observed are not due to measurement error. Different
grammes14 on muscle size can be assessed with USI. types of reliability examined for USI include intra-rater
reliability/repeatability within the same images, on dif-
ferent images taken within the same session and images
Contracted Muscles taken on different days. The latter is the most clinically
Measurement of contracting muscle may be more sensi- relevant scenario, as the complete scanning procedure as
tive for discriminating between health and pathology than well as scan interpretation and measurement technique
resting muscle.15,16 The TrA can be tested during volun- are being tested. Inter-rater reliability has also been
tary activity (e.g. abdominal drawing in manoeuvre) or examined between two or more investigators and between
automatic activity (e.g. active straight leg raise) test.13,14,17 experienced and novice investigators. The wealth of lit-
When TrA contracts and shortens the anterior abdominal erature cannot be covered here, but it indicates that USI
fascia slides/glides in a lateral direction and this move- is reliable for measuring various muscles. Most studies
ment is reduced in patients with low back pain.14 are on the abdominal and lumbar multifidus muscles (see
systematic reviews by Hebert et al.25 and Costa et al.26)
Relationship Between Muscle and studies have begun to include patient groups (e.g.
Koppenhaver et al.27). Reliability of measuring muscle
Size and Strength fascicle length and pennation angle,28 as well as measur-
The size of resting muscle is of potential value for pre- ing nerves has been demonstrated in several studies.29–32
dicting force-generating capacity when strength mea- Despite the lower reliability of thickness change with
surements are either not possible or appropriate due to contraction than resting thickness, the former is a better
pain or instability of structures. However, the relation- indicator of dysfunction (e.g. in back pain33). Lateral glide
ship between size and strength varies between muscles may also be a better indicator of muscle dysfunction than
and cannot be assumed to show high correlation.10,18 resting thickness.14,33
The remainder of the chapter is dedicated to dynamic
Perimuscular Connective USI, specifically biofeedback that is used clinically, and
measurement of motion, currently used primarily in
Tissue Thickness research but with clinical potential.
A study by Whittaker et al.19 has highlighted the impor-
tance of measuring connective tissue as well as muscle
thickness. They found that greater thickness of muscle BIOFEEDBACK OF MUSCLE FUNCTION
boundaries of the anterolateral abdominal muscles, as
well as the inter-recti distance, in patients with lumbo- According to a recent survey, 81% of physiotherapists
pelvic pain compared with healthy controls. These find- using USI use it as a biofeedback tool to aid rehabilita-
ings may reflect altered loading due to wasting of the tion.34 Studies have shown benefit from using USI for
rectus abdominis (RA) muscle. biofeedback, for example the ability to contract multifi-
dus in healthy participants35 improved, learning to con-
Validity of USI Against Other Imaging tract the pelvic floor muscles was achieved within five
minutes of training,36 and USI reduced the number of
Techniques and Electromyography trials needed to perform the abdominal hollowing exer-
The validity of USI for measuring muscle size has been cise in people with37 and without38 low back pain.
tested in various muscles against magnetic resonance However, Teyhen et al.39 did not find the same effect of
imaging, which is considered the gold standard. There is RUSI to enhance the ability of their group of patients
general agreement that USI provides accurate measure- with low back pain to perform the same exercise. Given
ments under static conditions at rest20 and also during the increasing recognition of the importance of motor
contraction.21 However, most studies have been restricted relearning, randomized controlled trials are needed to
to small groups of young, healthy participants and studies determine the role of RUSI as a biofeedback tool in
are needed in older healthy groups and patient popula- rehabilitation. The split-screen facility on a scanner can
tions to confirm validity. be useful for comparing the change in muscle thickness
The correlation between changes in muscle thickness from rest to contraction, as illustrated for multifidus and
during contraction has been studied using force and elec- the lateral abdominals in Figure 14-2.
tromyography. Increases in muscle thickness during con-
traction are not proportional to changes in force above
about 30% of maximal force, as demonstrated by a cur-
MEASURING TISSUE MOTION AND
vilinear relationship for TrA22 and lumbar multifidus23 MECHANICAL PROPERTIES OF
Conversely, McMeeken et al.24 found a linear relation- MUSCLE–TENDON UNIT
ship for TrA, but there were methodological differences
between studies. A great strength of USI is that it provides a non-invasive
means for quantifying tissue motion in vivo.5,40 This
has led to its use in rehabilitation research as a tool
Reliability to estimate the motion of muscles, tendons and nerves
Any assessment tool must be robust enough to produce associated with active and passive movements. By mea-
similar results on different occasions, so that any changes suring tissue displacement and strain it is possible to gain
 14  New Developments in Ultrasound Imaging in Physiotherapy Practice and Research 147

A B

C D

FIGURE 14-2  ■  Split-screen facility used for biofeedback. Sagittal view of lumbar multifidus (M) above the facet (F) joints (A) at rest
and (B) during contraction; note the increase in thickness measured by on-screen cursors (46.6 mm to 54 mm). Transverse view of
the lateral abdominal muscles (C) at rest and (D) during contraction; note the thickening of transversus abdominis (TrA) and internal
oblique (IO) muscles.

insights into the mechanical properties of the tissues in Valid and reliable measurement of muscle architec-
response to loading in both health and disease. tural features such as fascicle length and pennation angles
Movement of structures can be estimated using using B-mode ultrasound (Fig. 14-328) has enabled iden-
B-mode (brightness mode) images taken before and after tification of changes in these features under varying
an active or passive movement. Measurements can be loading conditions and comparison between population
made using electronic callipers on the ultrasound system groups.45–48 Furthermore, by tracking displacement of
or in image measurement software on exported images myofascial anatomical landmarks in combination with
or cine clips. This basic B-mode image analysis approach force measurements, it is possible to estimate mechanical
has proved useful in several research areas, for example properties of the muscle–tendon unit.49,50
measurement of transverse plane motion and deforma- The literature using USI to measure muscle architec-
tion of the median nerve in studies exploring aetiological tural features and mechanical properties is extensive and
factors in carpal tunnel syndrome41,42 and dynamic detailed discussion is beyond the scope of this chapter.
changes in acromio–humeral distance under varying The interested reader is directed to Magnusson et al.51
conditions.43,44 for an excellent discussion of the strengths and
148 PART II  Advances in Theory and Practice

A B

C D

FIGURE 14-3  ■  Sagittal view of triceps surae, illustrating muscle fascicle length (MFL) and pennation angle (PA) (A) at rest and
(B) during isometric contraction. Distal displacement of the musculotendinous junction (MTJ) of gastrocnemius (C) and (D) during
ankle dorsiflexion indicates lengthening of the muscle. GAS, Gastrocnemius muscle; SOL, Soleus muscle.

limitations of the general approach, and to Cronin et al.52 challenging (Fig. 14-4). Several approaches have been
for a review of USI measures of muscle–tendon complex developed to assist in such circumstances, including those
during walking. In addition, Magnusson et al.53 provides based on tissue Doppler principles and B-mode speckle
a thorough overview of how USI and other approaches tracking; as explained below.
have enhanced our understanding of in vivo tendon
function. Tissue Doppler Imaging (TDI)
While Doppler ultrasound modes are primarily used in
M-MODE the measurement of blood flow characteristics,5 it is pos-
sible to modify the technique to detect tissue motion.56
M-mode (motion mode) ultrasound provides an alterna- Studies using TDI-based approaches have been used to
tive to B-mode for tracking tissue motion.5 In M-mode, measure longitudinal motion of tendons and nerves57,58
a single selected scan line is used to display depth changes and for detection of onset of muscle activity.55,59 TDI-
of tissue over time. A potential benefit of M-mode is based approaches are well suited to tracking fast tissue
that several seconds of motion data can be displayed and motion, and good reliability and validity have been
measured from a single image, and for this reason it reported for some applications.59–62 There are potential
has been suggested as an alternative to B-mode for mea- limitations for detecting slow tissue movement63 and
suring abdominal wall muscle activity.54 High-frame rate measures may be open to substantial error, in particular
M-mode could also provide a non-invasive alternative to due to the angle dependence of this approach.57 A major
needle electromyography for detecting the onset of deep limitation to the basic TDI approach is that it assumes
muscle activity.55 A major limitation of this mode is that movement in one dimension only. Specialized ‘vector
it displays one-dimensional movement only (away or Doppler’ systems have been developed that can resolve
towards the ultrasound beam). two-dimensional movement of muscles and tendons64 but
this option is not typically available on ultrasound systems.
MOTION TRACKING USING TISSUE
DOPPLER AND B-MODE B-Mode Speckle Tracking
SPECKLE TRACKING B-mode speckle tracking techniques overcome the one-
dimensional and angle dependence limitations of TDI-
When tracking tissue motion in the absence of distinct based approaches.65 The basic principles of this approach
anatomical landmarks, for example when trying to involve the capture of a B-mode image sequence of the
measure longitudinal motion of peripheral nerves or tissue movement of interest. The image sequence is then
free tendon, relying on visual tracking of movement is analysed using tracking software that typically requires
 14  New Developments in Ultrasound Imaging in Physiotherapy Practice and Research 149

A B

C D

FIGURE 14-4  ■  Typical appearance of peripheral nerves and free tendons in longitudinal section: (A) median nerve; (B) sciatic nerve;
(C) flexor pollicis longus tendon; and (D) Achilles tendon. Note the apparent lack of clear anatomical landmarks that could be visu-
ally tracked during longitudinal movement. Also note the reduced ultrasound resolution of the more deeply placed sciatic nerve
compared to the more superficial median nerve.

the operator to select points or regions of interest within moves out of the ultrasound beam plane,72 although
the first frame of the image sequence. The grey-scale three-dimensional tracking techniques could address this
(‘speckle’) patterns within the selected regions are then problem.77 The success of the technique is also depen-
tracked from frame to frame using a mathematical match- dent on the quality of the image sequence captured,
ing algorithm that finds the best match in subsequent which may be influenced by several factors, including
frames and enables estimation of the displacement of the depth of the structure imaged (see Figs 14-4A and
tissue in two dimensions.40 14-4B). For more detailed discussion of technical aspects
The technique has been developed to allow concur- of B-mode speckle tracking and related approaches for
rent measurement of both longitudinal and superficial/ measuring displacement, the interested reader is directed
deep movement of nerves and tendons.66,67 An extensive to the papers by Korstanje et  al.,67 Loram et  al.72 and
series of studies using this approach on upper and lower Revell et  al.78
limb peripheral nerves have substantially enhanced our Developing a valid B-mode speckle tracking system
knowledge and understanding of in vivo nerve dynamics for measuring local strain is more challenging.79 While
in healthy and patient populations.68–71 The approach has there is evidence supporting the validity of this approach
also been applied to continuously track muscle fascicle in tendons,80 caution is required due to some inherent
movement as a non-invasive method for monitoring neu- limitations.81 Refinements to the standard B-mode
romotor activity in posture and locomotion,72 and to approach have been recommended to better capture local
facilitate studies exploring mechanical properties and strain.79 However, there are a range of existing techniques
behaviour of muscle.73 known as ‘elastography’ that should be well suited to the
Relative motion between adjacent structures can also measurement of local strain and mechanical properties in
be measured (e.g. between the median nerve, flexor neuromusculoskeletal tissues.
tendons and/or subsynovial connective tissue at the carpal
tunnel). Identification of relative movement ratios with
the consequent potential for shear force development ELASTOGRAPHY
may be relevant in the aetiology of entrapment syn-
dromes74 and tendinopathy.75 Differential strain within The basic principle common to all ultrasound-based elas-
layers of the same tendon under loading has also been tography approaches is that ultrasound is used to detect
identified using speckle tracking.76 the tissue response to perturbation that is either gener-
The validity of B-mode speckle tracking for measur- ated externally (e.g. by manual compression) or internally
ing displacement under well-controlled laboratory condi- (e.g. by muscle contraction). Primarily developed for use
tions is typically reported as high.66,67,72 The primary in cardiac and tumour detection applications, musculosk-
threat to validity in vivo is when the tissue of interest eletal elastography applications are emerging.82,83
150 PART II  Advances in Theory and Practice

Perhaps the most familiar elastography approach uses vascularity is another developing area with research and
manual compression of the tissues (via the transducer) as clinical potential, for example in the assessment of
the perturbing source. The deformation of the com- tendinopathies.92
pressed tissues is captured by the ultrasound and is dis- The predominant use of USI in physiotherapy has
played as a colour-coded map of relative tissue stiffness, been for musculoskeletal conditions, but since changes in
where localized areas of greater stiffness (e.g. tumours) the musculoskeletal system can occur in other conditions
can be identified. The estimation of deformation is based (e.g. respiratory and neurological disorders) USI is poten-
on correlation techniques similar to B-mode speckle tially useful. For example, USI of the diaphragm may
tracking but the raw ultrasound data are used, which provide a complimentary technique for assessing respira-
provides higher spatial and temporal resolution. Several tory function,93 the gastrocnemius muscle after stroke94
studies have explored the potential of this approach in and wrist extensors in tetraplegic patients.95 Mechanical
the assessment of tendon health, where identification of properties using USI motion tracking techniques have
regions of relatively reduced stiffness may be indicative been studied in patients with stroke,96 cerebral palsy97 and
of tendinopathy.84 Variations on the basic technique multiple sclerosis.98 The response of muscles to exercise
include using a controlled longitudinal stretching to programmes in patients with neurological conditions
provide a more functional loading source for tendon could be monitored using USI.
applications,85 and controlled electrical stimulation of All uses of USI in physiotherapy need standardized
muscle to standardize force applications.86 imaging protocols, with evidence of validity and reliabil-
An early form of elastography used tissue Doppler to ity, as well as normal reference values for comparison
detect the response to low-frequency vibration (‘sono- with clinical cohorts. The tissue motion techniques, in
elasticity imaging’87). An example of this approach is the particular, require further development to make them
‘Doppler imaging of vibrations’ developed to provide a more accessible, affordable and user friendly. Random-
measure of sacroiliac joint laxity.88,89 Vibration is applied ized controlled trials are needed to provide evidence of
to the ilium anteriorly, and the resultant relative move- the clinical and cost effectiveness of using USI to enhance
ment of the ilium and sacrum posteriorly at the sacroiliac clinical practice, both for aiding assessment and rehabili-
joint is captured by tissue Doppler and used to provide tation through biofeedback. Uses in research to investi-
an index of sacroiliac joint laxity. Studies using Doppler gate mechanisms of dysfunction and recovery also warrant
imaging of vibrations have informed assessment and further exploration.
management of pregnancy-related pelvic girdle pain,90 The ultimate goal is for USI to become a routine tool
and the approach has potential in other musculoskeletal in physiotherapy. For this aim to be achieved, formal
applications, for example in the assessment of myofascial training programmes are needed that are recognized by
trigger points.91 therapists’ national professional bodies and medical dis-
More recently a range of ‘dynamic’ elastography tech- ciplines. Eventually, basic USI training would become
niques using a single ultrasound transducer without the part of the undergraduate curriculum, both as a teaching
need for an external vibration source or manual compres- tool to aid teaching structural and functional anatomy
sion force have been developed.82 These techniques, and as a clinical tool for assessment and biofeedback.
which include supersonic shear wave imaging, are still Postgraduate training for specific clinical applications
considered to be at an evaluative stage83 but they have the and research would be needed. Education programmes
potential to provide a more repeatable and quantifiable will remain a challenge until uptake of USI becomes
measure of tissue mechanical properties.82,83 more widespread, to provide the infrastructure to support
practical training.

FUTURE DIRECTIONS
REFERENCES
The USI applications most readily available for routine 1. Teyhen DS. Rehabilitative Ultrasound Imaging Symposium, May
8–10, 2006, San Antonio, Texas. J Orthop Sports Phys Ther
clinical use and research are visual biofeedback and static 2006;36:A-1–17.
measurements of tissue characteristics from B-mode 2. Chhem RK, Kaplan PA, Dussault RG. Ultrasonography of the
images. These areas were included in the original defini- musculoskeletal system. Radiol Clin North Am 1994;32:275–89.
tion of RUSI in 2006. More recent uses of tissue motion 3. WHO. Training in diagnostic ultrasound: essentials, principles and
techniques require more sophisticated equipment and standards. Report of a WHO Study Group. World Health Organ
Tech Rep Ser 1998;875:i–46, back cover.
software, and are less well developed than the earlier 4. Van Holsbeeck M, Introcaso JH. Musculoskeletal Ultrasound, 2nd
RUSI techniques. The extended field of view provided edn. St Louis, MO, USA: Mosby; 2001. p. 648.
by panoramic ultrasound is a major advance for enabling 5. Kremkau FW. Diagnostic Ultrasound, Principles and Instruments,
the size of large muscles to be viewed and measured, as 7th edn. London: Saunders; 2005. p. 126, 142, 159.
6. Whittaker JL, Teyhen DS, Elliott JM, et al. Rehabilitative ultra-
well as length of tendons and nerves. As use of this spe- sound imaging: understanding the technology and its applications.
cific facility becomes more widespread, it will greatly J Orthop Sports Phys Ther 2007;37:434–49.
enhance research into the clinical utility of ultrasound. 7. Boyce S, Murray A, Jeffrey M. A review of musculoskeletal ultra-
Similarly, three-dimensional ultrasound provides more sound training guidelines and recommendations for sport and exer-
accurate and realistic assessments, particularly during cise medicine physicians. Ultrasound 2013;21:155–8.
8. Thain LMF, Downey DB. Sonography of peripheral nerves: tech-
motion of tissues, as out-of-plane activity is not captured nique, anatomy, and pathology. Ultrasound Q 2002;18:225–45.
by two-dimensional imaging. The use of power Doppler 9. Ryan ED, Rosenberg JG, Scharville MJ, et al. Test-retest reliability
ultrasound (see Table 14-1) to detect changes in tissue and the minimal detectable change for Achilles tendon length: a
 14  New Developments in Ultrasound Imaging in Physiotherapy Practice and Research 151

panoramic ultrasound assessment. Ultrasound Med Biol 2013; 33. Wong AYL, Parent EC, Funabashi M, et al. Do various baseline
39(12):2488–91. characteristics of transversus abdominis and lumbar multifidus
10. Young A, Stokes M, Crowe M. The size and strength of the quad- predict clinical outcomes in nonspecific low back pain? A systematic
riceps muscles of old and young men. Clin Physiol 1985;5: review. Pain 2013;154:2589–602.
145–54. 34. Potter CL, Cairns MC, Stokes MJ. Use of ultrasound imaging by
11. Stokes M, Hides J, Elliott J, et al. Rehabilitative ultrasound imaging physiotherapists: a pilot study to survey use, skills and training. Man
of the posterior paraspinal muscles. J Orthop Sports Phys Ther Ther 2012;17:39–46.
2007;37(10):581–95. 35. Van K, Hides JA, Richardson CA. The use of real-time ultrasound
12. Teyhen DS, Gill NW, Whittaker JL, et al. Rehabilitative ultra- imaging for biofeedback of lumbar multifidus muscle contraction
sound imaging of the abdominal muscles. J Orthop Sports Phys in healthy subjects. J Orthop Sports Phys Ther 2006;36:920–5.
Ther 2007;37(8):450–66. 36. Dietz HP, Wilson PD, Clarke B. The use of perineal ultrasound
13. Hodges PW, Moseley GL. Pain and motor control of the lumbo- to quantify levator activity and teach pelvic floor muscle exercises.
pelvic region: effect and possible mechanisms. J Electromyogr Int Urogynecol J Pelvic Floor Dysfunct 2001;12:166–8, discussion
Kinesiol 2003;13:361–70. 168–9.
14. Hides JA, Stanton WR, Wilson SJ, et al. Retraining motor control 37. Worth S, Henry S, Bunn J. Real-time ultrasound feedback and
of abdominal muscles among elite cricketers with low back pain. abdominal hollowing exercises for people with low back pain. NZ
Scand J Med Sci Sports 2010;20:834–42. J Physiother 2007;35:4–11.
15. Teyhen DS, Bluemle LN, Dolbeer JA, et al. Changes in lateral 38. Henry SM, Westervelt KC. The use of real-time ultrasound feed-
abdominal muscle thickness during the abdominal drawing-in back in teaching abdominal hollowing exercises to healthy subjects.
maneuver in those with lumbopelvic pain. J Orthop Sports Phys J Orthop Sports Phys Ther 2005;35:338–45.
Ther 2009;39(11):791–8. 39. Teyhen DS, Miltenberger CE, Deiters HM, et al. The use of
16. Teyhen DS, Williamson JN, Carlson NH, et al. Ultrasound char- ultrasound imaging of the abdominal drawing-in maneuver in sub-
acteristics of the deep abdominal muscles during the active straight jects with low back pain. J Orthop Sports Phys Ther 2005;35:
leg raise test. Arch Phys Med Rehabil 2009;90:761–7. 346–55.
17. Whittaker JL, Thompson JA, Teyhen DS, et al. Rehabilitative 40. Anderson T, McDicken WN. Measurement of tissue motion. Proc
ultrasound imaging of pelvic floor muscle function. J Orthop Sports Inst Mech Eng [H] 1999;213:181–91.
Phys Ther 2007;37:487–98. 41. Yoshii Y, Ishii T, Tung W-L, et al. Median nerve deformation and
18. Kanehisa H, Ikegawa S, Fukunaga T. Comparison of muscle cross- displacement in the carpal tunnel during finger motion. J Orthop
sectional area and strength between untrained women and men. Res 2013;31:1876–80.
Eur J Appl Physiol Occup Physiol 1994;68:148–54. 42. van Doesburg MHM, Henderson J, Yoshii Y, et al. Median nerve
19. Whittaker JL, Warner MB, Stokes M. Comparison of the sono- deformation in differential finger motions: ultrasonographic com-
graphic features of the abdominal wall muscles and connective parison of carpal tunnel syndrome patients and healthy controls.
tissues in individuals with and without lumbopelvic pain. J Orthop J Orthop Res 2012;30:643–8.
Sports Phys Ther 2013;43:11–19. 43. Seitz AL, McClure PW, Lynch SS, et al. Effects of scapular dyski-
20. Hides JA, Richardson CA, Jull GA. Magnetic resonance imaging nesis and scapular assistance test on subacromial space during static
and ultrasonography of the lumbar multifidus muscle. Comparison arm elevation. J Shoulder Elbow Surg 2012;21:631–40.
of two different modalities. Spine 1995;20:54–8. 44. Luque-Suarez A, Navarro-Ledesma S, Petocz P, et al. Short term
21. Hides J, Wilson S, Stanton W, et al. An MRI investigation into the effects of kinesiotaping on acromiohumeral distance in asymptom-
function of the transversus abdominis muscle during ‘drawing-in’ atic subjects: a randomised controlled trial. Man Ther 2013;18:
of the abdominal wall. Spine 2006;31:E175–8. 573–7.
22. Hodges PW, Pengel LHM, Herbert RD, et al. Measurement of 45. Kubo K, Kanehisa H, Fukunaga T. Gender differences in the vis-
muscle contraction with ultrasound imaging. Muscle Nerve 2003; coelastic properties of tendon structures. Eur J Appl Physiol
27(6):682–92. 2003;88:520–6.
23. Kiesel KB, Uhl TL, Underwood FB, et al. Measurement of lumbar 46. Narici MV, Binzoni T, Hiltbrand E, et al. In vivo human gastro­
multifidus muscle contraction with rehabilitative ultrasound cnemius architecture with changing joint angle at rest and during
imaging. Man Ther 2007;12:161–6. graded isometric contraction. J Physiol 1996;496:287–97.
24. McMeeken JM, Beith ID, Newham DJ, et al. The relationship 47. Narici MV, Maganaris CN, Reeves ND, et al. Effect of aging on
between EMG and change in thickness of transversus abdominis. human muscle architecture. J App Physiol 2003;95:2229–34.
Clin Biomech 2004;19(4):337–42. 48. Burgess KE, Graham-Smith P, Pearson SJ. Effect of acute tensile
25. Hebert JJ, Koppenhaver SL, Parent EC, et al. A systematic review loading on gender-specific tendon structural and mechanical prop-
of the reliability of rehabilitative ultrasound imaging for the quan- erties. J Orthop Res 2009;27:510–16.
titative assessment of the abdominal and lumbar trunk muscles. 49. Fukashiro S, Itoh M, Ichinose Y, et al. Ultrasonography gives
Spine 2009;34:E848–56. directly but noninvasively elastic characteristic of human tendon in
26. Costa LOP, Maher CG, Latimer J, et  al. Reproducibility of vivo. Eur J Appl Physiol Occup Physiol 1995;71:555–7.
rehabilitative ultrasound imaging for the measurement of abdomi- 50. Maganaris CN, Paul JP. In vivo human tendon mechanical proper-
nal muscle activity: a systematic review. Phys Ther 2009;89: ties. J Physiol 1999;521:307–13.
756–69. 51. Magnusson SP, Aagaard P, Dyhre-Poulsen P, et al. Load-
27. Koppenhaver SL, Hebert JJ, Parent EC, et al. Rehabilitative ultra- displacement properties of the human triceps surae aponeurosis in
sound imaging is a valid measure of trunk muscle size and activation vivo. J Physiol 2001;531:277–88.
during most isometric sub-maximal contractions: a systematic 52. Cronin NJ, af Klint R, Grey MJ, et al. Ultrasonography as a tool
review. Aus J Physiotherapy 2009;55:153–69. to study afferent feedback from the muscle-tendon complex during
28. Kwah LK, Pinto RZ, Diong J, et al. Reliability and validity of human walking. J Electromyogr Kinesiol 2011;21:197–207.
ultrasound measurements of muscle fascicle length and pennation 53. Magnusson SP, Narici MV, Maganaris CN, et al. Human tendon
in humans: a systematic review. J App Physiol 2013;114:761–9. behaviour and adaptation, in vivo. J Physiol 2008;586:71–81.
29. Cartwright MS, Demar S, Griffin LP, et  al. Validity and reli- 54. Bunce SM, Hough AD, Moore AP. Measurement of abdominal
ability of nerve and muscle ultrasound. Muscle Nerve 2013;47: muscle thickness using M-mode ultrasound imaging during func-
515–21. tional activities. Man Ther 2004;9:41–4.
30. Impink BG, Gagnon D, Collinger JL, et al. Repeatability of ultra- 55. Vasseljen O, Fladmark AM, Westad C, et al. Onset in abdominal
sonographic median nerve measures. Muscle Nerve 2010;41: muscles recorded simultaneously by ultrasound imaging and intra-
767–73. muscular electromyography. J Electromyogr Kinesiol 2009;19:
31. Tagliafico A, Cadoni A, Fisci E, et al. Reliability of side-to-side e23–31.
ultrasound cross-sectional area measurements of lower extremity 56. Heimdal A. Technical principles of tissue velocity and strain
nerves in healthy subjects. Muscle Nerve 2012;46:717–22. imaging methods. In: Marwick TH, Yu C-M, Sun JP, editors.
32. Tagliafico A, Martinoli C. Reliability of side-to-side sonographic Myocardial Imaging: Tissue Doppler and Speckle Tracking.
cross-sectional area measurements of upper extremity nerves in Oxford, UK: Blackwell Scientific Publications: Oxford; 2007.
healthy volunteers. J Ultrasound Med 2013;32:457–62. p. 3–16.
152 PART II  Advances in Theory and Practice

57. Hough AD, Moore AP, Jones MP. Reduced longitudinal excursion respiratory motion using 4D ultrasound. Phys Med Biol 2010;55:
of the median nerve in carpal tunnel syndrome. Arch Phys Med 3363–80.
Rehabil 2007;88:569–76. 78. Revell JD, Mirmehdi M, McNally DS. Musculoskeletal motion
58. Soeters JNM, Roebroeck ME, Holland WP, et al. Reliability of flow fields using hierarchical variable-sized block matching in ultra-
tendon excursion measurements in patients using a color Doppler sonographic video sequences. J Biomech 2004;37:511–22.
imaging system. J Hand Surg [Am] 2004;29:581–6. 79. Revell JD, Mirmehdi M, McNally D. Computer vision elastogra-
59. Pulkovski N, Schenk P, Maffiuletti NA, et al. Tissue Doppler phy: speckle adaptive motion estimation for elastography using
imaging for detecting onset of muscle activity. Muscle Nerve ultrasound sequences. IEEE Trans Med Imaging 2005;24:
2008;37:638–49. 755–66.
60. Holland WP, Buyruk HM, Hoorn E, et al. Tendon displacement 80. Brown PG, Alsousou J, Thompson M, et al. Ultrasound strain
assessment by pulsed Doppler tissue imaging: validation with a imaging measurement in Achilles tendons as a measure of healing
reciprocating string test target. Ultrasound Med Biol 1999;25: from rupture with controlled ankle motion. J Biomech 2012;45:S402.
1229–39. 81. Slagmolen P, Scheys L, D’Hooge J, et al. Letter: In regard to: ‘In
61. Hough AD, Moore AP, Jones MP. Peripheral nerve motion mea- vivo strain analysis of the intact supraspinatus tendon by ultrasound
surement with spectral Doppler sonography: a reliability study. speckles tracking imaging’ ( J Orthop Res 2011;29:1931–7).
J Hand Surg [Br] 2000;25:585–9. J Orthop Res 2012;29:1–3.
62. Mannion AF, Pulkovski N, Schenk P, et al. A new method for the 82. Gennisson J-L, Deffieux T, Fink M, et al. Ultrasound elastography:
noninvasive determination of abdominal muscle feedforward activ- principles and techniques. Diagn Interv Imag 2013;94:487–95.
ity based on tissue velocity information from tissue Doppler 83. Wu C-H, Chen W-S, Park G-Y, et al. Musculoskeletal sonoelas-
imaging. J Appl Physiol 2008;104:1192–201. tography: a focused review of its diagnostic applications for evaluat-
63. Oh S, Belohlavek M, Zhao C. Detection of differential gliding ing tendons and fascia. J Med Ultrasound 2012;20:79–86.
characteristics of the flexor digitorum superficialis tendon and sub- 84. De Zordo T, Fink C, Feuchtner GM, et al. Real-time sonoelastog-
synovial connective tissue using color Doppler sonographic raphy findings in healthy Achilles tendons. AJR Am J Roentgenol
imaging. J Ultrasound Med 2007;26:149–55. 2009;193:W134–8.
64. Eranki A, Bellini L, Prosser L, et al., editors. Measurement of 85. Brown PG, Alsousou J, Cooper A, et al. The AutoQual ultrasound
tendon velocities using vector tissue Doppler imaging: a feasibility elastography method for quantitative assessment of lateral strain in
study. Buenos Aires, Argentina: Annual International Conference post-rupture Achilles tendons. J Biomech 2013;46:2695–700.
of the IEEE Engineering in Medicine and Biology Society; 2010, 86. Lopata RGP, van Dijk JP, Pillen S, et al. Dynamic imaging of
31st August-4th September. skeletal muscle contraction in three orthogonal directions. J Appl
65. Bohs LN, Trahey GE. A novel method for angle independent Physiol 2010;109:906–14.
ultrasonic imaging. IEEE Trans Biomed Eng 1991;38:280–6. 87. Parker KJ, Doyley MM, Rubens DJ. Imaging the elastic properties
66. Dilley A, Greening J, Lynn B, et al. The use of cross-correlation of tissue: the 20 year perspective. Phys Med Biol 2011;56:R1–29.
analysis between high-frequency ultrasound images to measure lon- 88. Buyruk HM, Stam HJ, Snijders CJ, et al. Measurement of sacroiliac
gitudinal median nerve movement. Ultrasound Med Biol 2001;27: joint stiffness in peripartum pelvic pain patients with Doppler
1211–18. imaging of vibrations (DIV). Eur J Obstet Gynecol Reprod Biol
67. Korstanje J-WH, Selles RW, Stam HJ, et al. Development and 1999;83:159–63.
validation of ultrasound speckle tracking to quantify tendon dis- 89. de Groot M, Spoor CW, Snijders CJ. Critical notes on the tech-
placement. J Biomech 2010;43:1373–9. nique of Doppler imaging of vibrations (DIV). Ultrasound Med
68. Boyd BS, Gray AT, Dilley A, et al. The pattern of tibial nerve Biol 2004;30:363–7.
excursion with active ankle dorsiflexion is different in older people 90. Mens JMA, Damen L, Snijders CJ, et al. The mechanical effect of
with diabetes mellitus. Clin Biomech 2012;27:967–71. a pelvic belt in patients with pregnancy-related pelvic pain. Clin
69. Dilley A, Lynn B, Greening J, et al. Quantitative in vivo studies of Biomech 2006;21:122–7.
median nerve sliding in response to wrist, elbow, shoulder and neck 91. Ballyns JJ, Turo D, Otto P, et al. Office-based elastographic tech-
movements. Clin Biomech 2003;18:899–907. nique for quantifying mechanical properties of skeletal muscle.
70. Ellis RF, Hing WA, McNair PJ. Comparison of different neural J Ultrasound Med 2012;31:1209–19.
mobilization exercises upon longitudinal sciatic nerve movement: 92. McCreesh KM, Riley SJ, Crotty JM. Neovascularity in patellar
an in-vivo study utilizing ultrasound imaging. J Orthop Sports Phys tendinopathy and the response to eccentric training: a case report
Ther 2012;42:667–75. using power Doppler ultrasound. Man Ther 2013;18:602–5.
71. Ridehalgh C, Moore A, Hough AD. Normative sciatic nerve excur- 93. Harper CJ, Shahgholi L, Cieslak K, et al. Variability in diaphragm
sion during a modified straight leg raise test. Man Ther 2013;19: motion during normal breathing, assessed with B-mode ultrasound.
59–64. J Orthop Sports Phys Ther 2013;43:927–31.
72. Loram ID, Maganaris CN, Lakie M. Use of ultrasound to make 94. Cho KH, Lee HJ, Lee WH. Reliability of rehabilitative ultrasound
noninvasive in vivo measurement of continuous changes in human imaging for the medial gastrocnemius muscle in poststroke patients.
muscle contractile length. J Appl Physiol 2006;100:1311–23. Clin Physiol Funct Imaging 2014;34:26–31.
73. Herbert RD, Clarke J, Kwah LK, et al. In vivo passive mechanical 95. Gorgey AS, Timmons MK, Michener LA, et al. Intra-rater reli-
behaviour of muscle fascicles and tendons in human gastrocnemius ability of ultrasound imaging of wrist extensor muscles in patients
muscle-tendon units. J Physiol 2011;589:5257–67. with tetraplegia. PM R 2014;6:127–33.
74. Korstanje J-WH, Scheltens-De Boer M, Blok JH, et al. Ultrasono- 96. Zhao H, Ren Y, Wu Y-N, et al. Ultrasonic evaluations of Achilles
graphic assessment of longitudinal median nerve and hand flexor tendon mechanical properties poststroke. J Appl Physiol 2009;106:
tendon dynamics in carpal tunnel syndrome. Muscle Nerve 2012;45: 843–9.
721–9. 97. Zhao H, Wu Y-N, Hwang M, et al. Changes of calf muscle-tendon
75. Tian M, Herbert RD, Hoang PD, et al. Myofascial force transmis- biomechanical properties induced by passive-stretching and active-
sion between the human soleus and gastrocnemius muscles during movement training in children with cerebral palsy. J Appl Physiol
passive knee motion. J Appl Physiol 2012;113:517. 2011;111:435–42.
76. Arndt A, Bengtsson A-S, Peolsson M, et al. Non-uniform displace- 98. Hoang P, Saboisky JP, Gandevia SC, et al. Passive mechanical
ment within the Achilles tendon during passive ankle joint motion. properties of gastrocnemius in people with multiple sclerosis. Clin
Knee Surg Sports Traumatol Arthrosc 2011;20:1868–74. Biomech 2009;24:291.
77. Harris EJ, Miller NR, Bamber JC, et al. Speckle tracking in a
phantom and feature-based tracking in liver in the presence of
 CHAPTER 15 

Advances in Magnetic Resonance

Imaging (MRI) Measures
James Elliott  •  Graham Galloway  •  Barbara Cagnie  •  Katie McMahon

which highlight different processes. Contrast between

INTRODUCTION different tissues in MRI is dependent on a combination
of the concentration of the protons and their molecular
Magnetic resonance imaging (MRI) provides a map of environment. The greatest influences on contrast weight-
the distribution of hydrogen atoms, principally in water ing1 are the relaxation properties, which are largely
and fat molecules, through the use of radiofrequency dependent on molecular motion and also by the tech-
pulses and static and changing magnetic fields to produce nologist selecting and setting the different sequence
anatomical images of the body. Different tissue types and applications. However, the presence of relaxation agents
pathologies have their own signature.1 MRI does not use also has an influence and these agents may be either
ionizing radiation, making it particularly useful in moni- endogenous (e.g. iron) or exogenous (e.g. gadolinium).
toring longitudinal management of injury and disease. Each family of sequences has different applications and
MRI provides excellent soft tissue definition with a range disadvantages in musculoskeletal imaging. A brief guide
of contrasts that allow for a non-invasive visualization of to some of the terms is provided in Table 15-1. For more
tissues and abnormalities in multiple planes. Although information, the interested reader is encouraged to refer
still evolving and more expensive compared to other to McMahon et al.1 A user-friendly pocket guide to
imaging modalities (e.g. computed tomography, radiog- MRI acronyms across manufacturers is also available
raphy and ultrasound), MRI is being used increasingly to from Hitachi at http://www.hitachimed.com/idc/groups/
identify tissue changes at the microscopic, metabolic and hitachimedical/documents/supportingdocumentpdf/
macroscopic levels to determine any of the following: (a) poc_001960.pdf.
the severity and extent of injury or a disease process; (b) Changing the parameters (e.g. timing) of any of the
progress and response to treatments; (c) a specific under- families of sequences will lead to a different contrast
lying pathological cause and location; or (d) when specific in target tissues (Table 15-1). When investigating vas-
tissues are affected.2 cular tissues or muscle haemorrhaging, a gradient echo
MRI has long been an important tool for evaluating sequence is preferred. However, gradient echo sequences
the musculoskeletal system.2 There are many examples are very sensitive to tissue interfaces, of which there
where MRI is used in the diagnosis of relevant mus- are many in all joints, as well as metallic implants such
culoskeletal disease/injury,3–8 thus helping to direct as pins or screws. Their presence results in signal loss
appropriate treatment. There are not always consistent and geometric distortions in the surrounding areas. A
findings of patho-anatomical lesions that are related to spin echo sequence is less sensitive to disturbances
the clinical symptoms. However, advancing MRI tech- in the magnetic field and is a good option for visual-
nologies are providing mechanistic, diagnostic and pos- izing meniscal tears. There are steady-state or hybrid
sibly therapeutic-based information.9–25 These advancing sequences, which offer superior muscle/blood contrast
technologies are providing a glimpse into the physiologi- and can allow real-time imaging of joint motion.
cal, cognitive and affective processes26 that may be Trabecular bone and bone marrow are brighter in
associated with poor functional recovery and chronic proton density weighting than tendons and cortical bone.
pain-related disability in high-risk patients. The fol- General anatomical imaging can be performed with T1
lowing chapter will explore how MRI is being used weighting (where fat is bright and water is dark).
(and may be used) in neuromusculoskeletal research, However, if pathologies such as inflammation or fluid
what is being measured with various applications, and accumulation are suspected, T2 weighting will most
its uses and limitations. clearly reveal the extent of the effusions (Fig. 15-1).
Often the fat signal is suppressed to aid in the visualiza-
tion of pathological processes in a T2-weighted image. A
MRI CONTRASTS fat-suppressed acquisition using a short-tau inversion
recovery sequence, which nulls the signal from fat, has
It is first necessary to understand the fundamental area predictive capacity to identify denervated muscles in the
of MRI contrasts. There are a range of MRI contrasts, periphery (Fig. 15-2).2,7
153
154 PART II  Advances in Theory and Practice

TABLE 15-1  A Brief Guide to Different FAT/ WATER SEPARATION:

Sequences and Contrast
Weightings of Clinical MRI
MACROSCOPIC STRUCTURE OF MUSCLE
Applications Commonly Used in
Clinical observations of altered muscle structure and
Musculoskeletal Imaging
function on conventional MRI have been reported in
Sequence Gradient echo Sensitivity to iron-rich patients with neuromusculoskeletal complaints, such
family compounds and as low back pain,27–31 neck, head and shoulder girdle
vascularity, but has disorders,15,17,18,20–22,32–35 radiculopathy2,7 and peripheral
artefacts around metal neuropathies,36 rotator cuff pathology37 and chronic
implants like pins or
screws fibromyalgia.25 Recent conventional and advanced MRI
Spin echo Less sensitivity to metal evidence from our research in Brisbane, Australia20 and
implants, usually Chicago, USA (in preparation) has identified the unique
slower to acquire early expression of neck muscle degeneration (fatty infil-
Hybrid sequences Can be rapid sequences, trates) in patients following whiplash injury from a motor
(e.g. true-FISP offer great tissue/blood
or steady-state contrast and allow vehicle collision (MVC) who go on to develop chronic
sequences) real-time imaging pain-related disability.20 Such muscle changes are not
Contrast T1 Fat and meniscal tears present in patients with lower levels of initial pain or in
weighting will appear bright; patients with chronic non-traumatic neck pain,21 suggest-
fluids, muscles and ing traumatic factors play a role in altering the make-up
tendons are grey, air
and cortical bone are
and structure of the neck muscles. Furthermore, the pres-
black ence of a post-traumatic stress response mediated the
T2 Fluids like water and relationship between initial pain levels and the develop-
cerebrospinal fluid, as ment of neck muscle fat.20 While preliminary, these find-
well as fat appear ings demonstrate a relationship between symptoms of
bright; muscle and post-traumatic stress disorder (a psychological disorder)
tendons are grey, air
and cortical bone are and objective longitudinal MRI data for muscle degen-
black eration (a physical pathology), suggesting multiple neu-
T2* An additional relaxation ropsychobiological factors influence recovery rates
to T2, caused by local following an MVC. Questions regarding more informed
field changes. This is interventions for retarding (if not preventing) muscular
very sensitive to blood
oxygen level changes
degeneration remain. However, the prospect is that
and vascularity advanced, and currently available, MRI measures can
Proton density The more protons the provide spatio-temporal information on disease stage and
tissue contains, the progression. Ultimately, emerging MRI applications
brighter it is could be used to explore and inform interventions aimed
Diffusion Creates a sensitivity to at influencing functional recovery.
motion within the There are several MRI applications to measure the
tissue voxels, allowing
the investigation of macroscopic and microscopic expression of the fat and
tissue microstructure water composition of a muscle in neuromuscular disor-
ders.38,39 A dual acquisition method may be used, where

$ %

FIGURE 15-1  ■  Sagittal (A) T1-weighted and (B) T2-weighted magnetic resonance images of the cervical spine.
 15  Advances in Magnetic Resonance Imaging (MRI) Measures 155

$ %

FIGURE 15-2  ■  (A) Axial and (B) coronal short-tau inversion recovery images detailing increased signal intensity suggesting denerva-
tion of the right rectus femoris muscle in a patient with lumbar spine radiculopathy due to a herniated disc at L3/4.

FIGURE 15-3  ■  An example of whole body magnetic resonance imaging using a three-dimensional semi-automated segmentation
algorithm where the quantification of specific muscle volume and fat infiltration can be realized. For colour version see Plate 13.
(Images are courtesy of Dr Olof Dahlqvist-Leinhard, Linköping University, Sweden; Advanced MR Analytics http://amraab.se/).

a fat-suppressed image (water only) and a standard image chronic whiplash and incomplete spinal cord injury
(fat and water) are collected. Subtracting the first from [Elliott, manuscript in preparation]). Figure 15-3 details
the second yields a fat image. This type of acquisition a semi-automated segmentation algorithm that can be
does suffer from its reliance on the uniform frequency of used to calculate specific or whole-body muscle volume
fat across the whole volume of excitation, which is often and fat infiltration in rapid fashion. Figure 15-4 demon-
difficult to obtain especially at higher magnetic fields (3 strates an axial fat /water separation (fat only) image
Tesla and above). An alternative is the Dixon method,40 of the ankle plantar and dorsiflexors in one subject
where data are collected at two echo times; one when with incomplete spinal cord injury and one with chronic
water and fat are in-phase and one when water and fat (3 years duration) whiplash-related disability. Further-
are out of phase. The data can be combined in such a way more, recent investigation has validated such methodolo-
that they generate separate fat and water images. This gies against the gold-standard biopsy with histological
method is susceptible to short T2*, which is often the case confirmation.39
in musculoskeletal imaging. More sophisticated methods
collect data from more than two echoes to improve the
estimation of the fat and water images. These methods
have been applied successfully in the liver and musculo-
skeletal application using an iterative least squares solu-
MUSCLE FUNCTIONAL MRI:
tion called IDEAL.41 Such methodology provides MICROSCOPIC ACTIVATION AND
foundation for rapid data acquisition of whole-body FUNCTION OF MUSCLE
imaging42 which has implications for studying and quan-
tifying muscle degeneration in systemic38,43 and other Muscle functional MRI (mfMRI) offers a non-
neuromusculoskeletal disorders (e.g. fibromyalgia,25 invasive method to quantify changes in muscle
156 PART II  Advances in Theory and Practice

$ %

FIGURE 15-4  ■  Magnetic resonance (fat only) image of the right plantar (red) and dorsiflexors (blue) in (A) subject with incomplete
spinal cord injury and (B) subject with chronic whiplash-associated disorder. Note the increased signal throughout the plantar/
dorsiflexors in both subjects, suggestive of fatty infiltrates. Note: The posterior tibialis is highlighted in green. For colour version
see Plate 13.

physiology following the performance of exercise. The ADVANCED TECHNIQUES:

mfMRI technique is based on signal intensity changes MICROSCOPIC EVALUATION OF THE
due to increases in the relaxation time (T2) of tissue water MUSCLE AND NERVOUS SYSTEMS
following exercise. Specifically, exercise results in a slower
decay of the muscle water transverse magnetization, Magnetization Transfer Ratios
which causes an enhancement in signal intensity of the
activated muscles. As a consequence, activated muscles Magnetization transfer ratios (MTRs) are an indirect
look brighter on T2-weighted images when compared to measure of tissue stability, relying on the exchange of
muscles imaged in a resting state.44 The proposed under- magnetically saturated hydrogen nuclei (protons) between
lying physiological mechanism of this shift in T2 relax- solid tissue structures and free water.59,60 MTRs have
ation time is that the influx of fluid during activity is been widely studied as semi-quantitative metrics for mild
accompanied by an accumulation of osmolites (phos- and traumatic brain injury,61,62 and peripheral neuropa-
phate, lactate, sodium) in the cytoplasm and their pres- thy,36 and are used clinically in diagnostic studies of neu-
ence prolongs the relaxation time of soft-aqueous skeletal ronal degeneration in multiple sclerosis,63 Alzheimer’s
muscle.44 disease64–67 and Parkinson’s disease.68,69 Furthermore,
In contemporary research, mfMRI is an emerging MTR can be used to characterize the demyelination/
tool for assessing the extent of muscle activation (and degeneration of ascending and descending spinal path-
possibly function) following the performance of a task ways in patients with spinal cord injury to assess
and for the evaluation of neuromuscular adaptations as prognosis.70
a result of therapeutic interventions.13,32 Some studies Preliminary evidence (Elliott, manuscript in prepara-
utilizing mfMRI have investigated muscle activity pat- tion) suggests that the expression of muscle fatty infil-
terns during commonly prescribed clinically based exer- trates in the plantar and dorsiflexors (Fig. 15-4) in a small
cises.32,45–47 Other studies have evaluated muscle activity sample of patients with chronic whiplash could result
during exercise of the lower (knee extension, ankle from mild damage to descending white matter pathways
extension and flexion, running and cycling)48–50 and upper of the cervical spinal cord as detected from the MTR
extremities as well as the spine.32,46,51–53 It has been data. Such data provide a foundation for further prospec-
demonstrated that T2 shifts may be useful for non- tive investigations to quantify temporal losses in neural
invasive inferences regarding moderate levels of muscle substrates within specific descending and ascending
activity, but less valid for the lower and higher levels spinal cord pathways following traumatic spinal injuries.
of activity. Figure 15-5 details magnetization transfer contrast and
There are many clinical and preliminary experimental use of MTR in the spinal cord.
investigations to highlight changes in muscle activation
pattern as a result of pain.14,29,32,54–57 mfMRI has also
been used to non-invasively evaluate neuromuscular
Diffusion Weighted Imaging
adaptations as a result of resistance training. However, The microstructure of tissue can be assessed with an
there is a paucity of information in the literature to advanced technique known as diffusion weighted imaging
definitively ascribe and generalize its use to clinical (DWI). The sequences used in DWI are sensitive to
assessment.52,58 the motion of intracellular and extracellular water
 15  Advances in Magnetic Resonance Imaging (MRI) Measures 157

$ %

FIGURE 15-5  ■  Anatomically defined regions of interest (ROIs) on the (A) magnetization transfer (MT) and (B) non-MT-weighted image
over the ventromedial and dorsolateral (green in colour plate, arrows in this figure) primarily descending motor pathways and the
dorsal column (red in colour plate, circled in this figure) ascending sensory pathways of the cervical spinal cord. The non-
magnetization transfer (non-MT) scan (B) is identical except that the MT saturation pulse is turned off and run as a separate
co-registered acquisition. The MTR is calculated on a voxel-by-voxel basis using the formula of: MTR = 100*(non-MT − MT)/non-MT.
For colour version see Plate 14.

molecules and provide information on changes to the which utilizes T2 rather than T2* relaxation, giving it an
boundaries within the tissue. An increase in diffusion is advantage in complex structures such as the brain and
indicative of an increase in fluid or breakdown in cel- spine. Neuronal activity in the spinal cord has been
lularity (e.g. cysts or necrosis), whereas a decrease in mapped in response to normal processing of stimuli such
diffusion indicates a loss of permeability in the micro- as thermal changes and motor tasks, as well as the effect
structure (e.g. ischaemia and cell swelling). It is com- of trauma and disease processes.76
monly used to investigate neuromusculoskeletal tumours From a clinical perspective, spinal cord fMRI data may
as it allows determination of the extent of necrosis. DWI be used in clinical trials to provide information on the
can also be used to monitor treatment progression and site of action, efficacy and mechanisms of treatments, and
to estimate prognosis.71 Emerging applications use dif- may prove valuable in the diagnosis of diseases afflicting
fusion to gauge musculature changes and therapeutic the peripheral and central nervous systems.77 Such knowl-
response.19,72 For example, diffusion values can be used edge will greatly expand our understanding of the periph-
to investigate the loss of vertebral disc integrity in com- eral and central nervous system and the pathophysiological
pression fractures.72 Increased muscle diffusion values mechanisms underlying many of the common, yet enig-
may precede electrophysiological and histological evi- matic, disorders frequently assessed and managed by
dence of denervation.2,73 physiotherapists, worldwide.
As an example, thrust manipulation applied to the axial
and appendicular skeleton has long been shown to
Functional Magnetic Resonance improve the active range of motion, reduce self-reported
pain and improve function in groups of patients with
Imaging: Functional and Structural mechanical spinal and shoulder pain.78–80 While biome-
Functional magnetic resonance imaging (fMRI) is the chanical models have yet to explain the mechanisms by
process of observing signal changes due to blood oxygen- which manipulation works,81 preliminary fMRI evidence
ation level differences (BOLD).74 Neuronal activity is from a thoracic spine manipulation model82 and animal
highly correlated to blood oxygenation changes, and models of mobilization83 suggests that supraspinal mech-
fMRI allows the localization of these changes, although anisms may explain the attendant, albeit immediate,
it suffers low temporal resolution. There is a signal hypoalgesic effect. Future work, with larger datasets and
increase in a BOLD-sensitive sequence approximately different patient populations, should shed light on neuro-
4.5 seconds after a cognitive challenge, in response to the physiological mechanisms of manipulative procedures.
haemodynamic fluctuations of active tissue. Although
predominantly a neuroimaging technique for the brain, Caution
applications of fMRI to study the spinal cord are emerg-
ing. These applications sometimes use BOLD, but also fMRI is a potentially powerful method for evaluating
use a signal enhancement by extravascular water protons,75 regional brain and spinal cord activation. It can also be
158 PART II  Advances in Theory and Practice

used to determine the connectivity or interactions be- patient-centred outcomes, are all important components
tween regions, either when a subject is performing an of patient management. In short, healthcare practitioners
explicit task, or at rest. Numerous techniques have been worldwide can play a primary-care role through partici-
proposed to acquire and analyse fMRI data with the pri- pation in pathways that are based on diagnostic and
mary aim to find an optimal combination of methods to patient management algorithms.94–97 The judicious adher-
plot activated (or deactivated) brain regions (functional) ence to such algorithms can reduce practice variation,96
and understand relationships between them (structural). and ensure that our patients understand both the neces-
This requires the optimization of many aspects of (a) data sity for appropriate imaging studies and the negative
acquisition (e.g. duration of scan, spatial resolution, spa- influence of unnecessary imaging.98,99
tial smoothing during pre-processing) and (b) data analy-
sis, such as seed-based and independent component REFERENCES
analyses. Accordingly, the reader is encouraged to be a 1. McMahon KL, Cowin G, Galloway G. Magnetic resonance
cautious and informed consumer of the literature in re- imaging: the underlying principles. J Orthop Sports Phys Ther
gard to findings from fMRI studies and to understand the 2011;41:806–19.
2. Fritz RC, Domroese ME, Carter GT. Physiological and anatomical
complexities of such methodologies before definitively basis of muscle magnetic resonance imaging. Phys Med Rehabil
interpreting any/all available literature. This is a call to Clin N Am 2005;16:1033–51.
‘talk across fences’ in order to establish interdisciplinary 3. Bendszus M, Koltzenburg M, Wessig C, et al. Sequential MR
relationships whereby challenging clinical questions can imaging of denervated muscle: experimental study. AJNR Am J
Neuroradiol 2002;23:1427–31.
be interpreted, rigorously (and accurately) tested and 4. Bendszus M, Wessig C, Reiners K, et al. MR imaging in the dif-
translated. ferential diagnosis of neurogenic foot drop. AJNR Am J Neurora-
diol 2003;24:1283–9.
5. Bendszus M, Wessig C, Solymosi L, et al. MRI of peripheral nerve
MRI IN MUSCULOSKELETAL degeneration and regeneration: correlation with electrophysiology
and histology. Exp Neurol 2004;188:171–7.
CLINICAL PRACTICE 6. Bredella MA, Tirman P, Fritz RC, et al. Denervation syndromes of
the shoulder girdle: MR imaging with electrophysiologic.
When used appropriately, MRI studies can be a crucial Skeletal Radiol 1999;28:567–72.
component for managing a patient with a neuromuscu- 7. Carter GT, Fritz R. Electromyographic and lower extremity short
time to inversion recovery magnetic resonance imaging findings in
loskeletal complaint. MRI provides objective measures of lumbar radiculopathy. Muscle Nerve 1997;20:1191–3.
the damage to the neuromusculoskeletal system, making 8. Wessig C, Koltzenburg M, Reiners K, et al. Muscle magnetic reso-
it an excellent tool for accurate diagnosis, improved nance imaging of denervation and reinnervation: correlation with
understanding of the pathophysiology of disease and electrophysiology and histology. Exp Neurol 2004;185:254–61.
evaluating the efficacy of treatment regimens, which oth- 9. Apkarian AV. Functional magnetic resonance imaging of pain con-
sciousness: cortical networks of pain critically depend on what is
erwise are often based on the patients’ self-reporting of implied by ‘pain’. Curr Rev Pain 1999;3:308–15.
pain. MRI does not use radiation and so is non-invasive. 10. Apkarian AV, Hashmi JA, Baliki MN. Pain and the brain: specificity
Accordingly, it is the technique of choice for research and and plasticity of the brain in clinical chronic pain. Pain 2011;152
for longitudinal clinical studies. It is necessary to note (Suppl. 3):S49–64.
11. Baliki MN, Geha PY, Apkarian AV. Parsing pain perception
that a subset of patients will be incompatible for MRI, as between nociceptive representation and magnitude estimation.
there are a number of contraindications. Depending J Neurophysiol 2009;101:875–87.
upon the area to be imaged, these include, but are not 12. Baliki MN, Geha PY, Fields HL, et al. Predicting value of pain and
limited to, certain pacemakers, aneurysm clips, metallic analgesia: nucleus accumbens response to noxious stimuli changes
foreign bodies and claustrophobia. A full list of magnetic in the presence of chronic pain. Neuron 2010;66:149–60.
13. Cagnie B, Elliott J, O’Leary S, et al. Muscle functional MRI as an
resonance conditional and incompatible devices can be imaging tool to evaluate muscle activity. J Orthop Sports Phys Ther
found at www.mrisafety.com84 and interested readers are 2011;41:896–903.
encouraged to refer to Durbridge.85 14. Cagnie B, Elliott J, O’Leary S, et al. Pain-induced changes in
Ongoing research is further defining the role of MRI the activity of the cervical extensor muscles evaluated by muscle
functional magnetic resonance imaging. Clin J Pain 2011;27:
in evaluating disorders of the musculoskeletal system. 392–7.
Nevertheless, there are some negative aspects of MRI 15. Elliott J. Are there implications for morphological changes in neck
from a clinical perspective. For example, early MRI refer- muscles after whiplash injury? Spine 2011;36(Suppl. 25):S205–10.
rals of patients with acute low back pain on the basis of Review.
self-reported pain and without any other indication gen- 16. Elliott J, Cannata E, Christensen E, et al. MRI analysis of the size
and shape of the oropharynx in chronic whiplash. Otolaryngol
erally provide little benefit and contribute to poor out- Head Neck Surg 2008;138:747–51.
comes and often to a strong iatrogenic effect.86–88 A 17. Elliott J, Jull G, Noteboom JT, et al. Fatty infiltration in the cervi-
patient’s knowledge (or interpretation) of imaging abnor- cal extensor muscles in persistent whiplash-associated disorders: a
malities (e.g. a ‘bulging disc’) can actually decrease self- magnetic resonance imaging analysis. Spine 2006;31:E847–55.
18. Elliott J, Jull G, Noteboom JT, et al. MRI study of the cross-
perception of health and may lead to fear avoidance and sectional area for the cervical extensor musculature in patients
catastrophizing behaviours that may predispose people to with persistent whiplash associated disorders (WAD). Man Ther
chronicity.89,90 Accordingly, clinicians should understand 2008;13:258–65.
and refer to the available guidelines on appropriate use 19. Elliott J, Pedler A, Beattie P, et al. Diffusion-weighted magnetic
of and judicious referral for imaging.91, 92 resonance imaging for the healthy cervical multifidus: a potential
method for studying neck muscle physiology following spinal
Furthermore, the use of clinical pathways93 that reduce trauma. J Orthop Sports Phys Ther 2010;40:722–8.
the referral for inappropriate imaging studies, reduce 20. Elliott J, Pedler A, Kenardy J, et al. The temporal development of
costs of healthcare delivery and ultimately improve fatty infiltrates in the neck muscles following whiplash injury: an
 15  Advances in Magnetic Resonance Imaging (MRI) Measures 159

association with pain and posttraumatic stress. PLoS ONE 45. Cagnie B, D’Hooge R, Achten E, et al. A magnetic resonance
2011;6(6):e21194. imaging investigation into the function of the deep cervical flexors
21. Elliott J, Sterling M, Noteboom JT, et al. Fatty infiltrate in the during the performance of craniocervical flexion. J Manipulative
cervical extensor muscles is not a feature of chronic, insidious-onset Physiol Ther 2010;33:266–91.
neck pain. Clin Radiol 2008;63:681–7. 46. Elliott JM, O’Leary SP, Cagnie B, et al. Craniocervical orientation
22. Elliott JM, O’Leary S, Sterling M, et al. Magnetic resonance affects muscle activation when exercising the cervical extensors in
imaging findings of fatty infiltrate in the cervical flexors in chronic healthy subjects. Arch Phys Med Rehabil 2010;91:1418–22.
whiplash. Spine 2010;35:948–54. 47. O’Leary S, Cagnie B, Reeve A, et al. Is there altered activity of the
23. Elliott JM, Pedler AR, Cowin G, et al. Spinal cord metabolism and extensor muscles in chronic mechanical neck pain? A functional
muscle water diffusion in whiplash. Spinal Cord 2011;50:474–6. magnetic resonance imaging study. Arch Phys Med Rehabil
24. Elliott JM, Walton DM, Rademaker A, et al. Quantification of 2011;92:929–34.
cervical spine muscle fat: a comparison between T1-weighted and 48. Jenner G, Foley JM, Cooper TG, et al. Changes in magnetic reso-
multi-echo gradient echo imaging using a variable projection algo- nance images of muscle depend on exercise intensity, duration, not
rithm (VARPRO). BMC Med Imaging 2013;13:30. work. J Appl Physiol 1994;76:2119–24.
25. Gerdle B, Forsgren MF, Bengtsson A, et al. Decreased muscle 49. Kinugasa R, Akima H. Neuromuscular activation of triceps surae
concentrations of ATP and PCR in the quadriceps muscle of using muscle functional MRI and EMG. Med Sci Sports Exerc
fibromyalgia patients – A (31) P-MRS study. Eur J Pain 2013; 2005;37:593–8.
17:1205–15. 50. Ono T, Higashihara A, Fukubayashi T. Hamstring functions
26. Wager TD, Atlas LY, Lindquist MA, et al. An fMRI-based neuro- during hip-extension exercise assessed with electromyography and
logic signature of physical pain. N Engl J Med 2013;368: magnetic resonance imaging. Res Sports Med 2011;19:42–52.
1388–97. 51. Conley MS, Meyer RA, Bloomberg JJ, et al. Noninvasive analysis
27. Campbell WW, Vasconcelos O, Laine FJ. Focal atrophy of the of human neck muscle function. Spine 1995;20:2505–12.
multifidus muscle in lumbosacral radiculopathy. Muscle Nerve 52. Conley MS, Stone MH, Nimmons M, et al. Resistance training and
1998;21:1350–1353F. human cervical muscle recruitment plasticity. J Appl Physiol
28. Danneels LA, Vanderstraeten GG, Cambier DC, et al. CT imaging 1997;83:2105–11.
of trunk muscles in chronic low back pain patients and healthy 53. Mayer JM, Graves JE, Clark BC, et al. The use of magnetic reso-
control subjects. Eur Spine J 2000;9:266–72. nance imaging to evaluate lumbar muscle activity during trunk
29. Dickx N, Cagnie B, Achten E, et al. Changes in lumbar muscle extension exercise at varying intensities. Spine 2005;30:2556–63.
activity because of induced muscle pain evaluated by muscle func- 54. Falla D, Jull G, Hodges P. Neck pain patients demonstrate reduced
tional magnetic resonance imaging. Spine 2008;33:E983–9. EMG activity of the deep cervical flexors during performance of
30. Kader DF, Wardlaw D, Smith FW. Correlation between the MRI the craniocervical flexion test. Spine 2004;29:2108–14.
changes in the lumbar multifidus muscles and leg pain. Clin Radiol 55. Falla D, Bilenkij G, Jull G. Patients with chronic neck pain dem-
2000;55:145–9. onstrate altered patterns of muscle activation during performance
31. Paalanne N, Niinimäki J, Karppinen J, et al. Assessment of associa- of a functional upper limb task. Spine 2004;29:1436–40.
tion between low back pain and paraspinal muscle atrophy using 56. Falla D, Dall’Alba P, Rainoldi A, et al. Repeatability of surface
opposed phase magnetic resonance imaging a population-based EMG variables in the sternocleidomastoid and anterior scalene
study among young adults. Spine 2011;36:1961–8. muscles. Eur J Appl Physiol 2002;87:542–9.
32. Cagnie B, Dickx N, Peeters I, et al. The use of functional MRI to 57. Schomacher J, Farina D, Lindstroem R, et al. Chronic trauma-
evaluate cervical flexor activity during different cervical flexion induced neck pain impairs the neural control of the deep semispi-
exercises. J Appl Physiol 2008;104:230–5. nalis cervicis muscle. Clin Neurophysiol 2012;123:1403–8.
33. Elliott JM, Pedler AR, Jull GA, et al. Differential changes in muscle 58. Akima H, Ushiyama J, Kubo J, et al. Resistance training during
composition exist in traumatic and non-traumatic neck pain. Spine unweighting maintains muscle size and function in human calf.
2014;39:39–47. Med Sci Sports Exerc 2003;35:655–62.
34. Fernandez-de-Las-Penas C, Bueno A, Ferrando J, et al. Magnetic 59. Wolff SD, Balaban RS. Magnetisation transfer contrast (MTC)
resonance imaging study of the morphometry of cervical extensor and tissue water proton relaxation in vivo. Magn Reson Med
muscles in chronic tension-type headache. Cephalalgia 2007;27: 1989;10:135–44.
355–62. 60. Wolff SD, Eng J, Balaban RS. Magnetisation transfer contrast:
35. Sheard B, Elliott J, Cagnie B, et al. Evaluating serratus anterior method for improving contrast in gradient-recalled-echo images.
muscle function in neck pain using muscle functional magnetic Radiology 1991;179:133–7.
resonance imaging. J Manipulative Physiol Ther 2012;35:629–35. 61. Bagley LJ, McGowan JC, Grossman RI, et al. Magnetisation trans-
36. Sinclair CD, Morrow JM, Miranda MA, et al. Skeletal muscle fer imaging of traumatic brain injury. J Magn Reson Imaging
MRI magnetisation transfer ratio reflects clinical severity in 2000;11:1–8.
peripheral neuropathies. J Neurol Neurosurg Psychiatry 2012;83: 62. Sinson G, Bagley LJ, Cecil KM, et al. Magnetisation transfer
29–32. imaging and proton MR spectroscopy in the evaluation of axonal
37. Gladstone JN, Bishop JY, Lo IK, et al. Fatty infiltration and injury: correlation with clinical outcome after traumatic brain
atrophy of the rotator cuff do not improve after rotator cuff repair injury. AJNR Am J Neuroradiol 2001;22:143–51.
and correlate with poor functional outcome. Am J Sports Med 63. Dehmeshki J, Chard DT, Leary SM, et al. The normal appearing
2007;35:719–28. grey matter in primary progressive multiple sclerosis: a magnetisa-
38. Bley TA, Wieben O, Francois CJ, et al. Fat and water magnetic tion transfer imaging study. J Neurol 2003;250:67–74.
resonance imaging. J Magn Reson Imaging 2010;31:4–18. 64. Hanyu H, Asano T, Iwamoto T, et al. Magnetisation transfer mea-
39. Gaeta M, Scribano E, Mileto A, et al. Muscle fat fraction in neu- surements of the hippocampus in patients with Alzheimer’s disease,
romuscular disorders: dual-echo dual-flip-angle spoiled gradient- vascular dementia, and other types of dementia. AJNR Am J
recalled MR imaging technique for quantification a feasibility study. Neuroradiol 2000;21:1235–42.
Radiology 2011;259:487–94. 65. Hanyu H, Asano T, Sakurai H, et al. Magnetisation transfer mea-
40. Dixon W. Simple proton spectroscopic imaging. Radiology 1984; surements of the hippocampus in the early diagnosis of Alzheimer’s
153:189–94. disease. J Neurol Sci 2001;188:79–84.
41. Costa DN, Pedrosa I, McKenzie C, et al. Body MRI using IDEAL. 66. Hanyu H, Shimizu S, Tanaka Y, et al. Differences in magnetisation
Am J Roentgenol 2008;190:1076–84. transfer ratios of the hippocampus between dementia with Lewy
42. Schmidt GP, Reiser MF, Baur-Melnyk A. Whole-body imaging of bodies and Alzheimer’s disease. Neurosci Lett 2005;380:166–9.
the musculoskeletal system: the value of MR imaging. Skeletal 67. Kabani NJ, Sled JG, Chertkow H. Magnetisation transfer ratio in
Radiol 2007;36:1109–19. mild cognitive impairment and dementia of Alzheimer’s type.
43. Rönn M, Lind PM, Karlsson H, et al. Quantification of total and Neuroimage 2002;15:604–10.
visceral adipose tissue in fructose-fed rats using water-fat separated 68. Eckert T, Sailer M, Kaufmann J, et al. Differentiation of idiopathic
single echo MRI. Obesity (Silver Spring) 2013;21:E388–95. Parkinson’s disease, multiple system atrophy, progressive supra-
44. Meyer RA, Prior BM. Functional magnetic resonance imaging of nuclear palsy, and healthy controls using magnetisation transfer
muscle. Exerc Sport Sci Rev 2000;28:89–92. imaging. Neuroimage 2004;21:229–35.
160 PART II  Advances in Theory and Practice

69. Tambasco N, Pelliccioli GP, Chiarini P, et al. Magnetisation trans- 84. Shellock FG. Reference Manual for Magnetic Resonance Safety,
fer changes of grey and white matter in Parkinson’s disease. Implants, and Devices. 2013 edition.
Neuroradiol 2003;45:224–30. 85. Durbridge G. Magnetic resonance imaging: fundamental safety
70. Cohen-Adad J, El Mendili MM, et al. Demyelination and degen- issues. J Orthop Sports Phys Ther 2011;41:820–8.
eration in the injured human spinal cord detected with diffusion 86. Chou R, Fu R, Carrino JA, et al. Imaging strategies for low-back
and magnetisation transfer MRI. Neuroimage 2011;55:1024–33. pain: systematic review and metaanalysis. Lancet 2009;373:
71. Khoo MM, Tyler PA, Saifuddin A, et al. Diffusion-weighted 463–72.
imaging (DWI) in musculoskeletal MRI: a critical review. Skeletal 87. Chou R, Qaseem A, Owens DK, et al. Diagnostic imaging for low
Radiol 2011;40:665–81. back pain: advice for high-value health care from the American
72. Beattie P. Diffusion-weighted magnetic resonance imaging of the College of Physicians. Ann Intern Med 2011;154:181–9.
musculoskeletal system: an emerging technology with potential to 88. Webster BS, Bauer AZ, Choi Y, et al. Iatrogenic consequences of
impact clinical decision making. J Orthop Sports Phys Ther early magnetic resonance imaging in acute, work-related, disabling
2011;41:887–95. low back pain. Spine 2013;38:1939–46.
73. Holl N, Echaniz-Laguna A, Bierry G, et al. Diffusion-weighted 89. Ash LM, Modic MT, Obuchowski NA, et al. Effects of diagnostic
MRI of denervated muscle: a clinical and experimental study. information, per se, on patient outcomes in acute radiculopathy and
Skeletal Radiol 2008;37:1111–17. low back pain. AJNR 2008;29:1098–103.
74. Ogawa S. Finding the BOLD effect in brain images. Neuroimage 90. Fisher ES, Welch HG. Avoiding the unintended consequences
2012;62:608–9. of growth in medical care: how might more be worse? JAMA
75. Stroman PW. Magnetic resonance imaging of neuronal function in 1999;281:446–53.
the spinal cord: spinal fMRI. Clin Med Res 2005;3:146–56. 91. American College of Radiology Appropriateness Critera®. <http://
76. Agosta F, Valsasina P, Caputo D, et al. Tactile-associated recruit- www.acr.org/Quality-Safety/Appropriateness-Criteria>.
ment of the cervical cord is altered in patients with multiple scle- 92. Davis PC, Wippold FJ 2nd, Brunberg JA, et al. ACR appropriate-
rosis. Neuroimage 2008;39:1542–8. ness criteria on low back pain. J Am Coll Radiol 2009;6:401–7.
77. Kornelsen J, Mackey S. Potential clinical applications for spinal 93. Furhmans V. A novel plan helps hospital wean itself off pricey tests.
functional MRI. Curr Pain Headache Rep 2007;11:165–70. Wall St J 2007.
78. Childs JD, Fritz JM, Flynn TW, et al. A clinical prediction rule to 94. Boissonnault WG, Goodman C. Physical therapists as diagnosti-
identify patients with low back pain most likely to benefit from cians: drawing the line on diagnosing pathology. J Orthop Sports
spinal manipulation: a validation study. Ann Int Med 2004;141: Phys Ther 2006;36:351–3.
920–8. 95. Boissonnault WG, Badke MB, Powers JM. Pursuit and implemen-
79. Cleland JA, Childs JD, Fritz JM, et al. Development of a clinical tation of hospital-based outpatient direct access to physical therapy
prediction rule for guiding treatment of a subgroup of patients with services: an administrative case report. Phys Ther 2010;90:100–9.
neck pain: use of thoracic spine manipulation, exercise, and patient 96. Fritz J, Flynn TW. Autonomy in physical therapy: less is more.
education. Phys Ther 2007;87:9–23. J Orthop Sports Phys Ther 2005;35:696–8.
80. Mintken PE, Cleland JA, Carpenter KJ, et al. Some factors predict 97. Ross MD, Boissonnault WG. Red flags: to screen or not to screen?
successful short-term outcomes in individuals with shoulder pain J Orthop Sports Phys Ther 2010;40:682–4.
receiving cervicothoracic manipulation: a single-arm trial. Phys 98. Flynn TW, Smith B, Chou R. Appropriate use of diagnostic
Ther 2010;90:26–42. imaging in low back pain – a reminder that unnecessary imaging
81. Ross JK, Bereznick DE, McGill SM. Determining cavitation loca- may do as much harm as good. J Orthop Sports Phys Ther
tion during lumbar and thoracic spinal manipulation – Is spinal 2011;41:838–46.
manipulation accurate and specific? Spine 2004;29:1452–7. 99. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic reso-
82. Sparks C, Cleland JA, Elliott JM, et al. Using functional magnetic nance imaging vs radiographs for patients with low back pain: a
resonance imaging to determine if cerebral hemodynamic responses randomized controlled trial. JAMA 2003;289:2810–18.
to pain change following thoracic spine thrust manipulation in
healthy individuals. J Orthop Sports Phys Ther 2013;43:340–8.
83. Malisza KL, Gregorash L, Turner A, et al. Functional MRI involv-
ing painful stimulation of the ankle and the effect of physiotherapy
joint mobilisation. Magn Reson Imaging 2003;21:489–96.
 CHAPTER 16 

Musculoskeletal Pain in
the Human Brain:
INSIGHTS FROM FUNCTIONAL
BRAIN IMAGING TECHNIQUES
Michael Farrell

INTRODUCTION Components of Pain Experience

The fully integrated experience of pain includes discrimi-
Pain commonly occurs in association with musculoskel- native, affective and cognitive components.5 Pain dis-
etal disorders, and can be the most important problem crimination incorporates localization, intensity coding
from the patient’s perspective. The ideal way to address and the representation of qualitative attributes (e.g. sharp,
musculoskeletal pain is to resolve the underlying disor- dull, aching, etc.).6 The affective component of pain can
der, although this is not feasible in all cases and in some be a primary or secondary attribute.7 Unpleasantness is a
circumstances pain persists despite the resolution of mus- defining element of pain,8 and this intrinsic component
culoskeletal dysfunction. Musculoskeletal therapists are is primary to the felt state.9,10 Autonomic responses such
well placed to make a substantial contribution to the as changes of heart rate, blood pressure and cutaneous
management of pain in those patients who are troubled vasoconstriction may contribute a somatic expression to
by their symptoms in both the short and longer term. the primary unpleasantness of pain.11 More elaborate,
Management strategies should be grounded in an under- secondary emotional responses, such as fear or altered
standing of the underlying problem, and the treatment mood states, including anxiety and depression, are not
of persistent pain is no exception. Neural processes sub- essential for the experience of pain per se, but are common
sequent to noxious stimulation of somatic structures co-morbidities of persistent pain.12 The experience of
occur in peripheral, spinal and supraspinal components pain also involves cognitive processes including appraisal
of the nervous system, but ultimately pain is a function of the meaning of the sensation, which may involve
of the brain. The objective of this chapter is to discuss memory of past experiences, and can influence behav-
the representation of pain in the brain and to consider ioural and emotional responses.13,14
interactions between musculoskeletal therapies and
central pain processing. Functional Components
of the Pain Network
Nociceptive inputs to the brain project from the dorsal
THE BRAIN NETWORK FOR PAIN horn via the contralateral anterolateral portion of the
white matter of the spinal cord, and also arise from
Pain in humans is represented in a widely distributed homologous nuclei in the brainstem receiving primary
brain network that reflects the multidimensional nature afferents from the head and face. Ascending nociceptive
of the sensation.1 Evidence from studies involving inputs from the spinal cord project to two principal sites
patients with brain lesions and functional brain imaging in the brain: the brainstem via spinobulbar pathways and
studies of healthy people and clinical groups point to the thalamus via the spinothalamic tract.
a high level of integration among brain regions impli-
cated in pain processing.2,3 A single, critical pain region Spinobulbar Pathways
in the brain does not exist,4 which means that lesions
or antagonism of components of the pain network can Nociceptive inputs from the spinal cord project to nuclei
change the expression of the sensation but are unlikely in the brainstem including the periaqueductal grey (PAG)
to eradicate pain altogether. One way to understand and parabrachial region. Relays from these nuclei ascend
distributed pain processing is to ascribe functional attri- to subcortical regions, but also project to other regions
butes to regions incorporated in the network. In order in the brainstem. The two principal functions of spino-
to appreciate the neural integration requisite for pain bulbar pathways relevant to pain experience are descend-
it is first necessary to consider the functional components ing modulation of nociceptive processing in the spinal
of the sensation. cord and the control of autonomic responses.
161
162 PART II  Advances in Theory and Practice

The PAG is a midbrain region that has been impli- amygdala are mainly to the central part of the structure.32
cated in descending modulation of dorsal horn responses The amygdala plays a role in pain-related emotional
to nociceptive inputs from the periphery (Fig. 16-1C). responses, such as anxiety, and is also involved in the
Very early electrophysiological studies and neurosurgical conditioned fear that can be enlisted by painful
interventions showed that stimulation of the PAG was stimulation.33–35 Emotional responses associated with
associated with analgesia in animals and humans.15–17 activation in the amygdala are likely to be contingent on
Further animal studies established that the influence of projections to other cortical brain regions. It is salient to
the PAG on spinal processing was mediated via relay note when considering musculoskeletal pain that para-
through the rostral ventral medulla18 (Fig. 16-1E), and brachial pathways may be especially important for the
recent functional brain imaging studies have provided relay of nociceptive information from bone.36
evidence to support a similar role for this region in
humans.19 However, descending modulation of the dorsal Spinothalamic Pathways and Other
horn is not confined to inhibition. Stimulation of the Hemispheric Regions
rostral ventral medulla can lead to facilitation of nocicep-
tive processing in the spinal cord,20 and the rostral ventral Projections originating from the dorsal horn terminate
medulla has been implicated in the development of in two main regions of the thalamus: the ventroposterior
hyperalgesia subsequent to tissue injury and inflamma- lateral nucleus and the medially located intralaminar and
tion.21 Importantly, the PAG is subject to control by medial dorsal nuclei.37 The ventroposterior lateral nucleus
higher brain centres, including the prefrontal cortex.22,23 relays nociceptive input to the primary and secondary
Collectively, spinobulbospinal pathways and higher- somatosensory cortex. Projections from the medial thala-
order brain inputs to these pathways constitute a network mus terminate in the cingulate cortex, insula and prefron-
with significant implications for the experience of pain. tal cortex. A third region in the posterior part of the
Contributions of this modulating network to spinal cord ventromedial thalamus may receive input from the spi-
processing can dampen or exacerbate pain depending on nothalamic tract and project to the posterior part of the
a wide range of contingencies, and could provide partial insula,38 although the role of this pathway in nociception
explanation for the plasticity of pain reports encountered is disputed.39 Human functional brain imaging studies
in clinical practice. show pain activation throughout the projection sites of
Nociceptive inputs to the parabrachial nuclei24,25 (Fig. the ventroposterior lateral nucleus and medial thalamus,
16-1D) are relayed in turn to the hypothalamus and although the consistencies of these activations vary
amygdala,26–28 although these structures may also receive regionally. The insula and cingulate cortex are most reli-
direct spinal nociceptive inputs. This spinoparabrachial ably activated in association with pain, whereas activation
pathway contributes to autonomic responses accompany- in the primary somatosensory cortex is inconsistent2,40
ing pain and may influence the expression of affective (see Fig. 16-2). Additionally, brain regions not in receipt
components of the experience.29 The hypothalamus is a of direct input from nociceptive thalamic nuclei also acti-
key brain region for the control of autonomic and neu- vate during the experience of pain. Pain activations in
roendocrine functions contributing to homoeostasis, and regions such as the amygdala are a consequence of bulbar
this region is likely to mediate pain-related responses via inputs, whereas activations in other regions such as the
pathways to the PAG.30 In addition to a role in analgesia, basal ganglia and association cortices are dependent on
the PAG has been implicated in emotion-related behav- corticocortical and cortico-thalamo-cortical connections
iours such as flight and freezing, and is also involved in or direct spinal inputs.41,42
the sympatho-excitation and inhibition that can accom- Investigations in humans have provided insights into
pany these behavioural states.31 Parabrachial inputs to the the hemispheric brain regions implicated in functional

A B C D E
FIGURE 16-1  ■  (A) A midline sagittal view of the brain is provided to show the location of the brainstem, which is enclosed within
the dashed box. (B) The brainstem outlined in panel A is enlarged and transverse lines indicate the axial level of images displayed
in the remaining panels. The z-value refers to the distance in mm inferior to the anterior commissure. (C) An axial slice through the
midbrain shows pain activations encompassing the ventrolateral regions of the periaqueductal grey. The aqueduct is visible on the
image as a dark oval region at the midline between the symmetrical activations. (D) The parabrachial regions are incorporated within
the pain activations on this axial slice at the upper level of the pons. (E) An axial slice through the upper (rostral) part of the medulla
also cuts through the lowest portion of the pons (grey tissue highest in the panel). The pain activation overlays the midline nucleus
raphe magnus, which is the human homologue of the rostroventral medulla in animals. For colour version see Plate 15.
 16  Musculoskeletal Pain in the Human Brain 163

A B

C D

E F

FIGURE 16-2  ■  (A) A three-dimensional rendering of the left hemisphere of human brain is traversed by two yellow lines that indicate
the positions of axial slices shown in panels C and E. The z-values are the distances in mm of the lines above the anterior commis-
sure. (B) The hemispheres are viewed from above to show the position of a sagittal slice 2 mm into the left hemisphere (x = −2)
and a coronal slice 20 mm posterior to the anterior commissure (y = −20). The slices appear in panels D and F. (C) Pain activation
commonly occurs in the insula and prefrontal cortex (PFC). Regions within the basal ganglia, such as the putamen can also show
pain activation. (D) The thalamus is the projection site of inputs from the spinothalamic tract. The ventroposterior lateral nuclei of
the thalamus project to the primary (SI) and secondary (SII) somatosensory cortices. (E) The midcingulate cortex (MCC) almost
invariably activates in association with pain. The primary somatosensory cortex (SI) is less consistently activated during noxious
stimulation. Pain activation in the posterior parietal cortex (PPC) predominates in the right hemisphere for stimuli on either side of
the body, although the left PPC can also activate during pain. (F) The midcingulate cortex (MCC) is a midline structure that is proxi-
mal to, and has connections with, the supplementary motor area (SMA). For colour version see Plate 16.

components of the pain experience. Generally, distrib- This model proposes a lateral pathway incorporating the
uted regions represent individual dimensions of the pain ventroposterior lateral and its projection sites in the
experience, and regions within these networks are fre- primary and secondary somatosensory cortices that is
quently implicated in more than one functional process. involved in discriminative pain processes, and a medial
Schemas have been developed to encapsulate structure/ pathway including the medial thalamus, cingulate cortex,
function relationships, of which a model of medial and insula and prefrontal cortex that has been ascribed with
lateral pain pathways has been most frequently espoused.43 a role in the affective/motivational aspect of pain. The
164 PART II  Advances in Theory and Practice

general tenets of medial and lateral pain pathways are have important implications for understanding the vaga-
sound from a neuroanatomical perspective, but the ries of clinical presentations.4 The general approach of
empirical data from functional brain imaging studies these studies is to manipulate participants’ beliefs or
would suggest a high level of integration between the expectations about the meaning or nature of pain and to
constituent brain regions that is not consistent with a identify activation in brain regions that accompany
dichotomous division of functional processes.44 Out- decreases or increases in pain engendered by the experi-
comes from lesion studies and direct brain stimulation mental paradigm. These studies usually find two types of
also support the proposition that the neural substrates of response patterns. Firstly, the distributed pain network
pain functions are best conceptualized as distributed, shows levels of activation that correspond with partici-
dynamic, interdependent activations.3,45 pants’ reports, in that a reduction or exacerbation of pain
Intensity coding is a feature of almost all brain regions will be associated with decreased or increased levels of
implicated in pain processing. For instance, studies com- activation in pain regions, which suggests that a neuro-
paring responses to varied stimulus intensities show grad- biological process is operating, as distinct from a psycho-
uated responses in thalamus, insula, and the cingulate, logically mediated relabelling phenomenon.58 Secondly,
somatosensory and prefrontal cortices.46,47 These out- studies involving cognitive manipulation also show
comes are compatible with the behavioural observation regions where activation patterns are related to modula-
that most features of pain are closely related to intensity. tion. Typically, these patterns are not aligned with cogni-
As pain becomes more intense it also becomes more tive processing, nor with pain processing, but do show an
unpleasant, more salient, more threatening and more interaction between cognition and pain.59 In other words,
likely to arouse anxiety, etc. However, functional brain these activation patterns implicate regions as active con-
imaging studies that manipulate stimuli in the context of tributors to the modification of pain. The network of
matching tasks have identified a more circumscribed regions implicated in pain modulation is the same for
network involved in judgements of pain intensity. This paradigms that make pain more or less intense, and incor-
network includes insula and prefrontal regions that are porates the dorsolateral and ventromedial prefrontal cor-
distinct from posterior parietal cortex and dorsolateral tices, the pregenual cingulate cortex, thalamus, PAG and
prefrontal cortex that activate in association with pain rostral ventral medulla.60 Given the established role of
localization.48,49 Judgements of both intensity and local- the PAG and the rostral ventral medulla in descending
ization of pain are associated with activation in the cin- modulation of spinal processing, it would appear that
gulate cortex. Collectively, these findings resonate with thoughts about pain fundamentally change the level of
findings from other sensory modalities whereby ventrally nociceptive input to the brain.
directed processes code the ‘what’ and a dorsal stream
processes the ‘where’ of afferent inputs.50
The representation of pain unpleasantness is of con- THE PAIN NETWORK IN
siderable interest, given that this intrinsic attribute dis- MUSCULOSKELETAL DISORDERS
tinguishes pain from other, exteroceptive sensations like
vision and hearing that do not incorporate an affective The preceding discussion provided a broad outline of
component. It is likely that processes in the brainstem, pain regions and functions based on studies involving
hypothalamus and amygdala contribute to the unpleas- experimental pain. In many respects, the processing
antness of pain, although it is debatable whether activa- of pain under experimental conditions is likely to recruit
tion in these regions would equate with conscious similar mechanisms to those that operate under clinical
experience.7 Implicating other brain regions in the con- conditions. However, there are attributes of clinical
scious experience of pain unpleasantness is difficult to do pain that distinguish the experience from experimental
because pain unpleasantness and intensity are very closely pain paradigms and could potentially involve distinct
related. There are circumstances such as the repeated neural representations. Broadly speaking, commonalities
application of noxious heat and hypnotic suggestion and differences between experimental and clinical pain
where pain intensity and unpleasantness vary indepen- can be considered in the contexts of evoked and
dently, and in these cases the mid cingulate cortex shows spontaneous pain.
activation levels that most accurately reflect variance in
pain unpleasantness.11,51 A number of other unpleasant
interoceptive sensations also show this pattern of activa-
Evoked Pain in Musculoskeletal Disease
tion in the mid cingulate cortex.52–55 Like other intero- The modus operandi of many pain-processing experi-
ceptive sensations, the affective dimension of pain is a key ments is to compare and contrast regional signals mea-
attribute of the experience that increases the likelihood sured from the brain during the application of a noxious
of adaptive behaviours compatible with tissue integrity. extrinsic stimulus versus a no-stimulus or innocuous-
Consequently, it is notable that the mid cingulate cortex stimulus control.1 Regions showing significantly increased
has established connections to motor and premotor cor- levels of signal change during noxious stimulation com-
tices, and this circuitry may be involved in the motivation pared to control stimuli are ascribed with a role in pain
of actions that are compatible with pain avoidance or processing. Contrasts compatible with functional brain
relief.56,57 imaging can be applied in the context of musculoskeletal
The interaction between cognition and pain process- pain with varying degrees of ecological validity.
ing has received sustained attention among researchers Pain responses to the same stimulus modality at a site
who argue convincingly that this interplay is likely to unrelated to clinical pain can be compared between
 16  Musculoskeletal Pain in the Human Brain 165

healthy people and patients with a musculoskeletal condi- that permit meaningful tests of signal changes measured
tion to assess the effects of ongoing pain on central pro- with functional brain imaging techniques. Despite these
cessing of a novel stimulus. Generally, studies of this type difficulties there have been a handful of studies of spon-
are notably for comparable or slightly reduced pain acti- taneous musculoskeletal pain and the outcomes point to
vation in patients compared to healthy groups,2 and this important distinctions in the representation of ongoing
outcome may not be unexpected given that the relation- symptoms. Analyses based on spontaneous fluctuations of
ship between the stimulus and the clinical condition is intensity in chronic back and osteoarthritis pain have
tenuous at best. Nevertheless, studies of this type can identified activations in regions including the ventrome-
provide insights into other aspects of the pain experience dial prefrontal cortex, amygdala, nucleus accumbens and
when the experimental paradigm incorporates additional orbitofrontal cortex.64,66,70,71 A parsimonious explanation
components such as manipulation of cognition or asso- for this medial prefrontal–limbic network activation is
ciations with mood state. that the principal components of ongoing musculoskel-
Measures of central pain processing associated with etal pain are cognitive and emotional. The relative
stimulation of clinically relevant sites have shown differ- absence of regional activity elsewhere in the brain that
ences between patients with some clinical conditions and typically accompanies brief experimental pain stimuli,
controls that point to plasticity of responses. The most and is likely involved in sensory discrimination, would
readily apparent example of altered pain processing in a suggest that discriminative components have less func-
musculoskeletal condition is the impact of fibromyalgia tional relevance as pain persists. The outcomes of studies
on responses to noxious pressure. Patients with fibromy- of spontaneous pain await replication and expansion
algia show greatly enhanced activation throughout the before definitive conclusions can be reached, but results
pain network compared to healthy controls stimulated to date would suggest that caution should be exercised
with similar levels of pressure.61 This outcome corrobo- when making inferences about clinical pain processing on
rates the heightened sensitivity to pressure that is a hall- the basis of experimental pain paradigms involving brief
mark of the disease,62 but does not necessarily implicate extrinsic stimulation.
central processing as a causal mechanism because an
increase in central responses would also be expected if
peripheral inputs were up-regulated. However, there is MUSCULOSKELETAL PHYSIOTHERAPY
evidence that fibromyalgia patients show decreased pain AND PAIN PROCESSING
activation in a key modulation region, the pregenual cin-
gulate cortex, when compared to controls, suggesting an Commentaries advocating research into the interaction
impairment of endogenous analgesia in the clinical of musculoskeletal physiotherapy and central pain pro-
group.63 Similar studies involving pressure applied to the cessing in musculoskeletal disorders regularly appear in
knee in people with osteoarthritis and healthy controls the literature,72–74 but unfortunately very few empirical
have not shown differences of hemispheric activation studies have been published. Indeed, despite reasoned
between groups.64–66 This absence of effect is unexpected arguments that manual therapy is likely to recruit endog-
given that hyperalgesia under experimental conditions enous inhibitory circuits,75 there have been no reports in
and in neuropathic pain states is associated with changes support of this contention using imaging techniques that
in pain processing that point to fundamental differences provide functional neuroanatomical information. The
in the processing of pain from sensitized tissues,67 pos- limited information regarding pain processing and mus-
sibly reflecting the unique implications of these inputs for culoskeletal physiotherapy that has been published relates
physiological integrity.68 However, studies of pain from to behaviour-related changes and the application of
clinically relevant sites in musculoskeletal conditions are transcutaneous electrical nerve stimulation (TENS).76,77
scarce and consequently conclusions about the represen- In addition to widespread pain and tenderness, people
tation of hyperalgesia in osteoarthritis and similar condi- with fibromyalgia also demonstrate low levels of activity
tions should await further studies. compared to their healthy counterparts.78 The degree of
activity impairment in fibromyalgia bears a relationship
to pain sensitivity, in that the least active patients show
Central Processing of Spontaneous Pain the greatest levels of sensitivity to noxious thermal
Ongoing, spontaneous pain is the most common com- stimuli.77 The relationship between activity and pain sen-
plaint of people with musculoskeletal conditions. Indeed, sitivity extends to regional brain responses in fibromyal-
pain at rest or in association with movement among gia. Brain regions implicated in modulation, such as the
people with musculoskeletal disorders is probably the dorsolateral prefrontal cortex, show increasing levels of
most prevalent of any type of pain in the community at activation in association with increased activity, whereas
large.69 Consequently, it is not difficult to motivate studies the converse relationship is evident for activation in the
of central processing of spontaneous musculoskeletal somatosensory cortex, possibly reflecting diminished dis-
pain, yet experiments of this type are rarely reported. The criminative processing in the more active patients.77
paucity of literature relates to the mismatch between the These outcomes point to interesting interactions between
techniques of functional brain imaging and the behaviour motor programming and pain processing, and chapters
of spontaneous pain. As mentioned in the previous elsewhere in this book discuss these issues in detail.
section, functional brain imaging is dependent on con- Nevertheless, the association between activity and
trasts between different states. Spontaneous pain may not pain-related regional brain responses in people with
conveniently turn on and off nor vary in predictable ways fibromyalgia, supported by findings in other settings,79
166 PART II  Advances in Theory and Practice

provides considerable impetus to explore similar pro- 11. Rainville P, Bao QV, Chretien P. Pain-related emotions modulate
cesses in musculoskeletal conditions more generally. experimental pain perception and autonomic responses. Pain
2005;118(3):306–18.
TENS is occasionally used by musculoskeletal thera- 12. Magni G, Marchetti M, Moreschi C, et al. Chronic musculoskeletal
pists to relieve pain, and a recent meta-analysis lends pain and depressive symptoms in the National Health and Nutri-
support to the device as a management strategy in mus- tion Examination. I. Epidemiologic follow-up study. Pain 1993;
culoskeletal disorders.80 Measurement of laser-evoked 53(2):163–8.
13. Apkarian AV, Baliki MN, Geha PY. Towards a theory of chronic
potentials in healthy people has shown that TENS is pain. Prog Neurobiol 2009;87(2):81–97.
associated with an attenuation of key pain-related peaks 14. Turner JA, Dworkin SF, Mancl L, et al. The roles of beliefs,
in the electroencephalogram,81 which supports the con- catastrophizing, and coping in the functioning of patients with
clusion that the treatment can decrease levels of activa- temporomandibular disorders. Pain 2001;92(1–2):41–51.
tion in the pain network. A similar effect of TENS has 15. Hosobuchi Y, Adams JE, Linchitz R. Pain relief by electrical stimu-
lation of the central gray matter in humans and its reversal by
also been demonstrated using fMRI in patients with a naloxone. Science 1977;197(4299):183–6.
musculoskeletal condition.76 Additionally, the fMRI study 16. Mayer DJ, Wolfle TL, Akil H, et al. Analgesia from electrical
showed increased pain-related activation in the prefron- stimulation in the brainstem of the rat. Science 1971;174(4016):
tal and posterior parietal cortices that correlated with 1351–4.
17. Reynolds DV. Surgery in the rat during electrical analgesia induced
TENS-related levels of pain relief, suggesting that the by focal brain stimulation. Science 1969;164(3878):444–5.
device had recruited pain modulation circuits in the 18. Gebhart GF. Descending modulation of pain. Neurosci Biobehav
patients with subacromial impingement syndrome. Rev 2004;27(8):729–37.
19. Eippert F, Bingel U, Schoell ED, et al. Activation of the opioidergic
descending pain control system underlies placebo analgesia.
Neuron 2009;63(4):533–43.
CONCLUSIONS 20. Zhuo M, Gebhart GF. Characterization of descending inhibition
and facilitation from the nuclei reticularis gigantocellularis and
Pain is represented in the brain by a dynamic network that gigantocellularis pars alpha in the rat. Pain 1990;42(3):337–50.
subserves multiple functions requisite for integrated 21. Urban MO, Gebhart GF. Supraspinal contributions to hyperalge-
sia. Proc Natl Acad Sci U S A 1999;96(14):7687–92.
sensory experience. The pain network is notable for its 22. Duncan NW, Wiebking C, Tiret B, et al. Glutamate concentration
plasticity, which is aided by caudally orientated circuits in the medial prefrontal cortex predicts resting-state cortical-
that extend beyond the brain to exert influence on the subcortical functional connectivity in humans. PLoS ONE 2013;
lowest levels of central nociceptive processing in the 8(4):e60312.
spinal cord. Musculoskeletal pain that persists may have a 23. Keay KA, Bandler R. Parallel circuits mediating distinct emotional
coping reactions to different types of stress. Neurosci Biobehav Rev
unique representation in the human brain that empha- 2001;25(7–8):669–78.
sizes the emotional and cognitive dimensions of pain 24. Bester H, Chapman V, Besson JM, et al. Physiological properties
experience. Therapists have recognized that strategies of the lamina I spinoparabrachial neurons in the rat. J Neurophysiol
directed at pain processing have great potential in the 2000;83(4):2239–59.
25. Bester H, Matsumoto N, Besson JM, et al. Further evidence for the
management of musculoskeletal disorders given the involvement of the spinoparabrachial pathway in nociceptive pro-
demonstrable capacity of the network for endogenous cesses: a c-Fos study in the rat. J Comp Neurol 1997;383(4):
modulation. Clinicians and researchers involved in 439–58.
musculoskeletal physiotherapy have a clear rationale to 26. Bernard JF, Peschanski M, Besson JM. A possible spino (trigemino)-
develop and test new methods that target pain processing. ponto-amygdaloid pathway for pain. Neurosci Lett 1989;100(1–3):
83–8.
27. Jasmin L, Burkey AR, Card JP, et al. Transneuronal labeling of a
REFERENCES nociceptive pathway, the spino-(trigemino-)parabrachio-
1. Peyron R, Laurent B, Garcia-Larrea L. Functional imaging of brain amygdaloid, in the rat. J Neurosci 1997;17(10):3751–65.
responses to pain. A review and meta-analysis (2000). Clin Neuro- 28. Pan B, Castro-Lopes JM, Coimbra A. Central afferent pathways
physiol 2000;30(5):263–88. conveying nociceptive input to the hypothalamic paraventricular
2. Apkarian AV, Bushnell MC, Treede RD, et al. Human brain mecha- nucleus as revealed by a combination of retrograde labeling and
nisms of pain perception and regulation in health and disease. Eur c-fos activation. J Comp Neurol 1999;413(1):129–45.
J Pain 2005;9(4):463–84. 29. Benarroch EE. Pain-autonomic interactions: a selective review.
3. Garcia-Larrea L. Insights gained into pain processing from patients Clin Auton Res 2001;11(6):343–9.
with focal brain lesions. Neurosci Lett 2012;520(2):188–91. 30. Lumb BM. Hypothalamic and midbrain circuitry that distinguishes
4. Tracey I, Mantyh PW. The cerebral signature for pain perception between escapable and inescapable pain. News Physiol Sci
and its modulation. Neuron 2007;55(3):377–91. 2004;19:22–6.
5. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 31. Bandler R, Keay KA, Floyd N, et al. Central circuits mediating
1965;150(3699):971–9. patterned autonomic activity during active vs. passive emotional
6. Melzack R, Casey KL. Sensory, motivational and central control coping. Brain Res Bull 2000;53(1):95–104.
determinants of chronic pain: A new conceptual model. In: 32. Gauriau C, Bernard JF. Pain pathways and parabrachial circuits in
Kenshalo DR, editor. The Skin Senses. Springfield, IL: Chas the rat. Exp Physiol 2002;87(2):251–8.
C. Thomas; 1968. p. 423–39. 33. Ji G, Fu Y, Ruppert KA, et al. Pain-related anxiety-like behavior
7. Price DD. Psychological and neural mechanisms of the affective requires CRF1 receptors in the amygdala. Mol Pain 2007;3:13.
dimension of pain. Science 2000;288(5472):1769–72. 34. Neugebauer V, Li W, Bird GC, et al. The amygdala and persistent
8. Merskey H, Bogduk N. Classification of Chronic Pain, IASP Task pain. Neuroscientist 2004;10(3):221–34.
Force on Taxonomy. Seattle. USA: IASP Press; 1994. 35. Gao YJ, Ren WH, Zhang YQ, et al. Contributions of the anterior
9. Gracely RH, McGrath P, Dubner R. Validity and sensitivity of ratio cingulate cortex and amygdala to pain- and fear-conditioned place
scales of sensory and affective verbal pain descriptors: manipulation avoidance in rats. Pain 2004;110(1–2):343–53.
of affect by diazepam. Pain 1978;5(1):19–29. 36. Williams MC, Ivanusic JJ. Evidence for the involvement of the
10. Price DD, Harkins SW, Baker C. Sensory-affective relationships spinoparabrachial pathway, but not the spinothalamic tract or post-
among different types of clinical and experimental pain. Pain synaptic dorsal column, in acute bone nociception. Neurosci Lett
1987;28(3):297–307. 2008;443(3):246–50.
 16  Musculoskeletal Pain in the Human Brain 167

37. Hodge CJ Jr, Apkarian AV. The spinothalamic tract. Crit Rev Neu- 62. Wolfe F, Clauw DJ, Fitzcharles MA, et al. The American College
robiol 1990;5(4):363–97. of Rheumatology preliminary diagnostic criteria for fibromyalgia
38. Craig AD, Zhang ET. Retrograde analyses of spinothalamic projec- and measurement of symptom severity. Arthritis Care Res
tions in the macaque monkey: input to posterolateral thalamus. 2010;62(5):600–10.
J Comp Neurol 2006;499(6):953–64. 63. Jensen KB, Kosek E, Petzke F, et al. Evidence of dysfunctional pain
39. Graziano A, Jones EG. Widespread thalamic terminations of fibers inhibition in fibromyalgia reflected in rACC during provoked pain.
arising in the superficial medullary dorsal horn of monkeys and Pain 2009;144(1–2):95–100.
their relation to calbindin immunoreactivity. J Neurosci 2004; 64. Baliki MN, Geha PY, Jabakhanji R, et al. A preliminary fMRI study
24(1):248–56. of analgesic treatment in chronic back pain and knee osteoarthritis.
40. Farrell MJ, Laird AR, Egan GF. Brain activity associated with pain- Mol Pain 2008;4:47.
fully hot stimuli applied to the upper limb: a meta-analysis. Hum 65. Gwilym SE, Keltner JR, Warnaby CE, et al. Psychophysical and
Brain Mapp 2005;25(1):129–39. functional imaging evidence supporting the presence of central
41. Cavada C, Goldman-Rakic PS. Posterior parietal cortex in rhesus sensitization in a cohort of osteoarthritis patients. Arthritis Rheum
monkey: I. Parcellation of areas based on distinctive limbic and 2009;61(9):1226–34.
sensory corticocortical connections. J Comp Neurol 1989; 66. Parks EL, Geha PY, Baliki MN, et al. Brain activity for chronic
287(4):393–421. knee osteoarthritis: dissociating evoked pain from spontaneous
42. Chudler EH, Dong WK. The role of the basal ganglia in nocicep- pain. Eur J Pain 2011;15(8):843, e1–14.
tion and pain. Pain 1995;60(1):3–38. 67. Lanz S, Seifert F, Maihofner C. Brain activity associated with pain,
43. Treede RD, Kenshalo DR, Gracely RH, et al. The cortical repre- hyperalgesia and allodynia: an ALE meta-analysis. J Neural Transm
sentation of pain. Pain 1999;79(2–3):105–11. 2011;118(8):1139–54.
44. Brooks J, Tracey I. From nociception to pain perception: imaging 68. Lorenz J, Minoshima S, Casey KL. Keeping pain out of mind: the
the spinal and supraspinal pathways. J Anat 2005;207(1):19–33. role of the dorsolateral prefrontal cortex in pain modulation. Brain
45. Mazzola L, Isnard J, Peyron R, et al. Stimulation of the human 2003;126(Pt 5):1079–91.
cortex and the experience of pain: Wilder Penfield’s observations 69. Magni G, Caldieron C, Rigatti-Luchini S, et al. Chronic musculo-
revisited. Brain 2012;135(Pt 2):631–40. skeletal pain and depressive symptoms in the general population.
46. Coghill RC, Sang CN, Maisog JM, et al. Pain intensity processing An analysis of the 1st National Health and Nutrition Examination
within the human brain: a bilateral, distributed mechanism. J Neu- Survey data. Pain 1990;43(3):299–307.
rophysiol 1999;82(4):1934–43. 70. Howard MA, Sanders D, Krause K, et al. Alterations in resting-
47. Derbyshire SW, Jones AK, Gyulai F, et al. Pain processing during state regional cerebral blood flow demonstrate ongoing pain in
three levels of noxious stimulation produces differential patterns of osteoarthritis: an arterial spin-labeled magnetic resonance imaging
central activity. Pain 1997;73(3):431–45. study. Arthritis Rheum 2012;64(12):3936–46.
48. Oshiro Y, Quevedo AS, McHaffie JG, et al. Brain mechanisms sup- 71. Kulkarni B, Bentley DE, Elliott R, et al. Arthritic pain is processed
porting discrimination of sensory features of pain: a new model. in brain areas concerned with emotions and fear. Arthritis Rheum
J Neurosci 2009;29(47):14924–31. 2007;56(4):1345–54.
49. Lobanov OV, Quevedo AS, Hadsel MS, et al. Frontoparietal mech- 72. Moseley GL. Pain, brain imaging and physiotherapy–opportunity
anisms supporting attention to location and intensity of painful is knocking. Man Ther 2008;13(6):475–7.
stimuli. Pain 2013;154(9):1758–68. 73. Shacklock MO. Central pain mechanisms: A new horizon in manual
50. Reed CL, Klatzky RL, Halgren E. What vs. where in touch: an therapy. Aust J Physiother 1999;45(2):83–92.
fMRI study. Neuroimage 2005;25(3):718–26. 74. Zusman M. Forebrain-mediated sensitization of central pain path-
51. Tolle TR, Kaufmann T, Siessmeier T, et al. Region-specific encod- ways: ‘non-specific’ pain and a new image for MT. Man Ther
ing of sensory and affective components of pain in the human brain: 2002;7(2):80–8.
a positron emission tomography correlation analysis. Ann Neurol 75. Vicenzino B, Wright A. Managing pain: physical treatments.
1999;45(1):40–7. In: Strong J, Unruh AM, Wright A, et  al., editors. Pain: a Text-
52. Farrell MJ, Cole LJ, Chiapoco D, et al. Neural correlates coding book for Therapists. Edinburgh: Churchill Livingston; 2002.
stimulus level and perception of capsaicin-evoked urge-to-cough in p. 187–206.
humans. Neuroimage 2012;61(4):1324–35. 76. Kocyigit F, Akalin E, Gezer NS, et al. Functional magnetic reso-
53. Farrell MJ, Egan GF, Zamarripa F, et al. Unique, common, and nance imaging of the effects of low-frequency transcutaneous elec-
interacting cortical correlates of thirst and pain. Proc Natl Acad Sci trical nerve stimulation on central pain modulation: a double-blind,
U S A 2006;103(7):2416–21. placebo-controlled trial. Clin J Pain 2012;28(7):581–8.
54. Farrell MJ, Johnson J, McAllen R, et al. Brain activation associated 77. McLoughlin MJ, Stegner AJ, Cook DB. The relationship between
with ratings of the hedonic component of thermal sensation during physical activity and brain responses to pain in fibromyalgia. J Pain
whole-body warming and cooling. J Therm Biol 2011;36:57–63. 2011;12(6):640–51.
55. von Leupoldt A, Sommer T, Kegat S, et al. Dyspnea and pain share 78. McLoughlin MJ, Colbert LH, Stegner AJ, et al. Are women with
emotion-related brain network. Neuroimage 2009;48(1):200–6. fibromyalgia less physically active than healthy women? Med Sci
56. Dum RP, Levinthal DJ, Strick PL. The spinothalamic system Sports Exerc 2011;43(5):905–12.
targets motor and sensory areas in the cerebral cortex of monkeys. 79. Villamar MF, Wivatvongvana P, Patumanond J, et al. Focal modu-
J Neurosci 2009;29(45):14223–35. lation of the primary motor cortex in fibromyalgia using 4×1-ring
57. Perini I, Bergstrand S, Morrison I. Where pain meets action in the high-definition transcranial direct current stimulation (HD-tDCS):
human brain. J Neurosci 2013;33(40):15930–9. immediate and delayed analgesic effects of cathodal and anodal
58. Benedetti F, Mayberg HS, Wager TD, et al. Neurobiological stimulation. J Pain 2013;14(4):371–83.
mechanisms of the placebo effect. J Neurosci 2005;25(45): 80. Johnson M, Martinson M. Efficacy of electrical nerve stimulation
10390–402. for chronic musculoskeletal pain: a meta-analysis of randomized
59. Bantick SJ, Wise RG, Ploghaus A, et al. Imaging how attention controlled trials. Pain 2007;130(1–2):157–65.
modulates pain in humans using functional MRI. Brain 2002;125(Pt 81. Vassal F, Creac’h C, Convers P, et al. Modulation of laser-evoked
2):310–19. potentials and pain perception by transcutaneous electrical nerve
60. Tracey I. Getting the pain you expect: mechanisms of placebo, stimulation (TENS): a placebo-controlled study in healthy volun-
nocebo and reappraisal effects in humans. Nat Med 2010;16(11): teers. Clin Neurophysiol 2013;124(9):1861–7.
1277–83.
61. Gracely RH, Petzke F, Wolf JM, et al. Functional magnetic reso-
nance imaging evidence of augmented pain processing in fibromy-
algia. Arthritis Rheum 2002;46(5):1333–43.
 CHAPTER 17 

Advances in Electromyography
Deborah Falla  •  Dario Farina

techniques, intramuscular electromyography allows the

INTRODUCTION activity of deep muscles to be recorded.
In 1929, Adrian and Bronk2 proposed the first elec­
Electromyography (EMG), a technique for the acquisi­ trode for intramuscular EMG, the concentric needle.
tion and analysis of myoelectric signals, has contributed This needle electrode detects signals between the tip of
significantly to the understanding of function and dys­ a wire insulated in the cannula and the cannula. Other
function of the neuromuscular system and has become an needle electrodes have since been proposed, such as a
essential tool in modern musculoskeletal physiotherapy. modified version of the concentric needle that comprised
The detection, recording and analysis of myoelectric 12 insulated wires (array) in a slot in the cannula.5 With
signals provide a reproducible means of determining this system it was possible to estimate the size of the
disturbances in muscle activation in patients with muscu­ territory of individual motor units. Contrary to needles,
loskeletal disorders. EMG is typically applied in muscu­ wire electrodes are flexible and therefore can be used
loskeletal physiotherapy for the assessment of disturbed with minimal discomfort for the subject. Modern types
muscle function and for monitoring changes with reha­ of wire electrode technology include multiple-site detec­
bilitation. The EMG signal provides information at tion systems on flexible substrates,6 for a well-defined
several levels, such as the onset or offset of muscle activ­ and reproducible spatial arrangement of the detection
ity, the progress of muscle fatigue, the intensity of muscle points.
activation, the directional specificity of muscle activation, Classic electrodes for surface EMG detection are
the spatial distribution of muscle activity and the behav­ made of solid silver or gold, sintered silver and silver
iour of individual motor units. This chapter will present chloride, carbon, sponge saturated with electrolyte gel or
an overview of contemporary electrode detection systems, conductive hydrogel. In clinical applications, gelled elec­
review fundamental methods of EMG assessment as a trodes are preferred over dry electrodes since the pres­
means of evaluating neuromuscular impairment in pa­ ence of gel reduces the influence of movement artefacts
tients with musculoskeletal disorders, and will discuss the on the signal quality. The classic recording modality for
limitations of EMG evaluation. surface EMG is the bipolar derivation, in which the
recorded signal is the difference between two electrodes
placed on the muscle at a distance, which is typically
ELECTRODE SYSTEMS 10–20 mm. In addition to the bipolar derivation, surface
EMG can be acquired by monopolar systems or as the
The electrical activity associated with the contraction linear combination of the electrical activity detected by
of muscle fibres in motor units can be recorded using more than two electrodes. For example, the double dif­
either intramuscular or non-invasive (surface) detection ferential system consists of three electrodes whose signals
systems. Intramuscular EMG signals are detected with are summed with weights −1, 2 and −1 to increase the
needles or wires inserted into muscles. With respect to selectivity with respect to the bipolar system.
non-invasive techniques, intramuscular EMG has greater Modern electrode technology for surface EMG con­
selectivity. Depending on the type of intramuscular sists of multi-channel systems with tens to hundreds of
electrode used and its location, the recorded action electrodes arranged in linear arrays or bi-dimensional
potentials can be the result of the activity of a small grids (for a recent review see Farina et al.7). Among the
(1–3), moderate (15–20) or large (more than 20) number multi-channel surface EMG systems, the so-called high-
of muscle fibres.1 In neurophysiological investigations, density EMG is characterized by a large number of elec­
intramuscular recordings are often used to identify the trodes (usually in the order of hundreds), closely spaced
discharge times of individual motor units.2 In this appli­ between each other (common separation of 2.5–10 mm)
cation, the shape of the action potentials is used to (Fig. 17-1). These recordings provide a two-dimensional
identify the occurrences of the discharges of the active sampling of the electric potential distribution over a large
motor units. Although surface EMG signals can also surface area during muscle contraction.8,9 Unlike classic
be decomposed into individual motor unit activities,3,4 bipolar EMG applications, this method provides a topo­
the analysis of motor unit behaviour is usually more graphical representation of EMG amplitude, and can
accurate using intramuscular systems because of the high identify relative adaptations in the intensity of activity
degree of selectivity. Moreover, by contrast with surface within regions of the muscle.9
168
 17  Advances in Electromyography 169

FIGURE 17-1  ■  Advances in electrode systems. Multi-channel surface EMG electrode grid containing 192 electrodes. The electrode
grid provides two-dimensional sampling of the electric potential distribution over a large surface area (e.g. around the forearm)
during muscle contraction.

Forward slide (FS) Backward slide (BS) Forward tilt (FT) Backward tilt (BT)
A
Sternocleidomastoid Splenius capitis

Controls
BT * BT *
Neck pain

BS * BS *

FS FS
* *

FT FT
* *
50 70 90 110 50 70 90 110
B Onset (ms) Onset (ms)

FIGURE 17-2  ■  Delayed onset of muscle activity. (A) Patients with chronic neck pain and healthy controls stood on a moveable plat-
form and were exposed to randomized full body postural perturbations (8 cm forward slides, 8 cm backward slides, 10° forward
tilts and 10° backward tilts). (B) Mean and SD of the onset of the sternocleidomastoid and splenius capitis muscles in response to
the perturbations. Note the significantly (* = P < 0.05) delayed onset time of the neck muscles for the patients with neck pain regard-
less of the perturbation direction. (Reprinted with permission from Boudreau and Falla.23)

APPLICATIONS evaluating the EMG responses of spinal muscles to

postural perturbations have revealed delayed trunk
Timing of Muscle Activity muscle responses in back14–21 and neck pain22,23 (Fig.
17-2). Alterations in the timing of muscle activity have
Detection of the onset and termination of muscle activ­ been identified in other musculoskeletal pain conditions
ity during tasks such as postural perturbations can be such as long-standing groin pain24 and knee pain.25 EMG
used to enhance our understanding of neuromuscular has also been applied in clinical trials to confirm that
control and the impact of musculoskeletal disorders. the onset of muscle activation can be enhanced via train­
Various methods can be employed to assess the onset ing in patients with various musculoskeletal disorders
and offset of EMG bursts, ranging from visual deter­ including low back pain,26 neck pain27 and patellofemoral
mination10,11 to computer-based algorithms.12,13 Studies pain syndrome.28
170 PART II  Advances in Theory and Practice

Myoelectric Manifestations of Fatigue perturbations in the intracellular and extracellular K+

and Na+ gradient concentrations.40 These alterations
The characteristics of the surface EMG signal vary during depolarize the sarcolemma and t-tubular membranes that
sustained muscle contractions and these modifications reduce membrane excitability.39 The changes in CV
are usually termed as myoelectric manifestations of determine changes in the power spectral variables since
muscle fatigue.29–31 The application of EMG to monitor CV scales the EMG power spectrum towards lower fre­
fatigue is common due to the immediate changes that quencies.29,34,38,41,42 However, other factors, in addition
occur in the EMG signal from the onset of the contrac­ to CV, also influence spectral variables, such as the shape
tion which allows fatigue to be assessed during short- of the intracellular action potential, motor unit
duration contractions.31–33 synchronization43–45 and progressive motor unit recruit­
For the assessment of myoelectric manifestations of ment.46 Despite the large number of influencing factors,
fatigue, linear arrays of at least four electrodes are typi­ the high correlation usually observed between relative
cally applied. The most frequently monitored surface changes in CV and spectral variables in isometric
EMG variables are the mean or median power spectral conditions47–50 indicates that CV has a strong influence
frequencies, the signal amplitude estimates such as the on spectral variables.
average rectified value or root mean square, and muscle To analyse myoelectric manifestations of muscle
fibre conduction velocity (CV). The typical pattern fatigue in isometric conditions and allow comparison
observed during sustained, relatively high force contrac­ between different variables, different muscles and differ­
tions is a decrease in both the CV and spectral variables ent subjects, a fatigue plot is usually produced.51 The
over time,29,33–35 and an initial increase followed by a fatigue plot reports each surface EMG variable over time
decrease in signal amplitude (although amplitude trends (duration of contraction) after normalization relative to
are not as consistent as the spectral and CV trends).33,36,37 a reference value (typically the initial value) (Fig. 17-3).
The decrement of CV over time during sustained As demonstrated elsewhere,29 the fatigue plot highlights
isometric contractions33,38 is due to alterations of sarco­ differences in myoelectric manifestations of fatigue,
lemma excitability.39 The generation of action potentials which might be related to different pools of activated
induces cellular K+ efflux and Na+ and Cl− influx, causing motor units and muscle fibres.

Force ARV CV MNF

Norm. values (%)

110 300 120 120

100 100 100
200 80
90 80 60
80 100 60 40
0 5 10 15 20 0 5 10 15 20 0 5 10 15 20 0 5 10 15 20
A Time (s) Time (s) Time (s) Time (s)

300

250
Norm. values (%)

200

ARV
Force
150
CV
MNF

100

50
0 5 10 15 20
B Time (s)

FIGURE 17-3  ■  Fatigue plot. (A) Individual plots of the surface EMG variables average rectified value (ARV), conduction velocity (CV),
mean frequency (MNF) and force recorded from the anterior scalene muscle of a healthy control contracting at 25% of their maximum
voluntary neck flexion force. Plots are obtained by normalizing each variable with respect to the initial value of its own regression
line. (B) The time course of MNF, ARV, CV and force are combined to produce a ‘fatigue plot’. Note that although the force is main-
tained constant, the signal characteristics are modified from the onset of the contraction. Myoelectric manifestations of fatigue are
identified by an increase in ARV values with time and decrease in MNF and CV values.
 17  Advances in Electromyography 171

Greater myoelectric manifestations of fatigue have disorders. As an example, EMG studies have revealed
been identified in a number of musculoskeletal disorders, augmented superficial neck muscle activity during
including chronic low back and neck pain.52–58 Moreover, isometric contractions71–74 and functional upper limb
it has been shown that fatigue-related EMG variables activities75–77 in people with neck pain. Furthermore,
may have a diagnostic value.59 For example, the classifica­ increased co-contraction of trunk flexor and extensor
tion of individuals with low back pain with respect to muscles has been reported when a load is released unex­
controls reached approximately 90% accuracy when the pectedly from the trunk17 or during unexpected, multdi­
force values obtained from a maximum voluntary con­ rectional translation perturbations78,79 in low back pain.
traction were associated with the EMG spectral variables In addition, increased erector spinae activity has been
as features for the classification.60 observed during the stride80–82 and swing83,84 phase of gait
In more recent times, the estimation of CV and altera­ and bracing of the abdominal muscles is increased during
tions with fatigue have been monitored during fast an active straight leg raise.85 On the contrary, the activity
dynamic contractions, in addition to isometric tasks.61,62 of the deep cervical flexors (longus colli, longus capitis)71
Instantaneous mean power spectral frequency of the and deep extensors (semispinalis cervicis and multifi­
EMG signal can also be estimated with time-frequency dus)86,87 has commonly been found to be reduced in the
tools63 and used for muscle characterization in dynamic presence of neck pain. Likewise with low back pain, the
tasks.64 However, despite the strong association between tonic activity of the deep transversus abdominis may be
CV and spectral variables in isometric, constant force reduced during walking88 and during repetitive arm
contractions, these variables are poorly related during movements89 and the activity of the lumbar multifidus is
fast dynamic tasks when the number of active motor units decreased during trunk loading.90
fluctuates over time.65 This has been observed in several
experimental conditions (e.g. in high-load dynamic con­
tractions),66–69 which indicates that a direct estimation of
EMG Tuning Curves
CV is necessary to monitor fatigue during dynamic EMG tuning curves represent the intensity of muscle
activities. activity (amplitude) as a function of force direction and
have been used to study activation strategies of arm and
neck muscles.91–96 When tuning curves are consistent
EMG Amplitude among subjects, analysing the orientation and focus
The amplitude of the surface EMG is frequently used as (mean direction and spread of EMG activity, respectively;
a measure of the intensity of muscle activity and has often defined below) of EMG tuning curves in relation to mus­
been used as an indicator of muscle force. Since the culoskeletal mechanics has provided insight into central
surface EMG is a random signal, its amplitude cannot be nervous system (CNS) control.95
estimated as the peak value but rather needs statistical EMG tuning curves of neck muscles have been
estimators.70 Among the estimators of EMG amplitude, recorded by asking subjects to perform contractions at a
the average rectified value and root mean square are those predefined force (e.g. 15 N of force) with continuous
most often used. They correspond to the best (i.e. with change in force direction in the range 0–360° in the
minimal variability) estimators when the signal has a horizontal plane96 (Fig. 17-4A). During these circular
Gaussian (root mean square) or Laplacian (average recti­ contractions, the amplitude of the surface EMG is esti­
fied value) distribution of amplitude values. In practice, mated and represented as a function of the angle of force
they are equivalent and often used interchangeably in direction. The directional activation curves represent the
applications.70 modulation in intensity of muscle activity with the direc­
Although the amplitude of the surface EMG is related tion of force exertion and represent a closed area when
to the number of motor unit action potentials discharged expressed in polar coordinates. The line connecting the
(i.e. to the number of active units and their discharge origin with the central point (barycentre) of this area
rates), other factors influence its measure. Among these, defines a directional vector, whose length is expressed as
EMG amplitude is strongly influenced by the thickness of a percent of the mean average rectified value during the
the subcutaneous tissue, the length of the muscle fibres entire task. This normalized vector length represents the
and their orientation with respect to the electrodes.70 specificity of muscle activation with direction: it is equal
Moreover, amplitude values cannot be compared when to zero if the muscle is active in the same way in all direc­
different electrode systems or distances between elec­ tions and, conversely, it corresponds to 100% if the
trodes are used. For these reasons, normalization of the muscle is active in exclusively one direction (Fig. 17-4B).
EMG amplitude estimation is necessary for comparing In healthy subjects, neck muscles show well-defined
data across subjects or different muscles. Normalization of preferred directions of activation that are in accordance
the EMG amplitude is typically performed by expressing with their anatomical position relative to the spine.95–97
the value obtained during a sub-maximal task as a percent These observations suggest that the CNS copes with the
relative to the amplitude measured during a maximum vol­ anatomical complexity and redundancy of the neck
untary contraction or a reference voluntary contraction. muscles by developing consistent muscle synergies to
When patient populations are investigated, often a refer­ generate multidirectional patterns of force.95–97 However,
ence voluntary contraction is selected since a discrepancy recent studies have shown that patients with either
in strength likely exists between patients and controls. whiplash-induced neck pain or idiopathic neck pain have
Numerous studies have evaluated changes in the reduced specificity of neck muscle activity with respect
amplitude of muscle activation in various musculoskeletal to asymptomatic individuals87,96,98 (Fig. 17-4C).
172 PART II  Advances in Theory and Practice

0° 0° 50 0°
330 30 330 30 330 30
40
30
300 60 300 60 300 60
20
10

Degrees
270 90 270 90 0 270 90
–10
10
240 120 240 120 –20 240 120
20
–30
30
210 150 210 150 –40 210 150
180 180 40 180
µV –50
–50 –40 –30 –20 –10 0 10 20 30 40 50
A B C Degrees

FIGURE 17-4  ■  EMG tuning curves. (A) The subject performs a circular contraction in the horizontal plane at a defined force with
change in force direction in the range 0–360°. (B) During this task, the amplitude of the surface EMG is recorded and EMG tuning
curves are generated. The EMG tuning curve represents the modulation in intensity of muscle activity with the direction of force
exertion. The central point of the tuning curve defines a directional vector (dashed arrow), whose length is expressed as a percent
of the mean EMG amplitude during the entire task. This provides an objective measure of the directional specificity of muscle activ-
ity. (C) Data for the directional vector describing the specificity of sternocleidomastoid activity during the circular contraction per-
formed at 15 N of force. People with chronic neck pain displayed reduced values of directional specificity in the surface EMG of the
sternocleidomastoid muscle bilaterally (P < 0.05). Control data are presented in black and patient data in white. Squares represent
the left sternocleidomastoid and circles, the right sternocleidomastoid. (Reprinted with permission from Falla et al.96)

Polar plots or EMG tuning curves are also useful to Furthermore, a shift of activity towards the cranial region
display and compare the EMG amplitude of a muscle in of the upper trapezius muscle is observed in healthy indi­
response to multidirectional perturbations. For example, viduals during sustained shoulder abduction8,105,106 as
Figure 17-5 displays polar plots of the normalized EMG reflected by the change in the y-axis coordinate of the
amplitude of the left internal oblique, left erector spinae, root mean square map. This response reflects a greater
tibialis anterior and gastrocnemius muscles in response progressive recruitment of motor units within the cranial
to unexpected balance perturbations performed in 12 region of the upper trapezius muscle.105
directions in a group of individuals with and without low Redistribution of activity within the same muscle has
back pain.79 Note the increased activity in the gastrocne­ been shown to be functionally important to maintain
mius during backward perturbations (i.e. when acting as motor output in the presence of altered afferent feedback
a prime mover) in the control group and increased tibialis (e.g. pain or fatigue).8 This variation in activation within
anterior activation following perturbation directions in regions of the same muscle is potentially relevant to avoid
which the muscle would also act as a prime mover, namely overload of the same muscle fibres during prolonged
perturbation directions with a forward component. In activation and is of particular relevance for muscles com­
addition, the individuals with low back pain showed monly exposed to repetitive or sustained activation, such
reduced activation of the left internal oblique in direc­ as the upper trapezius muscle107 and the lumbar erector
tions with either a leftward or leftward/backward com­ spinae.108
ponent and increased left internal oblique activity during On the contrary, in the presence of either experimen­
perturbations in which the left internal oblique could tally induced muscle pain106,109,110 or clinical pain (e.g.
contribute to a hip/trunk strategy. fibromyalgia, low back pain),104,111 the redistribution of
activity to different regions of the muscle during sus­
tained contractions is reduced (Fig. 17-6). These findings
Distribution of Muscle Activity suggest that muscle pain prevents the adaptation of
Spatial heterogeneity in muscle activity has been observed muscle activity during sustained or repetitive contrac­
from multi-channel surface EMG recordings during sus­ tions as observed in non-painful conditions, which may
tained constant-force contractions,8,99 contractions of induce overuse of similar muscle regions with fatigue.
increasing load,99 and during dynamic contractions,100
which suggests a non-uniform distribution of motor units
or spatial dependency in the control of motor units.101,102
Muscle Synergies
To characterize the spatial distribution of muscle A long-lasting hypothesis in motor control is that the
activity, two coordinates of the centroid (centre of activ­ CNS adopts strategies that simplify the control of
ity) of the root mean square map (x- and y-axes coordi­ complex tasks by combining few motor modules.112 Unit
nates for the medial–lateral and cranial–caudal direction, burst generators,113 spinal force fields114 and muscle syn­
respectively) are typically calculated.8 Studies in asymp­ ergies115 have been proposed as modular elements. This
tomatic individuals show a change in the distribution of hypothesis has been indirectly verified by factorization of
activity over the lumbar erector spinae muscle during a multi-channel EMG signals (i.e. by analysing the dimen­
fatiguing sustained lumbar flexion contraction103 or sionality of EMG signals). During complex motor tasks,
during repetitive lifting104 as reflected by a shift of the it can be shown that the number of non-redundant signals
centroid towards the caudal region of the lumbar spine. necessary to explain the tasks is less than the number of
 17  Advances in Electromyography 173

Internal Oblique Erector Spinae

90 90
120 60 120 60

150 30 150 30

Forward
90
180 0 180 0
120 60 0 25 50 75 0 25 50 75
150 30
210 330 210 330
180 L R 0

240 300 240 300

Left 210 330 Right 270 270 Back pain
240 300 Tibialis Anterior Gastrocnemius Controls
270
90 90
120 60 120 60

150 30 150 30
Backward

180 0 180 0
0 25 50 75 0 25 50 75

210 330 210 330

240 300 240 300

A B 270 270
FIGURE 17-5  ■  EMG tuning curves in response to perturbations. (A) Experimental setup for support surface translations which shows
the directions of platform perturbations with the induced body sway resulting from perturbations in the cardinal directions (i.e. left,
forward, right and backward perturbations). Schematic stick figures are depicted with the subject facing to the right for the sagittal
plane views and are viewed from the back for the frontal plane views. (B) Polar plots of the normalized EMG amplitude of the left
internal oblique muscles, left erector spinae, tibialis anterior and gastrocnemius muscles in response to unexpected balance per-
turbations performed in 12 directions translations in a group of individuals with and without low back pain. (Reprinted with permission
from Jones et al.79)

Fibromyalgia Control
0–5 s 55–60 s 0–5 s 55–60 s
Cranial 140

120

100

80
y-axis

60

40

20

0 µV
Caudal
Medial x-axis Lateral
FIGURE 17-6  ■  Topographical mapping of muscle activity. Representative topographical maps (interpolation by a factor 8) of the EMG
root mean square value from the right upper trapezius muscle for a person with fibromyalgia and a control subject. Maps are shown
for the first and last 5 seconds of a 60-degree sustained shoulder abduction contraction. Areas of blue correspond to low EMG
amplitude and dark red to high EMG amplitude. Note the shift of activity in the cranial direction as the task progresses but for the
control subject only. For colour version see Plate 17. (Reprinted with permission from Falla et al.111)
174 PART II  Advances in Theory and Practice

active muscles. This is due to the redundancy of the demonstrated, for example, that experimental muscle
neuromuscular system. pain disrupts the normal synergistic muscle activation in
Factorization methods, such as non-negative matrix a subject-specific way.116
factorization,115 have been applied to extract the dimen­
sionality from multi-channel EMG recordings, which
are divided into so-called activation signals (in a lower
Single Motor Unit Behaviour
dimension) and muscle synergies. The original EMG The most detailed analysis of the neural control of move­
recording over multiple muscles is explained by the ment from EMG signals is at the level of individual motor
weighted sum (by the synergy coefficients) of the activa­ units. As indicated, this analysis has been possible with
tion signals. Using this factorization analysis, it has been intramuscular EMG recording systems for more than 80

400 µV

300 µV

200 µV

100 µV

0 µV

20 10.0
19
Discharge rate

18 Force
17
16 7.5
15 pps
15 10 pps

Force (% MVC)
14 Time 5 pps
13
12 5.0
MU number

11
10
9
8 2.5
7
6
5
4 0
3
2
1
1 2 3 4 5 6 7 8 9 10 11 12
A Time (s)

15
Discharge rate (pps)

16 10
5
MU number

15
15 10
5
1 2 3 4 5 6 7 8 9 10 11 12
B Time (s)
FIGURE 17-7  ■  Extraction of single motor unit discharge patterns from high-density surface EMG. (A) Motor unit discharge patterns
during an increasing (6 seconds) and decreasing (6 seconds) force isometric contraction (to 10% of the maximum) of the abductor
pollicis brevis muscle, as estimated from surface EMG recordings obtained with a 13 × 5 electrode grid. Each dot indicates a motor
unit discharge at a time instant. The grey thick line represents the exerted muscle force. The upper panel depicts the root mean
square EMG map under the electrode grid during the same muscle contraction. RMS values were calculated from signal epochs of
1-s duration. (B) The discharge times of two motor units from (A) are shown on a larger vertical scale to illustrate the discharge
rate modulation during the contraction. MU: motor unit. For colour version see Plate 18. (Reprinted with permission from Merletti
et al.119)
 17  Advances in Electromyography 175

years.2 More recently, however, it has been demonstrated REFERENCES

that the same information can be obtained from non- 1. Merletti R, Farina D. Analysis of intramuscular electromyogram
invasive muscle recordings, using high-density surface signals. Philos Trans A Math Phys Eng Sci 2009;367:357–68.
EMG signals (Fig. 17-7). In a series of studies, this direct 2. Adrian ED, Bronk DW. The discharge of impulses in motor nerve
approach of investigating the neural determinants of fibres: Part II. The frequency of discharge in reflex and voluntary
contractions. J Physiol 1929;67:i3–151.
movement has been shown to be feasible and accu­ 3. Gazzoni M, Farina D, Merletti R. A new method for the extrac­
rate.7,117,118 These new possibilities for the extraction of tion and classification of single motor unit action potentials from
information from the surface EMG have opened a new surface EMG signals. J Neurosci Methods 2004;136:165–77.
line of research in which the alterations of single motor 4. Holobar A, Zazula D. Correlation-based decomposition of surface
unit behaviour can be analysed in clinical conditions and electromyograms at low contraction forces. Med Biol Eng Comput
2004;42:487–95.
used to monitor the effects of therapies. 5. Buchthal F, Guld C, Rosenfalck P. Multielectrode study of
the territory of a motor unit. Acta Physiol Scand 1957;39:
83–104.
6. Farina D, Yoshida K, Stieglitz T, et al. Multi-channel thin-film
MONITORING CHANGE WITH electrode for intramuscular electromyographic recordings. J Appl
Physiol 2008;104:821–7.
REHABILITATION 7. Farina D, Holobar A, Merletti R, et al. Decoding the neural drive
to muscles from the surface electromyogram. Clin Neurophysiol
EMG is frequently used as a tool to document change 2010;121:1616–23.
in neuromuscular function with rehabilitation. High 8. Farina D, Leclerc F, Arendt-Nielsen L, et  al. The change
in spatial distribution of upper trapezius muscle activity is cor­
levels of repeatability of normalized EMG estimates related to contraction duration. J Electromyogr Kinesiol 2008;18:
have been shown for both the neck and back 16–25.
muscles,120,121 confirming the suitability of using EMG 9. Zwarts MJ, Stegeman DF. Multichannel surface EMG: basic
between sessions to monitor changes. EMG has been aspects and clinical utility. Muscle Nerve 2003;28:1–17.
10. Latash ML, Aruin AS, Neyman I, et al. Anticipatory postural
used to monitor the physiological efficacy of multiple adjustments during self inflicted and predictable perturbations in
physical therapy interventions, including exercise,122 Parkinson’s disease. J Neurol Neurosurg Psychiatry 1995;58:
mobilization/manipulation123,124 and taping.125,126 In rela­ 326–34.
tion to exercise, EMG has been used to determine the 11. Woollacott MH, von Hosten C, Rosblad B. Relation between
most appropriate exercise to prescribe to patients,127–130 muscle response onset and body segmental movements during
postural perturbations in humans. Exp Brain Res 1988;72:
to monitor improvement in muscle activation post- 593–604.
intervention26,27,131,132 and as a tool for biofeedback with 12. Karst GM, Willet GM. Onset timing of electromyographic activ­
training.133,134 ity in the vastus medialis oblique and vastus lateralis muscles in
subjects with and without patellofemoral pain syndrome. Phys
Ther 1995;75:813–23.
13. Merlo A, Farina D, Merletti R. A fast and reliable technique for
LIMITATIONS muscle activity detection from surface EMG signals. IEEE Trans
Biomed Eng 2003;50:316–23.
Intramuscular EMG has the important limitation of 14. Hodges PW, Richardson CA. Inefficient muscular stabilization
being an invasive procedure which often precludes its use of the lumbar spine associated with low back pain. A motor
control evaluation of transversus abdominis. Spine 1996;21:
as a monitoring tool that would require multiple inser­ 2640–50.
tions. Moreover, it is very selective and therefore may not 15. Hodges PW, Richardson CA. Feedforward contraction of trans­
well represent the activity of the muscle. On the other versus abdominis is not influenced by the direction of arm move­
hand, surface EMG suffers from opposite limitations due ment. Exp Brain Res 1997;114:362–70.
16. Cholewicki J, Silfies SP, Shah RA, et al. Delayed trunk muscle
to the lack of selectivity. For example, crosstalk is an open reflex responses increase the risk of low back injuries. Spine
problem in surface EMG recordings. The most appropri­ 2005;30:2614–20.
ate method has to be chosen for each specific investiga­ 17. Radebold A, Cholewicki J, Panjabi MM, et al. Muscle response
tion and its limitations taken into account when pattern to sudden trunk loading in healthy individuals and in
interpreting the results. patients with chronic low back pain. Spine 2000;25:947–54.
18. Reeves N, Cholewicki J, Milner T. Muscle reflex classification of
low-back pain. J Electromyogr Kinesiol 2005;15:53–60.
19. Jacobs J, Henry S, Jones S, et al. A history of low back pain associ­
CONCLUSION ates with altered electromyographic activation patterns in response
to perturbations of standing balance. J Neurophysiol 2011;106:
2506–14.
EMG is a fundamental tool in musculoskeletal physio­ 20. Boudreau S, Farina D, Kongstad L, et al. The relative timing of
therapy and has been successfully used for the assessment trunk muscle activation is retained in response to unanticipated
of disturbed motor control and to monitor the physio­ postural-perturbations during acute low back pain. Exp Brain Res
logical efficacy of multiple physical therapy interventions. 2011;210:259–67.
A number of analyses of the EMG signal can be per­ 21. MacDonald D, Moseley GL, Hodges PW. Why do some patients
keep hurting their back? Evidence of ongoing back muscle dys­
formed to gain insight into the peripheral status of the function during remission from recurrent back pain. Pain 2009;
muscle and the strategies used by the CNS to control 142:183–8.
movement and posture. This chapter has reviewed some 22. Falla D, Jull G, Hodges PW. Feedforward activity of the cervical
of the most frequently applied analyses in musculoskel­ flexor muscles during voluntary arm movements is delayed in
chronic neck pain. Exp Brain Res 2004;157:43–8.
etal physical therapy research, including both classic 23. Boudreau S, Falla D. Chronic neck pain alters muscle activation
methods for information extraction and more recent patterns to sudden movements. Exp Brain Res 2014;232(6):
developments. 2011–20.
176 PART II  Advances in Theory and Practice

24. Cowan SM, Schache AG, Brukner P, et al. Delayed onset of trans­ 49. Arendt-Nielsen L, Mills KR. The relationship between mean
versus abdominus in long-standing groin pain. Med Sci Sports power frequency of the EMG spectrum and muscle fibre conduc­
Exerc 2004;36:2040–5. tion velocity. Electroencephalogr Clin Neurophysiol 1985;60:
25. Boling MC, Bolgla LA, Mattacola CG, et al. Outcomes of a 130–4.
weight-bearing rehabilitation program for patients diagnosed with 50. Lowery MM, Vaughan CL, Nolan PJ, et  al. Spectral compres­
patellofemoral pain syndrome. Arch Phys Med Rehabil 2006; sion of the electromyographic signal due to decreasing muscle
87:1428–35. fiber conduction velocity. IEEE Trans Rehabil Eng 2000;8:
26. Tsao H, Hodges PW. Persistence of improvements in postural 353–61.
strategies following motor control training in people with recur­ 51. Merletti R, Lo Conte LR. Advances in processing of surface myo­
rent low back pain. J Electromyogr Kinesiol 2008;18:559–67. electric signals: Part 1. Med Biol Eng Comput 1995;33:362–72.
27. Jull G, Falla D, Vicenzino B, et al. The effect of therapeutic 52. Falla D, Rainoldi A, Merletti R, et al. Myoelectric manifestations
exercise on activation of the deep cervical flexor muscles in people of sternocleidomastoid and anterior scalene muscle fatigue in
with chronic neck pain. Man Ther 2009;14:696–701. chronic neck pain patients. Clin Neurophysiol 2003;114:488–95.
28. Cowan SM, Bennell KL, Hodges PW, et al. Simultaneous feed­ 53. Gogia PP, Sabbahi MA. Electromyographic analysis of neck
forward recruitment of the vasti in untrained postural tasks can be muscle fatigue in patients with osteoarthritis of the cervical spine.
restored by physical therapy. J Orthop Res 2003;21:553–8. Spine 1994;19:502–6.
29. Merletti R, Knaflitz M, De Luca CJ. Myoelectric manifestations 54. Roy SH, De Luca CJ, Casavant DA. Lumbar muscle fatigue and
of fatigue in voluntary and electrically elicited contractions. J Appl chronic lower back pain. Spine 1989;14:992–1001.
Physiol 1990;69:1810–20. 55. Kankaanpaa M, Taimelas S, Laaksonen D, et al. Back and hip
30. Merletti R, Rainoldi A, Farina D. Surface electromyography for extensor fatigability in chronic low back pain patients and con­
noninvasive characterization of muscle. Exerc Sport Sci Rev trols. Arch Phys Med Rehabil 1998;79:412–17.
2001;29:20–5. 56. Elfving B, Dedering A, Nemeth G. Lumbar muscle fatigue and
31. Merletti R, Roy S. Myoelectric and mechanical manifestations of recovery in patients with long-term low-back trouble: electromy­
muscle fatigue in voluntary contractions. J Orthop Sports Phys ography and health-related factors. Clin Biomech (Bristol, Avon)
Ther 1996;24:342–53. 2003;18:619–30.
32. De Luca CJ. The use of the surface EMG signal for performance 57. Dehner C, Schmelz A, Völker H, et al. Intramuscular pressure,
evaluation of back muscles. Muscle Nerve 1993;16:210–16. tissue oxygenation, and muscle fatigue of the multifidus during
33. Basmajian JV, DeLuca CJ. Muscles Alive: Their Functions isometric extension in elite rowers with low back pain. J Sport
Revealed by Electromyography. USA: Williams and Wilkins; Rehabil 2009;18:572–81.
1985. 58. Sung P, Lammers A, Danial P. Different parts of erector spinae
34. De Luca CJ. Myoelectrical manifestations of localized muscular muscle fatigability in subjects with and without low back pain.
fatigue in humans. Crit Rev Biomed Eng 1984;11:251–79. Spine J 2009;9:115–20.
35. Kramer CG, Hagg G, Kemp B. Real time measurement of muscle 59. Roy SH, De Luca CJ, Emley M, et al. Classification of back
fatigue related changes in surface EMG. Med Biol Eng Comput muscle impairment based on the surface electromyographic signal.
1987;25:627–30. J Rehabil Res Dev 1997;34:405–14.
36. Bigland-Ritchie B, Cafarelli F, Vollestad N. Fatigue of submaximal 60. Candotti C, Loss J, Pressi A, et al. Electromyography for assess­
static contractions. Acta Physiol Scand 1986;128(Suppl. 556): ment of pain in low back muscles. Phys Ther 2008;88:1061–7.
137–48. 61. Farina D, Pozzo M, Merlo E, et al. Assessment of average muscle
37. Moritani T, Muro M, Nagata A. Intramuscular and surface elec­ fiber conduction velocity from surface EMG signals during fatigu­
tromyogram changes during muscle fatigue. J Appl Physiol ing dynamic contractions. IEEE Trans Biomed Eng 2004;
1986;60:1179–85. 51:1383–93.
38. Brody LR, Pollock MT, Roy SH, et al. pH-induced effects on 62. Falla D, Farina D. Muscle fiber conduction velocity of the upper
median frequency and conduction velocity of the myoelectric trapezius muscle during dynamic contraction of the upper limb in
signal. J Appl Physiol 1991;71:1878–85. patients with chronic neck pain. Pain 2005;116:138–45.
39. Kossler F, Lange F, Caffier G, et al. External potassium and action 63. Choi HI, Williams WJ. Improved time-frequency representation
potential propagation in rat fast and slow twitch muscles. Gen of multicomponent signals using exponential kernels. IEEE Trans
Physiol Biophys 1991;10:485–98. Acoust Speech Sig Proc 1989;37:862–71.
40. McKenna MJ, Bangsbo J, Renaud JM. Muscle K+, Na+, and Cl 64. Bonato P, Gagliati G, Knaflitz M. Analysis of surface myoelectric
disturbances and Na+-K+ pump inactivation: implications for signals recorded during dynamic contractions. IEEE Eng Med
fatigue. J Appl Physiol 2008;104:288–95. Biol Mag 1996;15:102–11.
41. Stulen FB, DeLuca CJ. Frequency parameters of the myoelectric 65. Farina D, Fosci M, Merletti R. Motor unit recruitment strategies
signal as a measure of muscle conduction velocity. IEEE Trans investigated by surface EMG variables. J Appl Physiol 2002;92:
Biomed Eng 1981;28:515–23. 235–47.
42. Lindstrom L, Magnusson R, Petersen R. Muscle fatigue and 66. Masuda K, Masuda T, Sadoyama T, et al. Changes in surface
action potential conduction velocity changes studied with fre­ EMG parameters during static and dynamic fatiguing contrac­
quency analysis of EMG signals. Electromyogr Clin Neurophysiol tions. J Electromyogr Kinesiol 1999;9:39–46.
1970;10:341–56. 67. Merlo E, Pozzo M, Antonutto G, et al. Time-frequency analysis
43. Bigland-Ritchie B, Donovan EF, Roussos CS. Conduction veloc­ and estimation of muscle fiber conduction velocity from surface
ity and EMG power spectrum changes in fatigue of sustained EMG signals during explosive dynamic contractions. J Neurosci
maximal efforts. J Appl Physiol 1981;51:1300–5. Methods 2005;142:267–74.
44. Kleine BU, Stegeman D, Mund D, et al. Influence of motorneu­ 68. Pozzo M, Alkner B, Norrbrand L, et al. Muscle fiber conduction
ron firing synchronisation on SEMG characteristics in depen­ velocity during concentric and eccentric actions on a flywheel
dence of electrode position. J Appl Physiol 2001;91:1588–99. exercise device. Muscle Nerve 2006;34(2):169–77.
45. Stegeman D, Blok J, Hermens H, et al. Surface EMG models: 69. Falla D, Graven-Nielsen T, Farina D. Spatial and temporal
properties and applications. J Electromyogr Kinesiol 2000;10: changes of upper trapezius muscle fiber conduction velocity are
313–26. not predicted by surface EMG spectral analysis during a dynamic
46. Gazzoni M, Farina D, Merletti R. Motor unit recruitment during upper limb task. J Neurosci Methods 2006;156:236–41.
constant low force and long duration muscle contractions investi­ 70. Farina D, Merletti R, Enoka RM. The extraction of neural strate­
gated by surface electromyography. Acta Physiol Pharmacol Bulg gies from the surface EMG. J Appl Physiol 2004;96:1486–95.
2001;26:67–71. 71. Falla D, Jull G, Hodges PW. Patients with neck pain demonstrate
47. Milner-Brown HS, Stein RB, Yemm R. Changes in firing rate of reduced electromyographic activity of the deep cervical flexor
human motor units during linearly changing voluntary contrac­ muscles during performance of the craniocervical flexion test.
tions. J Physiol 1973;230:371–90. Spine 2004;29:2108–14.
48. Lindstrom L, Magnusson R. Interpretation of myoelectric power 72. Jull G, Kristjansson E, Dall’Alba P. Impairment in the cervical
spectra: a model and its applications. Proc IEEE 1977;65: flexors: a comparison of whiplash and insidious onset neck pain
653–62. patients. Man Ther 2004;9:89–94.
 17  Advances in Electromyography 177

73. Chiu TT, Law E, Chiu TH. Performance of the craniocervical 97. Blouin JS, Siegmund GP, Carpenter MG, et al. Neural control of
flexion test in subjects with and without chronic neck pain. superficial and deep neck muscles in humans. J Neurophysiol
J Orthop Sports Phys Ther 2005;35:567–71. 2007;98:920–8.
74. Descarreaux M, Mayrand N, Raymond J. Neuromuscular control 98. Lindstrom R, Schomacher J, Farina D, et al. Association between
of the head in an isometric force reproduction task: comparison neck muscle co-activation, pain, and strength in women with neck
of whiplash subjects and health controls. Spine J 2007;7: pain. Man Ther 2011;16:80–6.
647–53. 99. Holtermann A, Roeleveld K. EMG amplitude distribution changes
75. Szeto GP, Straker LM, O’Sullivan PB. A comparison of symptom­ over the upper trapezius muscle are similar in sustained and ramp
atic and asymptomatic office workers performing monotonous contractions. Acta Physiol (Oxf) 2006;186:159–68.
keyboard work 1: neck and shoulder muscle recruitment patterns. 100. Falla D, Farina D, Graven Nielsen T. Spatial dependency of tra­
Man Ther 2005;10:270–80. pezius muscle activity during repetitive shoulder flexion. J Elec­
76. Nederhand MJ, Ijzerman MJ, Hermens HJ, et al. Cervical muscle tromyogr Kinesiol 2007;17:299–306.
dysfunction in the chronic whiplash associated disorder grade II 101. Holtermann A, Roeleveld K, Karlsson JS. Inhomogeneities in
(WAD-II). Spine 2000;25:1938–43. muscle activation reveal motor unit recruitment. J Electromyogr
77. Falla D, Bilenkij G, Jull G. Patients with chronic neck pain dem­ Kinesiol 2005;15:131–7.
onstrate altered patterns of muscle activation during performance 102. Falla D, Farina D. Periodic increases in force during sustained
of a functional upper limb task. Spine 2004;29:1436–40. contraction reduce fatigue and facilitate spatial redistribution of
78. Henry S, Hitt J, Jones S, et al. Decreased limits of stability in trapezius muscle activity. Exp Brain Res 2007;182:99–107.
response to postural perturbations in subjects with low back pain. 103. Tucker K, Falla D, Graven-Nielsen T, et al. Electromyographic
Clin Biomech (Bristol, Avon) 2006;21:881–92. mapping of the erector spinae muscle with varying load and during
79. Jones S, Hitt J, DeSarno M, et al. Individuals with non-specific sustained contraction. J Electromyogr Kinesiol 2009;19:373–9.
low back pain in an active episode demonstrate temporally altered 104. Falla D, Gizzi L, Tschapek M, et al. Reduced task-induced varia­
torque responses and direction-specific enhanced muscle activity tions in the distribution of activity across back muscle regions
following unexpected balance perturbations. Exp Brain Res in individuals with low back pain. Pain 2014;155(5):944–53.
2012;221:413–26. 105. Falla D, Farina D. Non-uniform adaptation of motor unit dis­
80. van der Hulst M, Vollenbroek-Hutten M, Rietman J, et al. Back charge rates during sustained static contraction of the upper tra­
muscle activation patterns in chronic low back pain during pezius muscle. Exp Brain Res 2008;191:363–70.
walking: a “guarding” hypothesis. Clin J Pain 2010;26:30–7. 106. Falla D, Arendt-Nielsen L, Farina D. Gender-specific adaptations
81. Ahern D, Follick M, Council J, et al. Reliability of lumbar para­ of upper trapezius muscle activity to acute nociceptive stimulation.
vertebral EMG assessment in chronic low back pain. Arch Phys Pain 2008;138:217–25.
Med Rehabil 1986;67:762–5. 107. Westgaard RH. Muscle activity as a releasing factor for pain in
82. Vogt L, Pfeifer K, Banzer W. Neuromuscular control of walking the shoulder and neck. Cephalalgia 1999;19:251–8.
with chronic low-back pain. Man Ther 2003;8:21–8. 108. Andersson G, Ortengren R. Assessment of back load in assem­
83. Arendt-Nielsen L, Graven-Nielsen T, Svarrer H, et al. The influ­ bly line work using electromyography. Ergonomics 1984;27:
ence of low back pain on muscle activity and coordination during 1157–68.
gait: a clinical and experimental study. Pain 1996;64:231–40. 109. Madeleine P, Leclerc F, Arendt-Nielsen L, et al. Experimental
84. Lamoth C, Meijer O, Daffertshofer A, et al. Effects of chronic muscle pain changes the spatial distribution of upper trapezius
low back pain on trunk coordination and back muscle activity muscle activity during sustained contraction. Clin Neurophysiol
during walking: changes in motor control. Eur Spine J 2006;15: 2006;117:2436–45.
23–40. 110. Falla D, Arendt-Nielsen L, Farina D. The pain-induced change
85. O’Sullivan PB, Beales DJ, Beetham JA, et al. Altered motor in relative activation of upper trapezius muscle regions is indepen­
control strategies in subjects with sacroiliac joint pain during the dent of the site of noxious stimulation. Clin Neurophysiol
active straight-leg-raise test. Spine 2002;27:E1–8. 2009;120:150–7.
86. Schomacher J, Boudreau S, Petzke F, et al. Localized pressure pain 111. Falla D, Andersen H, Danneskiold-Samsøe B, et al. Adaptations
sensitivity is associated with lower activation of the semispinalis of upper trapezius muscle activity during sustained contractions
cervicis muscle in patients with chronic neck pain. Clin J Pain in women with fibromyalgia. J Electromyogr Kinesiol 2010;
2013;29(10):898–906. 20:457–64.
87. Schomacher J, Farina D, Lindstroem R, et al. Chronic trauma- 112. Bernstein N. The Co-ordination and Regulation of Movements.
induced neck pain impairs the neural control of the deep semispi­ Oxford: Pergamon; 1967.
nalis cervicis muscle. Clin Neurophysiol 2012;123:1403–8. 113. Grillner S. Control of locomotion in bipeds, tetrapods, and fish.
88. Saunders S, Rath D, Hodges P. Postural and respiratory activation In: Brooks V, editor. Handbook of Physiology. Bethesda, MD,
of the trunk muscles changes with mode and speed of locomotion. USA: Am Physiol Soc; 1981. p. 1179–236.
Gait Posture 2004;20:280–90. 114. Giszter SF, Hart CB, Silfies SP. Spinal cord modularity: evolution,
89. Hodges PW, Moseley GL, Gabrielsson A, et al. Experimental development, and optimization and the possible relevance to low
muscle pain changes feedforward postural responses of the trunk back pain in man. Exp Brain Res 2010;200:283–306.
muscles. Exp Brain Res 2003;151:262–71. 115. Tresch MC, Saltiel P, Bizzi E. The construction of movement by
90. MacDonald D, Moseley G, Hodges P. People with recurrent low the spinal cord. Nat Neurosci 1999;2:162–7.
back pain respond differently to trunk loading despite remission 116. Muceli S, Falla D, Farina D. Reorganization of muscle synergies
from symptoms. Spine (Phila Pa 1976) 2010;35:818–24. during multidirectional reaching in the horizontal plane with
91. Buchanan T, Rovai G, Rymer W. Strategies for muscle activation experimental muscle pain. J Neurophysiol 2014;111(8):1615–30.
during isometric torque generation at the human elbow. J Neuro­ 117. Holobar A, Minetto MA, Botter A, et al. Experimental analysis of
physiol 1989;62:1201–12. accuracy in the identification of motor unit spike trains from high-
92. Keshner EA, Campbell D, Katz RT, et al. Neck muscle activation density surface EMG. IEEE Trans Neural Syst Rehabil Eng
patterns in humans during isometric head stabilization. Exp Brain 2010;18:221–9.
Res 1989;75:335–44. 118. Holobar A, Minetto MA, Farina D. Accurate identification of
93. Flanders M, Soechting J. Arm muscle activation for static forces motor unit discharge patterns from high-density surface EMG
in three-dimensional space. J Neurophysiol 1990;64:1818–37. and validation with a novel signal-based performance metric.
94. van Bolhuis B, Gielen C. The relative activation of elbow-flexor J Neural Eng 2014;11(1):016008.
muscles in isometric flexion and in flexion/extension movements. 119. Merletti R, Holobar A, Farina D. Analysis of motor units with
J Biomech 1997;30:803–11. high-density surface electromyography. J Electromyogr Kinesiol
95. Vasavada AN, Peterson BW, Delp SL. Three-dimensional spatial 2008;18:879–90.
tuning of neck muscle activation in humans. Exp Brain Res 120. Falla D, Dall’Alba P, Rainoldi A, et al. Repeatability of surface
2002;147:437–48. EMG variables in the sternocleidomastoid and anterior scalene
96. Falla D, Lindstrom R, Rechter L, et al. Effect of pain on the muscles. Eur J Appl Physiol 2002;87:542–9.
modulation in discharge rate of sternocleidomastoid motor units 121. Dankaerts W, O’Sullivan P, Burnett A, et al. Reliability of EMG
with force direction. Clin Neurophysiol 2010;121:744–53. measurements for trunk muscles during maximal and sub-maximal
178 PART II  Advances in Theory and Practice

voluntary isometric contractions in healthy controls and CLBP 129. Schomacher J, Petzke F, Falla D. Localised resistance selectively
patients. J Electromyogr Kinesiol 2004;14:333–42. activates the semispinalis cervicis muscle in patients with neck
122. Jørgensen M, Andersen L, Kirk N, et al. Muscle activity during pain. Man Ther 2012;17:544–8.
functional coordination training: implications for strength gain 130. Andersen L, Andersen C, Mortensen O, et al. Muscle activation
and rehabilitation. J Strength Cond Res 2010;24:1732–9. and perceived loading during rehabilitation exercises: comparison
123. Ferreira M, Ferreira PH, Hodges PW. Changes in postural activ­ of dumbbells and elastic resistance. Phys Ther 2010;90:538–49.
ity of the trunk muscles following spinal manipulative therapy. 131. Søgaard K, Blangsted A, Nielsen P, et al. Changed activation,
Man Ther 2007;12:240–8. oxygenation, and pain response of chronically painful muscles to
124. Krekoukias G, Petty N, Cheek L. Comparison of surface electro­ repetitive work after training interventions: a randomized con­
myographic activity of erector spinae before and after the applica­ trolled trial. Eur J Appl Physiol 2012;112:173–81.
tion of central posteroanterior mobilisation on the lumbar spine. 132. Falla D, Jull G, Hodges P, et al. An endurance-strength training
J Electromyogr Kinesiol 2009;19:39–45. regime is effective in reducing myoelectric manifestations of cervi­
125. Greig A, Bennell K, Briggs A, et al. Postural taping decreases cal flexor muscle fatigue in females with chronic neck pain. Clin
thoracic kyphosis but does not influence trunk muscle electromyo­ Neurophysiol 2006;117:828–37.
graphic activity or balance in women with osteoporosis. Man Ther 133. Ma C, Szeto G, Yan T, et al. Comparing biofeedback with active
2008;13:249–57. exercise and passive treatment for the management of work-
126. Ng G, Wong P. Patellar taping affects vastus medialis obliquus related neck and shoulder pain: a randomized controlled trial.
activation in subjects with patellofemoral pain before and after Arch Phys Med Rehabil 2011;92:849–58.
quadriceps muscle fatigue. Clin Rehabil 2009;23:705–13. 134. Dellve L, Ahlstrom L, Jonsson A, et al. Myofeedback training and
127. Bressel E, Dolny D, Gibbons M. Trunk muscle activity during intensive muscular strength training to decrease pain and improve
exercises performed on land and in water. Med Sci Sports Exerc work ability among female workers on long-term sick leave with
2011;43:1927–32. neck pain: a randomized controlled trial. Int Arch Occup Environ
128. Okubo Y, Kaneoka K, Imai A, et al. Electromyographic analysis Health 2011;84:335–46.
of transversus abdominis and lumbar multifidus using wire elec­
trodes during lumbar stabilization exercises. J Orthop Sports Phys
Ther 2010;40:743–50.
 CHAPTER 18 

Non-invasive Brain Stimulation

in the Measurement and Treatment
of Musculoskeletal Disorders
Siobhan Schabrun  •  Caroline Alexander

People have been investigating cortical connections to potential, the relevant muscle will contract. This muscle
muscles since the 1800s by electrically stimulating the twitch is called a motor evoked potential (MEP; Fig.
brain and watching the muscle contract. Electrical stimu- 18-2) and can be recorded using electromyography.
lation to the motor cortex is still used today. It can be TMS can be used to deliver single pulses at low fre-
applied directly to the cortex to evaluate corticospinal quency (approximately one every 5–6 seconds). When
output during surgery or indirectly to the skull to stimu- used in this manner, TMS is a measurement tool that
late the cortex below. However, the stimulus intensity can provide information about corticomotor control of
required to overcome the resistance of the skull is high, movement.
and this is painful. This limitation was overcome and the
field of brain stimulation was revolutionized when, in
1985, Barker and colleagues used a magnetic stimulator SINGLE-PULSE TRANSCRANIAL
(transcranial magnetic stimulation; TMS) to induce an MAGNETIC STIMULATION
electrical charge in the cortex.1 Here, a short-lasting elec-
trical current is discharged through a wire coil inducing A number of physiological measures can be made using
a magnetic field, which in turn produces a short-lasting single-pulse TMS. These include corticomotor control
electrical charge in underlying brain tissue (Fig. 18-1). If of a particular muscle, excitability of the corticospinal
the coil is centred over the motor cortex, axons that pathway, investigation of intra- and inter-cortical neural
synapse with corticospinal pathways are stimulated and, networks and the effect of pathology or treatment
if the stimulus intensity is high enough to evoke an action on corticospinal control. These investigations require
knowledge of the optimal anatomical site for stimula-
tion. In the motor cortex this site is found by locating
either the ‘hotspot’ or the centre of gravity.2–6 The
site most easily found is the hotspot, which is defined
as the scalp site that evokes an MEP of greatest am-
plitude in the target muscle at the lowest stimulator
intensity.7 The hotspot can be located more accurately
by linking the position of the magnetic stimulator coil
to an individual’s brain scan;8,9 however, this is costly
and not used universally.

Cortical Representation Mapping

The hotspot is not the only site that will evoke an MEP
in the target muscle. Stimulating the area around this site
will also evoke the MEP. As the coil is positioned further
away from the hotspot, the amplitude of the MEP will
reduce until it disappears. This surface topography of the
corticomotor projection to a particular muscle can be
systematically mapped by moving the coil around a grid
placed over the scalp10 (Fig. 18-3). The averaged ampli-
tude of the MEPs evoked at each scalp site creates a map
of the cortical representation for a target muscle. These
FIGURE 18-1  ■  A short-lasting electrical current (anticlockwise maps provide information on the area, excitability
arrow) is discharged through a wire housed in a coil that can
be of varying shapes and sizes. This induces a magnetic field (volume) and amplitude-weighted centre (centre of
(dashed lines), which in turn produces a short-lasting electrical gravity) of the corticomotor representation. The size and
charge in underlying brain tissue (clockwise arrow). location of these maps have been used to explore the
179
180 PART II  Advances in Theory and Practice

impact of a painful stimulus or disorders such as focal hand Motor Evoked Potential Latency
dystonia, lateral epicondylalgia and low back pain on brain
architecture.11–14 Of interest, early evidence suggests that The latency of an MEP is the time between TMS pulse
non-invasive brain stimulation,15 peripheral electrical delivery and the onset of the evoked response in the target
stimulation16 and motor retraining17 strategies may be muscle (see Fig. 18-2). The latency is dependent on a
effective in normalizing aberrant cortical organization and number of factors, including the central and peripheral
improving symptoms in some clinical disorders. pathway distance, whether MEPs are recorded at rest or
during contraction and the number of synapses in the
pathway. Consequently, a monosynaptic pathway to a
Resting and Active Motor Threshold trunk muscle will have a shorter latency than a multisyn-
The motor (or MEP) threshold is the lowest stimulus aptic pathway to a lower limb muscle. MEP latency is
intensity that elicits an MEP at rest (resting motor measured at a consistent stimulus intensity (usually 1.2 or
threshold) or during muscle activation (active motor 1.5 times threshold) and the response to multiple stimuli
threshold). Threshold can be measured using a number are averaged. MEP latency has been reported as an
of different strategies,18–20 but resting motor threshold is outcome measure in healthy people and in people with
most commonly defined as the stimulus intensity required musculoskeletal problems.24,27,30,31 For example, the MEP
to elicit an MEP at rest of approximately 100 µV in at latency of the lower trapezius is longer in individuals with
least five of ten consecutive trials.19 Threshold is thought non-traumatic shoulder instability than for healthy indi-
to reflect neuronal membrane excitability and conse- viduals,29 suggesting a shift towards the use of alternate,
quently is increased by drugs that block sodium chan- more complex corticospinal pathways. Conversely, MEP
nels.21 Threshold is also influenced by the degree and latency has been reported as unchanged in individuals with
depth of a muscle’s cortical representation.7 For instance, chronic low back pain24 and chronic fatigue syndrome.30
lower limb, paraspinal and pelvic muscles have higher
motor thresholds than hand muscles. Motor thresholds
also differ in some clinical disorders.14,20,22–28 For example,
Motor Evoked Potential Amplitude
resting motor threshold is increased for erector spinae in MEP amplitude provides a measure of the excitability
individuals with chronic low back pain,24 for lower trape- of the corticomotor pathway to a target muscle, which
zius in non-traumatic shoulder instability29 and following is inclusive of both upper and lower motoneuron excit-
immobilization of hand muscles in healthy individuals.28 ability. When used in conjunction with measures of
These changes suggest a reduction in cortical excitability peripheral (e.g. M-wave) and spinal (e.g. F-wave or
in these muscles in these conditions. H-reflex) excitability it can also be used to estimate

0.1 mV

–0.1 mV

20 ms
FIGURE 18-2  ■  Averaged electromyographic activity of the quadriceps muscle, which is contracting at 10% of maximum voluntary
contraction. This is the result of ten stimuli over the hotspot for quadriceps, stimulating the contralateral motor cortex. The down-
ward dashed arrow points to the stimulus artefact. The upward arrow points to the onset of the motor evoked potential (MEP). The
time between the stimulus artefact and the onset of the MEP is the MEP latency. The downward arrow points to the mid part of the
silent period.
 18  Non-invasive Brain Stimulation in the Measurement and Treatment of Musculoskeletal Disorders 181

A Transcranial
Motor cortex
magnetic (M1)
stimulation
over scalp grid

Medulla

Corticospinal
tract
Spinal cord
Vertex
(Cz)

LES
E Motor cortical map B Paraspinal muscle
EMG recordings
DM

Vertex
(Cz)

D MEPs superimposed
C MEP recorded at each site
over scalp sites

FIGURE 18-3  ■  Mapping of the motor cortex using transcranial magnetic stimulation (TMS). (A) Stimuli over the motor cortex using
a figure-of-eight coil excite intracortical neurons that provide synaptic input to corticospinal cells. (B) In this example the area of
the motor cortex corresponding to the paraspinal muscles is excited and electromyographic recordings are made from short/deep
fascicles of multifidius (DM) and longissimus erector spinae (LES) at the L4 spinal level. (C) The descending volley from the TMS
pulse excites spinal motoneurons and results in a motor evoked potential (MEP), mainly in contralateral muscles. (D) MEPs are
recorded in both muscles from TMS stimuli applied at each point on a grid placed over the scalp and aligned to the vertex (Cz). 
(E) A three-dimensional map of MEP amplitude can then be created for a muscle. (Reproduced with permission from Tsao et al 2011;
Spine 2011: 36(21): 1721–7.)

changes in cortical excitability.32 As a result, MEP ampli- Recruitment Curves

tude is frequently used as a marker of neuroplasticity,
where increased MEP amplitude is thought to reflect Recruitment curves are constructed by gradually increas-
long-term potentiation of synaptic efficacy, and ing or decreasing the stimulus intensity while the target
decreased MEP amplitude, long-term depression of muscle is maintained at rest or at a constant level of
synaptic efficacy. This measure is particularly useful for contraction. The MEP amplitude is then plotted as a
evaluating the corticomotor effects of an intervention. function of the stimulus intensity. Figure 18-4 illustrates
For instance, MEP amplitudes are reduced in healthy a typical recruitment curve that fits a sigmoid shape. In
individuals following transcutaneous electrical nerve this example, the stimulus intensity is increased incre-
stimulation, suggesting a reduction in cortical excit- mentally by 5% of the output of the magnetic stimulator
ability, and an increase in response to neuromuscular and the MEP rises until full recruitment of muscle fibre
electrical stimulation, indicating that cortical excitability is achieved. The curve plateaus once full recruitment has
is enhanced.33–35 Such findings have relevance for the occurred. A number of outcome measures can be calcu-
use of these therapeutic techniques in clinical popula- lated from the recruitment curve.
tions; however, the variability of MEP amplitude can • The peak slope of the fitted recruitment curve
be high and may require studies with large sample sizes ([1/b]a/4), where a is the amplitude of the MEP at the
to establish differences. slope’s maximum and b is the slope parameter.
182 PART II  Advances in Theory and Practice

0.30
0.1 mV

0.25
20 ms

MEP amplitude (MEP/Mmax)

0.20

0.15

0.10

0.05

0.00
40 60 80 100

% Stimulus strength (% output of magstim)

$
FIGURE 18-4  ■  (A) Averaged electromyographic activity of the quadriceps muscle, which is active at 10% of maximum voluntary
contraction. Each trace is the result of three stimuli over the hotspot for quadriceps, stimulating the contralateral motor cortex at
increasing stimulus intensities. The downward arrow points to the stimulus artefact. The normalized amplitude of the averaged
MEPs can be plotted against stimulus intensity. (B) A curve can then be fitted to these points; here a sigmoid curve is fitted from
which outcomes such as the stimulus intensity that evokes a response equivalent to 50% of the maximum amplitude (upward arrow),
the peak slope of the curve and the peak amplitude of the curve can be calculated.

• The stimulus intensity that evokes a response equiva- this implies that the maximum amplitude of the MEP
lent to 50% of the maximum amplitude of the fitted can be achieved with minimum increase in stimulus
curve (often termed x50). intensity – a measure of recruitment gain. Conversely,
• The slope of the rising phase of the recruitment if the slope is shallow it suggests that greater stimulus
curve. intensity is required to evoke a response of equal ampli-
• The maximum MEP amplitude at the plateau (which tude. Recruitment curves were used by Nicotra and col-
can be normalized to the Mmax). leagues to examine the impact of surgery on corticospinal
These outcome measures reflect different features of the excitability in patients with cervical myelopathy.37 This
strength of corticospinal projection.36 For example, if pilot study demonstrated that the recruitment curve dif-
MEPs of equal amplitude are comparable across two fered between controls and patients revealing reduced
groups then one interpretation is that there is no dif- corticospinal excitability in the patient group. Many of
ference in excitability between groups. However, if one the parameters explored had not improved three months
group exhibits a steep slope in the recruitment curve, after surgery.
 18  Non-invasive Brain Stimulation in the Measurement and Treatment of Musculoskeletal Disorders 183

Cortical Silent Period is known as repetitive TMS (rTMS). A rapidly changing

magnetic field induces electrical currents in underlying
TMS given during a voluntary muscle contraction evokes neurons that are capable of inducing neuroplastic effects
a period of electromyographic silence, termed the corti- that outlast the period of stimulation. rTMS at high fre-
cal silent period (CSP), which can be evoked at a lower quencies (5–20 Hz) can facilitate,58,59 and at low frequen-
threshold than the MEP and can be seen immediately cies (0.2–1 Hz) suppress,60 neural activity and cortical
after the MEP (see Fig. 18-2). Reduced electromyo- excitability. Although few studies have investigated how
graphic (EMG) activity is influenced in the early stage long these effects persist, the duration appears dependent
(up to 60 ms) by spinal mechanisms such as Renshaw on the length and number of rTMS trains.61 rTMS can
inhibition, while the later stage is thought to be due to also be delivered in patterned trains. For example, three
cortical inhibitory interneurons activated by TMS.38–40 short, high-frequency trains of rTMS in theta-frequency
The duration, amplitude, gain and stimulus intensity (theta-burst stimulation) facilitate cortical excitability at
needed to evoke the CSP are typically recorded.41 Mea- intermittent intervals, and suppress cortical excitability
sures of the CSP have been found to correlate with some when delivered continuously.62 Thus rTMS is predomi-
musculoskeletal pathologies. For example, the stimulus nantly an intervention used to induce long-term poten-
intensity required to evoke a CSP in erector spinae is tiation or long-term depression-like effects in the cortex.
higher in people with low back pain compared to healthy This property of rTMS has been exploited as a treatment
individuals and increased stimulus intensity is correlated in psychiatric, neurological and musculoskeletal disor-
with level of disability (Oswestry Disability Index).24 In ders (see Neuromodulation: A New Treatment Strategy
contrast, the CSP is reduced in the facial muscles of indi- in Physiotherapy section).
viduals with migraine, suggesting a possible dysfunction rTMS effects on cortical excitability can also be used
of cortical inhibitory interneurons in this condition.42 to produce transient disruption of neural activity in local
and remote brain regions, creating a ‘virtual lesion’. This
approach is widely used to study structure–function rela-
Fatigue tionships in the human brain. For example, rTMS has
Motor fatigue arises from both peripheral and central been used to examine the relationship between cortical
sources, which can in part be explored using TMS. Here regions such as the primary motor cortex,63,64 primary
an individual is asked to maintain a brief but maximum sensory cortex65 or premotor areas66,67 with function
static contraction while TMS is delivered at an intensity during object manipulation. Here, rTMS is applied to the
to achieve a maximum amplitude MEP. Any additional relevant cortical region before or during a task. The
force evoked by the TMS over the force of the voluntary effect of disruption to a particular cortical area on task
contraction is indicative of a loss of voluntary drive to the performance is then evaluated, providing insight into the
muscle (termed central fatigue). If the muscle is then cortical control of a specific function. This information
worked to fatigue, any change in voluntary drive can be can be used to guide and inform rehabilitation.
plotted over time.43 These methods have been used to
investigate the contribution of central mechanisms to
fatigue in a range of different muscles44–46 in response NEUROMODULATION: A NEW
to substances such as caffeine and to a variety of
pathologies.47 TREATMENT STRATEGY
IN PHYSIOTHERAPY
PAIRED-PULSE TRANSCRANIAL Electrical and magnetic stimulation techniques, such as
MAGNETIC STIMULATION those described above, can be used not only to measure
human neural function but may also induce and enhance
Paired-pulse TMS can be used to explore intracortical, neuroplasticity for therapy. When used to modulate
intrahemispheric and interhemispheric neural networks.48 neural activity, non-invasive brain stimulation may
These protocols involve a conditioning stimulus given to promote adaptive, and suppress maladaptive, neural
a relevant brain region prior to a test stimulus given to modifications (‘plasticity’) and may have the potential to
the motor cortex. Depending on the site of stimulation expedite and enhance recovery. Neuromodulatory inter-
and interstimulus interval, a range of inhibitory and ventions can be applied in two ways: (a) as stand-alone
facilitatory cortical circuits can be investigated. These treatments that change the resting state of the cortex or
methods can provide information on how particular (b) as priming protocols that modulate cortical excitabil-
neural networks may be altered in conditions such as ity in an attempt to increase the brain’s receptiveness to
acute pain,49 fibromyalgia,23 chronic regional pain syn- subsequent treatments (for a review see Schabrun et al.68).
drome,50 chronic low back pain51 and fatigue,52–54 as well Priming the cortex is of particular interest to physio-
as following therapeutic or training interventions.55–57 therapists where clinical outcomes might be enhanced by
combining neuromodulation with traditional therapies
such as motor retraining, peripheral electrical stimulation
REPETITIVE TRANSCRANIAL (e.g. transcutaneous electrical nerve stimulation, func-
MAGNETIC STIMULATION tional electrical stimulation) or pharmacological treat-
ments. An overview of two common neuromodulatory
TMS can also be used to deliver repetitive pulses at high interventions, rTMS and transcranial direct current
frequencies (5–20 stimuli every seconds); in this form it stimulation (tDCS) is provided below.
184 PART II  Advances in Theory and Practice

cord injury, fibromyalgia, multiple sclerosis) pain has

Repetitive Transcranial been reduced by 58–63% following 5 days of anodal
Magnetic Stimulation tDCS to M1.81 A greater number of consecutive sessions
(ten as opposed to five daily sessions) produces longer-
rTMS has been used to varying effect in the treatment lasting effects, with pain relief lasting up to 60 days fol-
of chronic pain conditions such as neuropathic pain,69 lowing treatment.91 However, these findings need to be
complex regional pain syndrome,70 fibromyalgia,71–74 considered carefully, as a recent systematic review con-
pelvic and perineal pain75 and phantom limb pain.76,77 cluded there was still insufficient evidence from which to
The mechanisms that underpin any analgesic effect of conclude the effectiveness of tDCS for chronic pain, and
rTMS are not yet fully understood. However, it is responses to tDCS are known to be highly variable
hypothesized that rTMS may act on intracortical net- between individuals.82 Further high-quality studies are
works to restore defective inhibitory mechanisms78 and required.
may influence endogenous opioid systems.79 The dura-
tion of effect appears to be dependent on the frequency
of rTMS application, the protocol used and the clinical SAFETY CONSIDERATIONS
condition treated. For instance, ten daily sessions of
10 Hz rTMS to the motor cortex is reported to improve Brain stimulation techniques used to measure or induce
pain and quality of life for up to two weeks in individuals neural modifications are considered safe and painless
with fibromyalgia.73 Indeed, a recent systematic review in when current safety guidelines are followed. The only
fibromyalgia reported a significant and lasting impact on absolute contraindication to TMS and rTMS is the pres-
pain reduction beyond the period of stimulation using ence of metallic hardware in close proximity to the
high-frequency rTMS protocols.80 However, evidence stimulating coil.9,19 rTMS carries a small risk of seizure
for the effectiveness of rTMS in other pain conditions is induction particularly in those using pro-epileptogenic
limited by a small number of heterogeneous studies, medication, are epileptic, have had brain injury or when
small effect sizes and variable findings.81 Further work is rTMS protocols outside current safety guidelines are
needed to determine the clinical efficacy of this technique implemented.9,19 The use of tDCS in healthy subjects and
in chronic pain.82 across a range of pathological conditions has not resulted
in any significant adverse effects to date.96 However, it
must be noted that while single and multi-day applica-
Transcranial Direct Current Stimulation tions of tDCS and rTMS appear safe, there have been
Direct current is the uninterrupted flow of electric charge few studies of prolonged periods of stimulation or inves-
in a single direction. Also known as constant current or tigation of long-term effects in humans.
galvanism, the application of direct current to the human
body as a therapeutic tool is not new. Physiotherapists REFERENCES
have utilized direct current since the early 1900s for ion- 1. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimu-
tophoresis and wound healing.83,84 tDCS is a contempo- lation of human motor cortex. Lancet 1985;1:1106–7.
2. Borghetti D, Sartucci F, Petacchi E, et al. Transcranial magnetic
rary direct current application that involves a weak direct stimulation mapping: a model based on spline interpolation. Brain
current (less than 2 mA) delivered to the scalp via two Res Bull 2008;77:143–8.
surface sponge electrodes (20–35 cm2). The current pen- 3. MacKinnon CD, Quartarone A, Rothwell JC. Inter-hemispheric
etrates the cranium and modulates the resting membrane asymmetry of ipsilateral corticofugal projections to proximal
potential of underlying neurons. The resting membrane muscles in humans. Exp Brain Res 2004;157:225–33.
4. Miranda PC, de Carvalho M, Conceicao I, et al. A new method for
potential of neurons under the anode is increased, whereas reproducible coil positioning in transcranial magnetic stimulation
the resting membrane potential of neurons under the mapping. Electroencephalogr Clin Neurophysiol 1997;105:116–23.
cathode is reduced. This leads to increased or decreased 5. Ridding MC, Brouwer B, Miles TS, et al. Changes in muscle
neuronal firing rates85,86 and a subsequent increase or responses to stimulation of the motor cortex induced by peripheral
nerve stimulation in human subjects. Exp Brain Res 2000;
decrease in the excitability of brain circuits. Altered corti- 131:135–43.
cal excitability with tDCS is thought to reflect neuroplas- 6. Uy J, Ridding MC, Miles TS. Stability of maps of human motor
tic processes akin to long-term potentiation and long-term cortex made with transcranial magnetic stimulation. Brain Topogr
depression of synaptic efficacy.87 These effects can be 2002;14:293–7.
observed in the brain region under the electrodes and in 7. Rossini PM, Barker AT, Berardelli A, et al. Non-invasive electrical
and magnetic stimulation of the brain, spinal cord and roots: basic
distant neuronal circuits.78 principles and procedures for routine clinical application. Report
tDCS has been investigated in a variety of chronic pain of an IFCN committee. Electroencephalogr Clin Neurophysiol
conditions including low back pain,88 pelvic pain,89 fibro- 1994;91:79–92.
myalgia,90,91 multiple sclerosis92 and spinal cord injury.93 8. Boroojerdi B, Foltys H, Krings T, et al. Localization of the
motor hand area using transcranial magnetic stimulation and func-
Analgesia is thought to be produced by direct cortical tional magnetic resonance imaging. Clin Neurophysiol 1999;110:
effects on thalamic nuclei as well as downstream effects 699–704.
on the anterior cingulate cortex and upper brainstem.94,95 9. Rossi S, Hallett M, Rossini PM, et al. Safety, ethical considerations,
Stimulation parameters have comprised an intensity of and application guidelines for the use of transcranial magnetic
1–2 mA, a duration of 20–30 minutes, and single through stimulation in clinical practice and research. Clin Neurophysiol
2009;120:2008–39.
to multiple, consecutive daily treatments. The most 10. Byrnes ML, Thickbroom GW, Wilson SA, et al. The corticomotor
common application is anodal tDCS to the primary representation of upper limb muscles in writer’s cramp and changes
motor cortex (M1). In chronic pain conditions (spinal following botulinum toxin injection. Brain 1998;121(Pt 5):977–88.
 18  Non-invasive Brain Stimulation in the Measurement and Treatment of Musculoskeletal Disorders 185

11. Krause P, Forderreuther S, Straube A. TMS motor cortical brain 36. Boroojerdi B, Battaglia F, Muellbacher W, et al. Mechanisms influ-
mapping in patients with complex regional pain syndrome type I. encing stimulus-response properties of the human corticospinal
Clin Neurophysiol 2006;117:169–76. system. Clin Neurophysiol 2001;112:931–7.
12. Tsao H, Danneels L, Hodges PW. Individual fascicles of the para- 37. Nicotra A, King NK, Catley M, et al. Evaluation of corticospinal
spinal muscles are activated by discrete cortical networks in humans. excitability in cervical myelopathy, before and after surgery, with
Clin Neurophysiol 2011. transcranial magnetic stimulation: a pilot study. Eur Spine J
13. Tsao H, Danneels LA, Hodges PW. ISSLS prize winner: smudging 2013;22:189–96.
the motor brain in young adults with recurrent low back pain. Spine 38. Fecteau S, Lassonde M, Theoret H. Intrahemispheric dysfunction
(Phila Pa 1976) 2011;36:1721–7. in primary motor cortex without corpus callosum: a transcranial
14. Tsao H, Galea MP, Hodges PW. Reorganization of the motor magnetic stimulation study. BMC Neurol 2006;6:21.
cortex is associated with postural control deficits in recurrent low 39. Werhahn KJ, Behrang-Nia M, Bott MC, et al. Does the recruit-
back pain. Brain 2008;131:2161–71. ment of excitation and inhibition in the motor cortex differ? J Clin
15. Schabrun SM, Jones E, Elgueta-Cancino E, et al. Targeting chronic Neurophysiol 2007;24:419–23.
recurrent low back pain from the top-down and the bottom-up: a 40. Ziemann U, Netz J, Szelenyi A, et al. Spinal and supraspinal mech-
combined transcranial direct current stimulation and peripheral anisms contribute to the silent period in the contracting soleus
electrical stimulation intervention. Brain Stimul 2014;7:451–9. muscle after transcranial magnetic stimulation of human motor
16. Schabrun SM, Stinear CM, Byblow WD, et al. Normalizing motor cortex. Neurosci Lett 1993;156:167–71.
cortex representations in focal hand dystonia. Cereb Cortex 41. King NK, Kuppuswamy A, Strutton PH, et al. Estimation of corti-
2009;19:1968–77. cal silent period following transcranial magnetic stimulation using
17. Tsao H, Galea MP, Hodges PW. Driving plasticity in the motor a computerised cumulative sum method. J Neurosci Methods
cortex in recurrent low back pain. Eur J Pain 2010;14:832–9. 2006;150:96–104.
18. Awiszus F. On relative frequency estimation of transcranial mag- 42. Curra A, Pierelli F, Coppola G, et al. Shortened cortical silent
netic stimulation motor threshold. Clin Neurophysiol 2012; period in facial muscles of patients with migraine. Pain 2007;
123:2319–20. 132:124–31.
19. Groppa S, Oliviero A, Eisen A, et al. A practical guide to diagnostic 43. Todd G, Taylor JL, Gandevia SC. Measurement of voluntary acti-
transcranial magnetic stimulation: report of an IFCN committee. vation of fresh and fatigued human muscles using transcranial mag-
Clin Neurophysiol 2012;123:858–82. netic stimulation. J Physiol 2003;551:661–71.
20. Qi F, Wu AD, Schweighofer N. Fast estimation of transcranial 44. McKenzie DK, Bigland-Ritchie B, Gorman RB, et al. Central and
magnetic stimulation motor threshold. Brain Stimul 2011;4:50–7. peripheral fatigue of human diaphragm and limb muscles assessed
21. Ziemann U, Lonnecker S, Steinhoff BJ, et al. Effects of antiepilep- by twitch interpolation. J Physiol 1992;454:643–56.
tic drugs on motor cortex excitability in humans: a transcranial 45. Schabrun SM, Stafford RE, Hodges PW. Anal sphincter fatigue:
magnetic stimulation study. Ann Neurol 1996;40:367–78. is the mechanism peripheral or central? Neurourol Urodyn
22. Davey NJ, Puri BK, Catley M, et al. Deficit in motor performance 2011;30:1550–6.
correlates with changed corticospinal excitability in patients with 46. Todd G, Petersen NT, Taylor JL, et al. The effect of a contralateral
chronic fatigue syndrome. Int J Clin Pract 2003;57:262–4. contraction on maximal voluntary activation and central fatigue in
23. Mhalla A, de A, Baudic S, et al. Alteration of cortical excitability in elbow flexor muscles. Exp Brain Res 2003;150:308–13.
patients with fibromyalgia. Pain 2010;149:495–500. 47. Gruet M, Temesi J, Rupp T, et al. Stimulation of the motor cortex
24. Strutton PH, Theodorou S, Catley M, et al. Corticospinal excit- and corticospinal tract to assess human muscle fatigue. Neurosci-
ability in patients with chronic low back pain. J Spinal Disord Tech ence 2013;231:384–99.
2005;18:420–4. 48. Chen R. Interactions between inhibitory and excitatory circuits in
25. Strutton PH, Catley M, McGregor AH, et al. Corticospinal excit- the human motor cortex. Exp Brain Res 2004;154:1–10.
ability in patients with unilateral sciatica. Neurosci Lett 2003; 49. Schabrun SM, Hodges PW. Muscle pain differentially modulates
353:33–6. short interval intracortical inhibition and intracortical facilitation
26. Svensson P, Romaniello A, Wang K, et al. One hour of tongue-task in primary motor cortex. J Pain 2012;13:187–94.
training is associated with plasticity in corticomotor control of the 50. Eisenberg E, Chistyakov AV, Yudashkin M, et al. Evidence for
human tongue musculature. Exp Brain Res 2006;173:165–73. cortical hyperexcitability of the affected limb representation area in
27. Alexander CM. Altered control of the trapezius muscle in subjects CRPS: a psychophysical and transcranial magnetic stimulation
with non-traumatic shoulder instability. Clin Neurophysiol study. Pain 2005;113:99–105.
2007;118:2664–71. 51. Masse-Alarie H, Flamand VH, Moffet H, et al. Corticomotor
28. Facchini S, Romani M, Tinazzi M, et al. Time-related changes of control of deep abdominal muscles in chronic low back pain
excitability of the human motor system contingent upon immobili- and anticipatory postural adjustments. Exp Brain Res 2012;
sation of the ring and little fingers. Clin Neurophysiol 218:99–109.
2002;113:367–75. 52. Takahashi K, Maruyama A, Maeda M, et al. Unilateral grip fatigue
29. Alexander CM. Altered control of the trapezius muscle in subjects reduces short interval intracortical inhibition in ipsilateral primary
with non-traumatic shoulder instability. Clin Neurophysiol 2007; motor cortex. Clin Neurophysiol 2009;120:198–203.
118:2664–71. 53. Takahashi K, Maruyama A, Hirakoba K, et al. Fatiguing intermit-
30. Davey NJ, Puri BK, Nowicky AV, et al. Voluntary motor function tent lower limb exercise influences corticospinal and corticocortical
in patients with chronic fatigue syndrome. J Psychosom Res excitability in the nonexercised upper limb. Brain Stimul 2011;
2001;50:17–20. 4:90–6.
31. Romaniello A, Cruccu G, McMillan AS, et al. Effect of experimen- 54. Baumer T, Munchau A, Weiller C, et al. Fatigue suppresses ipsilat-
tal pain from trigeminal muscle and skin on motor cortex excit- eral intracortical facilitation. Exp Brain Res 2002;146:467–73.
ability in humans. Brain Res 2000;882:120–7. 55. Clark BC, Taylor JL, Hoffman RL, et al. Cast immobilization
32. Davey NJ, Smith HC, Savic G, et al. Comparison of input-output increases long-interval intracortical inhibition. Muscle Nerve
patterns in the corticospinal system of normal subjects and incom- 2010;42:363–72.
plete spinal cord injured patients. Exp Brain Res 1999;127:382–90. 56. Nordstrom MA, Butler SL. Reduced intracortical inhibition and
33. Andrews RK, Schabrun SM, Ridding MC, et al. The effect of facilitation of corticospinal neurons in musicians. Exp Brain Res
electrical stimulation on corticospinal excitability is dependent on 2002;144:336–42.
application duration: a same subject pre-post test design. J Neuro- 57. Rosenkranz K, Williamon A, Rothwell JC. Motorcortical excit-
eng Rehabil 2013;10:51. ability and synaptic plasticity is enhanced in professional musicians.
34. Chipchase LS, Schabrun SM, Hodges PW. Corticospinal excit- J Neurosci 2007;27:5200–6.
ability is dependent on the parameters of peripheral electric 58. Berardelli A, Inghilleri M, Rothwell JC, et al. Facilitation of muscle
stimulation: a preliminary study. Arch Phys Med Rehabil evoked responses after repetitive cortical stimulation in man. Exp
2011;92:1423–30. Brain Res 1998;122:79–84.
35. Chipchase LS, Schabrun SM, Hodges PW. Peripheral electrical 59. Pascual-Leone A, Valls-Sole J, Wassermann EM, et al. Responses
stimulation to induce cortical plasticity: a systematic review of to rapid-rate transcranial magnetic stimulation of the human motor
stimulus parameters. Clin Neurophysiol 2011;122:456–63. cortex. Brain 1994;117(Pt 4):847–58.
186 PART II  Advances in Theory and Practice

60. Muellbacher W, Ziemann U, Boroojerdi B, et al. Effects of low- stimulation (tDCS) to relieve pain. Brain Stimul 2008;
frequency transcranial magnetic stimulation on motor excitability 1:337–44.
and basic motor behavior. Clin Neurophysiol 2000;111:1002–7. 79. de Andrade DC, Mhalla A, Adam F, et al. Neuropharmacological
61. Fitzgerald PB, Fountain S, Daskalakis ZJ. A comprehensive review basis of rTMS-induced analgesia: the role of endogenous opioids.
of the effects of rTMS on motor cortical excitability and inhibition. Pain 2011;152:320–6.
Clin Neurophysiol 2006;117:2584–96. 80. Marlow NM, Bonilha HS, Short EB. Efficacy of transcranial direct
62. Huang YZ, Edwards MJ, Rounis E, et al. Theta burst stimulation current stimulation and repetitive transcranial magnetic stimulation
of the human motor cortex. Neuron 2005;45:201–6. for treating fibromyalgia syndrome: a systematic review. Pain Pract
63. Berner J, Schonfeldt-Lecuona C, Nowak DA. Sensorimotor 2013;13:131–45.
memory for fingertip forces during object lifting: the role of the 81. Plow EB, Pascual-Leone A, Machado A. Brain stimulation in the
primary motor cortex. Neuropsychologia 2007;45:1931–8. treatment of chronic neuropathic and non-cancerous pain. J Pain
64. Nowak DA, Voss M, Huang YZ, et al. High-frequency repetitive 2012;13:411–24.
transcranial magnetic stimulation over the hand area of the primary 82. O’Connell NE, Wand BM, Marston L, et al. Non-invasive brain
motor cortex disturbs predictive grip force scaling. Eur J Neurosci stimulation techniques for chronic pain. A report of a Cochrane
2005;22:2392–6. systematic review and meta-analysis. Eur J Phys Rehabil Med
65. Schabrun SM, Ridding MC, Miles TS. Role of the primary motor 2011;47:309–26.
and sensory cortex in precision grasping: a transcranial magnetic 83. Chipchase LS, Williams MT, Robertson VJ. Factors affecting cur-
stimulation study. Eur J Neurosci 2008;27:750–6. riculum content and the integration of evidence-based practice
66. Davare M, Andres M, Cosnard G, et al. Dissociating the role of in entry-level physiotherapy programs. J Allied Health 2007;
ventral and dorsal premotor cortex in precision grasping. J Neuro- 36:17–23.
sci 2006;26:2260–8. 84. Robertson V, Ward A, Low J, et al. Electrotherapy explained.
67. Davare M, Andres M, Clerget E, et al. Temporal dissociation 4th ed. 2006.
between hand shaping and grip force scaling in the anterior intra- 85. Miranda PC, Lomarev M, Hallett M. Modeling the current distri-
parietal area. J Neurosci 2007;27:3974–80. bution during transcranial direct current stimulation. Clin Neuro-
68. Schabrun SM, Chipchase LS. Priming the brain to learn: the future physiol 2006;117:1623–9.
of therapy? Man Ther 2012;17:184–6. 86. Wagner T, Valero-Cabre A, Pascual-Leone A. Noninvasive human
69. Hosomi K, Shimokawa T, Ikoma K, et al. Daily repetitive transcra- brain stimulation. Annu Rev Biomed Eng 2007;9:527–65.
nial magnetic stimulation of primary motor cortex for neuropathic 87. Nitsche MA, Seeber A, Frommann K, et al. Modulating parameters
pain: a randomized, multicenter, double-blind, crossover, sham- of excitability during and after transcranial direct current stimula-
controlled trial. Pain 2013;154:1065–72. tion of the human motor cortex. J Physiol 2005;568:291–303.
70. Pleger B, Janssen F, Schwenkreis P, et al. Repetitive transcranial 88. O’Connell NE, Cossar J, Marston L, et al. Transcranial direct
magnetic stimulation of the motor cortex attenuates pain percep- current stimulation of the motor cortex in the treatment of chronic
tion in complex regional pain syndrome type I. Neurosci Lett nonspecific low back pain: a randomized, double-blind exploratory
2004;356:87–90. study. Clin J Pain 2013;29:26–34.
71. Lee SJ, Kim DY, Chun MH, et al. The effect of repetitive trans­ 89. Fenton BW, Palmieri PA, Boggio P, et al. A preliminary study of
cranial magnetic stimulation on fibromyalgia: a randomized sham- transcranial direct current stimulation for the treatment of refrac-
controlled trial with 1-mo follow-up. Am J Phys Med Rehabil tory chronic pelvic pain. Brain Stimul 2009;2:103–7.
2012;91:1077–85. 90. Fregni F, Gimenes R, Valle AC, et al. A randomized, sham-
72. Mhalla A, Baudic S, Ciampi de AD, et al. Long-term maintenance controlled, proof of principle study of transcranial direct current
of the analgesic effects of transcranial magnetic stimulation in stimulation for the treatment of pain in fibromyalgia. Arthritis
fibromyalgia. Pain 2011;152:1478–85. Rheum 2006;54:3988–98.
73. Passard A, Attal N, Benadhira R, et al. Effects of unilateral repeti- 91. Valle A, Roizenblatt S, Botte S, et al. Efficacy of anodal transcranial
tive transcranial magnetic stimulation of the motor cortex on direct current stimulation (tDCS) for the treatment of fibromyal-
chronic widespread pain in fibromyalgia. Brain 2007;130: gia: results of a randomized, sham-controlled longitudinal clinical
2661–70. trial. J Pain Manag 2009;2:353–61.
74. Sampson SM, Rome JD, Rummans TA. Slow-frequency rTMS 92. Mori F, Codeca C, Kusayanagi H, et al. Effects of anodal transcra-
reduces fibromyalgia pain. Pain Med 2006;7:115–18. nial direct current stimulation on chronic neuropathic pain in
75. Louppe JM, Nguyen JP, Robert R, et al. Motor cortex stimulation patients with multiple sclerosis. J Pain 2010;11:436–42.
in refractory pelvic and perineal pain: report of two successful cases. 93. Fregni F, Boggio PS, Lima MC, et al. A sham-controlled, phase II
Neurourol Urodyn 2013;32:53–7. trial of transcranial direct current stimulation for the treatment
76. Pallanti S, Di RA, Antonini S, et al. Low-frequency rTMS over of central pain in traumatic spinal cord injury. Pain 2006;
right dorsolateral prefrontal cortex in the treatment of resistant 122:197–209.
depression: cognitive improvement is independent from clinical 94. Garcia-Larrea L, Peyron R, Mertens P, et al. Electrical stimulation
response, resting motor threshold is related to clinical response. of motor cortex for pain control: a combined PET-scan and elec-
Neuropsychobiology 2012;65:227–35. trophysiological study. Pain 1999;83:259–73.
77. Topper R, Foltys H, Meister IG, et al. Repetitive transcranial mag- 95. Strafella AP, Vanderwerf Y, Sadikot AF. Transcranial magnetic
netic stimulation of the parietal cortex transiently ameliorates stimulation of the human motor cortex influences the neuronal
phantom limb pain-like syndrome. Clin Neurophysiol 2003; activity of subthalamic nucleus. Eur J Neurosci 2004;20:2245–9.
114:1521–30. 96. Poreisz C, Boros K, Antal A, et al. Safety aspects of transcranial
78. Lefaucheur JP, Antal A, Ahdab R, et al. The use of repetitive trans­ direct current stimulation concerning healthy subjects and patients.
cranial magnetic stimulation (rTMS) and transcranial direct current Brain Res Bull 2007;72:208–14.
 CHAPTER 19 

Musculoskeletal Modelling
Mark de Zee  •  John Rasmussen

Erdemir et al.6 wrote an extensive review describing

INTRODUCTION different methods to estimate muscle forces using mus-
culoskeletal modelling. In this chapter the focus will be
Consideration of the load on the musculoskeletal system on musculoskeletal modelling based on inverse dynamics
is relevant in physiotherapy for both diagnosis and treat- and optimization. The theory behind this methodology
ment of musculoskeletal conditions. The first consider- will be explained and two examples will be given of how
ation is the cause of an injury that could be due to musculoskeletal modelling can be applied and what infor-
overloading of the musculoskeletal system in sports or in mation can be gained from these models.
occupational circumstances. The next step is to modify
the system via an intervention. This could be an exercise
intervention which aims to change the loading of the
musculoskeletal system. However, the therapist cannot
BASICS OF MUSCULOSKELETAL
quantify the load on different structures of the musculo- MODELLING BASED ON INVERSE
skeletal system and will not know how or in what way an DYNAMICS
intervention changes the load. Surface electromyography
(EMG) may provide an indication about the change in Biomechanics, as all mechanics, is essentially based on the
muscle coordination,1 but this technique does not provide laws of Newton. Newton’s second law states:
an indication about the load on different structures.
Knowledge of the muscle, ligament and joint reaction F = ma [1]
forces inside the human body may help to improve clini-
cal decision making or improve the understanding of a where F is the sum of forces acting on a body, m is the
specific treatment. However, single muscle forces, liga- mass of the body and a is its acceleration. In spatial coor-
ment forces and joint reaction forces are extremely dif- dinates, F and a are three-dimensional. As with any
ficult and in many cases impossible to measure in vivo. equation, we can determine one property if the other
The only viable possibility for estimating the forces properties are known. Let us presume that m is known.
inside the human body is to make use of computational This leaves us with the following two options:
modelling of the musculoskeletal system based on the 1. If we know the sum of forces, F, then we can deter-
laws of physics. mine the acceleration and thereby the motion.
There are many examples in the literature where the 2. If we know the motion and thereby the acceleration
technology of musculoskeletal modelling has been applied a, then we can determine the sum of forces that
within areas related to physiotherapy. For example, Pon- must have affected the body in order to generate
tonnier et al.2 demonstrated the use of musculoskeletal the motion.
modelling in occupational health by predicting the Newton’s second law applies to particles and can be
optimal bench height for meat cutting tasks. Alkjær et al.3 extended to rigid bodies and even to mechanisms (i.e.
investigated the function of the cruciate ligaments during several rigid bodies connected by joints) if m is inter-
a forward lunge exercise using a musculoskeletal model. preted as mass moment of inertia and mass, F as moments
Their study indicated that the posterior cruciate ligament and forces and a as angular and linear accelerations.
had an important stabilizing role in the forward lunge These equations are called the Newton–Euler equations
movement, while the anterior cruciate ligament did not and they are much more complicated than Newton’s
have any significant mechanical function during this task. second law, but they are essentially structured the same
Furthermore, they showed that the gluteus maximus way and describe the same relationships between masses,
muscle may play a role as a knee stabilizer in addition to forces and motions. So even for very complex mecha-
the hamstring muscles. Rasmussen et al.4 demonstrated nisms, such as the human body with its hundreds of
the use of musculoskeletal modelling to provide insight bones, we can determine the motion if we know the
in to the complex relationship of chair design and seat forces and vice versa.
posture on muscle activity and spinal joint forces. As a If we know the forces, we can define the motions, and
last example, Dubowsky et al.5 estimated the shoulder if we know the motions, we can determine the forces.
joint forces during wheelchair propulsion using a muscu- There is more than an academic difference to the two
loskeletal model of the upper limb and this model could approaches. It is very complicated experimentally to
be used to identify the optimal axle placement in order determine all the forces acting on the human body, since
to lower the forces on the shoulder joint. many of these come from muscles that are voluntarily or
187
188 PART II  Advances in Theory and Practice

involuntarily activated by the central nervous system.

However, several methods are available to capture
motions of living organisms, for instance by photogram-
metry, so motions can be found experimentally and can
be used to compute forces, whereas the opposite is com-
plicated. In many ergonomically relevant cases, the body
can be presumed to be static or analysed in certain key
frames and, in this case, the kinematics of the problem is
even simpler. The process of finding forces from motions
is called inverse dynamics.

A Simple Example
Let us consider the simplified example of a lifting task
as shown in Figure 19-1 and the associated free body
diagram in Figure 19-2.
Despite the anatomical reality we shall consider the
spinal joint as a perfect two-dimensional hinge in which
two reaction force components, Rx and Ry, are working.
We disregard the self-weight of the body segments and
consider the system loaded only by the gravity force of
the lifted load, Fg. We consider initially only the muscle
force, Fm, from a branch of the erector spinae muscle.
We start by the moment equilibrium about the spinal
joint:
FIGURE 19-1  ■  Illustration of a lifting situation.
Fg s1 − Fm s 2 = 0
⇓
Fg s1
Fm =
s2

Horizontal equilibrium yields:

Rx − Fmx = 0
⇓
Rx = Fmx = Fm cos(θ )

FIGURE 19-2  ■  Free body diagram for the force equilibrium about
All that remains now is to determine Ry from vertical a spinal joint.
equilibrium:

R y − Fmy − Fg = 0
⇓ The external force of just 200 N leads to internal forces
that are an order of magnitude larger, and this is typical
R y = Fmy + Fg = Fm sin(θ ) + Fg for the human body; our internal forces are larger than
most people imagine. The mechanical explanation is that
Let us insert some plausible numbers: the moment arms of the external forces are typically
larger than the moment arms of the muscles or, in physi-
ological terms, the moment arms of muscles correspond
θ = 30°, s1 = 0.5 m, s 2 = 0.04 m, Fg = 200 N to the thickness of limbs while the external forces’
moment arms correspond to the length of limbs. Although
This leads to the following forces in the system: the strength of our tissues is substantial, injuries can
occur when, for instance, we lift a heavy load.
Fm = 2500 N Despite this example being static, it is in reality inverse
dynamics in its simplest form: We know the posture and
Rx = 2169 N the velocity (in this case the velocity is zero) of the ele-
ments in the system, and we also know the external forces
R y = 1450 N acting on the system. With this input we can compute
 19  Musculoskeletal Modelling 189

the internal forces (i.e. the muscle force and the joint A graph of the activation development of the hundreds
reaction force). However, we can only do this by hand if of spinal muscles in the model for increasing pelvis tilt is
the situation is very simple. Muscle systems tend to be depicted in Figure 19-5.
complicated and the spine is a good example: it is three- The model shows a complex increase of muscle activa-
dimensional, it contains many degrees-of-freedom, it is tion levels for the model as a result of the postural change
actuated by many muscles, actually hundreds if we con- (Fig. 19-6). The primarily affected muscle groups are
sider all the different muscle fascicles and real-life loading branches of psoas major, quadratus lumborum and
situations are rarely static. obliquus internus, where the increase of activity level is
Coping with such complexities requires more compu- significant from 0 to more than 5%. The increase of
tational power and software systems particularly devel- muscle activation concerns both sides of the body.
oped for the purpose. The development of physiologically
realistic models for use in such systems is also a complex
task. Figure 19-3 shows an example.

EXAMPLE 1: SIMULATED CHANGES IN

LUMBAR MUSCLE ACTIVATION FROM
A PELVIC TILT
Back pain is a complex and generally poorly understood
problem, and back pain may even be associated with
other types of musculoskeletal pain.7 Numerous clinical8–10
and experimental studies11 have confirmed alterations in
back muscle activation as a result of back pain. However,
the changes of muscle activity in response to postural
change are complex and for unilateral pain they are not
confined to the ipsilateral side and they do not correlate
with the level of pain. It is possible that pain evolves
beyond the original injury through the process illustrated
in Figure 19-4. X
To investigate the potential for improved understand-
ing of back pain development through musculoskeletal
simulation, pelvis lateral tilt typical of one-sided back
pain was imposed in small steps on an otherwise sym-
metrical computational model12 of a standing individual, FIGURE 19-3  ■  Model of human lifting a load with spine and hip
and the reconfiguration of muscle loads was reviewed. flexion. The model is developed in the AnyBody Modelling Sys-
temTM and comprises more than 1000 individually activated
The pelvic tilt was accompanied by a compensatory muscles. The colour shading of the muscles indicates the level
lateral flexion of the lumbar spine in such a way that static of activity. X indicates the x-direction of the global coordinate
balance of the model was maintained. system. For colour version see Plate 19.

FIGURE 19-4  ■  Possible development of acute back pain.

 190 PART II  Advances in Theory and Practice

This model shows that a relatively small asymmetrical order to be able to control the head in three-dimensional
postural change as seen in Figure 19-5 requires a complex space the cervical spine has multiple muscles. Many of
reorganization of the muscle activation pattern. If the those muscles span several joints, which makes it very
duration of the pain requires maintenance of the asym- difficult to judge or predict a muscle action without per-
metrical posture constantly, the constant loading of forming a full multi-body analysis based on the equations
these muscles may lead to muscle soreness, injury and of motion. Recently, Schomacher et al.14 investigated the
evolving pain. recruitment of semispinalis cervicis muscle at the levels
of the second (C2) and fifth (C5) cervical vertebrae using
intramuscular EMG during isometric neck extensions.
EXAMPLE 2: UNDERSTANDING THE They found significantly greater EMG amplitude at C5
than at C2. This was explained by the fact that the exter-
RECRUITMENT OF THE SEMISPINALIS nal moment around C5–C6 is larger than the external
CERVICIS MUSCLE USING moment around C2–C3. One has to realize that the semi-
MUSCULOSKELETAL MODELLING spinalis cervicis is a complex muscle, with multiple fas-
cicles that originate from the transverse processes of the
The cervical spine is a complex structure with many upper five or six vertebrae and insert on the cervical
degrees of freedom and complicated kinematics.13 In spinous processes, with each fascicle spanning four to six
segments. This makes it indeed difficult to explain pre-
cisely the mechanical action without taking the full three-
Most muscles are dimensional multi-body analysis into account. The goal
12%
relatively of this example is to show that the recruitment of the
unaffected
semispinalis cervicis can be predicted using a musculo­
11%

skeletal model of the cervical spine purely based on the

10%

9%
equations of motion and optimization principles. More-
Muscle active state

8%
over, it will be demonstrated that the analysis will give
7%
additional information about the loading of the cervical
6%
spine.
5%

4%
Description of the Cervical Spine
3%
Model and Simulation
2% A few muscles are
1% significantly The three-dimensional musculoskeletal model of the cer-
0%
affected vical spine was built using the AnyBody Modelling
System (AnyBody Technology A/S, Aalborg, Denmark).
0.00 0.10 0.20 0.30 0.40 0.50 0.60 0.70 0.80 0.90 1.00

Fraction of movement
The model consists of nine rigid segments: skull, seven
FIGURE 19-5  ■  The effect of a gradual 15° pelvic lateral tilt on
muscle activation in the lumbar spine. For colour version see cervical vertebrae and the thoracic region. The joints
Plate 19. between the vertebrae from T1 to C2 are modelled as

FIGURE 19-6  ■  Alteration of muscle forces (illustrated by the thickness of each fascicle) from symmetrical standing (left) to 10° pelvic
lateral tilt (right). For colour version see Plate 19.
 19  Musculoskeletal Modelling 191

$ %
FIGURE 19-7  ■  Model of the cervical spine with (A) all the muscle and (B) the six fascicles of the semispinalis cervicis on the right
side. For colour version see Plate 20.

three degrees-of-freedom spherical joints, while the 100

joints between C2 and the skull are modelled as one T1C2
90
degree-of-freedom revolute joints. The locations of the T2C3
centres of rotations are based on the work of Amevo 80
et al.15 The model is equipped with 136 muscle actuators T3C4
70
and the muscle parameters are based on the work by Van T4C5
Activity (%)

60
der Horst.16 Figure 19-7A illustrates the cervical spine
T5C6
model and Figure 19-7B provides an illustration of how 50
the semispinalis cervicis was implemented in the model. 40 T6C7
The semispinalis cervicis is modelled as six independent 30
fascicles. The most cranial fascicle spans from T1 to C2,
while the most caudal fascicle spans from T6 to C7. The 20
maximal force these fascicles can produce in the model is 10
based on their physiological cross-sectional areas and 0
these values were based on the work by Van der Horst.16 0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5
The physiological cross-sectional area of the semispinalis Time (s)
cervicis is increasing from the cranial to caudal direction FIGURE 19-8  ■  The predicted activity of the six fascicles of the
starting with 0.13 cm2 for the most cranial fascicle to semispinalis cervicis during ramped extension. For colour
1.1 cm2 for the most caudal fascicle. version see Plate 20.
In the simulation, the model was forced to create a
ramped extension moment in 5 seconds from 0 to around
50% of the model’s maximum capacity in extension. This
was to mimic the ramped extension contractions in the For example the fascicle T1C2 starts its activation after
experiments reported by Schomacher et al.14 The activi- about 0.5 seconds while the T5C6 is active from the start.
ties of the different fascicles of the semispinalis cervicis Figure 19-9 shows the predicted absolute force levels
were now predicted for the generation of these ramped in the fascicles of the semispinalis cervicis during the
extension moments plus the reaction forces between the ramped extension. The difference between the caudal
vertebrae were determined. For these calculations the and cranial fascicles is now even more pronounced than
polynomial muscle recruitment was used with the power when only considering the predicted activity. The cranial
of three. It is assumed that all fascicles of all muscles work fascicles have small force levels below 2 N, while the
independently from each other. highest caudal fascicle reaches 25 N.
Figure 19-10 shows the predicted reaction forces
between the vertebrae. One should be aware that these
Results forces are the products of all muscle forces around the
Figure 19-8 shows the predicted activity for the six fas- cervical spine, and not only the semispinalis cervicis. It
cicles of the semispinalis cervicis during the ramped can be seen that the predicted forces increase from the
extension task. It can be seen that the three caudal fas- cranial to the caudal direction with the highest force of
cicles T6C7, T5C6 and T4C5 show much higher activity around 700 N occurring between T1 and C7. This is a
than the three cranial fascicles. The prediction also high force for a submaximal isometric neck extension
showed that the timing between the fascicles is different. contraction.
192 PART II  Advances in Theory and Practice

30 semispinalis cervicis in addition to the many other muscles

T1C2
of the cervical region. It is also interesting to note that
25 T2C3 Schomacher et al.14 observed an earlier recruitment of
T3C4
the caudal fascicles in comparison with the cranial fasci-
20
cles during the extension contraction. The model pre-
T4C5 dicted the same, but this prediction was purely based on
Force (N)

T5C6
the equilibrium equations and optimization as explained
15 in the paragraph about the basics of musculoskeletal
T6C7 modelling.
10 The biggest advantage of a musculoskeletal model is
that the output contains information which would not be
5 possible to measure in an experimental setup. The results
depicted in Figures 19-9 and 19-10 are an example of
0 this. The absolute forces in the fascicles of the semispi-
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 nalis cervicis show a clear distinction between the caudal
Time (s) and cranial regions. The combination of higher predicted
FIGURE 19-9  ■  The predicted force in the six fascicles of the activations and a larger cross-sectional area in the caudal
semispinalis cervicis during ramped extension. For colour region results in higher absolute forces in these fascicles.
version see Plate 20. The combination of all muscle forces around the cervical
spine leads to reaction forces between the cervical verte-
brae. Those reaction forces are also impossible to measure
800 in an experimental setup. The result that the highest
reaction forces are between the caudal vertebrae is not
700 surprising, since the external extension moment, which
C2C1
has to be balanced, increases linearly with the distance
C3C2 from the force vector on the skull. The model also gives
600
C4C3
an estimate of the quantity of each reaction force and
shows high forces between the caudal vertebrae. This
500
C5C4 may partially explain why most disc herniations are
C6C5 observed in the caudal region of the cervical spine.17
Force (N)

400 C7C6
T1C7 CONCLUSION AND PERSPECTIVES
300
Musculoskeletal modelling is generally used for two pur-
poses. The first purpose is to increase our understanding
200
of the loads working in the musculoskeletal system under
different circumstances, including in patients. The second
100 purpose is the use of musculoskeletal modelling in clini-
cal applications. As Erdemir et al.6 already indicated, the
0
use of musculoskeletal modelling in the clinic is still
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 limited, but promising developments are now taking
Time (s) place.
FIGURE 19-10  ■  The predicted reaction forces between the verte- One of the key requirements for using musculoskeletal
brae in the cervical spine during ramped extension. For colour modelling in the clinic is that the model resembles a
version see Plate 21. certain patient. So there is a need for patient-specific
modelling. Pellikaan et al.18 showed that with a combina-
tion of imaging technology and morphing algorithms
The goal of this example was to demonstrate that it is they were able to estimate subject-specific muscle attach-
possible to obtain detailed information from a relatively ment sites in the lower extremity in a fast and automated
simple analysis, namely a ramped extension moment in 5 manner.
seconds from 0 to around 50% of the model’s capacity. The second requirement for using musculoskeletal
The model predicts varying levels of activity in the dif- models in the clinic is the need for validation. When a
ferent fascicles of the semispinalis cervicis depending on model would be used for critical decisions in a treatment
the location of the fascicle. The complex experiment per- of a patient, the consequences of erroneous models can
formed by Schomacher et al.14 also showed that individ- be very serious. Recently, Lund et al.19 published a review
ual fascicles of the semispinalis cervicis muscle are about validation methods of musculoskeletal models and
activated partly independently. However, due to the inva- provided a number of recommendations. One of the rec-
sive nature of this experiment (fine-wire EMG), record- ommendations is a stronger focus on trend validation.
ings of the activity of the semispinalis cervicis were One of the promising uses of a musculoskeletal model in
limited to two levels, the C2 and C5 levels. In contrast, the clinic would be the investigation of so-called ‘what if’
the model gives information on all fascicles of the scenarios. For example, what would happen with the
 19  Musculoskeletal Modelling 193

reaction force in the knee if we could strengthen the 6. Erdemir A, McLean S, Herzog W, et al. Model-based estimation
vastus medialis? To answer these questions the model of muscle forces exerted during movements. Clin Biomech
2007;22(2):131–54.
parameters have to interact with each other in the correct 7. Hartvigsen J, Natvig B, Ferreira M. Is it all about a pain in the
way, and this can be tested using trend validation. An back? Best Pract Res Clin Rheumatol 2013;10;27(5):613–23.
example of a trend validation was the work of Pontonnier 8. Ferreira PH, Ferreira ML, Hodges PW. Changes in recruitment
et al.2 where they changed the bench height during simu- of the abdominal muscles in people with low back pain. Spine
2004;29(22):2560–6.
lated meat cutting tasks in a systematic way and the same 9. Lamoth CJC, Meijer OG, Daffertshofer A, et al. Effects of chronic
was done in the model. The EMG outputs of certain low back pain on trunk coordination and back muscle activity
shoulder muscles were then compared with the model during walking: changes in motor control. Eur Spine J 2006;15(1):
outputs as a function of bench height. 23–40.
In conclusion, musculoskeletal modelling provides a 10. Lamoth C, Meijer O, Wuisman P, et al. Pelvis-thorax coordination
in the transverse plane during walking in persons with nonspecific
multitude of quantitative information of the loading of low back pain. Spine 2002;27(4):E92–9.
the musculoskeletal system; information which would 11. Dickx N, Cagnie B, Achten E, et al. Changes in lumbar muscle
otherwise be very difficult or impossible to measure in activity because of induced muscle pain evaluated by muscle func-
vivo. Musculoskeletal models have therefore been used tional magnetic resonance imaging. Spine 2008;33(26):E983–9.
12. de Zee M, Hansen L, Wong C, et al. A generic detailed rigid-body
extensively in research. For widespread clinical use of lumbar spine model. J Biomech 2007;40(6):1219–27.
musculoskeletal models, further work is necessary, prog- 13. Bogduk N, Mercer S. Biomechanics of the cervical spine. I: Normal
ress is being made both with respect to imaging technol- kinematics. Clin Biomech 2000;15(9):633–48.
ogy to build patient-specific models and validation. 14. Schomacher J, Dideriksen JL, Farina D, et al. Recruitment of
motor units in two fascicles of the semispinalis cervicis muscle.
REFERENCES J Neurophysiol 2012;107(11):3078–85.
15. Amevo B, Worth D, Bogduk N. Instantaneous axes of rotation of
1. Hug F. Can muscle coordination be precisely studied by surface the typical cervical motion segments: a study in normal volunteers.
electromyography? J Electromyogr Kinesiol 2011 2;21(1):1–12. Clin Biomech 1991;6(2):111–17.
2. Pontonnier C, de Zee M, Samani A, et al. Strengths and limitations 16. van der Horst MJ. Human Head Neck Response in Frontal, Lateral
of a musculoskeletal model for an analysis of simulated meat cutting and Rear End Impact Loading: Modelling and Validation. Eind-
tasks. Appl Ergon 2014;45(3):592–600. hoven: Technische Universiteit Eindhoven; 2002.
3. Alkjær T, Wieland MR, Andersen MS, et al. Computational mod- 17. Mann E, Peterson CK, Hodler J. Degenerative marrow (modic)
eling of a forward lunge: towards a better understanding of the changes on cervical spine magnetic resonance imaging scans. Spine
function of the cruciate ligaments. J Anat 2012;221(6):590–7. 2011;36(14):1081–5.
4. Rasmussen J, Tørholm S, de Zee M. Computational analysis of the 18. Pellikaan P, van der Krogt MM, Carbone V, et al. Evaluation of a
influence of seat pan inclination and friction on muscle activity and morphing based method to estimate muscle attachment sites of the
spinal joint forces. Int J Ind Ergon 2009 1;39(1):52–7. lower extremity. J Biomech 2014;47(5):1144–50.
5. Dubowsky SR, Rasmussen J, Sisto SA, et al. Validation of a mus- 19. Lund ME, de Zee M, Andersen MS, et al. On validation of multi-
culoskeletal model of wheelchair propulsion and its application to body musculoskeletal models. Proc Inst Mech Eng [H] 2012;226(2):
minimizing shoulder joint forces. J Biomech 2008;41(14):2981–8. 82–94.
 CHAPTER 20 

Quantitative Sensory Testing:

Implications for Clinical Practice
Toby Hall  •  Kathy Briffa  •  Axel Schäfer  • 
Brigitte Tampin  •  Niamh Moloney

Sensory examination is a critical component of the assess- protocols QST can be used to evaluate the integrity of
ment of a wide range of clinical conditions, including the entire sensory system, including thinly myelinated Aδ
musculoskeletal and neuropathic disorders. Bedside fibres, unmyelinated C fibres and large-diameter Aβ
examination of the somatosensory system includes the fibres as well as the dorsal column and spinothalamic
assessment of touch/vibration/proprioception (large tract,3,7 assessing sensory pathways from the peripheral
myelinated Aβ fibres) pinprick/blunt pressure sensitivity receptor to the central cortex.2 It is unique in that it can
(small thinly myelinated Aδ and small unmyelinated C be used to measure the function of all sensory nerve fibres
fibres), cold (Aδ fibres) and heat (C fibres) sensitivity as well as the peripheral and central processing of sensa-
utilizing simple equipment such as cotton wool, tuning tion.8 It has the ability to quantify both loss and gain of
fork, tooth pick, digital pressure, and cold and warm sensory function, detecting even subtle changes in noci-
stimuli such as test tubes or coins (Table 20-1). Sensory ceptive pathways missed by conventional nerve conduc-
loss (loss of function) and/or gain of function (hypersen- tion tests, which can only assess loss of function in large
sitivity) would be documented; the borders of changes Aβ fibres.9 As a consequence, a number of aspects of
established and findings compared with the contralateral sensory function can be evaluated including the primary
side if symptoms are unilateral. The bedside assessment afferents that mediate innocuous and painful sensation,
may reveal a sensory deficit or evoke pain that can then central processes that further alter the character and sen-
be interpreted in the context of its location and distribu- sitivity of the primary afferents10 and the clinical mani-
tion. Limitations of the bedside examination are that festations of peripheral and central sensitization.4,11
stimulus intensities are generally not calibrated and
testing procedures are not standardized.1
Quantitative sensory testing (QST) is a complimen- IMPORTANCE OF STANDARDIZING
tary approach that utilizes some more sophisticated PROTOCOLS
equipment and standardized testing protocols to allow
quantification of the stimuli applied during testing. Con- A number of different QST protocols have been
sequently, QST delivers more precise outcomes. It is developed. Typically they include various mechanical
important to recognize, however, that QST is not an and thermal stimuli testing detection and pain
objective assessment of pain or sensation, nor is it specifi- thresholds.2,9,12
cally diagnostic.3 Rather, QST is a psychophysical method In order to generate reliable QST results it is critical
of assessment in which objective stimuli are applied and that the test stimulus and examination procedure are
subjects’ responses are quantified and recorded. Hence, standardized and protocols strictly adhered to. Variations
cognitive factors may influence a patient’s responses.4 in technical equipment used to generate stimuli and
QST can also be influenced by environmental factors associated factors such as the size of the stimulated area
such as ambient temperature and noise, and method- and rate of change of stimulus can influence the results
ological factors such as test protocol, instructions and and have implications for comparing data between
application of the test.5,6 QST can be used in research patients and between different research groups. For these
and clinical contexts. reasons normative data must be protocol-specific. More-
Despite strong research interest, incorporation of over, values vary according to the body site being mea-
QST procedures into clinical practice has been slow. This sured and, for some parameters, there are age- and
may be due to poor knowledge regarding standards for gender-related differences. It is imperative therefore that
application, lack of information about its clinical utility,1 reference data used for the interpretation of test results
and time-consuming procedures and costly equipment. have been collected using the same protocols and well-
The purpose of this chapter is to describe QST and its matched healthy controls. In many cases this means that
use in research, as well as its potential role in clinical the test laboratory must collect their own normative
practice. reference data.
The reliability of QST has been demonstrated in mul-
tiple studies.13–18 However, it has to be acknowledged that
QUANTITATIVE SENSORY TESTING all reliability data are protocol- and population-specific
and statistical analyses vary between reliability studies,
A variety of sensory stimuli can be used for QST (Table hence reliability coefficients are not necessarily compa-
20-1). With appropriate choice of stimuli and testing rable between studies. As with reference data, in view of
194
 20  Quantitative Sensory Testing: Implications for Clinical Practice 195

TABLE 20-1  Modalities, Receptors and Testing Methods2

Postulated
Mechanism of
Principal Receptors Hyperalgesia/ Clinical
QST Parameter Laboratory Test Clinical Test and Axon Type Allodynia Relevance
Mechanical
Vibration threshold Graded tuning fork Tuning fork Pacinian, Aβ Unknown Lemniscal
or vibrometer
Mechanical detection Calibrated von Frey Cotton wool Aβ Lemniscal
thresholds filaments
Punctate pain Pin or calibrated Toothpick Unencapsulated, Aδ Spinothalamic
thresholds sharp metal pin and C
pricks
Pressure pain Algometer Analogue Algometer, Intramuscular Unknown Spinothalamic
threshold thumb afferents, iii and iv
Aδ and C
Dynamic mechanical Brush, cotton wool, Brush, cotton wool, Meissner’s Pacinian, Central sensitization Lemniscal
Q-tip Q-tip hair follicle
Aβ and C
Wind-up Pin prick Toothpick Aδ Central sensitization, Spinothalamic
reduced inhibition

Thermal
Cold detection Computer-controlled Thermoroller, test Unencapsulated, Aδ Spinothalamic
threshold thermotester tubes, coins
Warm detection Thermoroller, test Unencapsulated, C Spinothalamic
threshold tubes, coins
Cold pain threshold Thermoroller, test Unencapsulated Central and Spinothalamic
tubes, ice cube, Aδ and C peripheral
cold pressor test sensitization,
reduced inhibition
Heat pain threshold Thermoroller, test Unencapsulated peripheral Spinothalamic
tubes Aδ and C sensitization

QST, Quantitative sensory testing.

the specificity of QST results to testing protocols, unless testing stimuli and protocols that are not part of the
published QST protocols are being adhered to strictly, it DFNS protocol.
would be prudent for most groups to undertake their own
well-designed reliability studies rather than assuming
reliability in their hands will be comparable to published TEST PARAMETERS
values.
In view of the specificity of results to testing param- Mechanical Quantitative Sensory Testing
eters, the German Research Network on Neuropathic Vibration Thresholds
Pain (DFNS) has developed a comprehensive battery of
quantitative sensory tests that combined, provide a Vibration thresholds are typically measured by a vibrom-
complete somatosensory profile17,19,20 for which there are eter or Rydel-Seiffer graded tuning fork19 (Fig. 20-1)
validation and normative data accumulating in the placed against a bony point where it is left until the vibra-
literature.21–23 It is comprised of seven tests that are used tion can no longer be felt. Reduced vibration sense
to measure 13 parameters. These tests are described in has been identified as an indicator for the presence
detail in the literature19 and will not be reproduced in of peripheral nerve damage in diabetic neuropathy,24,25
detail here; however, methods documented in this chapter in peripheral nerve injuries,26,27 cervical and lumbar
are part of the DFNS protocol. The DFNS also have radiculopathies28–32 and in patient groups with neuro-
processes and procedures in place to train clinicians and pathic pain.33 Reduced vibration sense in people with
researchers in QST in order to guarantee standardized non-specific neck–arm pain34–39 was proposed to reflect
QST between users. This could be advantageous for the presence of a minor neuropathy.34,35 However, the
clinics and research facilities wishing to incorporate QST finding of widespread vibration threshold alterations in
into their assessment and data collection regimens, as it this patient population40 suggests that altered central
would validate their use of DFNS reference data.22 processing,39 possibly secondary to pain,41 may be an
Another advantage of these protocols is that published important underlying mechanism explaining this
reliability data are available for comparison.17 Although finding. Furthermore, reduced vibration sense has
the standardized DFNS protocol has many advantages, it been documented in other musculoskeletal, non-
must be recognized that QST is a broader concept than neuropathic pain conditions such as knee and hip
just one protocol and there are many valid and reliable osteoarthritis,42,43 temporomandibular joint disorders44
196 PART II  Advances in Theory and Practice

FIGURE 20-2  ■  Mechanical detection threshold evaluation using

a calibrated filament.

FIGURE 20-1  ■  Vibration threshold evaluation using a graded

tuning fork.

and fibromyalgia.32,45 Therefore, any evidence of altered

vibration thresholds must be interpreted within the
context of the overall clinical presentation, rather than as
a stand-alone method of assessment. Increased vibration FIGURE 20-3  ■  Pressure pain threshold evaluation using a pres-
sensitivity (vibration allodynia) has been reported as an sure algometer.
indicator of altered central processing.46

the skin, gently brushing/stroking the skin with a cotton

Light Touch
wisp (3 mN), a cotton wool tip (100 mN) or a brush (200–
Mechanical detection thresholds are measured using cali- 400 mN). Light touch allodynia in an area of secondary
brated von Frey hairs that exert specific forces upon hyperalgesia is mediated by large myelinated Aβ fibres50
bending that vary according to the stiffness of the hair and results from sensitization of nociceptive neurons in
used (Fig. 20-2). Reduced mechanical detection can be the dorsal horn due to C fibre discharge.51–54 Dynamic
indicative of a peripheral nerve lesion if the topographic mechanical allodynia is considered the hallmark sign of
area follows a plausible neuroanatomical distribu- central sensitization.55
tion.27,30–32,45,47 Elevated mechanical detection thresholds
have also been found in people suffering from musculo- Pressure Pain Thresholds
skeletal pain disorders,48 joint arthropathies49 and fibro-
myalgia.21,32 In this regard, tactile hypoaesthesia does not Pressure pain thresholds are measured using a pressure
specifically indicate structural nerve fibre damage and algometer (Fig. 20-3). A flat probe is applied to the skin,
may relate to central nervous system plasticity.33 Careful pressure is gradually increased and the subject is asked to
mapping of the distribution of sensory changes may indicate the onset of pain. Loss of function (hypoaesthe-
enable identification of the location of nerve injury: sia) as well as a gain of function (hyperalgesia) can be
peripheral nerve, plexus, or nerve root. established. Pressure pain thresholds have been investi-
Heightened sensitivity to light touch is referred to as gated in a diverse range of disorders, including non-
mechanical allodynia that can be classified into static and specific neck–arm pain, cervical radiculopathy, neck
dynamic mechanical allodynia, depending on which stim- pain, whiplash-associated disorder, knee osteoarthritis,
ulus is used. Dynamic mechanical allodynia can be patellofemoral pain, low back pain and low-back-related
assessed using different degrees of soft contact force on leg pain.2,3,7–9,19,33,56 Increased pressure sensitivity has been
 20  Quantitative Sensory Testing: Implications for Clinical Practice 197

found within anatomically local and distal sites in people second given within the same location.19 A pain rating is
with whiplash-associated disorders, non-specific arm pain given for the first stimulus and for the series of ten pin-
and cervical radiculopathy when compared with asymp- pricks using a 0–100 scale. The pain rating of repeated
tomatic groups.28 Increased pressure sensitivity at a distal pinprick stimuli is divided by the pain rating of the single
point may suggest widespread sensitization, while local stimulus to provide the wind-up ratio.
changes alone may indicate peripheral nerve dysfunction.
Interestingly, in people undergoing total knee replace-
ment, pre-operative increased pressure pain sensitivity at
Thermal Quantitative Sensory Testing
a remote site (forearm), but not at the knee, showed a Thermal detection and pain thresholds (cold and heat)
weak (r = 0.37) but significant correlation with worse pain are measured using a thermal sensory testing device (Fig.
scores using the WOMAC at 1-year follow-up.49 Similar 20-5). A thermode is placed on the skin, the temperature
associations between QST measures and recovery were of which can be altered ramping up and down in precise
found across a range of different surgeries including increments, typically in 1°C per second. For the measure-
thoracic surgery,57 subacromial decompression58 and ment of detection thresholds the subject is asked to indi-
herniotomy.59 cate when they feel a change in temperature, for pain
thresholds the subject is asked to indicate as soon as the
stimulus becomes painful.
Mechanical Pain Thresholds
Thermal QST has been investigated in many common
Mechanical pain thresholds can be measured using cali- musculoskeletal pain disorders including non-specific
brated weighted pinprick stimulators19 (Fig. 20-4). The neck–arm pain, cervical radiculopathy, neck pain,
tip of the stimulator is gently placed on the skin and whiplash-associated disorder, knee osteoarthritis, patel-
maintained for a duration of 2 seconds and subjects are lofemoral pain, low-back-related leg pain among
asked to indicate if the stimulus feels sharp or blunt and/ others,1,6–9,19,33,56 with some variation in findings.
or if the stimulus is painful. Hyperalgesia to pinprick is Reduced thermal detection, indicated when the subject
induced by C fibre discharges and mediated by Aδ fibres takes longer to feel the change of temperature, can be
(heterosynaptic facilitation),60 leading to central sensiti- indicative of a loss of small nerve fibre function. Reduced
zation to the input of A fibre nociceptors.53 Loss of func- thermal detection was evident on the symptomatic side
tion may be indicative of neuropathy, while a gain of in patients with cervical and lumbar radiculopathy,29–31,63
function may be indicative of peripheral and central findings suggestive of nerve root damage. However, some
sensitization.53 studies demonstrated a bilateral loss of function in
patients with unilateral nerve injury.29–31,63–65 It is hypoth-
esized that bilateral hypoaesthesia may be mediated
Temporal Summation of Pain
by peripheral nerve damage-induced central plasticity.66
(Wind-Up Ratio)
Widespread hypoaesthesia was also present in whiplash
Wind-up is defined as the summation of repeated C fibre patients, suggestive of disordered central pain
input to produce an augmented response.61,62 Although processing.67
not fully understood, it is thought that the mechanism of Increased heat sensitivity implicates mechanisms of
wind-up relates to the depolarization of neurons and the peripheral sensitization and has been demonstrated in
activation of the N-methyl-D-aspartate receptor.62 This various musculoskeletal disorders.50,68 Cold sensitivity
process results in the progressive increase in the action measured in the patient’s main pain area is a common
potential discharge elicited by each C fibre stimulus, such sequel of peripheral nerve injury;27,69 however, it is not
that relatively brief input can produce rapid and long- necessarily associated with the presence of pain or nerve
lasting changes in excitability. Wind-up can be assessed damage, as evidenced in patients with painless nerve inju-
with thermal or punctate stimuli. ries,69 in patients with fibromyalgia70–72 and in patients
An example for the latter is the wind-up protocol of with depression without pain.71 Mechanisms underlying
the DFNS. The perceived magnitude of a single pinprick cold-evoked pain are still not fully understood and likely
stimulus is compared with that of a series of ten pinprick
stimuli of the same force repeated at a rate of one per

FIGURE 20-4  ■  Mechanical pain threshold evaluation. FIGURE 20-5  ■  Thermal detection and pain threshold evaluation.
198 PART II  Advances in Theory and Practice

include both peripheral and central nervous system is the variation in both normative and patient data due to
mechanisms.73–75 heterogeneity of participants (including age and gender)
and methodological differences between studies such as
the body region assessed and the specific QST protocols
used.7,19,31,32,77 The DFNS has published reference data
TEST SITE AND INTERPRETATION for their protocols for the cheek, dorsum of the hand,
OF QUANTITATIVE SENSORY dorsum of the foot and trunk for male and female adults
TESTING DATA in age decades from 20 to 70 years22 and there are some
reference data for children and juveniles.23
QST data are usually collected in the area of maximal Furthermore, there is a lack of consensus as to what
sensory disturbance, often the area of maximal pain, and cut-off values are meaningful for the interpretation of
a control area. The choice of test sites depends on the QST data, for example what constitutes a clinically
clinical question to be answered. For example, testing important side-to-side difference for thermal detection
sensory function at the primary area of pain provides thresholds.19,65 A cut-off of 15°C has been defined as cold
information about primary afferent function and periph- hyperalgesia;78 however, this score may fall within the
eral sensitivity as well as central sensitization, whereas 95% confidence interval of normative data.22 The DFNS
testing in anatomically remote areas can provide proposes the use of z-scores to analyse an individual’s data
information about central sensitization and central and ascertain the presence of sensory gain or sensory
processing. loss.7,19,31,32,77 Using this system, two standard deviations
For the assessment of neuropathic pain, sensation above/below the mean of reference data is considered
testing should be performed in the area of maximal pain. indicative of a pathological value.
Dermatomal sensory loss in patients with cervical/lumbar Profiling patients using QST involves analysing mul-
radiculopathy is indicative of nerve root damage,29–31 tiple parameters of sensory testing to evaluate the func-
whereby sensory loss in the main pain area supports the tion of sensory receptors, nerve fibres and their respective
presence of neuropathic pain.31,33,76 pathways to determine whether patients demonstrate
An important consideration for the interpretation of dominant features of loss or gain of function.19,33 An
QST data and comparison of QST data between studies example is shown in Figure 20-6. Subgroups of patients

4
CxRAD
Gain of function

NSNAP
3

1
Z-score

–1
Loss of function

–2

–3

–4

–5
CDT WDT TSL CPT HPT MDT MPT MPS WUR VDT PPT
FIGURE 20-6  ■  Sensory profiling. The z-score quantitative sensory testing sensory profiles are shown for the maximal pain area in
two patients presenting with neck–arm pain in the C7 dermatomal distribution. Healthy control subjects are represented by a z-score
of ‘zero’. The patient with cervical radiculopathy (CxRAD, filled circle) was characterized by sensory alterations in the maximal pain
area (reduced thermal, mechanical and vibration detection and reduced pressure pain sensitivity), indicating a loss of small and
large sensory nerve fibre function, suggestive of nerve root damage and the presence of neuropathic pain. The thermal, mechanical
detection and pressure pain thresholds were two standard deviations below the mean of reference data. The patient also demon-
strated cold hypersensitivity compared to the reference data. The QST profile of the patient with non-specific neck–arm pain (NSNAP,
open square) did not demonstrate any loss of function, but demonstrated heightened pressure sensitivity compared to reference
data. However the value was not above 2 standard deviations from the mean of reference data.CDT, Cold detection threshold; CPT,
Cold pain threshold; HPT, Heat pain threshold; MDT, Mechanical detection threshold; MPS, Mechanical pain sensitivity; MPT,
Mechanical pain threshold; PPT, Pressure pain threshold; TSL, Thermal sensory limen; VDT, Vibration detection threshold; WDT,
Warm detection threshold; WUR, Wind-up ratio.
 20  Quantitative Sensory Testing: Implications for Clinical Practice 199

with distinct somatosensory profiles have been identified 3. Hansson P, Backonja M, Bouhassira D. Usefulness and limitations
within one aetiology, illustrating the heterogeneity of of quantitative sensory testing: clinical and research application in
neuropathic pain states. Pain 2007;129(3):256–9.
pain disorders.7,19,31,32,77 Moreover, patients with similar 4. Wilder-Smith OH, Tassonyi E, Crul BJ, et al. Quantitative sensory
somatosensory profiles can be present across aetiologi- testing and human surgery: effects of analgesic management on
cally different groups.33,79 It has been proposed that these postoperative neuroplasticity. Anesthesiology 2003;98(5):1214–22.
trans-aetiological profiles reflect underlying pain mecha- 5. Verhagen AP, Scholten-Peeters GG, van Wijngaarden S, et al.
Conservative treatments for whiplash. Cochrane Database Syst Rev
nisms and that sensory profiling may have a role in match- 2007;(2):CD003338.
ing patients to the most appropriate interventions.19,79 6. Backonja MM, Walk D, Edwards RR, et al. Quantitative sensory
QST is generally not recommended as a stand-alone testing in measurement of neuropathic pain phenomena and other
method of assessment;2 however, it often adds value to sensory abnormalities. Clin J Pain 2009;25(7):641–7.
comprehensive assessment or as a component of a diag- 7. Meier PM, Berde CB, DiCanzio J, et al. Quantitative assessment
of cutaneous thermal and vibration sensation and thermal pain
nostic profile. For example, quantitative thermal thresh- detection thresholds in healthy children and adolescents. Muscle
old testing combined with skin biopsy has been Nerve 2001;24(10):1339–45.
recommended for the assessment of small-fibre involve- 8. Yarnitsky D, Granot M. Chapter 27 Quantitative sensory testing.
ment in diabetic neuropathy.2 Handb Clin Neurol 2006;81:397–409.
9. Arendt-Nielsen L, Yarnitsky D. Experimental and clinical applica-
tions of quantitative sensory testing applied to skin, muscles and
viscera. J Pain 2009;10(6):556–72.
CLINICAL UTILITY OF QUANTITATIVE 10. Sang CN, Max MB, Gracely RH. Stability and reliability of detec-
SENSORY TESTING IN PHYSIOTHERAPY tion thresholds for human A-beta and A-delta sensory afferents
determined by cutaneous electrical stimulation. J Pain Symptom
Manage 2003;25(1):64–73.
Persistent musculoskeletal pain disorders can be chal- 11. Cruccu G, Anand P, Attal N, et al. EFNS guidelines on neuropathic
lenging to manage by traditional methods of physiother- pain assessment. Eur J Neurol 2004;11(3):153–62.
apy. Systematic reviews reveal evidence of poor efficacy 12. Walk D, Sehgal N, Moeller-Bertram T, et al. Quantitative sensory
for physical treatments when given to patients with testing and mapping: a review of nonautomated quantitative
methods for examination of the patient with neuropathic pain. Clin
complex pain conditions such as whiplash-associated dis- J Pain 2009;25(7):632–40.
order4 or chronic non-specific low back pain.80 It has 13. Wylde V, Palmer S, Learmonth ID, et al. Test-retest reliability of
been suggested that this might be because of the ‘washout quantitative sensory testing in knee osteoarthritis and healthy par-
effect’81,82 whereby only a small subgroup of people with ticipants. Osteoarthritis Cartilage 2011;19(6):655–8.
a specific feature-set respond to this form of intervention. 14. Wang R, Cui L, Zhou W, et al. Reliability study of thermal quan-
titative sensory testing in healthy Chinese. Somatosens Mot Res
This may be due to the fact that such persistent condi- 2014;31(4):198–203.
tions comprise a constellation of different underlying 15. Moloney NA, Hall TM, O’Sullivan TC, et al. Reliability of thermal
mechanisms despite presenting with similar symptoms. quantitative sensory testing of the hand in a cohort of young,
Such symptoms may be explained by the complex inter- healthy adults. Muscle Nerve 2011;44(4):547–52.
16. Moloney NA, Hall TM, Doody CM. Reliability of thermal quan-
action of a number of factors in any single pain presenta- titative sensory testing: a systematic review. J Rehabil Res Dev
tion including ongoing tissue damage, psychosocial 2012;49(2):191–207.
co-morbidities, peripheral and central nerve injury, and 17. Geber C, Klein T, Azad S, et al. Test-retest and interobserver reli-
altered central processing of sensory stimuli.83 Identify- ability of quantitative sensory testing according to the protocol of
ing these factors may lead to enhanced, individualized the German Research Network on Neuropathic Pain (DFNS): a
multi-centre study. Pain 2011;152(3):548–56.
patient-focused care.84 An example of this can be seen in 18. Felix ER, Widerstrom-Noga EG. Reliability and validity of quan-
a mechanism-based classification system designed to titative sensory testing in persons with spinal cord injury and neu-
assist in the manual therapy management of low-back- ropathic pain. J Rehabil Res Dev 2009;46(1):69–83.
related leg pain.84 The validity of this classification system 19. Rolke R, Baron R, Maier C, et al. Quantitative sensory testing in
the German Research Network on Neuropathic Pain (DFNS):
has been established through the use of QST to establish standardized protocol and reference values. Pain 2006;123(3):
subgroups suitable for physical intervention.85,86 Addi- 231–43.
tional benefits of the use of mechanism-based classifica- 20. Rolke R, Baron R, Maier C, et al. Quantitative sensory testing: a
tion include improved patient satisfaction through better comprehensive protocol for clinical trials. Eur J Pain 2006;10(1):
diagnostic labelling, a clearer understanding of progno- 77–88.
21. Pfau DB, Krumova EK, Treede RD, et al. Quantitative sensory
sis, and the potential for mechanism-based therapeutic testing in the German Research Network on Neuropathic Pain
interventions that would specifically target the underly- (DFNS): reference data for the trunk and application in patients
ing pathophysiology.1,47–49,61 QST can assist in the inter- with chronic postherpetic neuralgia. Pain 2014;155(5):1002–15.
pretation of pain mechanisms underlying a patient’s 22. Magerl W, Krumova EK, Baron R, et al. Reference data for quan-
titative sensory testing (QST): refined stratification for age and a
clinical presentation and its application should be consid- novel method for statistical comparison of group data. Pain
ered in physiotherapy assessment and management 2010;151(3):598–605.
of acute as well as persistent musculoskeletal pain 23. Blankenburg M, Boekens H, Hechler T, et al. Reference values for
disorders. quantitative sensory testing in children and adolescents: develop-
mental and gender differences of somatosensory perception. Pain
REFERENCES 2010;149(1):76–88.
24. Gelber DA, Pfeifer MA, Broadstone VL, et al. Components of
1. Backonja MM, Attal N, Baron R, et al. Value of quantitative sensory variance for vibratory and thermal threshold testing in normal and
testing in neurological and pain disorders: NeuPSIG consensus. diabetic subjects. J Diabetes Complications 1995;9(3):170–6.
Pain 2013;154(9):1807–19. 25. Martin CL, Waberski BH, Pop-Busui R, et al. Vibration perception
2. Krumova EK, Geber C, Westermann A, et al. Neuropathic pain: is threshold as a measure of distal symmetrical peripheral neuropathy
quantitative sensory testing helpful? Curr Diab Rep 2012;12(4): in type 1 diabetes: results from the DCCT/EDIC study. Diabetes
393–402. Care 2010;33(12):2635–41.
200 PART II  Advances in Theory and Practice

26. Schmid AB, Soon BT, Wasner G, et al. Can widespread hypersen- ment: an exploratory study. Osteoarthritis Cartilage 2013;21(9):
sitivity in carpal tunnel syndrome be substantiated if neck and arm 1253–6.
pain are absent? Eur J Pain 2012;16(2):217–28. 50. Kilo S, Schmelz M, Koltzenburg M, et al. Different patterns of
27. Taylor KS, Anastakis DJ, Davis KD. Chronic pain and sensorimo- hyperalgesia induced by experimental inflammation in human skin.
tor deficits following peripheral nerve injury. Pain 2010;151(3): Brain 1994;117(Pt 2):385–96.
582–91. 51. Simone DA, Sorkin LS, Oh U, et al. Neurogenic hyperalgesia:
28. Chien A, Eliav E, Sterling M. Whiplash (grade II) and cervical central neural correlates in responses of spinothalamic tract
radiculopathy share a similar sensory presentation: an investigation neurons. J Neurophysiol 1991;66(1):228–46.
using quantitative sensory testing. Clin J Pain 2008;24(7):595–603. 52. Torebjork HE, Lundberg LE, LaMotte RH. Central changes in
29. Freynhagen R, Rolke R, Baron R, et al. Pseudoradicular and radic- processing of mechanoreceptive input in capsaicin-induced second-
ular low-back pain – a disease continuum rather than different ary hyperalgesia in humans. J Physiol 1992;448:765–80.
entities? Answers from quantitative sensory testing. Pain 53. Magerl W, Fuchs PN, Meyer RA, et al. Roles of capsaicin-
2008;135(1–2):65–74. insensitive nociceptors in cutaneous pain and secondary hyperalge-
30. Nygaard OP, Mellgren SI. The function of sensory nerve fibers in sia. Brain 2001;124(Pt 9):1754–64.
lumbar radiculopathy. Use of quantitative sensory testing in the 54. Woolf CJ, Max MB. Mechanism-based pain diagnosis: issues for
exploration of different populations of nerve fibers and derma- analgesic drug development. Anesthesiology 2001;95(1):241–9.
tomes. Spine (Phila Pa 1976) 1998;23(3):348–52, discussion 353. 55. Woolf CJ, Mannion RJ. Neuropathic pain: aetiology, symptoms,
31. Tampin B, Slater H, Hall T, et al. Quantitative sensory testing mechanisms, and management. Lancet 1999;353(9168):1959–64.
somatosensory profiles in patients with cervical radiculopathy are 56. Moloney N, Hall T, Doody C. Sensory hyperalgesia is character-
distinct from those in patients with nonspecific neck-arm pain. Pain istic of nonspecific arm pain: a comparison with cervical radiculopa-
2012;153(12):2403–14. thy and pain-free controls. Clin J Pain 2013;29(11):948–56.
32. Tampin B, Briffa NK, Slater H. Self-reported sensory descriptors 57. Yarnitsky D, Crispel Y, Eisenberg E, et al. Prediction of chronic
are associated with quantitative sensory testing parameters in post-operative pain: pre-operative DNIC testing identifies patients
patients with cervical radiculopathy, but not in patients with fibro- at risk. Pain 2008;138(1):22–8.
myalgia. Eur J Pain 2013;17(4):621–33. 58. Gwilym SE, Oag HC, Tracey I, et al. Evidence that central sensi-
33. Maier C, Baron R, Tölle TR, et al. Quantitative sensory testing in tisation is present in patients with shoulder impingement syndrome
the German Research Network on Neuropathic Pain (DFNS): and influences the outcome after surgery. J Bone Joint Surg Br
somatosensory abnormalities in 1236 patients with different neu- 2011;93(4):498–502.
ropathic pain syndromes. Pain 2010;150(3):439–50. 59. Aasvang EK, Gmaehle E, Hansen JB, et al. Predictive risk factors
34. Greening J, Lynn B. Vibration sense in the upper limb in patients for persistent postherniotomy pain. Anesthesiology 2010;112(4):
with repetitive strain injury and a group of at-risk office workers. 957–69.
Int Arch Occup Environ Health 1998;71(1):29–34. 60. Ziegler EA, Magerl W, Meyer RA, et al. Secondary hyperalgesia to
35. Greening J, Lynn B, Leary R. Sensory and autonomic function in punctate mechanical stimuli. Central sensitization to A-fibre noci-
the hands of patients with non-specific arm pain (NSAP) and ceptor input. Brain 1999;122(Pt 12):2245–57.
asymptomatic office workers. Pain 2003;104(1–2):275–81. 61. Woolf CJ. Central sensitization: implications for the diagnosis and
36. Jensen BR, Pilegaard M, Momsen A. Vibrotactile sense and treatment of pain. Pain 2011;152(3 Suppl.):S2–15.
mechanical functional state of the arm and hand among computer 62. Yaksh TL, Malmber AB, editors. Central Pharmacology of Noci-
users compared with a control group. Int Arch Occup Environ ceptive Transmission. 3rd ed. London: Churchill Livingstone; 1994.
Health 2002;75(5):332–40. 63. Tampin B, Slater H, Briffa NK. Neuropathic pain components are
37. Laursen LH, Jepsen JR, Sjogaard G. Vibrotactile sense in patients common in patients with painful cervical radiculopathy, but not
with different upper limb disorders compared with a control group. in patients with nonspecific neck-arm pain. Clin J Pain 2013;
Int Arch Occup Environ Health 2006;79(7):593–601. 29(10):846–56.
38. Pilegaard M, Jensen BR. An 18-month follow-up study on vibro- 64. Jaaskelainen SK, Teerijoki-Oksa T, Forssell H. Neurophysiologic
tactile sense, muscle strength and symptoms in computer users with and quantitative sensory testing in the diagnosis of trigeminal neu-
and without symptoms. Int Arch Occup Environ Health 2005; ropathy and neuropathic pain. Pain 2005;117(3):349–57.
78(6):486–92. 65. Leffler AS, Hansson P, Kosek E. Somatosensory perception in
39. Tucker AT, White PD, Kosek E, et al. Comparison of vibration patients suffering from long-term trapezius myalgia at the site over-
perception thresholds in individuals with diffuse upper limb pain lying the most painful part of the muscle and in an area of pain
and carpal tunnel syndrome. Pain 2007;127(3):263–9. referral. Eur J Pain 2003;7(3):267–76.
40. Moloney NA, Hall T, Doody CM. Pathophysiology in nonspecific 66. Davis KD, Taylor KS, Anastakis DJ. Nerve injury triggers changes
arm pain. Physical Therapy Reviews 2011;16:321–5. in the brain. Neuroscientist 2011;17(4):407–22.
41. Apkarian AV, Stea RA, Bolanowski SJ. Heat-induced pain dimin- 67. Chien A, Eliav E, Sterling M. Hypoaesthesia occurs with sensory
ishes vibrotactile perception: a touch gate. Somatosens Mot Res hypersensitivity in chronic whiplash – further evidence of a neuro-
1994;11(3):259–67. pathic condition. Man Ther 2009;14(2):138–46.
42. Shakoor N, Agrawal A, Block JA. Reduced lower extremity vibra- 68. Staud R, Weyl EE, Price DD, et al. Mechanical and heat hyperal-
tory perception in osteoarthritis of the knee. Arthritis Rheum gesia highly predict clinical pain intensity in patients with chronic
2008;59(1):117–20. musculoskeletal pain syndromes. J Pain 2012;13(8):725–35.
43. Shakoor N, Lee KJ, Fogg LF, et al. Generalized vibratory deficits 69. Kleggetveit IP, Jorum E. Large and small fiber dysfunction in
in osteoarthritis of the hip. Arthritis Rheum 2008;59(9):1237–40. peripheral nerve injuries with or without spontaneous pain. J Pain
44. Hollins M, Sigurdsson A, Fillingim L, et al. Vibrotactile threshold 2010;11(12):1305–10.
is elevated in temporomandibular disorders. Pain 1996;67(1): 70. Blumenstiel K, Gerhardt A, Rolke R, et al. Quantitative sensory
89–96. testing profiles in chronic back pain are distinct from those in
45. Koroschetz J, Rehm SE, Pontus H, et al. Quantitative sensory fibromyalgia. Clin J Pain 2011;27(8):682–90.
testing in patients suffering from fibromyalgia. Eur J Pain 71. Klauenberg S, Maier C, Assion HJ, et al. Depression and changed
2010;4(Suppl.):66. pain perception: hints for a central disinhibition mechanism. Pain
46. Courtney CA, Kavchak AE, Lowry CD, et al. Interpreting joint 2008;140(2):332–43.
pain: quantitative sensory testing in musculoskeletal management. 72. Pfau DB, Rolke R, Nickel R, et al. Somatosensory profiles in sub-
J Orthop Sports Phys Ther 2010;40(12):818–25. groups of patients with myogenic temporomandibular disorders
47. George SZ, Bishop MD, Bialosky JE, et al. Immediate effects of and fibromyalgia syndrome. Pain 2009;147(1–3):72–83.
spinal manipulation on thermal pain sensitivity: an experimental 73. Berglund B, Harju EL, Kosek E, et al. Quantitative and qualitative
study. BMC Musculoskelet Disord 2006;7:68. perceptual analysis of cold dysesthesia and hyperalgesia in fibromy-
48. Lewis C, Souvlis T, Sterling M. Sensory characteristics of tender algia. Pain 2002;96(1–2):177–87.
points in the lower back. Man Ther 2010;15(5):451–6. 74. de Medinaceli L, Hurpeau J, Merle M, et al. Cold and post-
49. Wylde V, Palmer S, Learmonth ID, et al. The association between traumatic pain: modeling of the peripheral nerve message. Biosys-
pre-operative pain sensitisation and chronic pain after knee replace- tems 1997;43(3):145–67.
 20  Quantitative Sensory Testing: Implications for Clinical Practice 201

75. Treede RD, Meyer RA, Raja SN, et al. Peripheral and central 81. Wand BM, O’Connell NE. Chronic non-specific low back pain –
mechanisms of cutaneous hyperalgesia. Prog Neurobiol 1992; sub-groups or a single mechanism? BMC Musculoskelet Disord
38(4):397–420. 2008;9:11.
76. Cruccu G, Sommer C, Anand P, et al. EFNS guidelines on neuro- 82. Rose S. Physical therapy diagnosis: role and function. Phys Ther
pathic pain assessment: revised 2009. Eur J Neurol 2010; 1989;69(7):535–7.
17(8):1010–18. 83. Curatolo M. Diagnosis of altered central pain processing. Spine
77. Westermann A, Krumova EK, Pennekamp W, et al. Different (Phila Pa 1976) 2011;36(25 Suppl.):S200–4.
underlying pain mechanisms despite identical pain characteristics: 84. Schäfer A, Hall T, Briffa K. Classification of low back-related leg
a case report of a patient with spinal cord injury. Pain 2012; pain – a proposed patho-mechanism-based approach. Man Ther
153(7):1537–40. 2009;14(2):222–30.
78. Bennett GJ. Can we distinguish between inflammatory and neuro- 85. Schäfer A, Hall T, Müller G, et al. Outcomes differ between sub-
pathic pain. Pain Res Manage 2006;11(Suppl. A):11A–15A. groups of patients with low back and leg pain following neural
79. Freeman R, Baron R, Bouhassira D, et al. Sensory profiles of manual therapy: a prospective cohort study. Eur Spine J 2011;
patients with neuropathic pain based on the neuropathic pain symp- 20(3):482–90.
toms and signs. Pain 2014;155(2):367–76. 86. Schäfer AG, Hall TM, Rolke R, et al. Low back related leg pain:
80. Rubinstein SM, van Middelkoop M, Assendelft WJ, et al. Spinal An investigation of construct validity of a new classification system.
manipulative therapy for chronic low-back pain: an update of a J Back Musculoskelet Rehabil 2014;27(4):409–18.
Cochrane review. Spine (Phila Pa 1976) 2011;36(13):E825–46.
 CHAPTER 21 

Outcome Measures in
Musculoskeletal Practice
Jonathan Hill

some sectors performance-related pay is on the horizon.

INTRODUCTION For clinicians treating patients with musculoskeletal dis-
orders, the importance of understanding OMs has there-
Outcome measures (OMs) are integral to improving fore never been so critical.
quality of treatment for patients with musculoskeletal This chapter aims to inform the reader about the
disorders (Box 21-1). Originally emerging from scientific complex world of OMs to ensure they are equipped to
research as robust instruments designed to objectively deal with this new context in which outcomes are embed-
evaluate treatment, OMs are now rapidly gaining a pivotal ded into every-day clinical practice (see Table 21-1).
position at the heart of services as part of the wider
agenda to put patient needs, interests and feedback at the
centre of care.1 It is increasingly acknowledged that ‘we TYPES OF OUTCOME MEASURES
can only be sure to improve what we can actually
measure’,2 and as a consequence urgent efforts are being A health outcome measure is an instrument that enables
made to make what is important measurable and not an observer to objectively evaluate an intended goal (typi-
simply what is measurable important. Patients’ views cally an improvement in health status) from a health-care
about their health and quality of care are increasingly activity (treatment). Outcomes exist for a wide range of
valued1 as part of the wider re-orientation away from purposes and it is therefore essential to choose an instru-
acute and episodic care, towards prevention, self-care, ment that has the appropriate properties for its intended
and better coordinated care.3 The ‘appropriateness’ of use. The most commonly used outcomes in musculosk-
patient-reported outcomes and their place within quality eletal practice are patient-reported outcome (PRO) mea-
improvement initiatives has gained ascendency as the sures, although some anthropometric instruments (e.g.
importance of the patient voice has increased. Propelled grip strength) and examiner-completed observation lists
by these political changes in health care combined with (e.g. Berg Balance Scale) are still used. PROs are a series
the impact of the IT revolution, seismic shifts are occur- of questions asked of the patient in order to gauge their
ring in the way OMs in musculoskeletal practice are used. views of their own health status. As a consequence PROs
OMs are more than just tools with which treatment is are not entirely ‘objective’, but in musculoskeletal health
evaluated and the quality of care is monitored. They are PROs are particularly valued as personal perceptions of
now equally involved in guiding clinicians whether or not clinical status are considered to be at least as valid as
to refer someone for treatment or to enable patients to indirect laboratory and radiographic data.1 PROs are
self-track their own health online. Commissioners of typically administered before and after treatment, increas-
musculoskeletal services are insisting that outcomes are ingly by electronic means, and are usually distinguished
collected in order to benchmark performance, and in from patient-reported experience measures (e.g. patient
satisfaction) and measures of patient safety (e.g. accident/
near-miss reporting) that are measured at a single time
point. It is important to note that quality of care can be
BOX 21-1  Case Example evaluated using various domains including measures of
Consider Mrs Jones with a 2-year history of osteoarthritic patient safety, experiences, clinical indicators as well
pain in her shoulders and left knee, who is now presenting as OMs.
to health care with a new episode of low back pain. When OM data from large numbers of patients
• What musculoskeletal health domains should be sys- are collected at two fixed time points, the mean dif-
tematically measured? ference between the two scores can be used to evaluate
• Is the impact severe enough for her to require a course the improvements in health care achieved. In this
of treatment? way PROs can act as a catalyst for organizational
• Could outcome measures improve the transition of change to raise standards. In the UK, this has already
care between practitioners? been evidenced through a National Programme of
• Is it possible that she could track her own health prog-
ress over time?
PRO reporting (http://www.ic.nhs.uk/proms) with per-
• How should her outcomes be presented, who should formance reports available online.4 These reports
see them and should her progress be comparable to identify the best and worst health-care providers for
others in a similar position? four elective secondary care surgery procedures, while
in The Netherlands there is for the first time an
202
 21  Outcome Measures in Musculoskeletal Practice 203

TABLE 21-1  COSMIN Definitions of Domains, Measurement Properties

and Aspects of Measurement Properties
Term

Aspect of A
Measurement Measurement
Domain Property Property Definition
Reliability The degree to which the measurement is free from
measurement error
Reliability The extent to which scores for patients who have not
(extended changed are the same for repeated measurement
definition) under several conditions: e.g. using different sets of
items from the same health-related patient-reported
outcomes (HR-PRO) (internal consistency); over time
(test-retest); by different persons on the same occasion
(inter-rater); or by the same persons (i.e. raters or
responders) on different occasions (intra-rater)
Internal consistency The degree of the interrelatedness among the items
Reliability The proportion of the total variance in the
measurements which is due to ‘true’† differences
between patients
Measurement error The systematic and random error of a patient’s score
that is not attributed to true changes in the construct
to be measured
Validity The degree to which an HR-PRO instrument measures
the construct(s) it purports to measure
Content validity The degree to which the content of an HR-PRO
instrument is an adequate reflection of the construct
to be measured
Face validity The degree to which (the items of) an HR-PRO
instrument indeed looks as though it is an adequate
reflection of the construct to be measured
Construct validity The degree to which the scores of an HR-PRO
instrument are consistent with hypotheses (for
instance with regard to internal relationships,
relationships to scores of other instruments, or
differences between relevant groups) based on the
assumption that the HR-PRO instrument validly
measures the construct to be measured
Structural validity The degree to which the scores of an HR-PRO
instrument are an adequate reflection of the
dimensionality of the construct to be measured
Hypotheses testing Idem Construct validity
Cross-cultural validity The degree to which the performance of the items on a
translated or culturally adapted HR-PRO instrument
are an adequate reflection of the performance of the
items of the original version of the HR-PRO instrument
Criterion validity The degree to which the scores of an HR-PRO
instrument are an adequate reflection of a ‘gold
standard’
Responsiveness The ability of an HR-PRO instrument to detect change
over time in the construct to be measured
Responsiveness Idem Responsiveness
Interpretability Interpretability is the degree to which one can assign
qualitative meaning – that is, clinical or commonly
understood connotations – to an instrument’s
quantitative scores or change in scores

initiative being organized by the Dutch Physiotherapy the Oxford Knees Score.7 The advantage of specific
Association to collect PROs for a national survey of instruments is that they are generally more sensitive to
musculoskeletal services. change than generic measures, making them better able
Some PROs are designed as generic instruments for to discriminate treatment effectiveness when comparing
all health conditions such as the EuroQol5 and SF-366 services (benchmarking) or treatments (clinical trials).
that measure overall health-related quality of life. There However, the advantage of generic measures is that they
is also a plethora of instruments specific to a particular can be used to compare changes in health across different
set of conditions or part of the body, for example patient and population groups. A common current
204 PART II  Advances in Theory and Practice

By placing a tick in one box in each group below, please indicate which statements best describe your
own health state today.

Mobility
I have no problems in walking about q
I have some problems in walking about q
I am confined to bed q

Self-Care
I have no problems with self-care q
I have some problems washing or dressing myself q
I am unable to wash or dress myself q

Usual Activities (e.g., work, study, housework, family or leisure activities)

I have no problems with performing my usual activities q
I have some problems with performing my usual activities q
I am unable to perform my usual activities q

Pain/Discomfort
I have no pain or discomfort q
I have moderate pain or discomfort q
I have extreme pain or discomfort q

Anxiety/Depression
I am not anxious or depressed q
I am moderately anxious or depressed q
I am extremely anxious or depressed q

To help people say how good or bad a health state is, we have drawn a Best
scale (rather like a thermometer) on which the best state you can imaginable
imagine is marked 100 and the worst state you can imagine is marked 0. health state
100
We would like you to indicate on this scale how good or bad your own
health is today, in your opinion. Please do this by drawing a line from
the box below to whichever point on the scale indicates how good or 9 0
bad your health state is today.
8 0
Your own
health state 7 0
today
6 0

5 0

4 0

3 0

2 0

1 0

0
Worst
imaginable
health state
FIGURE 21-1  ■  The EQ-5D. (UK (English) © 1990 EuroQol Group EQ-5D™ is a trade mark of the EuroQol Group.)
 21  Outcome Measures in Musculoskeletal Practice 205

recommendation is therefore that generic and specific Another type of outcome is provided by patient-
instruments are used in combination.1 generated measures, such as the patient-specific function
The EQ-5D is one of the most commonly used generic scale10 or the MYMOP.11 Their particular value is for goal
instruments and captures quality of life from five health setting and monitoring progress at a completely indi-
domains: mobility, self-care, usual activities, pain/ vidual level, which tends to make them more sensitive to
discomfort and anxiety/depression (Fig. 21-1). The change than conventional measures. However, policy
EQ-5D is known to lack responsiveness to change in makers tend not to favour these types of OMs as they are
musculoskeletal conditions and has therefore been super- less useful for group-level comparisons. It is therefore
seded by the EQ-5D-5L, which offers five rather than recommended that clinicians use a patient-generated
three levels within each domain making it more sensitive measure alongside conventional OMs to get the advan-
to changes in health.1 tages of both.12
There are literally thousands of condition-specific There are considerable clinical benefits of using
OMs available. One unresolved dilemma is how PROMs data to provide feedback at an individual level
‘condition-specific’ is specific enough, and can a broad to patients and clinicians during treatment to help
musculoskeletal tool be used instead of something which monitor progress. For example, in mental health services
is patho-anatomically specific? There is an obvious trade- positive results have been shown from systems that use
off between clinical practicality and accuracy and often real-time outcome data to identify failing patients with
clinicians will choose more generic tools, while research- rapid intervention to avoid poor response.13 It has also
ers will still want to use condition-specific measures. One been shown that using individual-level feedback to both
recently developed and validated brief multidimensional the patient and clinician improves attendance rates and
instrument designed specifically for clinicians is the Keele cost-effectiveness, without the need for additional clinical
Musculoskeletal Patient Reported Outcome Measure training or negative impact on the therapeutic process.14
(MSK-PROM).8 (Fig. 21-2). The MSK-PROM enables There is some evidence that formal patient monitoring
clinicians to quickly evaluate and monitor musculoskel- tools prevent clinicians from arbitrarily modifying treat-
etal health status using single questions for each health ment plans without sufficient cause.13 It seems that
domain. The tool was developed using musculoskeletal clinicians are sometimes tempted to modify treatment
patients and experts together to prioritize the most because they predict treatment failure based primarily
important health domains regarding independence from on their perception of the therapeutic relationship rather
others, physical function, pain intensity, work interfer- than on actual progress.14 It has also been reported that
ence, limitations in activities and roles that matter, quality greater benefits are seen when progress feedback is given
of life, understanding about how to deal with the condi- to clinicians and patients because this can prompt dis-
tion, anxiety/depression, overall impact and a patient- cussion that helps to empower patients about their
generated item about the severity of their worst symptom. treatment options, resulting in greater shared care
To avoid duplication the MSK-PROM is designed to planning.15
complement the widely used EQ-5D-5L with six addi- There are some OMs that have been specifically
tional items that considerably increase the responsiveness designed to facilitate clinical decision making such as the
of the EQ-5D-5L items when used alone.8 This brief tool Orebro Musculoskeletal Pain Screening Tool.16 This has
is freely available for clinicians to use and ensures that established cut-off thresholds for provision of cognitive
health domains which matter to patients are systemati- behavioural approaches alongside manual therapy to
cally monitored. prevent work absence. High-quality clinical trial evidence
Another key source of evidence for clinicians about is also available for the use of a brief questionnaire as part
which health domains should be measured in muscu­ of a stratified care approach for low back pain that
loskeletal practice is the International Classification of is designed to match patient profiles to treatment
Functioning, Disability and Health (ICF: http://www.icf subgroups.17
-research-branch.org/icf-core-sets-projects-sp-16410 Applications are increasingly being developed to
24398/musculoskeletal-conditions). The ICF provides facilitate easy implementation of PROs in practice.
a standard classification framework based on the bio­ For example the Care Response System (www
psychosocial model introduced by Engel9 and suggests .care-response.com) enables clinicians and patients to
the following categories: body functions and structures, collectively monitor progress and simultaneously provide
activity and participation restriction, environmental aggregated service-level outcomes. A further relatively
factors and personal factors. The most important health recent innovation in the use of PROs has been the
domains for a number of musculoskeletal conditions have development of OMs that are specifically designed to
been identified by the ICF for low back pain, chronic enable patients to track their own health status over
widespread pain, ankylosing spondylitis, osteoporosis, time, such as ‘Hows your health BC?’ (http://www
osteoarthritis and rheumatoid arthritis. Common .howsyourhealthbc.ca/). The purposes for using OMs
domains across conditions include symptom severity are therefore rapidly expanding and clinicians need
(pain intensity), function (physical function, social func- to make themselves aware of such developments.
tion, work function), general well-being/quality of life, However, it should be noted that research publications
global improvement, emotional functioning, participa- using these online technologies are lacking and evi-
tion restriction and environmental factors such as levels dence is urgently required to establish which outcomes
of support needed, independence, relationships with should be monitored in musculoskeletal practice (see
family/others and patient satisfaction. Box 21-2).
206 PART II  Advances in Theory and Practice

The Keele MSK-PROM for Monitoring Musculoskeletal Health

This questionnaire is about the health problem for which you are seeking treatment from this service. Place a
tick in one box for each question below to indicate which statement best describes your view today (from
‘never’ to ‘all the time’). Each column records a different treatment visit.

Q1. Needing help Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6

How often do you need help from others because of your symptoms?
Never 1
Rarely 2
Sometimes 3
Frequently 4
All the time 5

Q2. Work/daily routine Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6

How often have your symptoms interfered with your normal work/daily routine (including jobs around
the house)?
Never 1
Rarely 2
Sometimes 3
Frequently 4
All the time 5

Q3. Activities and roles Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6
How often are you prevented from doing activities and roles that matter to you?
Never 1
Rarely 2
Sometimes 3
Frequently 4
All the time 5

Q4. Severity of worst problem (e.g., sleep, fatigue, driving) Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6
Think about the one thing you have the most difficulty with. How often are you finding this difficult?
Never 1
Rarely 2
Sometimes 3
Frequently 4
All the time 5

Q5. Understanding how to deal with symptoms Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6
How often do you feel unsure about how to deal with your symptoms?
Never 1
Rarely 2
Sometimes 3
Frequently 4
All the time 5

Q6. Overall impact Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6

Overall, how often do your symptoms bother you?
Never 1
Rarely 2
Sometimes 3
Frequently 4
All the time 5
Any and all copyrights © in Questions 1–6, their order and layout vest in Keele University (May 2013).
The tool is scored by summing all 6 items together.

FIGURE 21-2  ■  The Keele Musculoskeletal Patient Reported Outcome Measure (MSK-PROM) for monitoring musculoskeletal health.
 21  Outcome Measures in Musculoskeletal Practice 207

BOX 21-2  Useful Resources to which a tool has a qualitative meaning for clinical
practice including how easy it is to score. The definitions
For more information, the following websites provide a and measurement properties of the main instrument
handy source of free information, including references to quality domains are provided in Table 21-1 directly using
key publications reporting on outcome measures. the COSMIN agreed definitions.
ProQolid (www.proqolid.org/) is a French database of
instruments that is publicly accessible, with payment
options for additional access PRACTICAL ISSUES IN COLLECTING
ICF provides a standard classification framework for
relevant health domains: http://www.icf-research
OUTCOME MEASURES
-branch.org/icf-core-sets-projects-sp-1641024398/
musculoskeletal-conditions The following practical issues are useful to agree before
The Omeract organization provides excellent advice starting to collect OMs:
on outcomes for use in rheumatology. http://www 1. Set a clear purpose for gathering data, and deter-
.omeract.org/ mine the inclusion/exclusion criteria, who has an
Oxford University has a searchable database of relevant interest in the information and who is affected by
outcome measures: http://phi.uhce.ox.ac.uk/ your plans.
The EuroQol Group website (www.euroqol.org) provides 2. Decide on the timing of your measures.
information on the EQ-5D instruments, and a search- 3. Include some baseline case-mix adjustment factors.
able references list. Users of the EQ-5D must register
4. Decide where and how the data will be collected.
their studies with the EuroQol Group and respect
the copyright on the instrument. However, the EQ-5D
is generally free-of-charge for academic research use, Set a Clear Purpose
and NHS users can now also use the EQ-5D under
an arrangement with the Department of Health At the outset it is essential to decide on the purpose of
The International Society for Pharmacoeconomics and collecting the outcome measure. Why do you want the
Outcomes Research provides useful material on information, who is needed to help, who do you want it
patient-reported outcome methods, concepts and for and which patient population is included/excluded?
studies on its website: www.ispor.org/ Gathering OMs from patients can be a little more
The UK Department of Health’s PROMs webpages complex than it may initially appear. To ensure reliable,
are located at: http://www.hscic.gov.uk/proms
rigorous evidence is obtained the process must be sys-
EU Musc net (http://www.eumusc.net/) provides an
online facility to collect and collate information on the tematic. Patients and clinicians prefer to complete out-
impact of musculoskeletal conditions across the EU comes where there is a direct relevance between the
Member States measurement and clinical decision making. It is also
The Musculoskeletal Elf provides digested research important to consider whether the collection of OMs
reviews including some about outcome measures: is constrained by a national policy, or by the service
http://www.themusculoskeletalelf.net commissioner/funders. The more integrated the data
The Assessment in Ankylosing Spondylitis (ASAS) group collection process to routine care the better and clearly
(www.asas-group.org) the patient population must be carefully specified.
The group for research and assessment of psoriasis and
psoriatic arthritis (GRAPPA) (www.grappanetwork.org)
The OMERACT/OARSI initiative for osteoarthritis Decide on the Timing
(www.oarsi.org/) and the fibromyalgia
MAPI Research Institute (http://mapigroup.com/) An important practical issue when collecting OMs is
The International Society for Quality of Life Research deciding when to evaluate change and the correct timing
(http://www.isoqol.org/). of measures. Evidence suggests that on average the
natural course of common musculoskeletal conditions
means patient symptom severity is at its worst at the point
of initial consultation to health care.18 This has implica-
THE DEVELOPMENT AND VALIDATION tions for outcome measurement, as it is therefore best to
OF OUTCOME MEASURES obtain the initial baseline measurement as near to the first
contact consultation as possible. This fact means that two
One challenge for clinicians in choosing musculoskeletal equally effective musculoskeletal services measuring
OMs is that the methodological quality of different improvements at first appointment and at 3-month
instruments varies considerably. The COSMIN guide- follow-up are still likely to see differences in their pooled
lines (http://www.cosmin.nl) are an internationally agreed outcome improvements if they assess patients with
source of the appropriate methods required for outcome slightly different episode durations. For example, this
measure development and validation. They suggest that might occur if one service permitted direct treatment
the quality of a health-related PRO can be assessed by access and the other only accepted referred patients (e.g.
testing an instrument’s reliability, validity, responsiveness by their general practitioner). This is because the average
and interpretability. As mentioned in the introduction, episode duration (and pain severity) of patients at initial
the perceived relevance and acceptability to patients (face assessment in each service may systematically differ,
validity) is increasingly important in the choice of out- giving the service obtaining the earliest baseline measure
comes used in practice. Another key area for clinicians is an advantage in achieving greater outcome improve-
the interpretability of the instrument, which is the degree ments. There are also likely to be systematic differences
208 PART II  Advances in Theory and Practice

if the follow-up time point is not the same with greater differences in population demographics and severity.
improvements seen with a longer gap between measured Using risk adjustment enables ‘raw’ PRO change scores
time points (until around 6 months follow-up depending to better reflect the outcomes achieved had the provider
on the condition). The timing of follow-up measures treated a national average case-mix of patients. This case-
should therefore be considered and where possible stan- mix or risk adjustment ensures that comparisons between
dardized, according to the natural course of the condition services can be made on a like-for-like basis, controlling
and the conceptual framework for the mechanism of for differences in local patient population characteristics
treatment in question. such as age, social deprivation and co-morbidities.
Methods to case-mix adjust PROs data have been pub-
lished,19 but the methodology for case-mix adjustment in
Case-Mix Adjustment musculoskeletal practice is still in its relative infancy.20 To
Another important practical issue is collecting the right guide clinicians a number of commonly used case-mix
case-mix adjusters that enable patient outcomes to be adjustment factors for collection alongside baseline OMs
compared between services by statistically correcting for are presented in Figure 21-3.

Musculoskeletal Case-mix Adjustment

1. How old are you (years)? 2. Gender: M F 3. Postcode

4. What is your current work situation?

I am retired
I am not in paid work, because of my health
I am not in paid work, but not because of my health (e.g. student) How many days off, in
I am in work and have not had time off work because of my health the last 3 months?
I am in work having had time off in the last 3 months
I am in work but am currently on sick leave because of my health

5. Have you come for treatment from: Your GP or nurse A&E (casualty) Other
Self-referral NHS Consultant

6. Which PART of your BODY is the main problem for which you are seeking treatment? (tick 1)
Shoulder Head Hip
Elbow Neck Knee
Wrist Back Ankle/foot
Hand Multi-site pain Other

7. In the last 3 months, how many times have you consulted healthcare for this problem?

8. For how long have you had your current episode of this main problem?

Number of Weeks Months Years

9. How much do you expect your condition will respond to treatment in this service?
It will get worse It will stay the same It will be cured
0 1 2 3 4 5 6 7 8 9 10

10. Do you feel that your problem is terrible and that it is never going to get any better?

Completely disagree Completely agree

0 1 2 3 4 5 6 7 8 9 10

11. How would you rate your general health and well-being for your age?
Please do this by giving a number from 0 to 100
(where 0 = poor health, and 100 = perfect health).
FIGURE 21-3  ■  Musculoskeletal case-mix adjustment.
 21  Outcome Measures in Musculoskeletal Practice 209

Data Collection Method useful to examine changes in performance when surveys

are repeated, for example at the same time each year. This
Another practical issue is where and how to collect OMs. also helps to measure the impact of any new initiatives
Due to the self-selection involved in patients’ ongoing that have been introduced. Findings can also be com-
treatment attendance, less selection bias is present when pared with results from others that are similar in size,
data are collected outside of the clinic setting. Evidence type, or location to identify where strengths and weak-
is growing for the use of text messaging to collect clinical nesses exist. Linking with other work brings many ben-
OMs21 due to its strengths as increasing numbers carry efits and will help you to interpret your data in the light
their phone with them at all times, providing high of the findings of others. A workshop with patient involve-
response rates and data collected from the patient’s ment is a good way to explore the issues and priorities in
natural environment. The limitations however, are that order to deliver a future quality improvement action plan
this technology is less familiar to elderly patients and that (see Box 21-3).
the questions have to be short with a limited number of
characters. Perhaps the greatest innovation for modern
data collection is with online facilities, with patients able SUMMARY
to choose how they are contacted (e.g. by text, email or
post) and its ability to present progress in real time. Such This chapter has highlighted the benefits from OMs for
systems also empower patients to be the owners of their evaluating treatment and monitoring the quality of care
own data and to decide with whom they share the infor- for clinicians working with patients with musculoskeletal
mation. Case-mix adjustment questions are typically disorders. The need for outcomes that have robust mea-
included and a range of reporting methods is available surement properties including reliability, validity and
according to the needs of the person accessing the data. clinical ‘appropriateness’ using the patient’s perspective
Further research is needed to identify the optimal has been noted. The chapter has also outlined advantages
methods to present data and to facilitate the clinical of using electronic online data collection alongside timely
consultation using such information. Leadership from feedback of patient scores to improve patient care and
professional organizations is also required to prevent experience. Other considerations discussed included ben-
hundreds of different and incompatible systems being efits from working collectively with other organizations
introduced. rather than in isolation to ensure standardization for
benchmarking, particularly in respect to the OMs used,
their timing and the case-mix adjusters captured. Clini-
ACTING ON INFORMATION cians who treat musculoskeletal disorders need to embrace
this new world where OMs are embedded into routine
A key consideration is how you will act on the informa- practice to assist clinical decision making and systemati-
tion received and how you will evaluate the impact of any cally monitor treatment in order to deliver the best care
changes made. The health-care context within which the possible to their patients.
information was collected (such as the type of access) and
the population surveyed should be clearly defined. It is
REFERENCES
1. Devlin N, Appleby J. Getting the Most Out of PROMs: Putting
Health Outcomes at the Heart of NHS Decision Making. London:
BOX 21-3  Recommendations for Choosing King’s Fund and Office of Health Economics; 2010. <http://
www.kingsfund.org.uk/sites/files/kf/Getting-the-most-out-of
an Outcome Measure -PROMs-Nancy-Devlin-John-Appleby-Kings-Fund-March
-2010.pdf>.
• Use patients to help chose appropriate outcome domains 2. Darzi A. High Quality Care For All: NHS Next Stage Review Final
• Consider whether the PROM is for primarily for research Report. Cm 7432. London: The Stationery Office; 2008. Available
or clinical practice at: <www.dh.gov.uk/dr_consum_dh/groups/dh_digitalassets/@dh/
• Consider at least one patient-generated item – as they are @en/documents/digitalasset/dh_085828.pdf>; [accessed on 30th
most sensitive to change Dec 2011.].
• Use a generic measure and condition-specific measure in 3. Candace I, Chris N, Nick G, et al. Transforming our health
care system: Ten priorities for commissioners. The Kings Fund.
combination
12th May 2011. Available at: <http://www.kingsfund.org.uk/
• Multidimensional measures are more feasible than unidi- publications/articles/transforming-our-health-care-system-ten
mensional outcomes -priorities-commissioners>.
• Measure at baseline with follow-up timed for conceptual 4. Health & Social Care Information Centre. Hospital Episode Sta-
framework of treatment tistics. <http://www.hesonline.nhs.uk/Ease/ContentServer?siteID=
• Discuss outcomes and monitor progress with patients as 1937&categoryID=1295>.
a powerful treatment tool 5. Brooks R. EuroQol: the current state of play. Health Policy (New
• Aim for consistency across services to help assist York) 1996;37:53–72.
benchmarking 6. Ware JE Jr. SF-36 Health Survey Update. Spine 2000;25:3130–9.
7. Dawson J, Fitzpatrick R, Murray D, et al. Questionnaire on the
• Collect key demographic characteristics to enable case-
perceptions of patients about total knee replacement. J Bone Joint
mix adjustment Surg Br 1998;80(1):63–9.
• Try to collect some of your data from outside the clinic 8. Hill JC, Thomas E, Hill S, et al. Development and validation of
setting (preferably online) the Keele Musculoskeletal Patient Reported Outcome Measure
• Do not forget permission is needed to use some outcome (MSK-PROM). Abstract for The British Pain Society 2014. 2014.
measures 9. Engel GL. The need of a new medical model: a challenge for
biomedicine. Science 1977;196:129–36.
210 PART II  Advances in Theory and Practice

10. Stratford P, Gill C, Westaway M, et al. Assessing disability and 17. Hill JC, Dunn KM, Lewis M, et al. A primary care back pain
change on individual patients: a report of a patient specific measure. screening tool: identifying patient subgroups for initial treatment.
Physiother Can 1995;47:258–63. Arthritis Rheum 2008;59(5):632–41.
11. Paterson C. Measuring outcome in primary care: a patient- 18. Mallen CD, Thomas E, Belcher J, et al. Point-of-care prognosis
generated measure, MYMOP, compared to the SF-36 health survey. for common musculoskeletal pain in older adults. JAMA Intern
Br Med J 1996;312:1016–20. Med 2013;173(12):1119–25.
12. McDowell I, Newell C. Measuring Health: A Guide to Rating 19. Austin PC. An introduction to propensity score methods for reduc-
Scales and Questionnaires. 2nd ed. New York: Oxford University ing the effects of confounding in observational studies. Multivariate
Press; 1996. Behav Res 2011;46(3):399–424.
13. Newnham EA, Page AC. Bridging the gap between best evidence 20. Resnik L, Liu D, Hart DL, et al. Benchmarking physical therapy
and best practice in mental health. Clin Psychol Rev 2009;10:1016. clinic performance: statistical methods to enhance internal validity
14. Miller SD, Duncan BL, Sorrell R, et al. The Partners for Change when using observational data. Phys Ther 2008;88:1078–87.
outcome management system. J Clin Psychol 2005;61:199–208. 21. Lemeunier N, Kongsted A, Axén I. Prevalence of pain-free weeks
15. Harmon C, Lambert MJ, Smart DW, et al. Enhancing outcome for in chiropractic subjects with low back pain – a longitudinal study
potential treatment failures: therapist/client feedback and clinical using data gathered with text messages. Chiropr Man Therap
support tools. Psychother Res 2007;17(4):379–92. 2011;19:28. doi:10.1186/2045-709X-19-28.
16. Linton SJ, Hallden K. Can we screen for problematic back pain?
A screening questionnaire for predicting outcome in acute and
subacute back pain. Clin J Pain 1998;14:209–15.
 SECTION 2 . 3

RESEARCH APPROACHES FOR

MUSCULOSKELETAL
PHYSIOTHERAPY
Research forms the basis and framework for evidence approach is particularly indicated. Second, other research
based physiotherapy practice. In order to be effective methods are discussed including quantitative methods
evidence based clinicians, it is important to have a broad which physiotherapist may be most familiar with in addi-
understanding of various research approaches. The astute tion to qualitative and mixed-method designs which are
clinician can then critically evaluate the results of research becoming more common-place in musculoskeletal phys-
studies and effectively integrate them into their practice iotherapy research. A key element of most research
as indicated. Researchers also benefit from an under- approaches is the inclusion of robust data which under-
standing of various research approaches; especially those pins a study’s findings and this is vital regardless of the
not familiar to them where different approaches can often type of study being undertaken. As such, the third chapter
shed new light on problematic research questions. will explore the concept of standardized data collection
This section will outline several research methods and the mechanisms for developing standardized data
commonly used in studies that are relevant to musculo- collection tools.
skeletal physiotherapy practice. First, clinical research Finally, research is of little use if it is not effectively
methods to test treatment effects are presented. The translated into clinical practice as well as to policy stake-
randomized controlled trial is the most common design holders and consumers with musculoskeletal pain. Suc-
to test the effect of treatment but other less familiar cessful translation of research is difficult and complex.
designs are also discussed including cross-over, diamond The final chapter of this section will focus on relevant
and factorial designs as well as randomized withdrawal research methods exploring the process of improving the
and expertise-based designs. Finally N-of-1 designs are implementation of research findings into physiotherapy
outlined together with situations where this study practice.

211
 C H A P T E R 2 2 

Clinical Research to Test

Treatment Effects
Anita Gross  •  Charlie Goldsmith  •  David Walton  •  Joy MacDermid

treating practi­tioner. Triangulating different categories

INTRODUCTION of outcome measures as the primary outcome may help
to reduce detection bias. For example, integrating soft
Clinical trial designs are powerful tools for ascertaining outcomes like self-report scales with hard outcomes
benefits, harms and patient recruitment for intervention. measure such as (a) performance-based outcomes (i.e.
Numerous treatment approaches have been pronounced Fit-HaNSA,9 Neck Walk Index10) where an external
as having great effects only to be shown to be useless or independent evaluator assesses the outcome; and (b) a
even harmful when subject to rigorous independent biological measure (i.e. serum marker tests11) in the
empirical evaluation.1 We will explore trial design options primary measure grouping could help manage detection
that optimize various objectives. bias. When using multiple outcome measures, inter-
pretation must consider both the potential for bias and
differential effects either across different types of out-
comes or overtime. Reporting bias impacts the size of
CLASSIC MULTIPLE GROUP the effect measure most. In the manual therapy sys-
PARALLEL DESIGN RANDOMIZED tematic reviews (Fig. 22-2, Table 22-2), 68% (mobiliza-
CONTROLLED TRIAL tion12)/77% (manipulation12)/94% (massage13) of trials
report on either immediate post or short-term outcomes;
The establishment of randomized controlled trials these are generally depicting a positive effect. There
(RCTs) dates back to the 18th century but became a is better reporting of intermediate or long-term
core element of health research with the advent of follow-up in exercise4 (48%) or manual therapy/exercise5
evidence-based medicine (practice) and is labelled one (42%) systematic reviews when contrasted against
of the top ten medical advancements.2,3 The classic reviews addressing solely manual therapies (6%) (see
format is a two-group parallel RCT (see Fig. 22-1). Table 22-2), thus giving a better estimate of the effect.
The Cervical Overview Group’s experience4–6 in sys- Finally, since many RCTs in orthopaedics have small
tematically reviewing RCTs on manual therapies and sample sizes, the potential for imprecise estimation and
exercise for neck pain confirms that challenges exist in flawed treatment recommendations is a primary concern.
the design and conduct of RCTs (see Table 22-1). The literature also reveals a lack of utilization of designs
These challenges point to the need for greater under- that might be more appropriate for multimodal inter-
standing of designs on the classic RCT as well as to ventions commonly used in conservative management.
consider both alternative RCT designs and the role for Thus larger and multicentre trials with designs discussed
concurrent observational data collection. Figure 22-2 in the next sections are needed.
shows the emerging biases inherent in the manual
therapy and exercise trial designs. A key source of bias
that needs to be considered in trial design and inter-
pretation is performance bias (blinding of participants
THE CROSS-OVER DESIGN, DIAMOND
and personnel); it is often impossible to blind the clini- DESIGN, FACTORIAL DESIGN AND
cian providing hands-on manual therapy or the exercise FRACTIONAL FACTORIAL DESIGN
interventions to the treatment assignment. This can be
even more problematic if the treating clinician is involved A cross-over design (Fig. 22-3) is particularly helpful
in assessment of the outcomes. Hence, in such situa- when one wants to compare two active therapies and
tions blinded evaluators play a critical role in reducing there is no response carry over between periods. The
bias. Patient-reported outcome measures (PRO) are not comparison between the two therapies has to overcome
directly influenced by the assessor and measures like within-patient variation, which makes the design more
the Numeric Rating Scale and Neck Disability Index7 precise than a two-group comparison in a single period.
are commonly used as primary outcomes in clinical The model fitted to these data also assumes that there is
research and practice.8 Yet self-report scales are still no interaction between time or period and the therapies.
considered to be soft outcomes, and can be influenced In addition, the disease process should be capable of
by patient recall and the patient’s desire to please their returning to baseline between the two periods, not
212
 Intervention
group
Outcome
Participants Stratification Randomization
assessment
Control
group
FIGURE 22-1  ■  A parallel two-group comparison randomized controlled trial design. An explanatory design aims to show that a treat-
ment works using a placebo comparison thus testing efficacy while a pragmatic design aims to allow clinicians to make a decision
by comparing the new active treatment relative to a standard treatment thus testing effectiveness. Stratification to balance key
modulating factors is commonly used prior to randomization. Both primary and secondary outcomes (response variables) are mea-
sures based on identified primary and secondary trial objectives.

TABLE 22-1  Randomized Controlled Trial Design Strengths, Challenges and Opportunities for
Redesign Considerations
Strengths Challenges Opportunities

Appropriately designed and Trials can be very expensive; there are There are alternative research designs
conducted RCT allow one to many regulatory issues affecting trials; that can mitigate challenges by
determine that a treatment regulatory and ethics issues vary reducing sample size requirements
causes a specific outcome across countries and pose challenges or improving validity
Concealment of allocation and for the conduct of large international Research priorities need to be set to
randomization results in a fair randomized trials: the burden of focus trials on priority questions
comparison by distributing recruitment and data collection can be CONSORT statement can guide trial
potential covariates equally difficult to integrate in clinical practice; design, CONSORT criteria are
across comparison groups often require dedicated research improving the reporting of trials
personnel that are not routinely Trial registry and Protocol publication
available prior to start of trial will limit
In trials using conservative management reporting bias
approaches such as manual therapy, Sound ‘biological’ framework is
the trials are not seeded in clearly needed to classify and characterize
understood ‘biology’; there are ‘the disorder’ being randomized and
difficulties with classifying spinal pain the nature and impacts of the
(many frameworks exist, e.g. complex interventions being tested
biopsychosocial)
Analysis can be easy in simple RCT The definition of optimal outcome is Emerging work on defining adverse
design; statistical analysis difficult; different outcomes may be events in manual therapy may
software has become more more important at different time points provide a frameworks6
user-friendly The definition of adverse events is
difficult to adjudicate
Need large number of patients to Challenges in multicentre trials Small trials may be needed for rare
minimize random errors; we contribute to a single site small trials diseases
need large trials of 1000 to 2000 that can fail to detect differences, If we do small trials we need better
observations or unbiased produce unstable results contributing small trials: protocols avoid
meta-analysis of moderate to to inconsistent conclusions across reporting bias; blending outcomes
large trials which collectively trials; single sites may have unique to reduce detection bias
includes a few thousand samples that are not easily To perform large trials in manual
observations generalizable therapy we need international
collaboration on trials; international
multicentre trials
Linking into large existing databanks
will reduce costs
Unit of randomization is the site
Web-based data collection enhances
the ability to collaborate across sites
Patients are resistant to some of the key
elements of clinical research design:
including that their treatment is
determined by chance, the burden of
follow-up, and the potential for not
receiving timely treatment if they are
in control group
Balance can be achieved in Sceptical if this balance can actually be Stratified block design can improve
prognostic factors if the trial is achieved if trials are small and mitigates confounders in
large enough; confounders are It can be important to know which design.
managed through stratification, patients are most likely to benefit from Statistical analyses can control for
the randomization process and certain treatments, so unless collection effect modifiers, if measured
design (subgroup analysis) thus of data on potential effect modifiers is The development of treatment based
patients with a better prognosis preplanned the study may not identify clinical prediction rules can increase
are not preferably treated those most likely to benefit the accuracy of treatment based
prognosis
Compliant patients may have Standardized measurement of treatment
better prognosis, regardless of fidelity, co-intervention and
treatment; use ITT analysis; keep compliance to care in rehab trials is
track of everyone, low loss to usually inadequate
follow-up rate In long trials for chronic disease, it is
difficult to adhere to the therapy and
is often polluted by co-intervention

Continued on following page

214 PART III  Advances in Clinical Science and Practice

TABLE 22-1  Randomized Controlled Trial Design Strengths, Challenges and Opportunities for
Redesign Considerations (Continued)
Strengths Challenges Opportunities

The use of appropriate mock Trial can be done poorly: The trial is Outcomes selection needs
procedures, hard outcome and busted if it uses surrogate outcomes, triangulation using self-report scale
blind adjudication of outcomes soft outcomes and if end points are strategies; observer/performance-
in RCTs help protect against measured solely in the immediate based outcomes with blind
patients who like their treatment post-treatment period or at short adjudication of outcomes;
and may report spuriously better follow-up biologically based outcomes with
outcomes unrelated to the blind adjudication of outcomes
mechanism of action
Blinding of the practitioner (treater) Pressure to produce appealing results is Expertise-based design helps balance
and hard outcomes (morbidity, especially strong in experts who differential treatment bias by only
i.e. performance based) or prefer one approach having experts in intervention A and
blended evaluation of outcomes experts in intervention B perform
usually helps to protects against the treatments
performance bias. For example,
unblinded practitioners who like a
treatment or are experts in a
treatment might report spuriously
better outcomes unrelated to the
mechanism of action
Dosage of the intervention can Difficult to determine dosage since cells Factorial design
easily be determined in large trials of care are very small
Benefits vs harm trade-offs can be Difficult to pick up adverse effects if they
determined. are rare or occur late or if the
Can determine adverse event rate investigator does not look hard
enough (or even look) for adverse
outcome
Adverse events law suites; pay out of
compensation for any adverse event
not only severe adverse event; even
those in control or what is part of
usual clinical course require
compensation for adverse events

Manual Therapy Manipulation or

and Exercise Exercise Massage Mobilization
Random sequence
generation (selection bias)
Allocation concealment
(selection bias)
Blinding of participant
(performance bias)
Blinding of personnel
(performance bias)
Blinding of outcome
assessor (detection bias)
Incomplete outcome
data (attrition bias)
Intention-to-treat
(attrition bias)
Selective reporting
(reporting bias)
Similarity of baseline
characteristics (other bias)
Co-interventions
avoided (other bias)
Compliance acceptable
(other bias)
Timing of outcome
assessment (other bias)
0% 25% 50% 75% 100% 0% 25% 50% 75% 100% 0% 25% 50% 75% 100% 0% 25% 50% 75% 100%
Low risk of bias Unclear risk of bias High risk of bias
FIGURE 22-2  ■  Risk of bias from four Cochrane systematic reviews of clinical trials for neck pain on manual therapy and exercise,5
exercise,4 massage13 and mobilization or manipulation.12
 22  Clinical Research to Test Treatment Effects 215

TABLE 22-2  Reporting Bias Impacts the Size of the Effect Measure Most in the Manual Therapy
Systematic Reviews
Follow-up Manual therapy and
period exercise (n = 26) Exercise (n = 21) Massage (n = 16) Manipulation (n = 39) Mobilization (n = 16)
LT 6/26 38% 6/21 29% 1/16 6% 4/39 10% 1/16 6%
IT 1/26 4% 4/21 19% 0/16 0% 5/39 13% 4/16 25%
IP or ST 15/26 58% 11/21 52% 15/16 94% 30/39 77% 11/16 68%

Positive effects are reported more often at immediate post treatment or in the short term such as 68% (mobilization12)/77%
(manipulation12)/94% (massage13). There is better reporting of intermediate or long-term follow-up in exercise4 (48%) or manual therapy
plus exercise5>(42%) systematic reviews when contrasted against reviews addressing solely manual therapies12 (6%), thus, giving a
‘better’ estimate of the true treatment effect.
IP, Immediate post treatment follow-up; ST, short-term follow-up; IT, Intermediate-term follow-up; LT, Long-term follow-up; n, number of
randomized controlled trials.

Intervention Control
period 1 period 2
Defined Outcome
Randomization
participants assessment
Control Intervention
period 1 period 2

FIGURE 22-3  ■  Cross-over design.

Control
Intervention period 2
period 1 Intervention
period 2
Defined Control
Randomization
population period 1

FIGURE 22-4  ■  Diamond design.

something that patients or clinicians would like to see in conduct, it means that all patients get exposed to the new
a chronic disease. If these assumptions cannot be reason- therapy being tested, an advantage over the Figure 22-1
ably assumed with the therapies and the condition being design, as this should minimize dropouts that expect to
studied, this design should be avoided. If there is an get the new therapy. Figure 22-4 shows a plot of the
interaction between time and the therapies, then the sta- response versus time type of graph for the diamond
tistical literature suggests that using the first period data design. An example of the diamond design, however,
alone should be used for statistical inference. This means without the plot, is shown using occupational therapy in
that the second period data are wasted and patients may patients with rheumatoid arthritis.14
be put at extra risk with little extra benefit. The factorial design (Table 22-3) is a design that is
The so-called diamond design (Fig. 22-4) describes the useful if the therapy has many separate components. If
shape of the response versus time plot when the therapy the therapy has at least two components with at least two
being evaluated is of patient benefit in both periods; the levels then a factorial design has groups created by mul-
control group has little benefit in the first period, but tiplying the number of levels in each factor together to
hopefully similar benefit during the second period as the create the experimental groups such as shown in Table
intervention group did during the first period. If the 22-3 with 4 duration levels and 3 frequency levels to
intervention group does not receive any additional create 12 experimental groups. Randomization here is to
therapy during the second period, then the magnitude of the 12 different groups. The main effects of each factor
the benefit lasting for the second period can be estimated. as well as all interactions are estimable from the complete
The design allows for the magnitudes of the intervention factorial design with multiple replicates. Factorial designs
benefit in the first period to be compared to the control using factors with at least three levels can also be mod-
benefit during the second period; something not available elled using response surface methods that allow the
for the single-period two-group design shown in Figure analyst to determine the optimal experimental conditions
22-1. While the diamond design takes twice as long to amongst the combination of factor levels. An example of
216 PART III  Advances in Clinical Science and Practice

a 2 × 2 factorial design is shown comparing a sleeping fraction of the complete factorial design as long as the
neck pillow and isometric neck exercises in patients with proper model for the data had no interaction between
chronic neck pain.15 therapy A and either B or C, then the main effect of factor
The special fractional factorial design (Table 22-4) is used A is still estimable, albeit with less efficiency than in the
when the combinations of the multiple therapies that are complete factorial design. Indeed the estimates would be
suggested in a factorial design may not be feasible clini- of similar magnitude to the estimate provided by the one
cally. For example, if a patient is referred to you for care, period – two-group design in factor A alone, yet, the
you may be uncomfortable putting patients into trial patients would NOT be denied effective therapies. Hope-
groups where the patients may not get a therapy that is fully, this design will minimize dropouts since all patients
proven to be efficacious. For example in a factorial design receive therapy of known benefit.
there is usually a group that gets no therapy. Suppose we
have three therapies at two levels each, one of which (A)
is a therapy of unknown efficacy and the other two (B, RANDOMIZED WITHDRAWAL AND
C) are therapies that many clinicians use alone or in EXPERTISE-BASED DESIGNS
combination. A full factorial design would have 23 = 8
groups as outlined in Table 22-4. The objective of the randomized withdrawal design
Groups 1 and 2 contain no therapy that is proven and (Fig. 22-5) is to assess the response to either reducing the
so many clinicians would be reluctant to put patients into dosage of a treatment or discontinuing it. This design is
these groups. On the other hand groups 3 to 8 get either an option when either: (a) there is a chronic disease where
therapy B or C or both. If we ran the design as a 3 4 participants have taken part in an effective therapy for a
prolonged period; the goal is to determine if life-long
therapy is necessary (i.e. withdrawal of maintenance chi-
TABLE 22-3  Factorial Design ropractic care); or (b) the efficacy of a treatment has not

Number of Treatment Doses

Frequency (per week)
Duration (weeks) 1 2 3
TABLE 22-4  Special Fractional Factorial Design
0 0 0 0 Group A B C
3 3 6 9
6 6 12 18 1 No No No
12 12 24 36 2 Yes No No
3 No Yes No
For a manual therapy (MT) dosage trial compared to standard care 4 Yes Yes No
(i.e. exercise), if one factor has three levels (frequency per 5 No No Yes
week) and the other four levels (duration of treatment in
weeks), the factorial design is the product of the number of 6 Yes No Yes
levels of the factors in the design, i.e. 3 × 4 = 12, where the 12 7 No Yes Yes
groups receive: (cell 1) neither of the two dosage factors = 0 8 Yes Yes Yes
times per week for 0 weeks, i.e. no MT just standard care;
(cell 2) the first of the two dosage factors but not the second = Groups 1 and 2 contain no therapy that is proven. On the other
standard treatment two times per week, (cell 4) the second of hand groups 3 to 8 get either therapy B or C or both. If the
the two dosage factors and not the first (1 time per week for 3 design is run as a 3 4 fraction of the complete factorial design
weeks = 3 sessions of MT), (cell 12) both of the dosage factors then the main effect of factor A is still estimable, albeit with
(3 times a week for 12 weeks = 36 sessions of MT). less efficiency than in the complete factorial design.

Lack of
efficacy
withdrawal

Active
intervention
Titrated
Screen Outcome
active Randomization
participants assessment
intervention Control
group

Adverse
event
withdrawal

FIGURE 22-5  ■  Randomized withdrawal design.

 22  Clinical Research to Test Treatment Effects 217

Expertise-based
intervention A
Outcome
Participants Stratification Randomization
assessment
Expertise-based
intervention B

FIGURE 22-6  ■  Expertise-based design.

been conclusively shown to be beneficial (i.e. withdrawal 7

of manual therapy from the proven combined manual
therapy/exercise treatment approach; is this combination 6
of care needed longer than in a short initial course of
care?). Limitations of such designs are that a highly 5
selected sample is assessed often having had an interven-

Hours worked
tion for years while those with adverse effects will have 4
had their therapy discontinued. The effect size in
such designs is overestimated and the adverse effect 3
underestimated.
In expertise-based designs (Fig. 22-6), randomization of 2
participants to experts in intervention ‘A’ or experts in
intervention ‘B’, ensures therapists perform only the pro-
1
cedure where they are expert. Differential expertise bias
can occur in a conventional RCT when there is a dispro-
portionate number of cases being performed by the 0
A B A
expert in intervention ‘A’ compared with the expert in Treatment phase
intervention ‘B’ and will bias results favouring interven-
FIGURE 22-7  ■  Traditional A–B–A type N-of-1 design with phases
tion ‘A’. Additionally, the unblinded clinician performing of: A: multiple baseline, B: Intervention.
intervention ‘A’, an intervention that they favour, may be
more meticulous in applying the procedure or subcon-
sciously prescribe effective co-interventions. This trial can vary along the expertise scale depending on whether
design is more feasible for therapists with expertise are an efficacy to effectiveness approach is preferred.
more willing to participate and perform only the
techniques/interventions in which they are expert. Com-
petence needs to be ensured in such trial designs. A clini- CLINICAL RESEARCH TO TEST
cian will also have ethical concerns enrolling patients into
trials where they perform a technique in which they feel TREATMENT EFFECTS: N-OF-1
inexperienced (i.e. manipulation + exercise versus mobi- TRIAL DESIGNS
lization + exercise).
One of the challenges that occur within trials with As has been described above, RCTs require large samples,
non-pharmacologic interventions is that the skill and sometimes require challenging analyses, can be costly in
experience of the treatment provider is integral to the terms of time and money, and the results are not directly
outcomes obtained. In the classic RCTs, treatment pro- transferable to making decisions regarding individual
viders provide both treatments including one where they patients. RCTs will, on occasion, also present ethical
have a more experience, a preference and greater experi- dilemmas for clinicians, where it is not ethically sound to
ence and the comparator which in some cases they only randomly allocate patients into treatment arms that are
perform within the trial. This can contaminate the assess- expected to be inferior (e.g. control or ‘sham’ groups).
ment of treatment efficacy. A potential solution is the Finally, trials require the generalization of the results of
expertise-based design where the patient consents to be a group (with variable results) to an individual.
randomized to treatment and as a result be treated by an N-of-1 or single-subject design (Fig. 22-7) provides an
expert clinician who can provide the treatment assigned.16 option to experimentally evaluate interventions in patients
This has potential to provide a ‘fair’ comparison of the with chronic conditions by randomly allocating treat-
two treatment options but also has challenges in execu- ment and comparing standardized outcome measures. In
tion. The participant must consent to having their clini- traditional N-of-1 studies, a multiple baseline period is
cian determined by a random process which can be followed by random allocation of treatment options.
challenging if they prefer a specific person, and a pre- Internal and external validity are strengthened with
screening strategy is needed to consent and allocate the addition of extra phases (e.g. A–B–A or A–B–A–C
patients. Further each site must have clinicians with expe- designs), consistent findings across several patients or
rience in both treatment options. However, the benefits consistency across environmental contexts. Where treat-
can include enhanced participation of clinicians and more ment is multimodal, one must avoid altering other aspects
valid comparisons. The definition of treating clinicians of care or co-intervention. N-of-1 trials work best when
218 PART III  Advances in Clinical Science and Practice

7
BOX 22-1  A Case Study to Basis the
Discussion of N-of-1 6
Design Options 5

Hours worked
John is a 35-year-old labourer whose primary job duties 4
involve lifting and carrying over uneven terrain at jobsites. 3
He has presented to physiotherapy for problems related to
low back pain which are preventing him from working a full 2
day. His primary goal is to resume full work duties and 1
hours. As the physiotherapist, you have decided the best
treatment for John’s low back pain is a combination of 0
0 1 2 3 4
manual mobilization for the lumbar spine, complemented
with an exercise programme to improve stability and strength Treatment phase
around the core, and the use of a hot pack or TENS for pain FIGURE 22-8  ■  N-of-1 sequential withdrawal design with phases
management. Currently he is only able to perform his of: (0–1) multiple baseline; (1–2) manual therapy, exercise and
regular job duties for an average of 2 hours per day before TENS; (2–3) manual therapy and exercise; (3–4) exercise only.
being limited by pain. This is down from a normal workload
of 8 hours per day.
an average of 2 hours per day at full duties. The interven-
tion approach including manual therapy, exercise and
TENS rapidly leads to improvement in his worked hours,
comparing two treatment alternatives and when return up to 5.5 hours per day. In the next phase, the TENS is
to a stable baseline occurs with removal of treatment (i.e. dropped, and gains are maintained with manual therapy
short washout). For example, comparing two different and exercise. In the final phase, the manual therapy piece
orthoses (splints) for carpometacarpal arthritis might is withdrawn and a slight regression is seen with exercise
provide an evidence-based answer as to which option will alone.
work best for a specific patient. However, in some cases Important consideration needs to be given to the order
it is unclear if all elements in a multimodal treatment of withdrawal and the threshold for a satisfactory
programme are needed, as illustrated in Box 22-1. The outcome. More burdensome interventions are often the
treatment decision in Box 22-1 is to offer a combination most logical to withdraw first unless theoretical rationale
of manual therapy, exercise and use of self-administered suggests otherwise. The threshold for a satisfactory
heating packs for pain management to improve number outcome may be based on existing literature (e.g. clini-
of hours worked at full job duties. The clinician may opt cally important difference) or on the patient’s individual
to conduct an N-of-1 study to evaluate treatment effec- goals. This is another advantage of this design. Using our
tiveness in this case. Figure 22-7 shows the traditional hypothetical example, a slight regression in worked hours
approach using an A–B–A design, with each phase lasting was noted in the final phase (exercise alone), down to 5
1 week. A positive treatment effect is indicated by the from 5.5 hours per day. Decisions regarding ongoing
increase in John’s average hours of full work duties with intervention can now be made using the data as a key
treatment and decay upon removal of treatment. While information source; is an additional half hour of worked
sound, there are two rather large pragmatic issues with hours per day worth the time and cost burden of clinic
this design and its interpretation. The first is on the visits for manual therapy treatments, or are the stake-
surface it appears as though John may require manual holders content at 5 hours per day and exercises that can
therapy, exercise and hot pack in perpetuity. The second be performed at home?
is, by virtue of conducting this study, the clinician has
withdrawn a clearly effective treatment and reduced the
patient’s ability to work for at least 1 week, counter to CONCLUSION
most ethical practice guidelines.
The withdrawal N-of-1 design may be a better option Understanding alternative design when the usual parallel
for evaluating elements of multimodal programmes.17 group design is not feasible will facilitate the choice of
This is an extension of the N-of-1 design intended spe- the most appropriate design for a given disorder–
cifically for reversible conditions that require multimodal treatment–outcome situation. Each design may help to
therapies. In a withdrawal design, the full set of therapies minimize systematic error such as selection bias, perfor-
is offered once a stable baseline is established. Assuming mance bias and detection bias. A traditional parallel
effectiveness has been established, one aspect of the group design is simple to understand but may be difficult
therapy is removed and another phase of repeated out- to recruit for due to the placebo-controlled arm. Facto-
comes is collected. If the condition worsens again, that rial designs require fewer patients and will answer two or
aspect of therapy can be re-introduced for another phase, more questions as well as their interaction, and thus save
and then a different aspect can be withdrawn. If removal time. The cross-over trial design allows patients to receive
of one aspect does not worsen the condition, the clinician both treatments in a pre-specified sequence and allows
may decide to subsequently remove a second aspect, and patients to act as their own control but assumes a stable
so on, until the gains can be maintained with the least disease or an absence of treatment-period interaction.
amount of intervention. Figure 22-8 is our hypothetical The diamond design allows for an assessment of a delayed
patient John who comes to the clinic only able to work start of treatment however at the start of the second phase
 22  Clinical Research to Test Treatment Effects 219

the patients are no longer comparable. The randomized therapy: Application to the cervical spine. J Orthop Sports Phys
withdrawal design reduces the time on a placebo since Ther 2010;40(8):455–63.
7. Cleland JA, Childs JD, Whitman JM. Psychometric properties of
only the responders and those without adverse events are the Neck Disability Index and Numeric Pain Rating Scale in
randomized. It however will overestimate the treatment patients with mechanical neck pain. Arch Phys Med Rehabil
effect. Expertise-based trial designs ensures therapists 2008;89:69–74.
perform only the procedure where they are expert, 8. MacDermid JC, Miller J, Côté P, et al. Use of outcome measures
in managing neck pain: an international multidisciplinary survey.
provide a ‘fair’ comparison of the two treatment options, The Open Orthop J 2013;7:506–20.
and enhances the participation of clinicians. Finally, for 9. MacDermid JC, Ghobrial M, Quirion K, et al. Validation of a new
rare disorders, the N-of-1 trials design aims to assess the test that assesses the functional performance of the upper extremity
effect of more than one treatment in one person and and neck (FIT-HaNSA) in patients with shoulder pathology. BMC
patients are more likely to adhere to the treatment. Just Musculoskelet Disord 2007;8:42.
10. Pierrynowski MR, Gross AR, Miles M, et al. Reliability of the
like cross-over designs, N-of-1 requires a stable chronic long-range power-law correlations obtained from bilateral stride
disease. Thus innovative methodology will help answer intervals in asymptomatic volunteers whilst treadmill walking. Gait
specialized questions and address specific concerns such Posture 2005;22(1):46–50.
as engagement of physiotherapists in trial participation 11. van Uum SH, Sauve B, Fraser LA, et al. Elevated content of cor-
tisol in hair of paitents with severe chronic pain: a novel biomarker
and encourage patient recruitment. for stress. Stress 2008;Nov 11(6):483–8.
12. Gross AR, Langevin P, Andres C, et al. Manipulation or mobiliza-
REFERENCES tion for neck pain. Cochrane Database Syst Rev 2014;(in press).
1. Chalmer I. Unbiased, relevant, and reliable assessments in health 13. Patel KC, Gross AR, Graham N, et al. Massage for mechanical
care: Important progress during the past century, but plenty of neck disorders. Cochrane Database Syst Rev 2012, Issue 9. Art.
scope for doing better. BMJ 1998;317:1167–8. No.: CD004871. doi:10.1002/14651858.CD004871.pub4.
2. Bull JP. The historical development of clinical therapeutic trials. 14. Helewa A, Goldsmith CH, Lee P, et al. Occupational therapy
J Chronic Dis 1959;10:218–48. home service on patients with rheumatoid arthritis. Lancet
3. Lilienfeld AM. Ceteris paribus: The evolution of the clinical trial. 1991;337(8755):1453–6.
Bull History Medicine 1982;56:1–18. 15. Helewa A, Goldsmith CH, Smythe HA, et al. Exercise and sleeping
4. Gross A, Kay TM, Paquin JP, et al. Exercises for mechanical neck neck support on patients with chronic neck pain: A randomized
disorders. Cochrane Database of Systematic Reviews 2015, Issue 1. clinical trial. J Rheumatol 2007;34(1):151–8.
Art. No.: CD004250. doi:10.1002/14651858.CD004250.pub5. 16. Devereaux PJ, Bhandari M, Clarke M, et al. Need for expertise
5. Miller J, Gross AR, Kay T, et al. Manual therapy with exercise for based randomised controlled trials. BMJ 2005;330(7482):88.
neck pain. Cochrane Database Syst Rev 2014;(in press). 17. Rusch FR, Kazdin AE. Toward a methodology of withdrawal
6. Carlesso LC, MacDermid JC, Santaguida P. Standardization of designs for the assessment of response maintenance. J Appl Behav
adverse event terminology and reporting in orthopaedic physical Anal 1981;14(2):131–40.
 CHAPTER 23 

Research Approaches to
Musculoskeletal
Physiotherapy
CHAPTER OUTLINE

Nicola Petty and Hubert van Griensven’s Introduction Ch 23.3  Mixed Methods Research  224
Ch 23.1  Quantitative Research  221 Hubert van Griensven
Lieven Danneels
Ch 23.2  Qualitative Research  223
Nicola Petty

NICOLA PETTY AND HUBERT VAN GRIENSVEN’S INTRODUCTION

Musculoskeletal (MSK) physiotherapy is a needed, which involves generating theory from

complex intervention delivered within a context observation, interviewing, etc.3
of human and very often physical interaction. The focus of the study may suggest the
Practitioners deliver a service to people within a type of data required. If statistics are involved
political, social and medical context. for instance, to compare the effect sizes of two
Consequently, a physiotherapy researcher is treatments, the data are numerical and the
faced with a host of interdependent aspects that research is quantitative in nature. Quantitative
may be investigated, such as the clinical effects researchers try to be as objective as possible
of a controlled intervention, the interaction and to minimize the influence of anything other
between therapist and patient, the way patients than predetermined controlled variables [see
experience their condition, or the political Chapter 23.1]. While this approach answers
context of health care. The choice of research particular questions very well, not
focus will suggest the type of data that need to all practice can be reduced to numbers.
be collected, the methods that may be used and A qualitative study may be needed where
the overall methodological approach that best understanding of people is sought and
suits the research. The predominantly therefore data consist of verbal and non-verbal
quantitative focus of current MSK physiotherapy communication, for example [see Chapter 23.2].
literature may have created the illusion that Finally, complex or new topics may benefit from
there is only one research approach.1 This a combination of qualitative and quantitative
chapter series aims to broaden the options for data in mixed methods research [see Chapter
the researching clinician by providing a brief 23.3]. Each of these three approaches comes
overview of available methodological choices. with certain assumptions about the nature of
In developing a research question, researchers reality (ontology) and what can be known
need to familiarize themselves with existing (epistemology).
literature in the field to consider what is known, The research approach and data type usually
and what is unknown and needs to be suggest the research method. Method refers to
investigated. Next, they may consider whether a specific instruments and techniques of data
subject requires a deductive or inductive collection, such as qualitative interviews,
approach. In the former the researcher surveys or measurement of strain or angle. It
formulates a hypothesis and then designs the also includes methods of data analysis such as
research to either support or disprove it, usually statistical comparison and thematic analysis of
on a statistical basis.2 However, if not enough is interview data. Methods of data collection are
known about a subject to generate a feasible not inextricably linked with specific approaches.
hypothesis, an inductive approach may be For instance, questionnaires may be used to

220
 23  Research Approaches to Musculoskeletal Physiotherapy 221

establish participants’ opinions by asking REFERENCES

multiple-choice questions, thus generating 1. Petty NJ, Stew G, Thomson OP. Ready for a paradigm
quantitative data. Conversely, the inclusion of shift? Part 1: introducing the philosophy of qualitative
free text sections in a questionnaire generates research. Man Ther 2012;17(4):267–74.
qualitative data. 2. Bowling A. Research Methods in Health – Investigating
The next three chapters discuss quantitative, Health and Health Services. Maidenhead: Open Univer-
qualitative and mixed methods research. Each sity; 2009.
3. Teddlie C, Tashakkori A. Foundations of Mixed Methods
chapter outlines the underlying theory of the
Research. Integrating Quantitative and Qualitative
approach as well as the methodologies, Approaches in the Social and Behavioral Sciences. Thou-
methods and potential questions. The sand Oaks, CA: Sage; 2009. p. 26–7.
concluding chapter lists a few recommended
texts for readers who require more detailed
information about specific research approaches.

CHAPTER 23.1  ■  QUANTITATIVE RESEARCH

Lieven Danneels

WHAT IS QUANTITATIVE RESEARCH? study can be either prospective or retrospective.

The feature that distinguishes a prospective from
Quantitative research methods have been the foundation a retrospective cohort is simply and solely whether
for traditional biomedical research for a long time.1 The the outcome of interest has occurred at the time
goal of quantitative research is to answer research ques- the investigator initiates the study. The prospective
tions or to test hypotheses.2 Quantitative methods cohort study is important for research on the aeti­
examine the effects of specified circumstances on an ology of diseases and disorders. Therefore, the
outcome of interest in ways that can be expressed numer- individuals are not randomly allocated to the
ically.3 Thus, quantitative research deals with measurable groups. The study starts with the identification of
characteristics, named parameters, variables or factors, the population and the exposure status (exposed/
and uses statistics to deduct conclusions.4,5 Quantitative not exposed groups) and follows them (over time)
research aims to determine the relationship between one for the development of disease. Retrospective cohort
thing (an independent variable) and another (a dependent studies use existing data collected in the past to
or outcome variable) in a population. identify the population and the exposure status
(exposed/not exposed groups) and determines at
present the (development) status of disease. They
METHODOLOGY AND METHODS use information that has usually been collected for
reasons other than research, such as administrative
Quantitative research designs can be descriptive/ data and medical records.
observational, experimental or quasi-experimental. • Case-control studies compare cases with controls.
Descriptive/observational studies allow for associations Individuals who have the outcome of interest (cases)
between variables to be investigated. In these studies, the are compared to individuals who do not have the
subjects are observed without otherwise intervening, thus outcome of interest (controls) by looking back in
a participant’s exposure and outcome status are observed time to identify the existence of possible causal
with no influence from the researcher. However, the evi- factors. Case-control studies have a retrospective
dence they provide is not strong enough to establish a character, because they focus on conditions in the
causal link. Several types of studies can be classified as past that might have caused subjects to become cases
descriptive studies: rather than controls.
• A case or a case series study is the simplest form. A case Besides the abovementioned group, there are the experi-
study reports data on only one subject. Descriptive mental studies, which are also referred to as intervention
studies of a few cases are called a case series. studies. This approach provides the best evidence about
• Cross-sectional studies analyse variables of interest in cause and effect. Instead of just observing the subjects, an
a sample of subjects once, and the relationships independent variable (e.g. the therapeutic intervention)
between them are determined. A cross-sectional is manipulated to determine the effects on the dependent
study examines a characteristic and an outcome in variables (i.e. the outcome). In an experiment, an effort
the same individuals at the same point in time. is made to identify and impose control over all other
• A cohort study is a study that follows over time a variables except one. Further distinction can be made
group of similar individuals (cohorts) who differ between an active and an attribute independent variable.
with respect to certain factors under study, to The active independent variable is a manipulated vari-
determine how these affect outcome. A cohort able, which is controlled within a specified period of time
222 PART II  Advances in Theory and Practice

during the study (e.g. group A receives therapy X and themselves to a group by choosing to participate in the
group B is undergoing therapy Y). The attribute inde- intervention or in the control group.6–10
pendent variable (e.g. ethnicity) is a measure of charac-
teristics of the person and not study-dependent.3,6
Experimental studies, also referred to as longitudinal or FINDINGS
repeated measures studies, can be subdivided into several
types. Statistics are a major tool in quantitative research. They
• A time series is the simplest experiment. One or more allow the researcher to sample a portion of the popula-
measurements are taken on all subjects before and tion and to use probability to decide whether the findings
after a treatment. A major problem with a time from the sample are likely to apply to the entire popula-
series is to determine the changes seen as being the tion.10 Statistical methods can be used to assess relation-
effect from nothing else but the treatment. ships between the variables measured.3 Interpretation of
• A crossover design might be a solution to this problem. the results should be done carefully. Significant findings
The subjects are given two treatments: one being may not reflect clinically important outcomes10 and find-
the real treatment, the other a control or reference ings might be clinically relevant although not statistically
treatment. Half of the subjects receive the real treat- significant.
ment first and the other half the control first. After
a period of time, sufficient to allow a treatment to
effect to wash out, the treatments are crossed SUMMARY
over. Multiple crossover designs involving several
treatments are also possible. A problem with such a Quantitative research provides important tools to answer
study design is that a long-term follow-up is not research questions that can be formulated as hypotheses.
possible. It should be noted, however, that quantitative research
• A controlled trial, with a control group and an experi- cannot answer all types of questions. In health care, a
mental group, is to be used if the researcher wants recognized error is the attribution of the properties which
to evaluate long-term effects, or when the treatment apply collectively to a group, to an individual. The critical
effect is unlikely to be washed out between measure- need is to understand where generality ends and indi-
ments. All subjects are measured but only half of viduality begins, and that requires merging the two types
them, the experimental group, receive the treat- of knowledge: quantitative and qualitative research are
ment. All subjects are then measured again and the complementary.1,3 The fundamental differences lie in the
change in the experimental group is compared with content of the research question to be answered.4
the change in the control group.
• The randomized controlled trial is believed to be the
‘gold standard’ to test the effectiveness of an inter- REFERENCES
vention. Individuals who do not have the outcome 1. Runciman WB. Qualitative versus quantitative research – balancing
of interest are randomly allocated to receive the cost, yield and feasibility. Qual Saf Health Care 2002;11(2):
146–7.
intervention (the experimental group), or standard 2. Vogelsang J. Quantitative research versus quality assurance, quality
of care or conventional treatment (the comparison improvement, total quality management, and continuous quality
group), or no intervention (the control group) and improvement. J Perianesth Nurs 1999;14(2):78–81.
are followed forward in time to determine whether 3. Lakshman M, Sinha L, Biswas M, et al. Quantitative vs qualitative
research methods. Indian J Paediatr 2000;67(5):369–77.
they experience the outcome of interest. 4. Bergsjo P. Qualitative and quantitative research – is there a gap, or
• In a single-blind controlled trial, the subjects are blind only verbal disagreement? Acta Obstet Gynecol Scand 1999;78(7):
to the identity of the treatment. In a double-blind 559–62.
controlled trial, both the subject and the researcher 5. Castillo-Page L, Bodilly S, Bunton SA. AM last page. Understand-
do not know what treatment the subjects receive ing qualitative and quantitative research paradigms in academic
medicine. Acad Med 2012;87(3):386.
until all measurements are taken. 6. Enarson DA, Kennedy SM, Miller DL. Choosing a research study
Likewise, the quasi-experimental research attempts to design and selcting a population study. Int J Tuberc Lung Dis
establish cause–effect relationships among the variables. 2004;8(9):1151–6.
In a quasi-experimental research approach, there is again 7. Key Elements of a Research Proposal Quantitative Design, <http://
www.bcps.org/offices/lis/researchcourse/develop_quantitative
a manipulated independent variable, but the participants .html>; [accessed on April 25th 2014].
are not randomly allocated to a group. In a strong quasi- 8. Hopkins WG. Quantitative Reserch Design Sportscience 4(1),
experimental design the participants are already in a few <sportsci.org/jour/0001/wghdesign.html>; 2000.
similar intact groups, but the treatment is randomly 9. Morgan GA, Gliner JA, Harmon RJ. Quantitative research
assigned. In a moderate strong quasi-experimental design, approaches. J Am Acad Child Adolesc Psychiatry 1999;38(12):
1595–7.
the participants are again in intact groups, but the 10. Dowrick AS, Tornetta P, Obremskey WT, et al. Practical research
treatment cannot be randomly appointed. And in a methods for orthopaedic surgeons. J Bone Joint Surg Am
weak quasi-experimental design the participants assign 2012;94(4):368–74.
 23  Research Approaches to Musculoskeletal Physiotherapy 223

CHAPTER 23.2  ■  QUALITATIVE RESEARCH

Nicola Petty

highlight some of the concepts considered so far in this

WHAT IS QUALITATIVE RESEARCH? chapter. The focus of the research was to explore the
learning transition of physiotherapists following a Mas-
Qualitative research may be described as ‘a form of social ter’s course in MSK physiotherapy.5 It was assumed that
enquiry that focuses on the way people interpret and the learning process was predominantly through social
make sense of their experiences and the world in which exchange with others (social constructionism). In relation
they live’.1 Qualitative research is sometimes referred to to methodology, a constructivist (as opposed to objectiv-
as naturalistic enquiry,2 which aims to understand the ist) grounded theory approach6 was chosen, as its assump-
social reality, such as behaviours, perspectives and experi- tions were compatible with social constructionism. It
ences of individuals, groups and cultures. was assumed that individuals would have unique learning
transitions and so individual interviews (not focus groups)
were used to collect data. The ontological and episte-
ONTOLOGICAL AND EPISTEMOLOGICAL mological position of the researcher acts as an overarch-
ASSUMPTIONS ing paradigm to the study and influences decision making
throughout the research process, from early inception
The potential for a researcher to understand the views to final write up.
of an individual, group or culture is not straightforward. In qualitative research the focus is on the views of
Reflecting on our everyday lives and our ability to people, their perceptions, meanings and interpretations
understand others (and ourselves for that matter) high- of a phenomenon within a particular context. The indi-
light the challenges faced by qualitative researchers. vidual or groups and the context are explored in all its
The views of an individual may be considered subjec- complexity and it is assumed that there are multiple con-
tive and constructed by the individual, and in this structed views of reality with the participants’ history,
situation the researcher seeks knowledge about the culture, setting, time and place shaping the phenomenon
meaning that the individual holds; this view would being explored. Researchers thus seek to understand
equate with the ontological position of idealism or (describe and explain) these individual meanings. This is
relativism.3 Qualitative researchers make explicit their done as far as possible in their natural setting as the
ontological assumptions about the nature of the reality context is considered part of the phenomenon and the
under investigation and these can lie on a continuum process of gathering data can, of itself, influence
from realism to idealism (or relativism).4 Closely related participants.
to the nature of what is being studied (ontology), is There is an acknowledgement of the subjectivity of the
what can be known about what is being studied (epis- researcher in qualitative research. The researcher’s
temology). A researcher may, for example, consider that history, culture, setting, time, place, etc. will influence all
an individual creates meaning through engagement with aspects of a research study and in particular data collec-
others (an epistemological stance of social construction- tion and analysis. The researcher is the primary instru-
ism) or that an individual constructs meaning in their ment of data collection, bringing their subjective self to
minds (an epistemological position of constructivism).3 the research and requires them to adopt a critically reflec-
Qualitative researchers make explicit their epistemologi- tive and reflexive stance.7 Researchers try to examine and
cal assumptions about what can be known about that understand the perceptions, actions and situations from
reality; these can lie on a continuum from positivism the participant’s point of view. This can be challenging
to interpretivism (or subjectivism).4 Whatever ontologi- when conducting research in one’s own professional
cal and epistemological positions are adopted, qualitative setting and may require an extended length of time to
researchers seek to ensure these positions are congruent make what is familiar appear strange. The researcher
with the methodology and methods used to explore a collaborates interdependently with participants who are
given topic. integral to the study and in some situations, particularly
in participatory action research, may act as co-researchers.
The quality of the researcher–participant relationship is
METHODOLOGY AND METHODS thus of critical concern in qualitative research.
Data can come from multiple sources such as obser-
There are a number of qualitative research methodolo- vation, interviews, documents, field notes and personal
gies available and these include case study, grounded reflections to develop understanding of individuals in
theory, ethnography, phenomenology, narrative enquiry, their context. Data, which are mostly in the form of
evaluation research, action and participatory action words, have primacy. Data collection and analysis
research, discourse analysis, hermeneutics and feminism. proceed together. Analysis and interpretation occur from
Each methodology comes with its own set of processes the beginning of the study and are built from the data
and procedures as well as underlying ontological and inductively, from the specific to the general. No initial
epistemological assumptions. An example of a qualitative hypothesis is developed at the start of the study; rather,
piece of research in MSK physiotherapy may serve to tentative working propositions are developed (analysis)
224 PART II  Advances in Theory and Practice

from initial data collection that is then modified in perspective of the patient or practitioner and the values
subsequent data collection. This iterative cycle of data that underpin their behaviour and motivation.
collection and analysis continues until there are robust Within MSK physiotherapy qualitative research ques-
propositions to conclude the study. Detailed (‘thick’) tions could include:
description of the data and context aim to uncover the • what is it like to live with chronic low back pain or
meanings of participants’ experiences and actions, which neck pain?
can provide theoretical and analytical description and • what triggers a person to seek physiotherapy?
interpretation and in some cases, theory development. • how do MSK physiotherapists decide to refer a
Study findings portray situated understandings that are patient on for further investigations?
reflective of the participants’ perceptions; findings are • how do MSK physiotherapists develop expertise?
therefore reported with a significant number of quota- • what do patients expect from MSK
tions from participants. physiotherapists?
• what is the nature of the patient–therapist
relationship?
FINDINGS
Qualitative research can gain insight into the world of SUMMARY
individuals, groups and/or cultures. Commonalities and
patterns may be identified across individuals. In some The theoretical foundations of qualitative research are
cases an explanation of a social process may be developed. compatible with, and appropriate for, investigation of
Thick description aims to allow the reader to put them- contemporary MSK practice. Each of the qualitative
selves into the situation of the participants and gain methodologies provides a particular perspective to under-
empathic and experiential understanding.1 The social stand the behaviour, perspective and experience of
world and meanings held by individuals and groups will patients and practitioners that help inform practice.
change over time, thus findings are temporary and uncer-
tain. Theoretical (rather than statistical) generalizations REFERENCES
are developed that may be transferable to other settings. 1. Holloway I. Basic Concepts for Qualitative Research. Oxford: Black-
The quality of the research is assessed though trustwor- well; 1997.
2. Lincoln YS, Guba EG. Naturalistic Inquiry. Beverly Hills: Sage;
thiness; this umbrella term includes credibility (findings 1985.
ring true), transferability (of findings to other situations), 3. Blaikie N. Approaches to Social Enquiry. Cambridge: Polity; 1993.
dependability of the study procedures and confirmability 4. Savin-Baden M, Major C. Qualitative Research, the Essential Guide
that the findings relate to the data.8 Strategies are put in to Theory and Practice. London: Routledge; 2013.
place during the research study to address each of these 5. Petty NJ. Towards Clinical Expertise: Learning Transitions Of Neu-
romusculoskeletal Physiotherapists. University of Brighton: Unpub-
aspects. lished DPT thesis; 2009.
6. Charmaz K. Constructing Grounded Theory. A Practical Guide
Through Qualitative Analysis. London: Sage; 2006.
WHEN MIGHT YOU USE 7. Finlay L, Gough B. Reflexivity. A Practical Guide for Researchers
QUALITATIVE RESEARCH? in Health and Social Sciences. Oxford: Blackwell Science; 2003.
8. Erlandson DA, Harris EL, Skipper BL, et al. Doing Naturalistic
Inquiry, A Guide to Methods. Newbury Park: Sage; 1993.
Qualitative research would, for example, enable explora-
tion of patient-centred care, understanding the

CHAPTER 23.3  ■  MIXED METHODS RESEARCH

Hubert van Griensven

WHAT IS MIXED METHODS RESEARCH? question.2–4 Researchers may formulate at least one quali-
tative and one quantitative question5 and should ensure
Traditionally most research has been done from either a that all research questions are open-ended and non-
quantitative perspective based on hypothesis and deduc- directional.3
tion, or an interpretative and usually inductive qualitative In MMR both qualitative and quantitative data are
perspective. Mixed methods research (MMR) utilizes integrated or connected in the overall study. All of the
both and may be defined/described as ‘the type of research study’s strands must be an essential part of the study, be
in which a researcher or team of researchers combines investigated with rigour and analysed fully.1 Their role
elements of qualitative and quantitative research and mutual relationship need to be considered through-
approaches (e.g. use of qualitative and quantitative view- out the design, execution and reporting of the entire
points, data collection, analysis, inference techniques) for study,10 even when one element of the study receives
the broad purposes of breadth and depth of understand- more emphasis.5 For example, the use of a patient ques-
ing and corroboration’.1 The choice of methods and the tionnaire in a quantitative investigation of a drug or other
way in which they are combined is driven by the research treatment does not constitute MMR, because the data are
 23  Research Approaches to Musculoskeletal Physiotherapy 225

rarely subjected to full qualitative analysis and are typi- competent researchers MMR can be more time-
cally represented numerically. consuming and more costly than single method research.15
Those with limited resources should therefore consider
focusing their research question so that it can be answered
WHEN MIGHT YOU USE MIXED using a single method.2 This is especially pertinent
METHODS RESEARCH? because the level of unpredictability increases with the
number of research methods, and more complex research
Rationales for undertaking MMR include the engage- does not necessarily yield more complete answers.17 In a
ment and recruitment of participants, the development sequential MMR study the initial phase may yield results
and testing of a research instrument, the investigation of that do not support the second phase as anticipated, while
interventions and the enhancement of a study’s signifi- a parallel design can produce findings which contradict
cance.7 MMR offers the potential to be both inductive each other.6,18 Although unexpected findings have the
and deductive, incorporate more views and provide potential to generate greater insight15 or a dialogue about
stronger inferences compared with single method the multiplicity of viewpoints,13 they may also be disrup-
studies.5 Some MMR researchers have utilized MMR tive. For example, the criteria for validity or rigour set
specifically to address issues of social justice.8,9 out at the design stage may not be appropriate for the
actual findings.2 Applications to commissioning bodies
and ethics panels may therefore have to be revised
METHODOLOGY AND METHODS significantly or completely.
A further difficulty is the exact way in which qualita-
Only key design options for MMR studies will be dis- tive and quantitative findings should be combined, which
cussed here, although many others are possible. A sequen- is the subject of discussion among MMR scholars.1,4,19
tial study may be undertaken when one type of data is Even in sequential MMR studies where analysis and
needed for the development of a subsequent study phase.10 interpretation of one phase are completed before starting
For instance, a large survey may be used to identify the the next, integration of the findings remains essential.
most appropriate topics and participants for subsequent Direct comparison of data may require the transforma-
interviews, or a focus group may be used to generate a tion of at least one set of data, for instance by qualitizing
theory that is then tested with statistical methods. Alter- quantitative data or vice versa,3 which is likely to raise
natively, a researcher may decide to investigate qualitative objections from mono-method researchers of either per-
and quantitative aspects of a phenomenon in parallel.10 suasion. Mixed methods researchers may find themselves
Other design possibilities include embedding one type of under pressure to discuss only the part of their study that
investigation within another10 or the statistical analysis of is acceptable to a particular audience when writing up or
agreement between codings of qualitative interview presenting their findings.14
data.11
In addition to the best design for their study, research-
ers need to consider at which stage or stages mixing of SUMMARY
qualitative and quantitative aspects will take place.10 Both
must be considered at the design stage and throughout MMR involves the combination and integration of quali-
the study.6 In a sequential study, mixing takes place as data tative and quantitative data and research methods. As a
are collected. Mixing during data analysis may be done consequence, it offers the possibility of investigations
through triangulation or conversion of the results for with greater scope and depth than mono-method research
direct comparison,12 elaboration of one arm on the approaches. However, MMR adds its own complications
other,12 or the use of a dialectic approach, which invites and considerations to those associated with each method
dialogue about paradoxical and conflicting results.13 used, so it should only be considered if the research ques-
Alternatively, the arms of a study may be conducted and tion cannot be answered by a quantitative or qualitative
analysed separately, with mixing not taking place until the method alone.
interpretation phase. Finally, mixing takes place at every
stage of the research process in the fully integrated design.5
CONCLUSION
This chapter has provided a brief overview of three
DIFFICULTIES ASSOCIATED WITH research approaches to enable the reader to make an
MIXED METHODS RESEARCH informed choice when planning a research study. The
choice for a specific methodology is driven by the research
Although MMR is an exciting field of research, it is not question, which has to be considered carefully. For
without its difficulties and controversies. Researchers further reading, the following texts are recommended:
who wish to truly integrate the findings of qualitative and
quantitative methods must have a firm grasp of both.14
MMR may therefore be problematic to researchers who
Quantitative Research
have a background in only one approach or are new to Bowling A 2009 Research methods in health – inves-
research,15 although changes in the way research methods tigating health and health services. 3 ed. Maiden-
are taught are likely to change this.16 That said, even for head: Open University
226 PART II  Advances in Theory and Practice

Hicks C 2009 Research Methods for Clinical Thera- 5. Teddlie C, Tashakkori A. Foundations of Mixed Methods Research.
pists: Applied Project Design and Analysis. 2 ed. Integrating Quantitative and Qualitative Approaches in the Social
and Behavioral Sciences. Thousand Oaks, CA: Sage; 2009.
Edinburgh: Churchill Livingstone 6. Brannen J. Mixing methods: the entry of qualitative and quantita-
tive approaches into the research process. Int J Soc Res Methodol
2005;8(3):173–84.
Qualitative Research 7. Collins K, Onwuegbuzie A, Sutton I. A model incorporating the
rationale and purpose for conducting mixed-methods research in
Braun V, Clarke V 2013 Successful qualitative research, special education and beyond. Learn Disabil: Contemp J 2006;4(1):
a practical guide for beginners. Los Angeles: Sage 67–100.
Savin-Baden M, Major C 2013 Qualitative research, 8. Mertens D. Transformative paradigm. Mixed methods and social
the essential guide to theory and practice. London: justice. J Mixed Methods Res 2007;1(3):212–25.
Routledge 9. Mertens D. Emerging advances in mixed methods: addressing
social justice. J Mixed Methods Res 2013;7(3):215–18.
Silverman D 2013 A very short, fairly interesting and 10. Creswell J, Plano-Clark V. Designing and Conducting Mixed
reasonably cheap book about qualitative research. Methods Research. 2nd ed. Thousand Oaks, CA: Sage; 2011.
Los Angeles: Sage p. 66–96.
11. Castro F, Kellison J, Boyd S, et al. A methodology for conducting
integrative mixed methods research and data analyses. J Mixed
Mixed Methods Research Methods Res 2010;4(4):342–60.
12. Greene J, Caracelli V, Graham W. Toward a conceptual framework
Creswell J, Plano-Clark V 2011 Designing and con- for mixed-method evaluation designs. Educ Eval Policy Anal
ducting mixed methods research. 2 ed. Thousand 1989;11(3):255–74.
Oaks, CA: Sage 13. Greene J. Mixed Methods in Social Enquiry. San Francisco: Wiley;
2007. p. 69.
Teddlie C, Tashakkori A 2009 Foundations of mixed 14. Bryman A. Barriers to integrating quantitative and qualitative
methods research. Integrating quantitative and research. J Mixed Methods Res 2007;1(1):8–22.
qualitative approaches in the social and behavioral 15. Johnson R, Onwuegbuzie A. Mixed methods research: a research
sciences. Thousand Oaks, CA: Sage paradigm whose time has come. Educ Res 2004;33(7):14–26.
16. Hesse-Biber S, Johnson R. Coming at things differently: future
directions of possible engagement with mixed methods research.
REFERENCES J Mixed Methods Res 2013;7(2):103–9.
1. Johnson R, Onwuegbuzie A, Turner L. Toward a definition of 17. Bergman M. The good, the bad, and the ugly in mixed methods
mixed methods research. J Mixed Methods Res 2007;1(2):112–33. research and design. J Mixed Methods Res 2011;5(4):271–5.
2. Bryman A. Paradigm peace and the implications for quality. Int J 18. Morgan D. Practical strategies for combining qualitative and quan-
Soc Res Methodol 2006;9(2):111–26. titative methods: applications to health research. Qual Health Res
3. Onwuegbuzie A, Leech N. Linking research questions to mixed 1998;8(3):362–76.
methods data analysis procedures. Qual Rep 2006;11(3):474–98. 19. Tashakkori A, Teddlie C. Putting the human back in ‘human
4. Greene J. Is mixed methods social inquiry a distinctive methodol- research methodology’: the researcher in mixed methods research.
ogy? J Mixed Methods Res 2008;2(1):7–22. J Mixed Methods Res 2010;4(4):271–7.
 CHAPTER 24 

Standardized Data Collection,

Audit and Clinical Profiling
Ann Moore

INTRODUCTION place, as well as a range of other possible knowledge area

developments.
As can be seen from other chapters in this section of the The author, with a number of colleagues, has worked
text, there are many different approaches to research that on the development of a range of standardized data col-
are relevant and essential to underpin musculoskeletal lection tools for use in musculoskeletal physiotherapy
physiotherapy. One of the key elements of most research since the mid-1990s and has published a master class on
approaches is the inclusion of robust data that can under- this topic area that describes the development processes
pin the study’s findings, for example demographic data, in detail and also documents its historical development.2
clinical data, service delivery data, historical data and In this paper we defined a standardized data collection
objective clinical data, which can be used often to explain tool as:
why particular approaches to care have particular effects
on a particular profile of patients. These data can also be ‘an agreed instrument which enables data concerning
used for clinical profiling and to inform clinical audit patients, therapists and/or healthcare settings and
activities. approaches to be collected unambiguously by a range of
In addition there are various ways in which data col- practitioners in a number of different settings’.2
lection and appropriate use of data can contribute to the
care of patients, the quality of service delivery, marketing The definition asserts that this would allow data to be
of services, production of business cases, and quality shared and understood by practitioners working in the
enhancement of the provision of services, together same organization, as well as across multiple organiza-
with cost-effectiveness calculations, outcomes of care, tions countrywide or potentially worldwide. The impor-
improvement of patient experiences and patient satisfac- tant things to note here are that if a tool is needed, then
tion and also job satisfaction of those involved in the data in order for it to work effectively or for clinicians to use
collection and interpretation of the data. the tool effectively, the tool must be developed in a robust
In research terms standardized data collection can help and rigorous way which, in itself, requires some research
to rigorously profile research participants for inclusion, activity. In addition, a process has to be in place for pilot-
or for consideration for inclusion, in aspects of a research ing the tool, and adapting the tool based on feedback
study. It can also enable further explanation of findings from pilot studies. This process will be discussed in the
of studies focusing on profiling participants and how they rest of this chapter.
have reacted to different types of interventions included If data are being shared then of course the data col-
in the study concerned. In addition, standardized data lected must be anonymized to protect the identity of
collection can help to further develop understandings of individual patients and ethics approval for the activity
qualitative findings, for example what patient profiles must be gained. Data collected can include aspects of
appear to impact on their experiences and perhaps their patients’ demographics, service delivery, process and type
expectations of certain techniques/approaches. One can of care, referral pathways, clinical findings, outcomes of
only carry out such analyses of data if the data have been care, costs of care, profile of care providers, content of
collected robustly and rigorously with no room for ambi- care and factors that may have influenced care and the
guity. This chapter explores the concept of standardized outcome of care.
data collection and the mechanisms for developing stan- The reason that standardized data collection is impor-
dardized data collection tools. tant is that all health agendas and policies across the
world are focusing on the quality issues relating to inno-
vative, effective and efficient services that meet health-
CONTEXT care needs. As economic growth continues to be slow in
many countries and health-care costs often represent the
Research, as defined broadly by Bailey1 is ‘any activity largest proportion of government expenditure, hospital
which increases knowledge’. Standardized data collection staffs are increasingly being required to provide good-
is a mechanism by which musculoskeletal clinicians can quality information to commissioners of health care to
increase the knowledge of the work they undertake, the support their service. This could relate to value for
profiles of patients that they treat, the clinical approaches money, demonstrably high-quality patient outcomes
that they are taking, and how and when treatment takes and also in widening access and providing choice in
227
228 PART II  Advances in Theory and Practice

health-care provision. In this context standardized data with NHS hospital trusts in the United Kingdom and
collection can help with the following: with private practitioners via PhysioFirst, the private
• Sourcing evidence to demonstrate improved quality physiotherapy practitioner organization in the UK, and
of care and improvement of services. also with osteopaths in the United Kingdom via the
• Benchmarking outcomes against other similar and General Osteopathic Council. This work has led to a
perhaps competitive service providers. number of publications that detail the work2,11,12 and
• Monitoring the productivity of the workforce. other reports published on line.
• Delivering high-quality evidence-based services and There is no doubt that data emanating from practice
auditing impact of services. need to be recorded in a systematic and accessible way.
• Being able to match resources with projected health It is important that the reasons why data are needed and
needs. what purpose the data will serve, as well as a detailed plan
• Setting appropriate staffing levels in all areas of of what data are to be collected and how, is created.13
service delivery. Data can be used for both clinical and research purposes
• Providing data concerning service delivery and out- (i.e. it can be used to identify research questions relevant
comes to all stakeholders. to practice, to categorize/profile patients using diagnostic
• Auditing clinical services against standards. information, to provide descriptive/demographic data
• Providing evidence on which commissioning deci- [e.g. age, height, weight, psychosocial circumstances,
sions can be based. etc.]).
• Facilitating patient profiling, especially if combined The information may be used to predict the patient
with screening tools and validated and reliable outcome in the future, determine the suitability of par-
patient-recorded outcome measures. ticular interventions for particular patient profiles, inform
• Identifying meaningful research questions for the the dosage and frequency of interventions, classify
profession/speciality. patients into profiling groups and indicate possible rela-
It is well recognized that good-quality data are the tionships between two or more factors across a range of
foundation of good-quality information and that when patients with similar characteristics. The data/information
decision makers use information well, services improve.3 can also be used to detect changes in patient profiles
People who make decisions include patients and users of (diagnostic or personal) which can help further under-
services who can chose particular hospitals/practices, cli- standing and give more details of the patient’s situation
nicians and treatment approaches, professionals who and enable comparison of patients to take place.
exercise judgement on treatments and approaches, man- The data collection methods, however, can also focus
agers who prioritize service delivery and politicians who heavily on service delivery if required, for example the
allocate resources for health care.3 number of treatments needed, the expertise available/
The Audit Commission3 defined good-quality data as needed, costs of treatments, quality of the patient experi-
the statistics, facts, numbers and records that can be orga- ence, and a range of other possibilities depending on the
nized and analysed into information that answers a spe- need for the data collection which have been identified.
cific need. Six characteristics of good-quality data were The data collected can be qualitative or quantitative,
published by the Audit Commission4 in a report Volun- again depending on the need and relevance of the data,
tary Data, Quality Standards: and data collection tools to answer particular questions
• Accuracy – data need to be accurate for their may already be available.
intended purpose.
• Validity – data need to be recorded and used in
compliance with relevant requirements. DEVELOPMENT OF A STANDARDIZED
• Reliability – data need to reflect stable and consis- DATA COLLECTION TOOL
tent data collection processes across collection
points and over time. The methods most commonly used in the development
• Timelines – data should be captured as quickly as of a standardized data collection tool are consensus
possible after the event or activity and must be avail- methods. This involves bringing an expert team, or iden-
able for use within a reasonable time period. tifying an expert team that can work at a distance, rele-
• Relevance – data captured should be relevant to the vant to the topic area (i.e. experts in musculoskeletal
purposes for which they are used. physiotherapy, in health delivery policy, users of muscu-
• Completeness – data requirements need to be clearly loskeletal services, etc.). In this context the expert team
specified based on information needs.4 identifies and agrees why a standardized collection tool
For many years then, the concept of standardized data is needed and necessary and what it is hoped it will
collection has been in growth and utilized in many areas achieve.
of health practice, and there is substantial agreement that There are two consensus methods that can be utilized
quality data collection is inextricably linked to quality for this process. Firstly, there is the Delphi process and
improvement.5 Standardized data collection has also been secondly, the nominal group technique.14
used in various health specialities, including tropical
medicine,6 sports medicine,7,8 neurological physiother-
apy9 and cardiopulmonary settings.10 THE DELPHI PROCESS
In relation to musculoskeletal physiotherapy settings
the author has been involved in standardized data collec- The Delphi process or technique was developed by
tion developments and applications since 1994, working Dalkey and Helmer in 196315 and also discussed by
 24  Standardized Data Collection, Audit and Clinical Profiling 229

Linstone and Turoff.16 It is a technique commonly used nominal group needs to include representatives of all
to achieve consensus opinion on certain topic areas and stakeholders in the standardized data collection tool.
has been used in studies, particularly those looking at There could be more than one nominal group, but the
developing research priorities.17,18 The Delphi technique outcome of each group discussion needs to be shared and
is designed to achieve group communication via ques- discussed so that members of all groups understand the
tions online or in paper copy and, eventually, consensus concern and/or the priorities of the different groups.
with regard to specific issues, for example research prior-
ity setting17 (i.e. to seek out information which may gen-
erate a consensus on the majority of a respondent group).
Process of Standardized Data Collection
The Delphi process includes a panel of ‘experts’19 to Development Utilizing a Nominal Group
take part in up to four iterations/rounds of a questionnaire- Technique
type approach. In the Delphi process the panel of experts
is set up together with a Delphi team of collators. The • The organizer should carry out a literature search
expert panel receives postal, email or web-based ques- to see if any standardized data collection tools are
tionnaires on the research question or area of interest. available and relevant.
Examples of sample questions include: what should be • Preliminary work with several experts will be needed
included in a standardized data collection tool for mus- to identify appropriate discussion points/questions.
culoskeletal physiotherapy to highlight the quality of • A group or groups of experts need to be developed
patient care and service delivery? What topic areas should depending on the area in question, to come together
be included in the tool? Why should they be included? for a discussion.
It is usual for each participant to be asked to give a ratio- • Groups of patients, as well as clinicians, managers,
nale for the inclusion of certain topic areas. other health professionals can be involved depend-
The completed questionnaires are then sent back to ing on the topic area.
the collation team to analyse and collate the responses, • The individuals involved must have appropriate
and then another more structured questionnaire, includ- expertise and experience and interest in the topic
ing the entire panel’s views, is again sent out to the expert area.
panel members for completion. In this round the partici- • Groups will normally meet for approximately two
pants are usually asked to rank topics in order of agree- hours and the facilitator should be an expert on the
ment or importance. The expert panel members send discussion topic or be a credible non-expert.20
back their comments and the second round results are
collated and analysed; further rounds continue until con- A Nominal Group Technique
sensus is reached. Usually four rounds are sufficient.
Although the Delphi process allows participants to be
Protocol as an Example
anonymous, it does not enable further discussion and • Introductions and explanation of purpose and pro-
therefore it may detract from individuals’ understanding cedure (5 to 10 minutes).
of issues that are held by other members of the expert • Silent generation of ideas by all members of the
panel. However, it has advantages where an international group who write their thoughts down without dis-
perspective is needed and the group cannot be brought cussion with others (10 minutes).
together. • Sharing of all participants’ ideas and facilitator
records all the ideas and comments. In addition,
participants should write down any new ideas that
arise as a result of these discussions (15 to 30
NOMINAL GROUP TECHNIQUE minutes).
• The group discussion then takes place. Participants
The most common method used as a consensus method- seek more explanation/details of any ideas that are
ology is a nominal group technique. This technique was not clear to them and the facilitator controls the
first described by Delbecq and Van de Ven in 1971.20 discussion, but allows all participants the opportu-
They described it as a method to facilitate effective group nity to speak and feed in ideas (30 to 45 minutes).
decision making in social psychological research.20 Their • Voting and ranking process then takes place, priori-
process is clearly explained in a further paper.21 Usually tizing and confirming recorded ideas in relation to
a nominal group would consist of five to ten participants. the initial question.
The nominal group technique is often considered a • At this point immediate results are available to all
mixed-methods approach as it can utilize qualitative and participants and the meeting concludes.22
quantitative methods. With the development of a standardized data collection
The purpose of the group is to firstly identify why the tool, several meetings will often be necessary to cover the
data are needed and then to generate ideas for topics to complexities of the situation and the discussions around
be included in the data collection and eventually to decide it. For an overall example of the procedure, see Moore
how the data collection topics will be populated; for et al.2
example, if one is collecting data concerning whiplash The findings from the nominal group technique are
what classification system for whiplash will be utilized to rarely the finishing point, hence the process shown below.
capture the severity/mechanisms of the whiplash injury? The detailed discussion of the topics to be included and
This can be quite a complex process and the group how the answers are to be recorded is complex, but
needs to be well controlled during early discussions. The agreement/consensus will mean that ambiguity of the
230 PART II  Advances in Theory and Practice

standardized data collection will be low, at the first pilot cervical spine dysfunction, whiplash, exercise prescrip-
(see Fig. 24-1) tion, over-60s, shoulder dysfunction, knee dysfunction
Details and characteristics of consensus methods and sports injuries. These tools have often been used in
including the Delphi process and nominal group tech- Snapshot surveys due to their length. A short-form stan-
niques have been published by Fink et al.,23 as well as dardized data collection tool is now being developed for
Jones and Hunter;14 the Delphi technique has more daily and routine use in private practice.
recently been discussed in detail by Hsu and Sandford.24 Standardized data collection tools can be used in paper
It is useful to note that a manual of operation and copy, electronically via data sticks, or web-based data
completion and use of the tool for all participants is found storage, but obviously if data are being shared then it
to be very useful. To date, Moore et al.2 have undertaken must be anonymized. Usually data systems can be easily
nine projects, developed nine standardized data collec- modified to keep such data confidential and in an anony-
tion tools that include a general tool for low back pain, mized fashion.

Formulate a representative expert panel

Share motivation for the project (the panel's values

and needs in terms of the type of data to be collected)

Round table discussions regarding the content of the tool

Draft outline tool tabled for further discussion and modification

Refinement of tool to develop topic statements/questions and possible responses (this may need a
sequence of expert panel meetings depending on complexity). It is always useful to use existing
tools/topics that are available and have face/content validity to avoid reinventing the wheel

When the tool has been refined to the expert panel's satisfaction, pilot the tool with two members
of the panel in their own practice settings for one or two days for feasibility of use

Some refinement may then be discussed and implemented by the expert panel

Carry out a larger pilot if this is a local project with a few selected staff naive to the tool's development
for a 2-week period and ask for feedback on the tool and its use

Refine the tool as necessary and then pilot the tool with all staff in the location for a 2-week period.
Ask for feedback at the end of this period

If this is a local project choose the best time period to collect the data to maximize the time
(e.g. not over the Christmas period!)

Collect all the data and carry out the analysis.

(The data can be collected in paper format or electronic format, depending on the resources available)

Disseminate the findings

(to staff teams, the profession)

FIGURE 24-1  ■  Flow chart depicting the developmental process.

 24  Standardized Data Collection, Audit and Clinical Profiling 231

There are advantages of standardized data collection 2. Moore AP, Bryant E, Oliver G. Masterclass – development and use
for patients, practitioner therapists, managers for prac- of standardised data collection tools to support and inform muscu-
loskeletal practice. Man Ther 2012;17(6):489–96.
tices and for the musculoskeletal speciality. If data can be 3. Audit Commission. In the Know: Using Information to Make
collected across regions, countries, or even across the Better Decisions – A Discussion Paper. Audit Commission Publica-
world using the same format, it provides very powerful tions; 2008.
information. In addition to the positive benefits of stan- 4. Audit Commission. Voluntary Data – Quality Standards. Audit
Commission Publications; 2007.
dardized data collection already described, the data col- 5. Needham DM, Sinopoli DJ, Dinglas VD, et al. Improving data
lected can be utilized to set standards for clinical audit quality control in quality improvement projects. Int J Qual Health
purposes. Care 2009;21(2):145–50.
Clinical audit has been defined as systematically 6. Taylor T, Olola C, Valim C, et al. Standardised data collection for
looking at procedures used for diagnosis, care and treat- multi-centre clinical studies of severe malaria in African children:
establishing the SMAC network. Transcr R Soc Trop Med Hyg
ment, examining how associated resources are used and 2006;100(7):615–22.
investigating the effect care has on the outcome and 7. Finch CF, Valuri G, Ozanne-Smith J. Injury surveillance during
quality of life for the patient.25 medical coverage of sporting events – development and testing of
The use of data from research and standardized data a standardised data collection form. J Sci Med Sport 1999;2(1):
42–56.
collection and evaluation of service delivery and out- 8. Fuller CW, Ekstrand J, Junge A, et al. Consensus statement on
comes has been emphasized by authors including Øvret- injury definitions and data collection procedures in studies of foot-
veit26 as being an important area for development in ball (soccer) injuries. Br J Sports Med 2006;40(3):193–201.
clinical practice in the setting of standards which can then 9. Crow JL, Harmeling BC. Development of a consensus and
be audited. Clinical audits of course are founded on the evidence-based standardised clinical assessment and record form
for neurological inpatients: the Neuro dataset. Physiotherapy
need to monitor and improve quality of care and the audit 2002;88(1):33–46.
cycle largely focuses on the structure, process and out- 10. Jones P, Harding G, Wiklund I, et al. Improving the process and
comes of treatment. Standardized data collection tools outcome of care in COPD: development of a standardised assess-
can, when necessary, be focused on deriving data much ment tool. Prim Care Respir J 2009;18(3):208–15.
11. Fawkes C, Leach CMJ, Mathias S, et al. Development of a data
needed to inform standard setting in clinical environ- collection tool to profile osteopathic practice: use of a nominal
ments. The importance of well-informed and timely group technique to enhance clinician involvement. Man Ther
standard setting cannot be underestimated and the results 2014;19(2):119–24.
of a well-constructed quality audit of clinical activities 12. Fawkes C, Leach CMJ, Mathias S, et al. A profile of osteopathic
and outcomes can be extremely powerful. care in private practices in the United Kingdom: a national pilot
using standardised data collection. Man Ther 2014;19(2):125–30.
Together with detailed clinical subjective and objec- 13. Wade DT. Editorial. Assessment, measurement and data collection
tive data and the use of validated and reliable outcome tools. Clin Rehabil 2004;18:233–7.
measures, standardized data can be utilized to develop 14. Jones J, Hunter D. Consensus methods for medical and health
patient clinical profiles that may be very helpful in the services research. Br Med J 1995;331(7001):376–80.
15. Dalkey NC, Helmer O. An experimental application of the Delphi
development of treatment strategies and in formulating method to the use of experts. Manage Sci 1963;9(3):458–67.
clinical research questions. The data can also be a power- 16. Linstone HA, Turoff M. The Delphi Method: Technique
ful tool to influence commissioners of health services. and Applications. Massachussetts: Addison-Wesley Publishing
There are, however, some barriers to the use of stan- Company.; 1975.
dardized data collection tools. In a paper by Russek 17. Rushton A, Moore A. International identification of research
priorities for postgraduate theses in musculoskeletal physiotherapy
et al.,27 attitudes were highlighted that may impact on using a modified Delphi technique. Man Ther 2010;15(2):
standardized data collection tool use. Firstly, there is the 142–8.
inconvenience of collecting data in terms of the time 18. Rankin G, Rushton A, Olver P, et al. Chartered Society of Physio-
taken. Secondly, the necessity to ensure appropriate therapy’s identification of national research priorities for physio-
therapy using a modified Delphi technique. Physiotherapy
training takes place with regard to the standardized data 2012;98(3):260–72.
collection methods, so that large and high-quality data- 19. Dalkey NC. An experimental study of group opinion. Futures
bases can be constructed, i.e. training is needed in the 1969;1(5):408–26.
operational definition and data collection procedures and 20. Delbecq AL, Van de Ven AH. A group process model for problem
it is of course highly relevant that computerized patient identification and program planning. Appl Behav Sci 1971;
7:466–91.
documentation systems can streamline data collection 21. Delbecq AL, Van de Ven AH, Gustafson DH. Group Techniques
and increase clinicians’ efficiency. The notion of the for Program Planning: A Guide to Nominal and Delphi Process.
inconvenience of data collection, however, can be quickly Glenview Illinois: Scott, Foresman & Company; 1975.
rationalized with individuals if overall data produced is 22. Potter M, Gordon S, Hamer P. The nominal group technique: a
useful consensus methodology in physiotherapy research. N Z J
shared and discussed with them in an informative and Physiother 2004;32(3):126–30.
constructive way. This often enables individuals who may 23. Fink A, Kosecoff J, Chassin M, et al. Consensus methods: charac-
be sceptical about the need for data collection to be teristics and guidelines for use. Am J Public Health 1984;74:
brought up to speed with the impact that relevant data 979–83.
may have on a wide range of stakeholders including 24. Hsu CC, Sandford BA. The delphi technique: making sense of
consensus. Practical Assessment, Research and Evaluation 2007;
patients, carers, managers, commissioners and other 12(10):1–8.
health professionals. 25. Department of Health. Clinical Audit: Meeting and Improving
Standards in Health Care. London: HMSO; 1993.
26. Øvretveit J. Evaluating Health Interventions. Milton Keynes: Open
REFERENCES University Press; 1998.
1. Bailey DM. Research for the Health Professional: A Practical 27. Russek L, Wooden M, Ekedahl S, et al. Attitudes toward stan-
Guide. Philadelphia: FA Davis Company; 1991. dardised data collection. Phys Ther 1997;77(7):714–29.
 CHAPTER 25 

Implementation Research
Simon French  •  Sally Green  • 
Rachelle Buchbinder  •  Jeremy Grimshaw

INTRODUCTION Timely implementation of evidence into clinical

practice ensures that people who require health care
The availability of high-quality research evidence is not receive the most contemporary, effective and safest care.
sufficient to ensure high-quality health care is delivered, However, in many cases, research findings do not result
and the translation of research evidence into practice is in a change in clinical practice or health-care policy.
difficult and complex. Implementation research, or trans- Using musculoskeletal health care as an example, in many
lational research, explores the most effective ways to inte- cases diagnostic tests are not being used appropriately
grate research evidence into clinical practice and health (e.g. too few bone density scans for osteoporosis diagno-
policy. This chapter focuses on relevant research methods sis,13 or too many plain X-rays for low back pain14,15) and
exploring the process of improving the implementation interventions with established effectiveness are not being
of research findings into physiotherapy practice. The use used in practice (e.g. too few people with hip fracture
of theory, and theoretical frameworks, in implementation receive osteoporosis treatment to prevent further frac-
research is also discussed, including their use in the ture16). Also, interventions are being used before there is
process of developing implementation interventions established evidence to support them, and in some
designed to change clinical practice. instances, being used despite research demonstrating
they are ineffective and/or harmful (e.g. vertebroplasty
for vertebral compression fractures,17,18 opioid prescrip-
WHAT IS THE PROBLEM? tion for low back pain19 and arthroscopy for osteoarthritis
of the knee20).
Many people receiving health care are not receiving the Physiotherapists generally hold favourable attitudes
best possible care through a failure of their health-care towards evidence-based practice.21–23 However, these
providers to incorporate up-to-date research evidence positive attitudes alone do not guarantee best possible
into clinical practice. Researchers continuously produce patient care informed by the latest research. Many health-
new findings that can contribute to effective and efficient care workers, including physiotherapists, base clinical
health care as long as this research is implemented into decisions on potentially outdated knowledge obtained
practice. A common mechanism for synthesizing and during their physiotherapy education, or on personal
disseminating high-quality research-supported informa- experience, rather than being informed by findings from
tion to clinicians is in the form of a clinical practice up-to-date research.21,24–27
guideline. Guideline recommendations have the poten- The process of implementing research evidence into
tial to improve the quality and safety of health care, but an individual clinician’s practice and subsequent improve-
only with effective dissemination and uptake into clinical ment of patient health outcomes can be a long and
practice. In many clinical areas this does not occur and complex one.2 Much emphasis is placed on dissemina-
there is a gap between actual clinical practice and rec- tion of research evidence, for example by making clinical
ommended, evidence-based practice.1 practice guidelines available, or presentation at educa-
Evidence–practice gaps exist where there is variability tional meetings. But ensuring clinician awareness of
between best recommended practice and actual clinical the evidence is only the beginning of the process and
practice. There are numerous examples of evidence– other aspects of translation into practice have received
practice gaps in different clinical settings, in different less attention. In busy clinical environments clinicians
countries and for different clinical conditions, both in must not only remember the evidence, but also actively
diagnosis and treatment,2–12 resulting in some patients decide to vary their practice when relevant to an indi-
receiving care that is inappropriate, unnecessary or even vidual patient. In addition, if the evidence is contrary
harmful.1 For example, an Australian study determined to the clinician’s preconceived ideas and opinions, this
the percentage of health-care encounters at which care may limit acceptance and uptake of the new informa-
was in line with evidence-based or consensus-based tion.28 Even if the evidence is applicable to the clini-
guidelines.3 Overall, Australian patients in the study cian’s setting and it is accepted, they may not have the
received appropriate care at an average of 57% of eligible appropriate skills, training or equipment to be able to
encounters during 2009 and 2010, and for people with implement the evidence. Finally, the evidence also needs
low back pain or osteoarthritis, the percentage of encoun- to be acceptable and feasible to patients, and patient
ters with appropriate care were 72% and 43%, benefit relies upon adherence to the agreed course of
respectively. action.2
232
 25  Implementation Research 233

required to provide rigorous methods for improving the

WHAT IS IMPLEMENTATION uptake of evidence into clinical practice so patients
RESEARCH? receive the best care. However, there exists a ‘poverty of
research’ to inform decisions about how to improve the
To date, little is known about the best way to promote delivery of health care and there is great opportunity and
the uptake of research evidence into clinical practice. scope to conduct research to improve the uptake of evi-
Implementation research aims to evaluate the most effec- dence into clinical practice.12
tive and efficient means of achieving this. Implementa-
tion research is a field of health service research that
explores the development, delivery and evaluation of WHAT ARE THE TYPES OF
strategies and methods to implement research evidence IMPLEMENTATION RESEARCH?
into practice.29 Implementation research can study any
aspect of implementing evidence into practice, including A wide range of qualitative and quantitative research
exploring the factors affecting implementation, the pro- methods can be used in implementation research. Imple-
cesses of implementation, and the results of implementa- mentation research can be classified into three categories:
tion.30 Implementation researchers focus on understanding descriptive, evaluative and methodological implementa-
and influencing the process of uptake of evidence into tion research. Table 25-1 provides simple examples of the
practice by applying and developing theories on why different types of implementation research that fall within
health-care providers and policy makers do what they do, these three categories.
and on how to improve their performance through facili- Descriptive implementation research is investigation
tating the use of evidence in their decision making.31 conducted to describe current practice. This typically
The practice of, and research about, improving the includes observational research, using qualitative or
uptake of evidence into health-care practice and policy is quantitative methods, to determine what is occurring in
relatively new. Reflecting this, there are inconsistencies practice and to attempt to understand why practitioners
in the literature about the best term to use to describe conduct practice in this way. This research explores
this field.32 To add to the confusion, some of these terms whether an evidence–practice gap exists, and if so, the
have attempted to capture the entire process of research extent of this gap and the likely reasons for the gap.
to practice or policy, some parts of the process, and some Evaluative implementation research is the conduct of
terms have been used interchangeably.33 Some of the effectiveness studies of interventions that aim to improve
more common terms used in the literature include imple- the uptake of research into clinical practice. Evaluative
mentation research, knowledge translation research, implementation research generates substantive knowl-
translational research, research translation, research uti- edge about how to implement research into practice.
lization, quality improvement research, knowledge trans- This typically includes quantitative study designs to test
fer and exchange, and dissemination and implementation the effects of an intervention, such as uncontrolled or
research. In this chapter we will use the term ‘implemen- controlled before-and-after studies, interrupted time
tation research’. series studies, non-randomized controlled clinical trials
Advances in implementation research have the poten- and individual participant or cluster randomized con-
tial to improve patient care. Implementation research is trolled trials.34,35 Of these, the randomized controlled

TABLE 25-1  Different Implementation Research Categories with Examples

Implementation
Aim Research Category Examples
Describing practice Descriptive Demonstrating the extent to which clinicians practice according to
recommendations of an evidence-based clinical practice guideline (CPG),
e.g. a survey shows high rate of X-ray use for acute low back pain (LBP)
Understanding practice: Descriptive Determining reasons why clinicians do, and do not, practice in accordance
barriers and enablers with the CPG, e.g. focus groups with clinicians find that they feel
analysis pressure from patients to order an X-ray
Evaluation studies Evaluative Randomized controlled trial of an intervention to change health-care
providers’ behaviour, e.g. randomize clinicians to receive negotiation
skills or not, then measure X-ray referral rates between groups
Implementation Methodological Using theoretical exploration and modelling to develop an intervention to
intervention design overcome barriers to practicing in accordance with the CPGs, e.g.
modelling suggests providing clinicians with negotiation skills will assist
them when patients with acute LBP demand an X-ray
Assessing intervention Methodological Strategies to ensure that an intervention is delivered as planned and an
fidelity evaluation of this, e.g. document how many clinicians receive
negotiation skills training, and evaluating the content of the training
Methods development Methodological Research across all the different categories, contributing to the methods of
each, e.g. the development of techniques to analyse cluster randomized
controlled trials evaluating implementation strategies
234 PART II  Advances in Theory and Practice

trial is the most methodologically robust of the evaluative financial, organizational and regulatory interventions.42
implementation research designs. The other designs have EPOC has developed a taxonomy of implementation in-
greater risk of bias, but may be appropriate in certain terventions that describes interventions used to improve
situations, such as when a randomized controlled trial is clinical practice. Table 25-2 lists some of these interven-
not feasible or ethical to conduct. tions and gives some examples relevant to the physio-
Methodological implementation research is a study therapy profession.
conducted into the different methodological components
of the implementation process. This category of research
flows from, and informs, the conduct of both descriptive
and evaluative implementation research. The study
HOW ARE INTERVENTIONS DEVELOPED
designs utilized for this research are varied, and will typi- THAT AIM TO INCREASE
cally include qualitative and mixed-methods research. IMPLEMENTATION OF RESEARCH?
As implementation research is a relatively new field it
requires foundational research to build the science, devel- Complex interventions, which are interventions made up
oping and testing hypotheses about why health profes- of a number of components, are typically employed in
sionals, patients and health organizations do what they studies aiming to implement evidence into clinical prac-
do and how to improve their performance in clinical tice. Development of complex interventions for imple-
practice.12 mentation research requires careful planning to ensure
that the intervention specifically targets what requires
change. Given the high proportion of trials of complex
WHICH INTERVENTIONS HELP TO interventions in this area that do not show which inter-
CHANGE CLINICAL PRACTICE? ventions are effective in which situations, and the need
to improve practice in line with evidence, researchers
A systematic review published in 2010 synthesized all should provide a strong rationale for the development of
studies of knowledge translation strategies in allied their interventions.44 This will ensure that the theoretical
health, including physiotherapy.36 Only nine published basis and feasibility of the intervention have been estab-
studies involving physiotherapists could be found. The lished prior to embarking upon a costly implementation
authors concluded that equivocal results, low method- project.
ological quality and outcome-reporting bias did not allow The science of developing complex interventions to
them to recommend one particular knowledge transla- change practitioner behaviour is at an early stage of
tion strategy over another to improve allied health prac- development.12 Only a minority of trials of complex
tice. Although there are few studies specifically targeting implementation interventions have published details
physiotherapists, evidence from systematic reviews of about how and why the intervention tested was devel-
other professionals might be useful because their findings oped.41,45 Details of the theoretical basis, delivery and
are likely to be transferrable. measures of the process of care targeted by these inter-
Complex interventions designed to increase the uptake ventions are often lacking, making it difficult to know
of evidence into clinical practice can be termed implemen- what exactly has been evaluated and how to replicate the
tation interventions. Implementation interventions have intervention in other settings.
been extensively evaluated and the results synthesized in Pharmaceutical interventions are evaluated in ran-
a number of systematic reviews.37–40 Grimshaw and col- domized controlled trials only after there is a strong
leagues summarized the findings of 235 studies evaluat- rationale for their use, based on empirical evidence of
ing implementation interventions designed to improve their mechanism of effect in animals and from modelling
the uptake of clinical practice guidelines.41 The most studies.46 Pre-clinical studies then aim to elucidate the
common interventions evaluated included reminders, mechanism of effect in humans by measuring surrogate
dissemination of educational materials, audit and feed- outcomes. In other words, it takes many years and much
back, educational outreach, patient-directed interven- preliminary research before a drug is tested in definitive
tions and multifaceted interventions consisting of a trials. The same principle could apply for interventions
combination of these strategies. Overall, the majority of designed to change clinical practice; however, the need
the studies reported that the implementation interven- for change in practice is urgent and we cannot afford to
tions evaluated resulted in modest to moderate improve- wait many years using a pharmaceutical model of devel-
ments in care. However, the improvements varied both opment. More explicit consideration of barriers to change
within and across interventions. Despite the large number and mechanisms of action of potential implementation
of previous implementation studies, there is currently no interventions, underpinned by a theory or rationale that
strong basis for selecting a particular implementation attempts to explain how and why the intervention may
intervention to overcome a particular implementation effect change, would likely enhance the field.
problem. Implementation of evidence into practice often
The Cochrane Effective Practice and Organisation requires behaviour change. This behaviour change may
of Care (EPOC) Review Group publishes Cochrane be required at the general population or patient level, at
Systematic Reviews of interventions designed to im- the clinician level or health-care practice level (including
prove health-care delivery and health-care systems non-clinical staff), at a regional health-care level or at a
(http://epoc.cochrane.org/). EPOC reviews include policy level. Behaviour change is complex and there are
continuing education, quality assurance, informatics, many recommendations and approaches in the literature
 25  Implementation Research 235

TABLE 25-2  Examples of Interventions Designed to Change Health Professional Clinical Behaviour
Type of Intervention Subgroups Examples
Professional Distribution of educational Distribution of clinical practice guidelines via mass mailings
interventions materials
Educational meetings Clinicians participating in conferences
Educational outreach visits Use of a trained person who meets with a clinician in their
practice settings to give information with the intent of
changing the clinician’s practice
Local opinion leaders Use of providers nominated by their clinician colleagues as
‘educationally influential’
Audit and feedback A summary provided to a clinician of their clinical health-care
performance over a specified period of time
Reminders Patient- or encounter-specific information, provided verbally,
on paper or on a computer screen, which is designed or
intended to prompt a clinician to recall information
Marketing Survey of health-care providers to identify barriers to change
and subsequent design of an intervention that addresses
identified barriers
Mass media Targeting the general population about best practice
management of a particular health condition via the media
(including television, radio, newspapers, social media, etc.)
Financial interventions Provider interventions A new fee-for-service is introduced into a clinical practice
Organizational Revision of professional Use of allied health assistants
interventions roles
Clinical multidisciplinary Creation of a new team of health professionals to include
teams different clinical disciplines
Case management A new coordination of assessment, treatment and
arrangement for referrals for specific clinician groups
Changes in medical records Changing from paper to computerized records
systems
Regulatory interventions Changes in medical liability Expanded scope of practice

Adapted from the Cochrane Effective Practice and Organisation of Care Group intervention taxonomy.43

proposing one way or another, or multiple approaches, Step 1: Who needs to do what differently?
to achieve sustained behaviour change.47
Various conceptual and theoretical frameworks are Action: Systematically identify the evidence–practice gap
available when considering the development of imple-
mentation interventions to improve the uptake of research
into clinical practice.33,48–54 A systematic scoping review Step 2: Using a theoretical framework, which barriers and
in 2010 identified 33 frameworks designed for use by enablers need to be addressed?
researchers to guide research dissemination activities.51
However, there is no specific guidance available to choose Action: Systematically identify the barriers and enablers
to change
one framework over another for a specific clinical situa-
tion or for a specific evidence–practice gap.
One suggested approach, developed by the authors of
this chapter, is to use a series of questions in a streamlined Step 3: Which intervention components could overcome the
modifiable barriers and enhance the enablers?
approach moving directly from identified theoretical
domains relevant to the implementation problem to Actions: Select evidence-based behaviour change techniques
behaviour change techniques.44 Figure 25-1 outlines the that address barriers and enablers; combine techniques into a
four steps of this framework. By answering these ques- deliverable intervention; and test the intervention feasibility
tions, researchers, practitioners or policy makers, wishing and acceptability
to develop implementation interventions to overcome
evidence–practice gaps, can utilize a systematic theoreti-
cally informed method to develop implementation Step 4: How will we measure behaviour change?
interventions.
Action: Evaluate the intervention using an appropriate
The approach outlined in Figure 25-1 involves exam- research design
ining a potential evidence–practice gap and, if it is present,
developing a means to overcome this gap. The first step FIGURE 25-1  ■  A conceptual framework designed to guide
is to systematically identify the evidence–practice gap researchers, practitioners and decision-makers to systemati-
itself. This involves determining high-quality evidence, cally develop implementation interventions.44
236 PART II  Advances in Theory and Practice

in the form of a systematic review and/or clinical practice One proposed option to achieve this is to use behavioural
guideline, which suggests a particular health-care prac- theory, or behaviour change theory, to underpin the
tice should or should not be undertaken. Then clinical design of complex interventions aimed at implementing
practice needs to be examined to determine the extent to evidence into clinical practice.46,63–65
which this practice is, or is not, occurring. For example, Theory can explain how different events relate to one
United Kingdom (UK) National Institute of Health and another and may predict how these phenomena will
Clinical Excellence (NICE) guidelines for osteoarthritis relate under different conditions.66 Proponents of the use
made treatment recommendations based on high-quality of theory in the design of implementation interventions
evidence.55 However, a survey of physiotherapists showed argue that theories have the potential to provide under-
that while some of the guideline’s recommendations standing of how societies work, how organizations
including recommending exercise, undertaking patient operate and why people behave in certain ways.67 Behav-
education and encouragement of patient self-management iour change scientists propose that the development of
were generally undertaken by physiotherapists, physio- theoretical models for predicting when health-care pro-
therapists continued to use treatment modalities that the fessionals are likely to respond to different interventions
guidelines did not endorse.56 would provide a framework for effective implementa-
The next step is to systematically identify the barriers tion.64 This premise is built on an understanding that the
and enablers to clinical practice behaviour change. Using uptake of evidence into practice depends on human
this information, evidence-based behaviour change tech- behaviour, and so interventions aiming to change clinical
niques can be selected to address these barriers and practice may be improved by drawing on theories of
enablers. Behaviour change techniques can then be com- human behaviour that have been extensively developed
bined into a deliverable intervention, and this interven- and tested for use in changing the health behaviour of
tion should be tested for feasibility and acceptability. individuals.68,69
Importantly, consideration of system factors is also Explaining and changing a health-care professional’s
required to ensure that there is general system support practice behaviour could be informed by the use of
for any proposed clinician behaviour change. For theory.70 However, to date implementation intervention
example, efforts to change general population and clini- development appears to be largely based on simple,
cian behaviour in response to a mass media campaign mostly unstated, models of human behaviour, or com-
for back pain was much more successful in Australia in monly when it is reported that an intervention has been
comparison to other countries, in part explained by the theory-based, a systematic process has not been fol-
coexistence of supportive legislation and health policy lowed.47 In the Grimshaw and colleagues systematic
that supported that change.57 Finally, the intervention review discussed earlier,41 only 27% of included studies
should be evaluated using an appropriate research used theory and/or psychological constructs, and when
design. theory was reported as used it was often not explained
how the theory explicitly informed the design of the
intervention.45 There is a growing body of evidence dem-
onstrating that interventions based on theory may be
DOES THEORY HAVE A ROLE IN more effective in changing behaviour than those that are
COMPLEX INTERVENTION not.65
DEVELOPMENT? Currently, our understanding of factors that influence
health-care professional clinical practice and optimal
A possible explanation for the disappointing effects dem- approaches to modify their behaviour in line with research
onstrated to date for many complex interventions evidence is incomplete. Research into the uptake of evi-
designed to change health professional behaviour is the dence into practice using a theoretical base to support the
use of inadequate methods for their development,58 and choice and development of interventions is yet to be
a lack of consideration of the ‘whole system’.59 Without widely applied and tested. Consequently, the interpreta-
appropriate rationale to underpin their design, interven- tion of study results of the evaluations of these interven-
tions may not be ideally suited to the context in which tions into health-care practice is limited.46 This has led
they are delivered or to the behaviour they are attempting to calls for more research into implementation interven-
to change, nor designed to overcome the barriers to tions that are based on specific theories of behaviour
change. The lack of an explicit process for development change.47,63,71–73 However, a significant challenge to using
means that previous evaluations of complex interventions theories is choosing an appropriate theory for the context
have provided little information on determining how or in which the change is required.
why they were either effective or ineffective, and there is
little opportunity to determine the potential factors that
may have modified the effects. Without information on
this process it is also difficult for others to be informed HOW BEST SHOULD THEORY BE USED
about the application of the intervention to another IN IMPLEMENTATION RESEARCH?
setting or context. There is growing evidence in the lit-
erature suggesting that the design of complex implemen- Multiple theories and frameworks of individual and orga-
tation interventions requires a more systematic approach nizational behaviour change exist, and often these theo-
with a strong rationale for the chosen design and explicit ries have conceptually overlapping constructs.71,74,75 Only
reporting of the intervention development process.60–62 a few of these theories have been tested in robust research
 25  Implementation Research 237

in health-care settings. There is currently no systematic 4. Davis D, Evans M, Jadad A, et al. The case for knowledge transla-
basis for determining which among the various theories tion: shortening the journey from evidence to effect. BMJ
2003;327(7405):33–5.
available predicts behaviour or behaviour change most 5. Schuster MA, McGlynn EA, Brook RH. How good is the quality
precisely,76 or which is best suited to underpin implemen- of health care in the United States? Milbank Q 1998;76(4):517–63,
tation research.69,71 509. Review.
Using a broadly based theoretical framework for 6. McGlynn EA, Asch SM, Adams J, et al. The quality of health care
delivered to adults in the United States. N Engl J Med 2003;
behaviour change, rather than a single theory, may allow 348(26):2635–45.
a more comprehensive examination of potential barriers 7. Leatherman S, Sutherland K. Quality of care in the NHS of
and enablers, and possible mechanisms linking them to England. BMJ 2004;328(7445):E288–90.
the target clinical behaviour. The Theoretical Domains 8. Schoen C, Davis K, How SK, et  al. U.S. health system performance:
Framework is a broad-based, comprehensive, framework a national scorecard. Health Aff (Millwood) 2006;25(6):w457–75.
9. Seddon ME, Marshall MN, Campbell SM, et al. Systematic review
for designing implementation interventions offering a of studies of quality of clinical care in general practice in the UK,
broad coverage of potential change pathways;77,78 however, Australia and New Zealand. Qual Health Care 2001;10(3):152–8.
other theoretical frameworks, or specific theories, could 10. Steel N, Bachmann M, Maisey S, et al. Self reported receipt of care
be used. consistent with 32 quality indicators: national population survey of
adults aged 50 or more in England. BMJ 2008;337:a957.
It is unlikely that there will be one theory (and one 11. Bodenheimer T. The American health care system – the move­
implementation intervention) that will apply equally well ment for improved quality in health care. N Engl J Med 1999;
to every setting and every intervention.79 The complex 340(6):488–92.
interaction of barriers and facilitators to change may 12. Grol R, Berwick DM, Wensing M. On the trail of quality and safety
influence the success of an intervention designed to in health care. BMJ 2008;336(7635):74–6.
13. Elliot-Gibson V, Bogoch ER, Jamal SA, et al. Practice patterns in
implement evidence into practice. An understanding of the diagnosis and treatment of osteoporosis after a fragility fracture:
these barriers and facilitators is considered an essential a systematic review. Osteoporos Int 2004;15(10):767–78.
step in developing an effective implementation interven- 14. Gandjour A, Telzerow A, Lauterbach KW. European comparison
tion.71 A theory that can attempt to explain these barriers of costs and quality in the treatment of acute back pain. Spine
2005;30(8):969–75.
and facilitators could be used to develop a theory-based 15. Walker BF, French SD, Page MJ, et al. Management of people with
intervention for implementation research. acute low-back pain: a survey of Australian chiropractors. Chiropr
For example, in their study of 45 physiotherapists in Man Therap 2011;19(1):29.
various settings in Sweden, who participated in 11 focus 16. Majumdar SR. Recent trends in osteoporosis treatment after hip
group interviews, Dannapfel and colleagues used Self- fracture: improving but wholly inadequate. J Rheumatol 2008;
35(2):190–2.
Determination Theory to understand physiotherapists’ 17. Buchbinder R, Osborne RH, Ebeling PR, et al. A randomized trial
use of research evidence in practice.24,25 By using a theo- of vertebroplasty for painful osteoporotic vertebral fractures.
retical framework in their qualitative analysis, they were N Engl J Med 2009;361(6):557–68.
able to systematically make recommendations about how 18. Kallmes DF, Jarvik JG, Osborne RH, et al. Clinical utility of verte-
broplasty: elevating the evidence. Radiology 2010;255(3):675–80.
to improve the use of evidence in physiotherapy practice, 19. Mafi JN, McCarthy EP, Davis RB, et al. Worsening trends in the
including the potential to tailor educational programmes management and treatment of back pain. JAMA Internal Medicine
to better account for differences in motivation among 2013;173(17):1573–81.
physiotherapists, using physiotherapists as change agents 20. Bohensky MA, Sundararajan V, Andrianopoulos N, et al. Trends in
and creating favourable conditions to encourage autono- elective knee arthroscopies in a population-based cohort, 2000–
2009. Med J Aust 2012;197(7):399–403.
mous motivation by way of feelings of competence, 21. Heiwe S, Kajermo KN, Tyni-Lenne R, et al. Evidence-based prac-
autonomy and a sense of relatedness. tice: attitudes, knowledge and behaviour among allied health care
professionals. Int J Qual Health Care 2011;23(2):198–209.
22. Nilsagård Y, Lohse G. Evidence-based physiotherapy: a survey of
CONCLUSION knowledge, behaviour, attitudes and prerequisites. Adv Physiother
2010;12(4):179–86.
23. Jette DU, Bacon K, Batty C, et al. Evidence-based practice: beliefs,
Translation of research evidence into practice is complex attitudes, knowledge, and behaviors of physical therapists. Phys
and does not happen automatically. Well-designed imple- Ther 2003;83(9):786–805.
mentation interventions are required to improve clinical 24. Dannapfel P, Peolsson A, Nilsen P. What supports physiotherapists’
use of research in clinical practice? A qualitative study in Sweden.
practice, but currently there is limited research in phys- Implement Sci 2013;8:31.
iotherapy settings to guide the choice of effective inter- 25. Dannapfel P, Peolsson A, Stahl C, et al. Applying self-determination
ventions to improve practice. The design and evaluation theory for improved understanding of physiotherapists’ rationale
of implementation interventions aiming to improve the for using research in clinical practice: a qualitative study in Sweden.
Physiother Theory Pract 2014;30(1):20–8.
uptake of research into physiotherapy practice should be 26. Filbay SR, Hayes K, Holland AE. Physiotherapy for patients fol-
informed by theory and science. lowing coronary artery bypass graft (CABG) surgery: limited
uptake of evidence into practice. Physiother Theory Pract
2012;28(3):178–87.
REFERENCES 27. Li LC, Bombardier C. Physical therapy management of low back
pain: an exploratory survey of therapist approaches. Phys Ther
1. Grimshaw JM, Eccles MP, Lavis JN, et al. Knowledge translation 2001;81(4):1018–28.
of research findings. Implement Sci 2012;7(1):50. 28. Festinger L. A Theory of Cognitive Dissonance. Stanford, CA:
2. Glasziou P, Haynes B. The paths from research to improved health Stanford University Press; 1957.
outcomes. Evid Based Med 2005;10(1):4–7. 29. Eccles M, Mittman B. Welcome to Implementation Science. Imple-
3. Runciman WB, Hunt TD, Hannaford NA, et al. CareTrack: assess- ment Sci 2006;1(1):1.
ing the appropriateness of health care delivery in Australia. Med J 30. Peters DH, Adam T, Alonge O, et al. Implementation research:
Aust 2012;197(2):100–5. what it is and how to do it. BMJ 2013;347:f6753.
238 PART II  Advances in Theory and Practice

31. Rubenstein LV, Pugh J. Strategies for promoting organizational and 55. National Institute for Health and Clinical Excellence (NICE).
practice change by advancing implementation research. J Gen Osteoarthritis: the care and management of osteoarthritis in adults.
Intern Med 2006;21(Suppl. 2):S58–64. NICE Clin Guide 2008;59.
32. Rabin BA, Brownson RC, Haire-Joshu D, et al. A glossary for dis- 56. Walsh NE, Hurley MV. Evidence based guidelines and current
semination and implementation research in health. J Public Health practice for physiotherapy management of knee osteoarthritis.
Manag Pract 2008;14(2):117–23. Musculoskeletal Care 2009;7(1):45–56.
33. Graham ID, Logan J, Harrison MB, et al. Lost in knowledge transla- 57. Gross DP, Deshpande S, Werner EL, et al. Fostering change in
tion: time for a map? J Contin Educ Health Prof 2006;26(1):13–24. back pain beliefs and behaviors: when public education is not
34. Eccles M, Grimshaw J, Campbell M, et al. Research designs for enough. Spine J 2012;12(11):979–88.
studies evaluating the effectiveness of change and improvement 58. van Bokhoven MA, Kok G, van der Weijden T. Designing a quality
strategies. Qual Saf Health Care 2003;12(1):47–52. improvement intervention: a systematic approach. Qual Saf Health
35. Grimshaw J, Campbell M, Eccles M, et al. Experimental and quasi- Care 2003;12(3):215–20.
experimental designs for evaluating guideline implementation 59. Loisel P, Buchbinder R, Hazard R, et al. Prevention of work dis-
strategies. Fam Pract 2000;17(Suppl. 1):S11–16. ability due to musculoskeletal disorders: the challenge of imple-
36. Scott SD, Albrecht L, O’Leary K, et al. Systematic review of menting evidence. J Occup Rehabil 2005;15(4):507–24.
knowledge translation strategies in the allied health professions. 60. Des Jarlais DC, Lyles C, Crepaz N. Improving the reporting
Implement Sci 2012;7:70. quality of nonrandomized evaluations of behavioral and public
37. NHS. Getting evidence into practice. Eff Health Care 1999;5(1). health interventions: the TREND statement. Am J Public Health
38. Oxman AD, Thomson MA, Davis DA, et al. No magic bullets: a 2004;94(3):361–6.
systematic review of 102 trials of interventions to improve profes- 61. Baker EA, Brennan Ramirez LK, Claus JM, et al. Translating and
sional practice. CMAJ 1995;153(10):1423–31. disseminating research- and practice-based criteria to support
39. Bero LA, Grilli R, Grimshaw JM, et al. Closing the gap between evidence-based intervention planning. J Public Health Manag Pract
research and practice: an overview of systematic reviews of inter- 2008;14(2):124–30.
ventions to promote the implementation of research findings. The 62. Boutron I, Moher D, Altman DG, et al. Extending the CONSORT
Cochrane Effective Practice and Organization of Care Review statement to randomized trials of nonpharmacologic treatment:
Group. BMJ 1998;317(7156):465–8. explanation and elaboration. Ann Intern Med 2008;148(4):
40. Davis DA, Taylor-Vaisey A. Translating guidelines into practice. A 295–309.
systematic review of theoretic concepts, practical experience and 63. ICEBeRG (The Improved Clinical Effectiveness through Behav-
research evidence in the adoption of clinical practice guidelines. ioural Research Group). Designing theoretically-informed imple-
CMAJ 1997;157(4):408–16. mentation interventions. Implement Sci 2006;1:4.
41. Grimshaw JM, Thomas RE, MacLennan G, et al. Effectiveness and 64. Sanson-Fisher RW, Grimshaw JM, Eccles MP. The science of
efficiency of guideline dissemination and implementation strate- changing providers’ behaviour: the missing link in evidence-based
gies. Health Technol Assess 2004;8(6):iii–iv, 1–72. practice. Med J Aust 2004;180(5):205–6.
42. Grimshaw J, Shepperd S, Pantoja T, et al. Cochrane Effective Prac- 65. Marteau T, Dieppe P, Foy R, et al. Behavioural medicine: changing
tice and Organisation of Care Group. About The Cochrane Col- our behaviour. BMJ 2006;332(7539):437–8.
laboration (Cochrane Review Groups (CRGs) 2013(4) Art. No.: 66. Bem S, Looren de Jong H. Theoretical Issues in Psychology: An
EPOC. Introduction. 2nd ed. London; Thousand Oaks, California: Sage;
43. Cochrane Effective Practice and Organisation of Care Group 2006.
(EPOC). Data collection checklist, section 2. 2007. Available from: 67. Reeves S, Albert M, Kuper A, et al. Why use theories in qualitative
<http://www.epoc.cochrane.org/>; [Accessed 13 January, 2015.]. research? BMJ 2008;337:a949.
44. French SD, Green SE, O’Connor DA, et al. Developing theory- 68. Armitage CJ, Conner M. Social cognition models and health behav-
informed behaviour change interventions to implement evidence iour: a structured review. Psychol Health 2000;15(2):173–89.
into practice: a systematic approach using the Theoretical Domains 69. Lippke S, Ziegelmann JP. Theory-based health behavior change:
Framework. Implement Sci 2012;7(1):38. developing, testing, and applying theories for evidence-based inter-
45. Davies P, Walker AE, Grimshaw JM. A systematic review of the use ventions. Appl Psychol 2008;57(4):698–716.
of theory in the design of guideline dissemination and implementa- 70. Sales A, Smith J, Curran G, et al. Models, strategies, and tools.
tion strategies and interpretation of the results of rigorous evalua- Theory in implementing evidence-based findings into health care
tions. Implement Sci 2010;5:14. practice. J Gen Intern Med 2006;21(Suppl. 2):S43–9.
46. Eccles M, Grimshaw J, Walker A, et al. Changing the behavior of 71. Grol RP, Bosch MC, Hulscher ME, et al. Planning and studying
healthcare professionals: the use of theory in promoting the uptake improvement in patient care: the use of theoretical perspectives.
of research findings. J Clin Epidemiol 2005;58(2):107–12. Milbank Q 2007;85(1):93–138.
47. Michie S. Designing and implementing behaviour change interven- 72. Greenhalgh T, Robert G, Macfarlane F, et al. Diffusion of innova-
tions to improve population health. J Health Serv Res Policy tions in service organizations: systematic review and recommenda-
2008;13(Suppl. 3):64–9. tions. Milbank Q 2004;82(4):581–629.
48. Craig P, Dieppe P, Macintyre S, et al. Developing and evaluating 73. Thompson DS, Estabrooks CA, Scott-Findlay S, et al. Interven-
complex interventions: the new Medical Research Council guid- tions aimed at increasing research use in nursing: a systematic
ance. BMJ 2008;337:a1655. review. Implement Sci 2007;2:15.
49. Campbell M, Fitzpatrick R, Haines A, et al. Framework for design 74. Ferlie EB, Shortell SM. Improving the quality of health care in the
and evaluation of complex interventions to improve health. BMJ United Kingdom and the United States: a framework for change.
2000;321(7262):694–6. Milbank Q 2001;79(2):281–315.
50. Bartholomew LK, Parcel GS, Kok G. Intervention mapping: a 75. Ashford A. Behavioural Change in Professional Practice: Support-
process for developing theory- and evidence-based health educa- ing the Development of Effective Implementation Strategies
tion programs. Health Educ Behav 1998;25(5):545–63. Report No 88. Newcastle upon Tyne: Centre for Health Services
51. Wilson PM, Petticrew M, Calnan MW, et al. Disseminating Research; 1998.
research findings: what should researchers do? A systematic scoping 76. Noar SM, Zimmerman RS. Health Behavior Theory and cumula-
review of conceptual frameworks. Implement Sci 2010;5:91. tive knowledge regarding health behaviors: are we moving in the
52. Estabrooks CA, Thompson DS, Lovely JJ, et al. A guide to knowl- right direction? Health Educ Res 2005;20(3):275–90.
edge translation theory. J Contin Educ Health Prof 2006; 77. Michie S, Johnston M, Abraham C, et al. Making psychological
26(1):25–36. theory useful for implementing evidence based practice: a consen-
53. Damschroder LJ, Aron DC, Keith RE, et al. Fostering implemen- sus approach. Qual Saf Health Care 2005;14(1):26–33.
tation of health services research findings into practice: a consoli- 78. Cane J, O’Connor D, Michie S. Validation of the theoretical
dated framework for advancing implementation science. Implement domains framework for use in behaviour change and implementa-
Sci 2009;4:50. tion research. Implement Sci 2012;7(1):37.
54. Zidarov D, Thomas A, Poissant L. Knowledge translation in physi- 79. Grimshaw J, Eccles M, Tetroe J. Implementing clinical guidelines:
cal therapy: from theory to practice. Disabil Rehabil 2013;35(18): current evidence and future implications. J Contin Educ Health
1571–7. Prof 2004;24(Suppl. 1):S31–7.
 PA RT I I I

ADVANCES IN
CLINICAL SCIENCE
AND PRACTICE

239
This page intentionally left blank
 SECTION 3 . 1

PRINCIPLES OF MANAGEMENT

One of the key characteristics of modern musculoskeletal for the patient. Pain is a multifaceted entity from biologi-
physiotherapy is the use of multimodal approaches to the cal and individual perspectives and to reflect this, the pain
management of musculoskeletal disorders reflecting their experience, physical interventions for pain management
biopsychosocial dimensions. This section on principles of and educational approaches are overviewed. In addition,
management presents some of the main features and a further chapter considers cognitive and behavioural
systems to be considered in modern musculoskeletal influences on physiotherapy practice with strategies
physiotherapy management. which clinicians may use to help their patients in their
Approaches to assessment and management of muscu- daily practice.
loskeletal disorders have become more complex and mul- The advances in knowledge of the very familiar areas
tifaceted over the years. In the first instance, the way for the musculoskeletal physiotherapist, namely in the
clinicians may make decisions in terms of approach to articular, neuromuscular and nervous systems are fea-
assessment and choice of management methods can be tured. Chapters have been dedicated to the areas of
based on a range of models (e.g. clinical reasoning, sub- manipulative therapy management, the management of
grouping, clinical prediction rules, clinical guidelines and the nervous system, the very large area of therapeutic
evidence-based practice). A chapter discussing these exercise where re-education of motor control, strength
models for management prescription has been included and endurance are considered as well as management of
to contextualize these approaches to assist the clinician the sensorimotor system in terms of proprioception and
appraise them in respect of their own clinical practice. postural control. A chapter also considers adjuvant pain
Good communication is fundamental for every suc- management strategies that are used by physiotherapists
cessful therapeutic relationship. Thus it was considered (electrophysical agents, acupuncture/dry needling,
important to reflect on several aspects of communication taping), realizing the importance to have as much damp-
including the use of language, the communication of risk ening of pain as possible to facilitate rehabilitative
and approaches to patient education to highlight the exercises.
importance of the awareness of communication styles and In summary, this section focuses on the fundamental
approaches in providing patient-focused care. principles involved in musculoskeletal physiotherapy and
There are many features for the clinician to consider their rationales to inform delivery of quality care for
when assessing and treating individuals with musculo­ patients.
skeletal disorders. Pain management is usually a priority

241
 CHAPTER 26 

Clinical Reasoning and Models for

Clinical Management
Peter Kent  •  Jan Hartvigsen

Clinical reasoning is the foundation for rational patient need to adjust to a changing body of knowledge that
care in musculoskeletal and other health conditions. It responds to the publication of new research findings.
includes the ability to think critically, to weigh different This has proven to be difficult because the education of
types of knowledge and evidence, and to reflect upon how musculoskeletal clinicians such as physiotherapists, chi-
a clinical conclusion has been reached, for example, about ropractors and osteopaths has traditionally been grounded
diagnosis and treatment.1 In this chapter we discuss dif- in profession-specific traditions and belief systems,
ferent clinical reasoning models used in musculoskeletal and not in dynamic, evidence-based, clinical problem
health care, including the roles of clinical guidelines, solving.9,10 Consequently, modern musculoskeletal clini-
clinical prediction rules, stepped care, adaptive care, clin- cians, in addition to their clinical skills, ideally are capable
ically important subgroups and stratified care. of appraising different types of scientific studies.
Observational studies inform us about the incidence,
prevalence, course, prognosis and risk of health condi-
EVIDENCE-BASED CLINICAL tions, while intervention studies inform us about the
REASONING effect of treatments or other interventions. The synthesis
of evidence in systematic reviews and meta-analyses sum-
Whether you are managing patients with similar clinical marizes results of multiple comparable studies within a
presentations in roughly the same way according to a field of interest (Fig. 26-1). Because more tightly designed
predefined system, or whether you are more adaptive in studies provide more trustworthy results, they carry
customizing management strategies for patients based on greater scientific weight. Therefore knowledge and skills
their individual needs and presentation, you are using a in the appraisal of scientific literature enable clinicians to
clinical reasoning model. While models can vary greatly make rational and evidence-based decisions about diag-
in their flexibility and content, the interpretive matrix nostic procedures, therapeutic efficacy, prognosis and
that clinicians apply to each and every patient encounter clinical impact.11–15 However, in musculoskeletal care, as
is by definition a clinical reasoning model – whether they many areas of clinical interventions and management are
are conscious of it or not. under-researched, clinical reasoning is mostly informed
Currently, evidence-based practice is the dominant by evidence that is patchy and imperfect.
clinical reasoning model. This is in contrast to models
focused on traditions or beliefs, such as opinion-based
models promoted by people teaching particular treat- BOX 26-1  Key Points
ment techniques, location-based models based on local
traditions, or authority-based models that are based on • Clinical reasoning is inherent in solving clinical prob-
opinions of respected and experienced clinicians.2–5 This lems, making a diagnosis or prognosis and formulating a
fundamental shift in clinical decision-making is primarily clinical management plan
the result of the explosion in research activity over the • Evidence-based practice involves clinical reasoning that
includes best-available scientific evidence, clinician expe-
last 30 years, but also the growing demand for clinical
rience and patient preference
accountability from funders and the medico-legal system, • Scientific evidence in musculoskeletal care is greater than
and more recently, a recognition of the importance of ever before, but still quite incomplete
patients in shared decision-making.6–8 So, in addition to • Good clinical reasoning models allow for new knowledge
traditions and clinician judgement, contemporary clinical to change clinical practice
reasoning also embraces the contribution of evidence and
patient input.3
In an evidence-based health-care environment, clini-
cians need to be able to read, appraise and apply scientific SOURCES OF EVIDENCE
evidence to prognosis, diagnosis and the treatment of
individual patients. This is because evidence-based clini- Information on recent evidence is available from a range
cal reasoning and life-long learning practices have become of sources including electronic databases such as PubMed
core competences required for clinicians to be able to (www.ncbi.nlm.nih.gov/pubmed) – the world’s largest
adapt to changing standards of good clinical practice. In free search engine of published peer-reviewed literature –
musculoskeletal care, this poses particular challenges, as and Trip Database (www.tripdatabase.com) – a broader
the evidence base is incomplete. Therefore, clinicians database indexing and providing links to peer-reviewed
242
 26  Clinical Reasoning and Models for Clinical Management 243

Observational studies Intervention studies

Meta- Meta-
analyses/ analyses/ Synthesis of evidence
systematic systematic
reviews reviews
ht
eig

Cohort Randomized
w
ific

clinical trials
ent
sci

Case control Controlled clinical trials Designed studies

ing
eas
r
Inc

Cross-sectional Pre-post design studies

Case series Case series

Clinical observations
Case reports Case reports

FIGURE 26-1  ■  Hierarchy of evidence for observational/epidemiological studies and intervention studies. Designed studies and syn-
theses of the evidence carry increasing scientific weight and are therefore shown higher up in the pyramids.

scientific papers plus clinical guidelines, reports, patient

information material and opinion statements. These and TABLE 26-1  Sources of Evidence to Inform
other resources can be used to inform best practice based Clinical Reasoning
on scientific evidence (e.g. clinical guidelines, systematic Source Definitions
reviews, clinical trials, prediction rules, case series, case
studies). In contrast, other sources are more experiential, Original (primary) Individual diagnostic, therapeutic,
research prognostic or clinical impact
such as, using a patient’s response to clinical tests and studies that provide varying
initial response to treatment to guide subsequent treat- levels of evidence (clinical trials,
ment decisions, and drawing on clinicians’ previous cohort studies, case series, case
experience. studies)
Different types of research findings provide different Clinical prediction Clinically useful rules for the
types of evidence and have different uses in clinical rules selection of diagnostic
procedures, clinical assessment
decision-making (Table 26-1 and Fig. 26-1). Summaries techniques and treatment, or for
of evidence from multiple studies are communicated in estimating prognosis
systematic reviews and meta-analyses. Clinical guidelines Systematic Syntheses of original research on a
are based on systematic reviews of the literature but reviews/ single topic, that are designed to
usually also take into account local circumstances regard- meta-analyses give the most precise estimate of
(a) how good a diagnostic
ing feasibility, side effects and costs. Systematic reviews procedure is; (b) how effective a
and meta-analyses generally convey greater certainty specific treatment is; or (c) how
than individual studies, but clinicians still need to assess prognostic a clinical feature is
the generalizability of these findings to their particular Clinical guidelines Overviews that aim to synthesize
clinical setting and the demographic characteristics of best-available evidence into
their patients. clinically interpretable principles
and procedures

INDUCTIVE AND DEDUCTIVE

CLINICAL REASONING
exercises, he/she is using deductive reasoning – from the
When using inductive reasoning, we develop generaliza- general to the specific. Deductive reasoning is inherent
tions from specific observations, whereas in deductive in almost all physiotherapy management of musculoskel-
reasoning, we develop specific hypotheses from general etal conditions, because working from general principles
principles.16,17 Clinical reasoning includes both inductive to concrete decisions about specific patients is at the core
reasoning and deductive reasoning, with deductive rea- of clinical practice.
soning being the mainstay of patient management. For Some deductive-based clinical reasoning models allow
example, a clinician who remembers evidence that some for repeated recalibration of the management plan based
patients with lumbar disc lesions respond well to direc- on monitoring a patient’s response to treatment. Exam-
tional preference-based exercises and then decides that ples of these are stepped care models and adaptive care
the best treatment for a specific patient would be such models.
244 PART III  Advances in Clinical Science and Practice

Stepped Care and Adaptive Care injury and also in the clinic. This prediction rule was
designed and validated for use in hospital emergency
Stepped care is where the intensity, complexity and departments. In an initial validation study of 1096 adults
costs of care are ‘stepped up’ based on the complexity in two hospitals, the rule had a sensitivity of 1.0 (95% CI
of a patient’s presentation or response to initial care.18–20 0.94 to 1.0) for identifying clinically important fractures,
The principle is to commence care with ‘first-line’ and the probability of fracture, when the decision rule
low-intensity, low-cost diagnosis and treatment and was negative, was 0% (95% CI, 0% to 0.4%).24 This rule
only progress to more intense, complex and costly is designed to be extremely sensitive – to not miss any
management strategies in those patients who do not clinically important fractures – and yet in this study the
improve adequately or present with obvious reasons rule would have reduced the rate of unnecessary X-ray
for more costly and intense diagnostic procedures and/ referrals by 28%. Replication in external validation
or therapy. Therefore, individualized stepped care is studies is a very important step in the development of
a time-dependent strategy that Tiemens and Von Korff21 clinical prediction rules, and near-identical results for the
describe as being based on three assumptions: (a) dif- Ottowa Knee Rule were obtained in a subsequent study
ferent levels of care are required for different people; of 3907 patients in four hospitals.25 Also important in the
(b) a monitoring of outcomes is often required to assessment of clinical prediction rules are impact analysis
determine the right level of care for individual patients; studies26 that examine whether such rules work in non-
and (c) health system effectiveness and cost efficiency experimental conditions in routine clinical care settings
can be improved by progressing patients from lower (prediction rule practicality and acceptance).
to higher levels of care based on their outcomes. In An example of a clinical prediction rule for treatment
principle, stepped care may apply both within the range selection in patients with acute non-specific low back
of management/treatment options that an individual pain is Flynn’s Manipulation Prediction Rule.27 Initial
clinician can self-administer, and also to the range of results indicated that patients who were positive on this
options available for co-management of patients with prediction rule were more likely to benefit from spinal
musculoskeletal conditions. For example, a patient with manipulation and range of movement exercises than from
recurrent patellar dislocation might initially be com- a low-stress aerobic and lumbar spine strengthening
menced on a progressive exercise and taping programme. programme.28 Patients were ‘rule positive’ if they met
However, a monitoring of their adherence, treatment any four out of these five criteria: symptom duration of
response and outcomes may subsequently indicate that less than 16 days; no symptoms distal to the knee; score
use of a patellar brace, modification of functional/sports less than 19 on a fear-avoidance measure; at least one
activities and referral for an opinion from a sports hypomobile lumbar segment; and at least one hip with
medicine physician or orthopaedic surgeon would be more than 35° of internal rotation. Overall at 1-week
useful next steps. In the management of musculoskeletal follow-up in this clinical trial, 44% of participants
conditions, care is often progressed on the basis of improved with the manipulation (defined as a 50% or
patient response to treatment rather than diagnosis more improvement in their baseline activity limitation
alone. scores). However, 92% who were rule positive improved
Adaptive care is a closely related strategy for individu- with the manipulation (positive likelihood ratio = 13.2)
alizing patient care that uses decision rules to guide versus only 7% who were rule negative (negative likeli-
whether, how and when to alter clinical management.22 hood ratio = 0.1). These results are promising, as this
The main distinction between stepped care and adaptive simple prediction rule appears to identify subgroups of
care is that the latter uses more formalized clinical guide- people for whom manipulation is, or is not, effective.
lines to specify the way in which care should be tailored However, similar to the Ottawa Knee Rule, there is a
for individual patients. Adaptive care strategies are also need for independent external validation studies that test
called adaptive interventions and dynamic treatment this rule using the same treatments and determine
regimens.23 whether it is generalizable to, and feasible for use in,
other clinical settings.
Classifying patients in diagnosis or treatment can go
CLINICAL PREDICTION RULES beyond simple clinical prediction rules and may involve
more complex classification systems. An example is
Clinical prediction rules are often simple, memorable Classification-Based Cognitive Functional Therapy for
rules for selecting clinical assessment techniques or people with chronic non-specific low back pain.29 This
treatment. targeted treatment approach contains a comprehensive
An example of a prediction rule for the selection of a decision-making algorithm that classifies patients based
clinical assessment technique is the Ottowa Knee Rule, on the assessment of multiple health domains (physical
which is a rule designed to help clinicians determine impairment, pain, activity limitation, functional loss,
whether an X-ray is required in patients who have an psychological adaptation). A recent randomized con-
acute knee injury.24 This prediction rule states that an trolled trial showed clinically important improvements
X-ray is required only in patients who have one or more in outcomes for people with chronic non-specific low
of the following: age 55 years or older, tenderness at the back pain treated with this approach when compared
head of the fibula, isolated tenderness of the patella, an with current best practice manual therapy and exercise.30
inability to flex to 90°, or an inability to bear weight Over the 12-month follow-up period, the group of
(unable to take four steps) both immediately after the patients treated with this approach had more than twice
 26  Clinical Reasoning and Models for Clinical Management 245

the improvement in pain and activity limitation than these technologies, clinicians are provided with value-
those receiving the control treatment. This is also an adding information that they can choose whether to
example of a physiotherapy management approach for include in their clinical reasoning. This information is
which components have been systematically validated,31 not intended to replace the role of individual clinicians
including its reproducibility,32,33 prior to its clinical effi- taking responsibility for clinical decision-making about
cacy being examined in a clinical trial. individual patients because only the clinician sees the
patient in his or her entirety and there is always a need
for clinical decisions to be adaptive and responsive to
TECHNOLOGY AND PAPER-BASED individual circumstances. One example of a computer
AIDES FOR CLINICAL REASONING algorithm designed to inform musculoskeletal clinical
reasoning is an electronic nomogram that classifies the
Technology-based assistance for clinical reasoning gait characteristics of children with spastic diplegia which
involves the use of phone/tablet applications and com- can also be used for monitoring their gait outcomes.34
puter algorithms embedded in electronic patient record Using three simple clinical measures as inputs – leg
systems and clinical care databases (Table 26-2). Using length in metres, stride length in metres and cadence in
steps per minute – the computer algorithm characterizes
and compares the child’s neuromuscular function and
classifies it into one of five characteristic patterns. The
TABLE 26-2  Features of Technology-Assisted principle is that changes in cluster membership provide
and Paper-Based Aids for Clinical an objective measure of improvement in the child’s neu-
Reasoning romuscular function, using measures obtained with only
simple clinical equipment: a stopwatch, tape measure,
Definitions Strengths/Weaknesses and talcum powder.
Technology Assisted – Computer-Based Another example of web-based computer algorithms
Questionnaires or Algorithms designed to inform clinical reasoning is the Focus On
Phone/tablet Strengths: Therapeutic Outcomes system (FOTO Inc. Knoxville,
applications, or • Automated scoring TN, USA). On the basis of standardized, validated base-
functions • May be more sensitive and
embedded in patient-specific than
line questions that are answered by the patient, the
electronic patient paper-based systems, as system calculates, for a range of musculoskeletal condi-
records/clinical they can be compared with tions, the patient’s baseline functional status and pre-
information large normative datasets dicted functional status taking into account such factors
systems • May provide novel or more as age, episode duration, severity and co-morbidities,
precise information, or may
automatically synthesize based on a large normative dataset. The clinician can
information from disparate then (a) base clinical decisions on the predicted change
sources in functional status, predicted outcome, and predicted
• Easy storage and retrieval of number of patient visits to achieve that outcome, which
information
• May include skip logic to
are based on the collective performance of other phys-
reduce questionnaire length iotherapists; and (b) measure and document actual func-
• Can include multiple tional status at the time of discharge from care. This
languages allows for benchmarking of performance against a risk-
Weaknesses: adjusted average for similar patients, by effectiveness
• Require technology literacy
• Need to be integrated into (functional outcome), by efficiency (number of visits) and
the clinical encounter in by patient satisfaction.
ways that do not excessively An example of a paper-based questionnaire or algo-
interrupt the workflow and rithm is the STarT Back Tool.35 The STarT Back Tool is
clinician/patient engagement
• Require ongoing expert IT
a simple nine-item questionnaire that classifies patients
support with non-specific low back pain into one of three care
streams. This classification is based on an estimate of
Paper-Based Questionnaires or Algorithms each patient’s risk of a poor outcome (low risk; medium
Printed questionnaires Strengths: risk; high risk) plus an estimate of the complexity of his
or printed scoring • Easy to complete
algorithms, such as • Do not require technology or her presentation, that results in an estimate of the
nomograms* literacy complexity of intervention that is likely to be required
Weaknesses: (minimal intervention/reassurance; manual therapy and
• Require manual scoring and exercise; manual therapy, exercise and psychologically
therefore the scoring informed physiotherapy). In a recent clinical trial, STarT
method needs to be simple
and time-efficient Back Tool classification-based treatment showed modest
• Harder to store information improvements in patient outcomes and overall treatment
• May provide less costs (primarily by reducing unnecessary treatments for
sophisticated information low-risk patients), compared with usual GP/physiotherapy
*A nomogram is a visual method for predicting a patient’s score
care.36 Noteworthy in this approach is that clinicians
on an unobserved or unmeasured clinical feature, when their retain considerable flexibility in their choice of treatment
score on related clinical features is known. for the medium-risk and high-risk subgroups.
246 PART III  Advances in Clinical Science and Practice

of poor outcome). However, within a care pathway, such

STRATIFIED HEALTH CARE AND as for the high-risk group, targeted treatment decisions
TREATMENT EFFECT MODIFICATION can be informed by knowledge of treatment effect modi-
fication, that is, identifying which high-risk patients are
Stratified health care is similar to stepped care and adap- likely to respond to a particular available treatment and
tive care models in that they all seek to match the right which patients are better suited to different treatment
treatment to the right patient at the right time. Some- methods. In addition, response to treatment in a given
times these concepts co-exist or overlap in the same stratified care pathway may determine subsequent steps
setting. However, stratified health care in its pure form that merge the stratified and stepped care approaches.
is designed for decision making about care pathways Another concept with similar wording to treatment
during the initial clinical encounter, rather than relying effect modification is treatment effect mediation and,
on a time-dependent response to treatment. although these concepts are often confused, they are
Stratified care targets treatment to patient subgroups quite different (Table 26-3). While treatment effect mod-
based on characteristic patient profiles, such as their ification aims at matching the individual patient to the
prognostic risk, the suspected underlying causal mecha- best treatment, treatment effect mediation is a method
nisms of their health condition or their likely response to for testing theories about causal links between a treat-
a particular treatment.37 The idea of stratified health care ment and an outcome45 and so it seeks to understand how
is popular because it is seen as a method: (a) to tailor and why – and not if – a treatment works or does not
treatment to specific, sometimes biologically or psycho- work. A hypothetical mediational analysis might test
logically distinct, individuals; (b) to maximize treatment whether the effect of a treatment (such as stabilization
response, reduce harm or both, and; (c) to rescue treat- exercises for people with whiplash) on an outcome (such
ment that fails to show an overall effect by identifying as activity limitation) occurs via a change in some modifi-
subgroup(s) for whom it is effective.38 able intermediate variable (such as reduced fear of move-
Stratified care is closely related to the concept of treat- ment). If this were the case, then the effect of the
ment effect modification, which confusingly is also some- treatment might be increased by also deliberately treating
times called treatment effect moderation and treatment the intermediate variable. In musculoskeletal research,
effect subgrouping. Research into treatment effect modi- mediation analysis is becoming more common as it has
fication seeks to identify patients with distinct clinical the capacity to inform the design and delivery of more
profiles (phenotypes) who respond best to particular effective interventions.46 Again, the goal is that in the
treatment.37 It is based on the concept that not all patients medium term, robust evidence of effect mediation will
respond to the same extent to a given treatment and the become available to assist musculoskeletal clinicians in
recognition that research methods exist to identify such optimizing treatment effects.
patient phenotypes. This is also seen as a means to
perform research that more closely mimics current clini-
cal practice and the hope that research targeting clinically
important subgroups will result in the demonstration of
THE CHALLENGE OF MAKING CLINICAL
larger treatment effects. REASONING MODELS RELEVANT TO
Treatment effect modification research is more techni- THE CARE OF INDIVIDUAL PATIENTS
cally and procedurally demanding than traditional two-
group clinical trials,39 and although the appropriate The clinical reasoning models that we have discussed
methods vary depending on the specific research question above attempt to integrate or provide best-available evi-
being asked,40 these methods are now well defined.39,41–44 dence to clinicians in forms that are accessible, under-
Given the current research interest in treatment effect standable and useful in reducing uncertainty at the time
modification, the goal is that in the medium term, robust of the clinical encounter. One of the challenges in provid-
evidence of treatment effect modification will become ing this evidence is to extend findings from the group or
available that assists musculoskeletal clinicians in their subgroup level and make them as accurate as possible at
clinical reasoning. the individual patient level. One way in which researchers
Clinical reasoning models can include both stratified are working on this challenge is by exploring the use of
care and treatment effect modification.37 For example, a Bayesian statistical methods to create clinical reasoning
stratified care model, such as the STarT Back Tool, may tools.47 Bayesian methods have a number of advantages
identify preferred care pathways for patients based on that hold the promise of their being more adaptive and
their prognostic profile (low risk, medium risk, high risk patient-specific than previous methods.48,49 For example,

TABLE 26-3  Treatment Effect Modification and Effect Mediation – How Are They Different?
Treatment effect The identification of symptoms or This information is often the basis for a clinical
modification signs that indicate a patient’s likely prediction rule
response to a specific treatment
Treatment effect A method to identify factors that are This information helps with understanding the
mediation causally linked to treatment response mechanisms by which a treatment is effective, how
it could be more effective, or why it is ineffective
 26  Clinical Reasoning and Models for Clinical Management 247

they are able to incorporate and respond to clinical infor- such as disability, beyond the factors operating at the
mation that may only emerge during an episode of care level of individuals.52,57–60
(such as initial response to treatment and the results of One example of a physiotherapy clinical reasoning
subsequent tests), and are therefore better able to model method that follows the biomedical model is the Mechan-
the dynamic temporal nature of a clinical trajectory. They ical Diagnosis and Therapy approach to the management
are also able to model the causal relationships underlying of spinal pain.61 This popular assessment approach62 clas-
that trajectory. As they are based on probability, Bayesian sifies patients into treatment subgroups using validated
models typically result in outputs that clinicians find diagnostic procedures.63,64 Although this approach classi-
intuitive to understand, such as ‘this patient has a 73% fies patients on the basis of their physical impairment and
probability of improving by a clinically important amount pain characteristics rather than patho-anatomical diagno-
by 6 weeks if he or she receives this treatment regimen’. sis, it nonetheless is based on the biomedical model to
the extent that it does not incorporate psychological and
social factors. A more recent physiotherapy clinical rea-
BOX 26-2  Key Points soning model – Classification-Based Cognitive Func-
• Deductive reasoning is the mainstay of patient manage- tional Therapy – does incorporate psychosocial factors
ment because working from general principles to con- because in addition to considering physical impairment
crete decisions about specific patients is at the core of and pain, this classification system clusters patients into
clinical practice subgroups based on cognitive constructs (negative back
• Deductive-based clinical reasoning models, such as pain beliefs, fear, hypervigilance, anxiety, low mood), life-
stepped care and adaptive care models, incorporate the style behaviours (activity avoidance, poor pacing) and
repeated monitoring of a patient’s response to treatment maladaptive movement (loss of movement awareness,
as a means to regularly calibrate the management plan protective and avoidance behaviours).29,65
• Other models of clinical reasoning are based on identify- Despite emerging evidence that embracing the bio-
ing clinically important subgroups of patients by way of
psychosocial model may be more effective,30,36 and the
clusters of their symptoms and signs. Some of these
models involve clinical prediction rules and classification intuitive appeal of managing the ‘whole person’ in mus-
systems, and are based on technology assistance or paper- culoskeletal patient care, there is evidence that many cli-
based questionnaires and algorithms nicians, including physiotherapists, frequently do not
• Stratified health care and the concept of treatment effect assess the psychosocial aspects of their patients66 and are
modification are based on a recognition that not all often uncomfortable addressing these aspects.67,68 Many
patients respond to the same extent to a given treatment do not feel they possess adequate skills or training to deal
effectively with psychosocial obstacles to recovery.67,69
Perhaps this is because clinical education and culture
THE BIOPSYCHOSOCIAL MODEL – WHY have historically been too biomedically focused70 and
have largely failed to adopt the biopsychosocial model.52
DEALING WITH THE PHYSICAL IS In response to this, a more psychologically informed
OFTEN NOT ENOUGH practice71 has recently been promoted and the model of
the psychologically informed physiotherapist72 has been
Currently, the dominant conceptual framework in mus- implemented in some settings, such as in the training of
culoskeletal disorders is the biopsychosocial model put physiotherapists to manage high-risk patients under the
forward by, among others, Gordon Waddell in the mid- STarT Back Tool model. This can be seen as a ‘middle
1980s.50,51 This model suggests that taking a purely bio- way’ between traditional biomedically focused physio-
medical perspective may limit one’s understanding of therapy and cognitive-behavioural therapy71 because
musculoskeletal disorders. This is because for many indi- this training equips physiotherapists with skills to recog-
viduals the fundamental problem is not their experience nize and influence modifiable psychological risk factors
of pain, which can often be temporary, but rather their for the development of unnecessary pain-associated
own and society’s views and responses to their pain.52 Yet disability.
the concept of a ‘diagnosable disease’ is still central to
most clinical reasoning in musculoskeletal health care, as
diagnosis and staging of the condition identify the BOX 26-3  Key Points
involved abnormal body function plus its pathological
cause, and, at least theoretically, indicate appropriate • Much current management of musculoskeletal disorders
treatment and prognosis. However, there is now good is centred around a biological or biomedical paradigm
evidence showing that in musculoskeletal health, psycho- • The biopsychosocial model encourages clinicians to
logical factors (such as fear-avoidance beliefs, anxiety, include in their clinical reasoning their patient’s psycho-
depression, poor coping strategies, poor self-efficacy and logical and social barriers to recovery
pre-existing somatization) are important predictors of • In musculoskeletal care, some of these psychosocial bar-
poor outcomes, and play significant roles in the transition riers are believed to be modifiable
• Many clinicians currently do not assess these aspects and
from acute to persistent pain and disability.53–56 In fact, feel inadequately trained or uncomfortable to address
often these are more strongly associated with outcome them
than biomedical factors. Similarly, social factors (social • Recent developments in clinical education have led to the
arrangements, health and disability structures and local model of the psychologically informed physiotherapist
cultural beliefs) have been shown to influence outcomes,
248 PART III  Advances in Clinical Science and Practice

7. Edwards A, Elwyn G. Shared Decision Making in Health Care:

FUTURE DIRECTIONS FOR CLINICAL Achieving Evidence-Based Patient Choice. Shared Decision
Making in Health Care. 2nd ed. Oxford UK: Oxford University
REASONING AND MANAGEMENT Press; 2009.
8. Informed Medical Decisions Foundation. 2013. From: <http://
The volume of clinical and epidemiological research in www.informedmedicaldecisions.org>; [retrieved 31 December
musculoskeletal health is increasing and it is changing the 2013].
9. Parsons S, Harding G, Breen A, et al. Will shared decision making
face of musculoskeletal health care and the role of phys- between patients with chronic musculoskeletal pain and physio-
iotherapists and other health-care providers. The prin- therapists, osteopaths and chiropractors improve patient care? Fam
ciples behind clinical reasoning will remain, but clinicians Pract 2012;29(2):203–12.
will face new evidence that will challenge their beliefs and 10. Foster NE, Hartvigsen J, Croft PR. Taking responsibility for the
routines and require the development of new practice early assessment and treatment of patients with musculoskeletal
pain: a review and critical analysis. Arthritis Res Ther 2012;14(1):205.
patterns. For example, clinicians are likely to be expected 11. Guyatt GH, Oxman AD, Kunz R, et al. Rating quality of evidence
to systematically screen patients for risk of chronicity and strength of recommendations: going from evidence to recom-
using psychological and social instruments, in addition to mendations. BMJ 2008;336(7652):1049–51.
the physical clinical examination, in order to make 12. Guyatt GH, Oxman AD, Kunz R, et al. Rating quality of evidence
and strength of recommendations: incorporating considerations
evidence-based, biopsychosocially informed, decisions of resources use into grading recommendations. BMJ 2008;
about prognosis and therapy. Stepped diagnosis and care 336(7654):1170–3.
that reserves expensive testing and therapy for patients 13. Guyatt GH, Oxman AD, Vist G, et al. Rating quality of evidence
with clear indications and evidence of benefit, and care and strength of recommendations GRADE: an emerging consensus
stratified according to predefined criteria will gradually on rating quality of evidence and strength of recommendations.
BMJ 2008;336:924–6.
be implemented with the emergence of new evidence and 14. Schünemann HJ, Oxman AD, Brozek J, et al. Grading quality of
the desire for more cost-effective health care. Wearable, evidence and strength of recommendations for diagnostic tests and
discrete and affordable devices to monitor activity and strategies. BMJ 2008;336(7653):1106–10.
motion will become common so that physiotherapists 15. Jaeschke R, Guyatt GH, Dellinger P, et al. Use of GRADE grid to
reach decisions on clinical practice guidelines when consensus is
and other clinicians can capture information in real time elusive. BMJ 2008;337:a744.
about the activities of patients and thereby improve com- 16. Edwards I, Jones M, Carr J, et al. Clinical reasoning strategies in
pliance with prescribed exercises (Actigraph, Pensacola, physical therapy. Phys Ther 2004;84:312–30.
USA; actigraphcorp.com). Also, motion sensing and 17. Pottier P, Hardouin JB, Hodges BD, et al. Exploring how students
analysis technology to assist the assessment of movement, think: a new method combining think-aloud and concept mapping
protocols. Med Educ 2010;44(9):926–35.
movement patterns, posture and work practices will 18. Hartvigsen J, Natvig B, Ferreira M. Is it all about a pain in the
extend physiotherapists’ capacity to evaluate patients in back? Best Pract Res Clin Rheumatol 2013;27:613–23.
the clinic and in their daily functional activity, and these 19. Roos E, Juhl C. Osteoarthritis 2012 year in review: rehabilitation
data – whether from occupational, rehabilitation, sport, and outcomes. Osteoarthr Cartil 2012;20:1477–83.
20. Von Korff KM, Moore JC. Stepped care for back pain: activating
recreation or daily living settings – will require new forms approaches for primary care. Ann Intern Med 2001;134:911–17.
of clinical reasoning (dorsaVi Ltd, Melbourne, Australia; 21. Von Korff M, Tiemens B. Individualized stepped care of chronic
www.dorsavi.com). illness. West J Med 2000;172(2):133–7.
Importantly, patients will be informed and will expect 22. Amirall D, Compton SN, Gunlicks-Stoessel M, et al. Designing a
to participate in decisions about their own care pilot sequential multiple assignment randomized trial for develop-
ing an adaptive treatment strategy. Stat Med 2012;31:1887–902.
management.6–8 Information technology will be a useful 23. Murphy SA. Optimal dynamic treatment regimes. J R Stat Soc
vehicle for disseminating evidence to both patients Series B 2003;65:331–55.
and clinicians, and interactive platforms for informed 24. Stiell IG, Greenberg GH, Wells GA, et al. Prospective validation
decision-making based on the presentation and circum- of a decision rule for use of radiography in acute knee injury. JAMA
1996;275:611–15.
stances of individual patients will become common. 25. Stiell IG, Wells GA, Hoag RH, et al. Implementation of the
High-quality evidence and ready access to care are fun- Ottawa Knee Rule for the use of radiography in acute knee injuries.
damental components in modern societies. However, JAMA 1997;278:2075–9.
good clinical reasoning from well-educated clinicians will 26. Moons KG, Royston P, Vergouwe Y, et al. Prognosis and prognos-
remain the foundation for good health care. tic research: what, why and how? BMJ 2009;338:b375.
27. Flynn T, Fritz JW, Whitman M, et al. A clinical prediction rule
for classifying patients with low back pain who demonstrate short-
term improvement with spinal manipulation. Spine 2002;27(24):
REFERENCES 2835–43.
1. Anderson KJ. Factors Affecting the Development of Undergradu- 28. Childs JD, Fritz JM, Flynn TW, et al. A clinical prediction rule to
ate Medical Students’ Clinical Reasoning Ability. PhD Thesis, The identify patients with low back pain most likely to benefit from
University of Adelaide; 2006. spinal manipulation: a validation study. Ann Intern Med 2004;
2. Sackett D, Richardson W, Rosenberg W, et al. Evidence-Based 141(12):920–8.
Medicine: How to Practice & Teach EBM. 1st ed. Edinburgh: 29. O’Sullivan P. Diagnosis and classification of chronic low backpain
Churchill Livingstone; 1998. disorders: maladaptive movement and motor control impairments
3. Sackett DL, Rosenberg WM, Gray JA, et al. Evidence based medi- as underlying mechanism. Man Ther 2005;10:242–55.
cine: what it is and what it isn’t. BMJ 1996;312(7023):71–2. 30. Vibe Fersum K, O’Sullivan P, Skouen JS, et al. Efficacy of
4. Hoffmann T, Bennett S, Del Mar C. Evidence-Based Practice classification-based cognitive functional therapy in patients with
Across the Health Professions. Australia: Elsevier; 2009. non-specific chronic low back pain: a randomized controlled trial.
5. Isaacs D, Fitzgerald D. Seven alternatives to evidence based medi- Eur J Pain 2012;17(6):916–28.
cine. BMJ 1999;319:1618. 31. Dankaerts W, O’Sullivan P. The validity of O’Sullivan’s classifica-
6. Trede F, Higgs J. Collaborative decision making. In: Higgs JJM, tion system (CS) for a sub-group of NS-CLBP with motor control
Loftus S, Christensen N, editors. Chapter 4 in Clinical Reasoning impairment (MCI): overview of a series of studies and review of the
in the Health Professions. Elsevier Health Sciences; 2008. p. 520. literature. Man Ther 2011;16(1):9–14.
 26  Clinical Reasoning and Models for Clinical Management 249

32. Dankaerts W, O’Sullivan PB, Straker LM, et al. The inter-examiner 54. Mallen CD, Thomas E, Belcher J, et al. Point-of-care prognosis
reliability of a classification method for non-specific chronic low for common musculoskeletal pain in older adults. JAMA Intern
back pain patients with motor control impairment. Man Ther Med 2013;173(12):1119–25.
2006;11(1):28–39. 55. Pincus T, Burton A, Vogel S, et al. A systematic review of psycho-
33. Fersum KV, O’Sullivan PB, Kvåle A, et al. Inter-examiner reliabil- logical factors as predictors of chronicity/disability in prospective
ity of a classification system for patients with non-specific low back cohorts of low back pain. Spine 2002;27(5):E109–20.
pain. Man Ther 2009;14(5):555–61. 56. Nicholas MK, Linton SJ, Watson PJ, et al. Early identification and
34. Vaughan CL, O’Malley MJ. A gait nomogram used with fuzzy management of psychological risk factors (‘yellow flags’) in patients
clustering to monitor functional status of children and young adults with low back pain: a reappraisal. Phys Ther 2011;91:737–53.
with cerebral palsy. Dev Med Child Neurol 2005;47(6):377–83. 57. Anema JR, Schellart AJM, Cassidy JD, et al. Can cross country
35. Hill JC, Dunn KM, Lewis M, et al. A primary care back pain differences in return-to-work after chronic occupational back pain
screening tool: identifying patient subgroups for initial treatment. be explained? An exploratory analysis on disability policies in a six
Arthritis Rheum 2008;59(5):632–41. country cohort study. J Occup Rehabil 2009;19:419–26.
36. Hill JC, Whitehurst DG, Lewis M, et al. Comparison of stratified 58. Fransen M, Woodward M, Norton R, et al. Risk factors associated
primary care management for low back pain with current best with the transition from acute to chronic occupational back pain.
practice (STarT Back): a randomised controlled trial. Lancet Spine 2002;27(1):92–8.
2011;378(9802):1560–71. 59. Lippel K, Lötters F. Public insurance systems: A comparison of
37. Foster NE, Hill JC, O’Sullivan P, et al. Stratified models of care. cause-based and disability-based income support systems. In: Loisel
Best Pract Res Clin Rheumatol 2013;27:649–61. PaA JR, editor. Handbook of Work Disability: Prevention and
38. Hingorani AD, Windt DA, Riley RD, et al. Prognosis research Management. New York: Springer Science+Business Media; 2013.
strategy (PROGRESS) 4: Stratified medicine research. BMJ 60. Loisel P, Buchbinder R, Hazard R, et al. Prevention of work dis-
2013;346:e5793. ability due to musculoskeletal disorders: the challenge of imple-
39. Hancock M, Herbert R, Maher CG. A guide to interpretation of menting evidence. J Occup Rehabil 2005;15:507–24.
studies investigating subgroups of responders to physical therapy 61. McKenzie R, May S. Lumbar Spine, Mechanical Diagnosis and
interventions. Phys Ther 2009;89(7):698–704. Therapy. 2nd ed. Waikanae, New Zealand: Spinal Publications Ltd;
40. Kent P, Hancock M, Petersen DH, et al. Choosing appropriate 2003.
study designs for particular questions about treatment subgroups. 62. Battié MC, Cherkin DC, Dunn R, et al. Managing low back pain:
J Man Manip Ther 2010;18(3):147–52. attitudes and treatment preferences of physical therapists. Phys
41. Kent P, Keating JL, Leboeuf-Yde C. Research methods for Ther 1994;74(3):219–26.
subgrouping low back pain. BMC Res Meth 2010;10:62. 63. Donelson R, Aprill C, Medcalf R, et al. A prospective study of
doi:10.1186/1471-2288-10-62. centralization of lumbar and referred pain: a predictor of symptom-
42. Rothwell P. Subgroup analysis in randomised controlled trials: atic discs and annular competence. Spine 1997;22(10):1115–22.
importance, indications, and interpretation. Lancet 2005;365(9454): 64. Long A, Donelson R, Fung T. Does it matter which exercise? A
176–86. randomized control trial of exercise for low back pain. Spine
43. Royston P, Moons KG, Altman DG, et al. Prognosis and prognos- 2004;29(23):2593–602.
tic research: developing a prognostic model. BMJ 2009;338:b604. 65. O’Sullivan PB. Lumbar segmental ‘instability’: clinical presentation
44. Altman DG, Vergouwe Y, Royston P, et al. Prognosis and prognos- and specific stabilizing exercise management. Man Ther
tic research: validating a prognostic model. BMJ 2009;338:b605. 2000;5(1):2–12.
45. Mansell G, Kent P, Kamper S. Why and how back pain interven- 66. Kent P, Keating JL, Taylor NF. Primary care clinicians use variable
tions work: what can we do to find out? Best Pract Res Clin Rheu- methods to assess acute nonspecific low back pain and usually focus
matol 2013;27(5):685–97. on impairments. Man Ther 2009;14:88–100.
46. van der Windt DA, Dunn KM. Preface. Best Pract Res Clin Rheu- 67. Sanders T, Foster NE, Bishop A, et al. Biopsychosocial care and
matol 2013;27:571–3. the physiotherapy encounter: physiotherapists’ accounts of back
47. van Gerven MA, Taal BG, Lucas PJ. Dynamic Bayesian networks pain consultations. BMC Musculoskelet Disord 2013;14:65.
as prognostic models for clinical patient management. J Biomed doi:10.1186/471-2474-14-65.
Inform 2008;41:515–29. 68. Shaw WS, Pransky G, Winters T, et al. Does the presence of psy-
48. Verduijn M, Peek N, Rosseel PM, et al. Prognostic Bayesian net- chosocial ‘yellow flags’ alter patient-provider communication for
works I: Rationale, learning procedure and clinical use. J Biomed work-related, acute low back pain? J Occup Environ Med
Inform 2007;40:609–18. 2009;51:1032–40.
49. Verduijn M, Rosseel PM, Peek N, et al. Prognostic Bayesian net- 69. Savage R, Armstrong D. Effect of a general practitioner’s consult-
works II: an application in the domain of cardiac surgery. J Biomed ing style on patients’ satisfaction: a controlled study. BMJ
Inform 2007;40:619–30. 1990;301(6758):968–70.
50. Waddell G. A new clinical model for the treatment of low-back 70. Shepard KF. Thirty-eighth Mary McMillan Lecture: are you
pain. Spine 1987;12(7):632–44. waving or drowning? Phys Ther 2007;87:1543–54.
51. Waddell G. Preventing incapacity in people with musculoskeletal 71. Main CJ, George SZ. Psychologically informed practice for man-
disorders. BMJ 2006;77–78:55–69. agement of low back pain: future directions in practice and research.
52. Pincus T, Kent P, Bronfort G, et al. Twenty-five years with the Phys Ther 2011;91:820–4.
biopsychosocial model of low back pain – is it time to celebrate? A 72. Craik RL. A convincing case – for the psychologically informed
report from the Odense Forum XII. Spine 2013;38(14):2118–23. physical therapist. Phys Ther 2011;91(5):606–8.
53. Gatchel RJ, Peng YB, Peters ML, et al. The biopsychosocial
approach to chronic pain: scientific advances and future directions.
Psychol Bull 2007;133:581–624.
 CHAPTER 27 

Communicating with Patients

CHAPTER OUTLINE

Editor’s Introduction Ch 27.2  Patient Education: A Collaborative

Approach  254
Ch 27.1  Patient-Focused Practice and
Communication: Use of Communication Lynne Caladine  •  Jane Morris
in the Clinical Setting  250 Ch 27.3  Communicating Risk  258
Ruth Parry Roger Kerry

EDITOR’S INTRODUCTION

One of the key elements of a successful patient– region. This enables them to make an informed
therapist relationship is personal one-to-one choice about the treatment that they receive.
communication. In the absence of good-quality One of the key areas highlighted by
communication, patients’ satisfaction can be musculoskeletal physiotherapists, as part of a
reduced and patients’ expectations may not be multimodal approach to treatment, is education.
achieved. In addition, the opportunity for mutual A person-centred approach to communication
understanding between the patient and the and how educational strategies and concepts
clinician may be lost. Intelligence in the use of are articulated by the physiotherapist are vital in
language in the therapeutic setting is vital in ensuring that the pedagogic (educational)
maintaining an empathetic and trusting element of a multimodal approach is appropriate
relationship which contributes to successful and effective. Thus this chapter focuses on these
treatment outcomes. three important components: the use of
Frequently, patients need to be informed language in the clinical setting, the
about possible risks, for example the risk that communication of relative risk of treatments and
may occur as a result of proposed high-velocity patient education.
thrust manipulative procedures to the cervical

CHAPTER 27.1  ■  PATIENT-FOCUSED PRACTICE AND

COMMUNICATION: USE OF
COMMUNICATION IN THE
CLINICAL SETTING
Ruth Parry
‘reaching common ground’ and so on. Fortunately, a
INTRODUCTION growing body of research is providing explicit descrip-
tions of practices through which we can implement these
Substantial evidence shows that the content and style of kinds of communication.
clinicians’ communication influence patient outcomes In this section I consider evidence from this growing
including: attendance at subsequent appointments, body of research. This research uses the conversation
adherence with prescribed activities, symptom resolu- analytic approach, which entails systematically analysing
tion, functional outcomes and reported satisfaction.1,2 recordings of naturally occurring interactions to identify
The evidence indicates that effective communication and describe the structure and functioning of communi-
entails treating the patient as an active participant, cation behaviours.4–8 First, I will outline features of com-
in-depth discussion of their problem(s), providing oppor- munication that one needs to grasp in order to analyse
tunities to ask questions, offering positive feedback and one’s own communication and that of patients and col-
emotional support, giving clear instructions and endeav- leagues (Box 27-1). Then I describe the structure and
ouring to reach common ground about the nature of the functioning of some specific practices relevant for working
problem and what needs to be done.1–3 While these with patients. In doing so, I provide a brief introduction
insights are helpful, practitioners need to know precisely to conversation analytic findings and make recommenda-
how to go about ‘treating patients as active participants’, tions for further reading.
250
 27  Communicating with Patients 251

BOX 27-1  Some Key Features of BOX 27-2  Strategies by Which Practitioners
Communication Can Work to Build Common
Ground
• The details of communication matter: meaning is built
not just by what is said, but how and when it is said • Asking patients about their views and understandings
• Communication is sequentially structured • Encouraging them to respond
• Any particular communicative task or action can be • Designing what you say in relation to what the
done in a variety of ways, and these have different patient says
consequences • Stepwise building of agreement
• Each of our communicative ‘moves’ does several things at • ‘You tell me first’ sequences
the same time • Online commentary about your examination findings
• Communication is more than information exchange: • Explaining reasons
through communication we build relationships and • Making positive and specific recommendations before
identity – who we are to one another making any negative recommendations

SOME KEY FEATURES OF another (trustworthy therapist, cooperative patient, etc.),

COMMUNICATION make sense of one another’s actions, wishes and per-
spectives; and build and maintain relationships with one
Firstly, we should notice that not only what we say, but another.
how and when we say it is important: details are highly
significant for meaning-making.9 These details include
wording, pauses, intonation, gesture, gaze and so on. To SOME SPECIFIC PRACTICES FOR
illustrate: consider all the different ways you can pro- BUILDING TOWARDS COMMON GROUND
nounce words such as ‘Oh’ or ‘Yeah’, and notice how
vastly their meanings differ depending on how you say Inevitably, therapists and patients will have different per-
them and at what conversational juncture you say them. spectives and understandings on physiotherapy-related
Secondly, communication is structured in sequences – matters. As noted, the research evidence suggests it is
think of greetings, or the question and response series important that practitioners at least try to build common
during initial patient assessments. Therefore, when we ground about treatment activities, recommendations and
think about communication, we should think of it sequen- decisions, and about the rationale underpinning them.
tially, i.e. in terms how what we do shapes what the Box 27-2 lists some relevant strategies, and I describe
patient can and does say, and how this in turn shapes what them below.
we can and do say.
Thirdly, any particular communication task or activity
can be done in multiple ways. For instance, we can seek Pursuing Patients’ Contributions, and
information from another person via a quizzical look, by Designing What You Say in Relation to
repeating what they have said in a puzzled tone of voice,
or by asking indirect or direct questions.10 Each different
Their Contributions
way of attempting a communication task will have differ- Perhaps the simplest strategy for reaching common
ent consequences for what the other person does and ground is asking questions, and – if you do not get the
says, and for how they perceive you. Some communica- answer you need – asking again, or asking somewhat dif-
tion tasks that are frequent in physiotherapy have been ferently. Once a patient has responded, building common
studied in great detail, for instance, different ways of ground entails designing what you say in relation to their
seeking patients’ views,11–13 ways in which patients convey response.
their views,14 and different ways of making treatment
recommendations.15–17 This research helps illuminate Stepwise Building of Agreement
how different ways of doing things have different conse-
quences; for instance, how different question formats This practice can be particularly useful where there are
more or less strongly encourage in-depth or ‘on-topic’ some obstacles to building common ground. An illustra-
responses.13 tive example can be found in Box 27-3, a transcript of
Fourthly, it is important to recognize that commu- part of a physiotherapy session involving a patient who is
nication is the fundamental means by which we do receiving inpatient rehabilitation after acute stroke. The
things with one another, and furthermore that every focus of the fairly lengthy session has been on sitting
communicative action does more than one thing at once. balance.
When I ask a patient to do a movement I not only Analysis of some features I don’t examine here can be
request her physical efforts, but also convey that this found elsewhere.19 Notice that as the episode begins, a
is what therapy is and that I have therapeutic knowledge difference between the patient’s and therapist’s positions
and skills. When the patient responds with a movement, becomes evident (L1–18). The therapist ‘pursues’ the
they not only perform the action, they also convey patient’s response and the patient resists, culminating in
things like cooperation and effort.18 Communication is voicing a reason why he cannot answer (L18). At this
the key means by which we convey who we are to one point, the therapist begins building agreement in a
252 PART III  Advances in Clinical Science and Practice

BOX 27-3  Transcribed Episode from Physiotherapy Illustrating Stepwise Building of Agreement
Parry_S4Ph9PaUT1/2.55 (simplified)
1 T Have you ‘ad enough?
2 (0.3)
3 P No I’m not bothered ((flat tone)) (0.2) ‘s up to you entirely
4 (0.3)
5 T No it’s not (0.2) doesn’ matter to us (it’s up to) you
6 P Mm
7 (1.0)
8 P Oh. Think you (.) Think you achieved something?
9 T D’you think you achieved something?
10 (1.0)
11 P Not up to me it’s up to you (.) teacher
12 T hh uh huh the teacher ((patient and therapist are smiling))
13 T No
14 (0.3)
15 T It’s what you want. you gotta get better [‘aven’t] you
16 P [ahh ((quietly))]
17 T [yeah?]
18 P [No] but I can – I don’t know what’s better.
19 T Alright. Well to be able to sit was your first goal
20 P Ye[s]
21 T [an]d you achieved it
22 P Yes
23 T So you have achieved something
24 P (I’ve) achieved something yes.
25 T Yeah.
26 (0.5)
27 P Mm
28 T Very good
29 (0.2)
30 T Uhm, still sometimes Joe, you’re you are falling this way?
31 P Yes I know,
((The next minute or two are not included in this transcript. During them, the therapist, and to a degree
the patient talk about future treatment plans and what needs to be worked on. Then the therapist refers back
to the higher level of assistance the patient needed in order to sit up earlier during the treatment session))
32 T … but we don’t need three ((meaning no longer needing three people to help him stay sitting up))
33 P Mm, ahm
34 T So you must be better
35 P Must be better hu hum
36 T Try and keep yer … ((instructions follow as the patient is assisted to get dressed))

T = therapist
P = patient
Underline = emphasized word or syllable
[talk]
[talk] = overlapping talk
(0.x) = gap of silence of more than a tenth of a second
((text)) = supplementary descriptive information

stepwise manner. First, she cites a goal that it seems the coming to a conclusion (L34) that directly refers back to
patient had agreed to at the start of the session (L19). the patient’s claim not to know ‘what’s better’ (L18).
That is, she raises something about which she can reason- Thus, common ground appears to be reached.
ably expect agreement, and this proves to be the case By the way, you may have noticed that I am being
(L20). The therapist then builds another ‘step’, it too rather tentative about whether common ground is ‘really’
results in agreement (L21,22) and then another (L23,24). reached. In line with conversation analytic practice, I take
A minute or so later, we see the same patterning: the the position that we cannot KNOW, we can only INFER
therapist raises something about which she can predict what someone actually feels or thinks – what is inside
the patient will agree, and she keeps building upon this, someone’s head. This is the case whether we are
 27  Communicating with Patients 253

communicating with one another, or analysing that

communication. Make Positive, Specific
Recommendations First
‘You Tell Me First’ Sequences
Conversation analytic research in primary care medicine
The ‘perspective display’, or ‘you tell me first’ sequence, has described how recommendations can be negatively
has been documented in contexts where clinicians deliver or positively formulated and has found that positive,
bad news.20–22 In musculoskeletal physiotherapy, this specific recommendations are more likely to be accepted.15
might be informing a footballer that they have severe Negative recommendations include ‘You don’t need anti-
damage to a ligament and need surgery, or explaining biotics’ or, to give a more physiotherapeutic example,
to someone hoping for a quick fix for their low back ‘You need to stop playing football for 4 weeks’. The
pain that they need a lengthy pain management and research indicated that if a practitioner’s first recom-
cognitive behavioural therapy programme. In these mendation is a negative one, this is much more likely
sequences, the clinician seeks the view of the person to be met with resistance and arguments than when
consulting them before they deliver any specific news, their first recommendation is a positive and specific one,
then the clinician goes on to deliver the news in ways for example, ‘I think the best thing to do at this point
that are fitted to the patient’s perspective.20–24 This prac- would be to elevate your head at night, have plenty
tice has particular advantages when there is a chance the of fluids to drink’. In our physiotherapy example, the
recipient of the news may disagree with and/or be highly therapist might want to first describe specific interven-
distressed by it. It allows us to shape our news delivery tions (e.g. ultrasound, joint mobilization) and a specific
to the patient’s own understandings and perspectives, home exercise programme, BEFORE recommending the
and to accomplish news delivery in a ‘cautious’, relatively patient stops playing football. While we cannot be certain
gentle manner. that someone who has agreed to something will actually
comply, it seems sensible nevertheless to make our
Online Commentary About Your recommendations maximally likely to be met with
agreement.
Examination Findings Readers are directed towards other research on ways
Another practice found to be effective in building of working towards common ground and providing
common ground with patients – and in forestalling dis- patients with opportunities to be active participants.12,29–33
agreements – is online commentary.25–27 This entails the
clinician providing the patient with information – ‘com-
mentary’ – about what she is seeing and finding on physi- CONCLUDING REMARKS
cal examination. This paves the way towards common
ground about what is (or is not) wrong, and thus what I have only been able to scratch the surface of the vast
should be done about it. In terms of physiotherapy, one and important body of evidence about the structure and
might consider deploying online commentary when functioning of communication practices. Furthermore,
examining a patient who in your clinical judgement has there are some highly relevant areas of communication
incorrect assumptions about their condition. For instance, (body movement, facial expression, touch) that are still
commentary indicating ‘no problem’ or ‘non-serious not well researched. On a more positive note, a key
problem’ may be helpful for building common ground message is that when reflecting on and developing one’s
with a patient who thinks a damaged joint is stopping own and other’s communication skills, it is helpful to be
them from various activities, whereas examination shows aware that there are always different ways – different
the absence of any serious damage. communication practices – by which one can attempt any
particular activity. Few if any will always be the right
Explaining Reasons for Treatments thing to do, or always the wrong thing to do. Rather, it
is best to consider communication practices as having an
and Recommendations array of pros and cons; trying to be conscious and analyti-
Explaining reasons seems an obvious means of working cal about these is a good way of developing one’s own
towards common ground. However, in everyday life, practice. Finally, it is important to be very clear that good
people only provide reasons when they suspect that communication takes time: time for staff training, devel-
others might understand their actions as surprising or opment, support and reflection, and – very importantly –
problematic. People also tend not to ask others to explain sufficient contact time with patients themselves.34
their reasons (‘Why are you doing that?’) because doing
so can be interpreted as showing a lack of trust and REFERENCES
respect. Thus ‘social’ pressures tend to work against pro-
1. Stewart M. Effective physician-patient communication and health
viding reasons in everyday life and, indeed, in physio- outcomes: a review. Can Med Assoc J 1995;152(9):1423–33.
therapy.28 Nevertheless, some therapists manage to 2. Brown J, Stewart M, Ryan BL. Outcomes of patient-provider inter-
‘opportunistically’ squeeze in talk about reasons. In par- action. In: Thompson T, Dorsey A, Miller K, et al., editors. Hand-
ticular, when a patient directly or indirectly refers to their book of Health Communication. Mahwah NJ.: Lawrence Erlbaum
physical limitations, besides giving some kind of reassur- Associates; 2003. p. 141–61.
3. Hall AM, Ferreira PH, Maher CG, et al. The influence of
ance and/or sympathy, some therapists go further by the therapist-patient relationship on treatment outcome in
‘tacking on’ explanations about how therapy activities can physical rehabilitation: a systematic review. Phys Ther 2010;
manage or alleviate these physical limitations.28 90(8):1099–110.
254 PART III  Advances in Clinical Science and Practice

4. Clayman SE, Gill VT. Conversation analysis. In: Hardy M, Bryman 20. Maynard DW. Bearing bad news in clinical settings. In: Dervin B,
A, editors. Handbook of Data Analysis. Beverly Hills: Sage; 2004. editor. Progress in Communication Sciences. New Jersey: Ablex;
p. 589–606. 1991a. p. 143–72.
5. Heritage J. Conversation analysis and institutional talk: analysing 21. Maynard DW. The perspective-display series and the delivery and
data. In: Silverman D, editor. Qualitative Research: Theory, receipt of diagnostic news. In: Boden D, Zimmerman D, editors.
Method and Practice. London: Sage; 2004. p. 222–45. Talk and Social Structure. Cambridge: Polity Press; 1991b. p.
6. Heritage J, Clayman S. Talk in Action: Interactions, Identities, and 164–94.
Institutions. Chichester: Wiley-Blackwell; 2010. 22. Maynard DW. How to tell patients bad news: the strategy of ‘fore-
7. Parry R. Video-based conversation analysis. In: Bourgeault I, casting. Cleve Clin J Med 1997;64(4):181–2.
DeVries R, Dingwall R, editors. Sage Handbook of Qualitative 23. Maynard DW. On clinicians co-implicating recipients’ perspective
Methods in Health Research. London: Sage; 2010. p. 373–96. in the delivery of diagnostic news. In: Drew P, Heritage J, editors.
8. Sidnell J, Stivers T. The Handbook of Conversation Analysis. Talk At Work. Cambridge: Cambridge University Press; 1992. p.
Malden MA: Wiley-Blackwell; 2013. 331–58.
9. Sidnell J. Conversation Analysis. Chichester: Wiley-Blackwell; 24. Lutfey K, Maynard DW. Bad news in Oncology: how physician
2010. and patient talk about death and dying without using those words.
10. ten Have P. Talk and institution: a reconsideration of the ‘Asym- Soc Psychol Q 1998;61(4):321–41.
metry’ of doctor-patient interaction. In: Boden D, Zimmerman 25. Heritage J, Stivers T. Online commentary in acute medical visits:
DH, editors. Talk and Social Structure. Cambridge: Polity Press; a method of shaping patient expectations. Soc Sci Med 1999;49:
1991. p. 138–63. 1501–17.
11. Heritage J, Robinson J, Elliott MN, et al. Reducing patients’ unmet 26. Mangione-Smith R, Stivers T, Elliott M, et al. Online commentary
concerns in primary care: the difference one word can make. J Gen during the physical examination: a communication tool for avoiding
Intern Med 2007;22(10):1429–33. inappropriate antibiotic prescribing? Soc Sci Med 2003;56:313–20.
12. Heritage J. Questioning in medicine. In: Freed A, Ehrlich S, editors. 27. Heritage J, Elliott MN, Stivers T, et al. Reducing inappropriate
Why do you Ask?’: The Function of Questions in Institutional antibiotics prescribing: the role of online commentary on physical
Discourse. Oxford: Oxford University Press; 2009. p. 42–68. examination findings. Patient Educ Couns 2010;81(1):119–25.
13. Parry R, Land V, Seymour J. How to communicate with patients 28. Parry R. Practitioners’ accounts for treatment actions and recom-
about future illness progression and end of life: a systematic review. mendations in physiotherapy: when do they occur, how are they
BMJ Support Palliati Care 2014. mjspcare-2014-000649. Published structured, what do they do? Sociol Health Illn 2009;31(6):835–53.
Online First: 24 October 2014; doi:10.1136/bmjspcare-2014 29. Stivers T, Heritage J. Breaking the sequential mold: answering
-000649. ‘more than the question’ during comprehensive history taking. Text
14. Gill VT, Pomerantz A, Denvir P. Pre-emptive resistance: patients’ 2001;21(1/2):151–85.
participation in diagnostic sense-making activities. Sociol Health 30. Collins S, Drew P, Watt I, et al. ‘Unilateral’ and ‘bilateral’ practi-
Illn 2010;32(1):1–20. tioner approaches in decision-making about treatment. Soc Sci
15. Stivers T. Non-antibiotic treatment recommendations: delivery Med 2005;61:2611–27.
formats and implications for patient resistance. Soc Sci Med 31. Boyd E, Heritage J. Taking the patient’s medical history: question-
2005;60:949–64. ing during comprehensive history taking. In: Heritage J, Maynard
16. Clark SJ, Hudak PL. When surgeons advise against surgery. Res D, editors. Communication in Medical Care: Interactions Between
Lang Soc Interac 2011;44(4):385–412. Primary Care Physicians and Patients. Cambridge: Cambridge
17. Toerien M, Shaw R, Duncan R, et al. Offering patients choices: a University Press; 2006. p. 151–84.
pilot study of interactions in the seizure clinic. Epilepsy Behav 32. Robinson J, Heritage J. Physicians’ opening questions and patients’
2011;20:312–20. satisfaction. Patient Educ Couns 2006;60(3):279–85.
18. Parry RH. The interactional management of patients’ physical 33. Peräkylä A, Ruusuvuori J, Lindfors P. What is patient participation:
incompetence: a conversation analytic study of physiotherapy inter- Reflections arising from the study of general practice, homeopathy
actions. Sociol Health Illn 2004;26(7):976–1007. and psychoanalysis. In: Collins S, Britten N, Ruusuvuori J, et al.,
19. Parry RH. Communication Between Stroke Patients and Physio- editors. Patient Participation in Health Care Consultations. Maid-
therapists, PhD Thesis, University of Nottingham. British library enhead: Open University Press/McGraw-Hill Education; 2007.
reference DXN054515. 2002. EThOS ID 247132 http:// 34. Parry R. Communication and compassion need time and support:
ethos.bl.uk/OrderDetails.do?did=1&uin=uk.bl.ethos.247132. insights from end of life care. Int J Ther Rehabil 2013;20(10):
Copy available from the author. 478–9.

CHAPTER 27.2  ■  PATIENT EDUCATION:

A COLLABORATIVE APPROACH
Lynne Caladine  •  Jane Morris

Patient education is a relatively new development and can The term ‘patient education’ and other terms such as
be traced from the early 1970s.1 Since that time there has ‘health education’ and ‘health promotion’ are often used
been an increasing emphasis on the concept of patient- interchangeably, which may lead to some confusion.
centred care,2 with increased patient involvement in deci- Patient education has been defined as ‘a planned system-
sion making about their own health and promotion of atic, sequential, and logical process of teaching and learn-
self-care.3 During this period there has also been signifi- ing provided to patients and clients in all clinical settings’.4
cant growth in information technology, including the The same author considered patient education to include
development of the internet, giving opportunities for wide health education which ‘concentrates mostly on wellness,
access to medical information and advice. Patient educa- prevention and health promotion’.4
tion forms part of the role of a wide range of health Physiotherapists and other health professionals have a
professional groups but has developed at different rates. variety of roles, including that of educator. In this role
It is also a separate discipline in some countries (e.g. they support the learning experiences of peers, colleagues
the USA). and students as well as patients and their carers. Key
 27  Communicating with Patients 255

aspects of the educator role in relation to the learner have 2. Select approaches to facilitate the learning.
been identified as facilitator, assessor and evaluator.5 3. Assess the learning (i.e. check whether the patient
Despite being a demanding role it is an aspect for which understands and has learnt).
there is often very little formal preparation or recogni- 4. Evaluate your own practice as an educator through
tion. In a recent study physiotherapists acknowledged self-reflection, peer feedback or more formal
their educator role and reported that a high percentage feedback.
(more than 50%) of their interactions with patients
included educational activities.6,7 These communications
might include explanations, instructions (verbal or CONSIDER THE CHARACTERISTICS OF
written), teaching exercises and assessing understanding. THE LEARNER (E.G. PATIENT OR CARER)
The author also suggested that the terms (e.g. verbs and
metaphors) used when discussing aspects of patient edu- Several pertinent issues related to the individual learner
cation may give some insight into educational/pedagogic are noted below.
approaches likely to be adopted by individual thera-
pists.6,7 The expert therapists in a study in the USA were
distinguished by:
What Are the Patient’s Learning Needs?
By finding out what the patient already knows, relevant
‘a patient-centred approach to care characterised by to their current condition, his or her learning needs can
patient empowerment through education … with an be identified and prior experience recognized. This may
emphasis on problem solving and cultivation of a patient- be achieved by the use of a modified learning agreement
practitioner relationship’.8 (or learning contract). The physiotherapist and the
patient collaborate and contribute equally to this process.
More recently this was reinforced by another author The format of the learning agreement need not be
complex and could be based on those in wide use with
‘education that is tailored to the individual or to a group students.
is perhaps the most important component of the expertise To give an example of how a modified learning agree-
of the contemporary physical therapist to effect health ment might be used, a possible case scenario (Table 27-1)
behaviour change along with the individual’s motivation for a recently retired 60-year-old male who has been
to effect such change’.9 diagnosed with osteoarthritis of the knee joint is pre-
sented below. He has had an active job as a project
Despite this recognition, education related to students as manager in the construction industry and is a keen golfer.
learners has received more attention than education of His present condition is limiting his ability to pursue his
patients in the literature over recent years. However, hobby. He has good eyesight and hearing and no other
there is a substantial literature base across health profes- disabilities.
sional contexts that uses patient education as a treatment The alternative name for a learning contract is a
intervention in research studies. In such studies ‘patient ‘negotiated learning agreement’ and the latter more accu-
education’ is often used as a generic category to be com- rately reflects their intended collaborative and construc-
pared against a treatment intervention of interest to the tive nature. More information about learning contracts
researchers. It is worth noting that there is wide variation may be accessed through various websites including
in the operational definition of patient education in such http://www.learningace.com/doc/5825504/8fd61966eeb
studies and seldom consideration of the related educa- ed03ac44fb0a905b63823/learningcontracts/.
tional approaches or methods (sometimes referred to as
pedagogy). What Are the Learner’s (Patient’s)
In relation to student education there has been a
marked shift in emphasis over the last two decades.
Personal Characteristics?
‘Teacher-centred’ approaches of the past, based on the A wide range of personal characteristics may influence a
belief that knowledge can be transmitted from one indi- patient’s readiness or ability to learn. These may include
vidual to another have given way to more ‘student- age, cultural background, learning styles and preferences,
centred’ approaches which focus on the needs of the and additional needs (including visual impairment,
learner and change the teacher’s role to one of facilitator hearing impairment, dyslexia and ability to communicate
of learning, helping people to learn. There are parallels effectively). How will you adapt your approach in response
that can be drawn between student-centred teaching and to these characteristics?
patient-centred care when patients are recognized as Many of the learners (patients) will be adults and an
learners and the traditional, paternalistic, practitioner- understanding of Knowles’ ideas,10 including his princi-
centred approach to patient education is joined, if not ples of adult learning, may help to guide the approaches
replaced by, one in which the patient takes a more active to patient education that therapists choose to adopt.
part in self-care. In adopting a more patient-centred Adult(s):
approach to patient education the principles of student- • are internally motivated and self-directed
centred learning can be readily transferred and are listed • are goal-orientated
below and then expanded upon: • need to see the relevance
1. Consider the characteristics of the learner (e.g. • are practical
patient or carer). • like to be respected
256 PART III  Advances in Clinical Science and Practice

TABLE 27-1  Possible Format for a Patient Education Learning Agreement

Patient’s name:
Therapist’s name:
Diagnosis: – Osteoarthritis R Knee joint
Date of learning agreement:
Date(s) of review:

What Do the Patient and

Therapist Agree the Patient How Will the Learning Be Date by Which This
Needs to Learn? Achieved? How Will the Learning Be Assessed? Will Be Achieved
Basic anatomy of the knee • Hand out with drawings of key • Patient will self-assess As appropriate
joint structures • Therapist will check understanding (at next visit)
• Use of anatomical model through discussion
• Explanation by therapist
Basic pathology of the knee • As above plus referral to • As above • As above
joint website
Exercises to strengthen knee • Demonstration by therapist • Demonstration by patient • As above
extensors and flexors • Guidance and correction by • Assessment of muscle strength
therapist to help patient carry • Measurement of muscle bulk
out the exercises • Patient’s reflective log
• Hand out if appropriate
• Written instructions on number
and frequency of exercises
Exercises to improve • As above • Demonstration by patient • As above
mobility of the knee joint • Measurement of joint range

Concrete
Patient encounter
experience
Assessment/treatment/
(Doing/having an
management
experience)

Active Reflective
Collaborative reflective Collaborative reflective
experimentation observation
discussion encouraging discussion to identify
(Planning/trying out (Reviewing/reflecting
patient (or carer) to needs/goals.
what you have learnt) on the experience)
self-assess. Identify Patient strategies to
what worked well, what achieve learning goals
could have been done are put in place including
differently. elements of education
Modify if necessary
Abstract
conseptualization
(Concluding/learning
from the experience)

FIGURE 27-1  ■  Learning cycle based on Kolb (1984). Patient begins to

self-manage

• bring life experiences and knowledge to learning

FIGURE 27-2  ■  Collaborative patient education learning cycle.
experiences.
The vast array of past and continuing experience that
learners can draw upon can form a basis for further learn-
ing based on Kolb’s ideas11 and his experiential learning
cycle (Fig. 27-1). This may equally apply to the therapist SELECT APPROACHES TO FACILITATE
developing their practice as an educator or be applied to THE LEARNING
the patient as a learner.
Figure 27-1 outlines Kolb’s classic learning cycle in Once the patients’ learning needs have been established,
which experience is formalized as the basis for learning learning outcomes can be identified. It is then necessary
and builds upon previous knowledge through reflection. to decide how these outcomes can be achieved. Facilita-
We suggest that a more collaborative version might be tion is about helping and enabling rather than telling and
appropriate when helping patients and their carers to persuading. Once you have identified what needs to be
learn. Figure 27-2 identifies the phases of a collaborative learnt you may select from what Cross et al. referred to
patient education learning cycle. as a ‘toolkit’.5 They have identified ways in which
 27  Communicating with Patients 257

TABLE 27-2  Examples of Therapist-Centred and More Patient-Centred Approaches

to Patient Education
Example of Type of Examples of Therapist-Centred/
Learning Transmission Approach Examples of Patient-Centred/Facilitatory Approach
Knowledge/information Verbal explanation from 1. Find out what the patient already knows about the
about a condition (e.g. therapist. condition. Use this as a base to suggest other sources of
low back pain) Provision of information leaflet information (which might include leaflets) appropriate for
their learning characteristics. Allow the opportunity for
questions and discussion
2. Work with group of patients with similar learning needs
and draw on their experiences. Your role is to facilitate
discussion rather than provide all information. Consider
principles of peer learning and problem-based learning
Practical skills (e.g. Giving an information leaflet. Use leaflet and demonstration if appropriate but observe,
exercises for core Demonstration of a set of correct and help patient to adapt for own needs and
stability) exercises learning characteristics
Use anatomical models to aid explanation of rationale.
Respond to questions by linking to current understanding
Allow the opportunity for questions and progress difficulty
of the exercises based on subsequent assessment and
discussion with the patient
Use of equipment Provision of instruction leaflet. Demonstrate use of the equipment; explain how it should
Demonstration by therapist be used; get the patient to try
Use their self-assessment and your observations as a basis
for correction
Continue until performance is at a suitable standard
Ask questions to ensure/support understanding
Health promotion Provision of information sheet Assess current level of understanding through observation/
questioning, identify learning needs
Direct patient to website(s) and follow up
If possible provide opportunity for group discussion
facilitated by therapist

learning can be facilitated in the practice setting. As well ASSESS THE LEARNING
as structuring learning, guidance is given on fostering
collaboration and promoting empowerment. Dreeben4 In the same way that student learning needs to be assessed
also addressed approaches to facilitate patient learning in in academic or clinical settings, therapists responsible for
a comprehensive way. patient education also need to check whether the patient
Some examples of ways in which patient learning may understands and has learnt. As a patient educator you
be facilitated are outlined in Table 27-2. These include may need to check understanding through questions,
‘traditional’ therapist-centred approaches and more observation and exploration of how the patient has incor-
patient-centred strategies. A combination is likely to be porated, for example, exercises and new information into
most effective. Aim for a balance of providing informa- functional activity. This will form a basis for deciding
tion (transmission) to the patient and facilitating patient collaboratively with the patient how to proceed with the
learning (helping people to learn). There may be times management of their condition or injury.
when it is appropriate to explain something verbally or
give patients a well-constructed information leaflet, but
it is also necessary to consider drawing on strategies that EVALUATE YOUR OWN PRACTICE
help patients to become more independent as learners in AS AN EDUCATOR
order to manage their condition. Group discussion is an
example of how patients’ prior knowledge and expertise When supporting student learning evaluating the educa-
of a condition can be used to help others (which may tional episode is an important part of the cycle. Feedback
include the therapist) to learn. A recent master class by obtained from the learner helps to guide the educator in
Sadlo12 on the use of problem-based learning with stu- making improvements to their strategies for the future.
dents on placement in the practice learning environment Suggestions are made below for how evaluation might be
contains some content which may be transferable to adapted for use with patients as learners.
certain groups of patients as learners. • Seek verbal feedback from a patient or group of
When directing patients to websites for information patients about an educational interaction or episode.
about their condition therapists will also need to ensure • Devise a simple form to gather written feedback
that they have a way of evaluating the quality of these about aspects of an educational episode.
sources. There are many guides available for critical • Be alert to occasions in your clinical practice which
appraisal of research articles but this site13 includes con- involve you as a ‘teacher’. Take time to review
sideration of websites. individual educational patient interactions using a
258 PART III  Advances in Clinical Science and Practice

reflective model such as that of Gibbs.14 Use a recent ‘provision’ of information. Therapists are encouraged to
example of patient education to try this. You might reflect on their own educational practice with patients.
choose to talk this through with a trusted colleague.
How might your patient education practice change REFERENCES
in response to this reflection? 1. Hoving C, Visser A, Dolan Mullen P, et al. A history of patient
• Consider whether your teaching is based on a belief education by health professionals in Europe and North America:
from authority to shared decision making education. Patient Educ
that knowledge can be transmitted between a teacher Couns 2010;78:275–81.
and a learner or whether you think of it as helping 2. Mead N, Bower P. Patient-centredness: a conceptual framework
to facilitate learning. Thinking about the language and review of the empirical literature. Soc Sci Med 2000;51(7):
you use when discussing your involvement in educa- 1087–110.
tion with colleagues may be a guide. What sort of 3. Deccache A, Van Ballekom K. From patient compliance to empow-
erment and consumer’s choice: evolution or regression? An over-
verbs and metaphors do you use? Use of terms such view of patient education in French speaking European countries.
‘giving’, ‘delivery’, ‘getting it through’ might suggest Patient Educ Couns 2010;78(3):282–7.
that your ideas and approach to teaching are closer 4. Dreeben O. Patient Education in Rehabilitation. Sudbury, MA:
to transmission than facilitation. Whereas ‘support’, Jones & Bartlett; 2010.
5. Cross V, Moore A, Morris J, et al. The Practice-Based Educator –
‘guiding’, ‘working with’ when related to education A Reflective Tool for CPD and Accreditation. Chichester: Wiley;
may indicate a more collaborative, facilitatory and 2006.
patient-centred approach. 6. Caladine L. Physiotherapists’ construction of their role in patient
• Note the way that your peers and colleagues talk education. Doctoral thesis. University of Brighton; 2011.
about patient education (the terms and figures of 7. Caladine L. Physiotherapists’ construction of their role in patient
education. Int J Practice-based Learn Health Soc Care 2013;1(1):37–
speech they use – their discourse) and the approaches 49. doi:10.11120/pblh.2013.00005.
they adopt. Is there a link between their discourse 8. Resnik L, Jenssen GM. Using clinical outcomes to explore the
and their approach? Do they predominantly follow theory of expert practice in physical therapy. Phys Ther 2003;
a transmission or a facilitation model? 83(12):1090–106.
9. Dean E. Physical therapy in the 21st century (Part 2): evidence-
based practice within the context of evidence-informed practice.
Physiother Theory Pract 2009;25(5–6):354–68.
SUMMARY 10. Knowles M. The Adult Learner: A Neglected Species. 4th ed.
Houston: Gulf Publishing; 1990.
Developments in patient education are driven by an 11. Kolb D. Experiential Learning: Experience as the Source of Learn-
ing and Development. New Jersey: Prentice-Hall; 1984.
increasing emphasis on more patient-centred approaches 12. Sadlo G. Using problem-based learning during student placements
to care, self-management of health and financial impera- to embed theory in practice. Int J Practice-based Learn Health Soc
tives. Parallels have been identified here between patients Care 2014;2(1):6–19. doi:10.11120/pblh.2014.00029.
as learners and students as learners, noting that the prin- 13. Engle M. Evaluating web sites: criteria and tools. Online avail-
able from: <http://www.library.cornell.edu/olinuris/ref/research/
ciples of student-centred education may be applied with webeval.html#context>; 2014 [May 2014].
patients. Approaches to patient education which include 14. Gibbs G. Learning by doing: A guide to teaching and learning
collaboration and facilitation of learning may be more methods. Oxford Centre for Staff and Learning Development,
effective in some situations than traditional transmission- Oxford Polytechnic. Further Education Unit, London. <http://
based approaches alone with their heavy reliance on the www2.glos.ac.uk/gdn/gibbs/ch4_3.htm#4.3.5>; 1988.

CHAPTER 27.3  ■  COMMUNICATING RISK

Roger Kerry

Risk is the probability that an event will give rise to using numerical ranges can worsen understanding, cred-
harm.1 As healthcare professionals, communicating risk ibility, and perceptions of risk.3 This section aims to
is central to all our interactions. Risks associated with provide some clarity and guidance on risk communication
manual therapy might include rare and severe events (e.g. by focusing on three key areas: understanding risk; com-
death, stroke), or common and mild ones (e.g. transient munication tools; and framing risk.
unwanted responses to treatment). Given these associa-
tions, we have a responsibility to consider and commu-
nicate risk as best we can. This section summarizes UNDERSTANDING RISK
evidence on the best ways to communicate risk in order
to optimize shared decision making. Healthcare professionals are poor at understanding
Risk communication has become increasingly impor- numbers.2,4 Gigerenzer et al reported only 25% of sub-
tant with the publication of data and evidence-based prac- jects correctly identified 1 in 1000 as being the same as
tice. In contrast to traditional ‘gut feelings’ about risk, it 0.1%, coining the phrase ‘collective statistical illiteracy’
is becoming possible to make data-informed judgements. in relation to health statistics users.5 Education and
Despite this numerical dimension, there is still uncer- numeracy levels have little impact on risk judgement or
tainty in understanding and communicating risk.2 Para- understanding.6,7 Consensus on the best ways for health
doxically, communicating uncertain risk judgements professionals to communicate risk is lacking.8 These facts
 27  Communicating with Patients 259

create barriers to communication, and can lead to aber- research reports where authors want to exaggerate
rant use of research-generated data.9 Regardless of this, differences.13
a numerical interpretation of probability is an important
aspect of the clinicians’ understanding of risk. Risk com- ‘If the absolute risk is low, even if the relative risk is
munication should be inclusive of the numerical proba- significantly increased to exposed individuals, the actual
bility of an unwanted event happening, together with the risk to exposed individuals will still be very low’14
effect of this on a patient; importance of the effect; and
the context in which the risk might occur.10 A related statistic to absolute risk is number needed to
harm (NNH). NNH is the inverse of the absolute risk
‘every representation of risk carries its own connotations difference. Although NNH might seem to hold informa-
and biases that may vary according to the individual’s tive content,15 a recent Cochrane review concluded that
perspective concerning the way the world works’11 this was poorly understood by patients and clinicians.16
In summary both RR (including ORs) and NNH are
poor means of communicating risk, and AR should be
Understanding Probabilities favoured.4,17
What does 5% mean? Is this the same as 0.05? Does 5
out of 100 mean the same thing as 50 out of 1000? Do Probabilities Versus Natural Frequencies
the odds of 1 : 20–for say the same as 19 : 1–against? These
are all mathematically valid expressions of the same data So far we have considered risk expressed as some sort of
relating to probability judgement, but can and do mean probability. Alternatively, natural frequencies (NF) can
different things. But what actually is a 5% risk? If I said be a clearer way of representing risk.16,18 NFs are joint
you had a 5% chance of increased pain following inter- occurrences of two events (e.g. positive result on a clinical
vention X, how do you interpret that? Does this mean test and the presence of a condition). In terms of risk
you might be one of the 5 out of 100 people who will prediction, we may be familiar with probabilistic ideas
experience pain? Or that in every 100 patients I treat, 5 of specificity, sensitivity, positive predictive value, etc.
experience pain? Does it mean if you had 100 treatments, Although commonly used (e.g. these form the core of
you would experience pain 5 times? Does it mean that in clinical predication rules), these statistics are a consistent
5% of the time, people experience pain? Or that 5 out of source of confusion and error.19–21 Reports have sug-
every 100 manual therapists induce pain to all their gested that the human mind might be better evolved to
patients? Is this 5% epistemological (i.e. it is already understand risk in terms of NFs.22,23 NFs are absolute
decided that you will have pain, but you just do not know frequencies arising from observed data. Risk representa-
it yet to the degree of 5%) or is it aleatory (i.e. a com- tion using NFs avoids the complex statistics of probabil-
pletely random notion to the degree of 5% that you will ity expression, while maintaining the mathematical rigour
or will not experience pain)? These variables should be and Bayesian logic necessary to calculate risk.
considered when communicating risk.
The first stage in effective communication is establish-
ing the reference class to which the probability relates (e.g. COMMUNICATION TOOLS
time, location, person). In using population data for risk
communication, most of the time the reference class will Stacey et al. found that use of decision aids can improve
be historical (i.e. data from past events are used to inform patients’ knowledge and perception of risk, and improve
the chance of the next event). Embedding a new individual shared decision making.24 Such aids include visual repre-
event in data from a past population should carry some sentations of risk, and these have many desirable proper-
additional judgement, as new informative knowledge may ties (e.g. reveal otherwise undetected data patterns, attract
be ignored. Spiegelhalter ’s report of pre-Obama odds on attention and evoke specific mathematical operations).25
a black US President is a good example: 43 43 of past US Specific types of aids are useful for specific types of risk
Presidents were white, indicating a statistical prediction (e.g. bar charts for group comparisons, line graphs for
of almost certainty of a 44th white President.11 temporal interactions among risk factors, pie-charts for
showing risk proportions, etc.).26 Icon arrays are also used
to display population proportions, and rare events can be
Relative Versus Absolute Risk demonstrated in magnified or circular images. Figures
Misinterpretations of absolute and relative risk contrib- 27-3 and 27-4 shows examples of graphical images used
ute to data users’ anxieties and misunderstandings.12 for communicating common and rare events.
Absolute risk (AR) can be the prevalence (or incidence),
or indicate the absolute difference in risk between two
groups. Relative risks (RR) – and their counterparts, odds FRAMING RISK
ratios (OR) – are products of the division of AR in each
group, to form a relative difference. RRs may help to The way risk is framed is considered important for
make comparative judgements (e.g. ‘this is riskier than effective communication.1 Framing presents logically
that’). This way of communicating is encouraged in equivalent information in different ways. Generally,
evidence-based medicine. However, RRs are more per- risks can be framed positively (gain-framed) or nega-
suasive and make differences in risk appear larger than tively (loss-framed). We might gain-frame the risk of
they are.5 They are over-reported in lay-press and stroke following manual therapy as ‘you are very unlikely
260 PART III  Advances in Clinical Science and Practice

Transient neurological adverse

events following cervical
manipulation
100

90 19.4 out of 100 people

exhibit this property

80 80.6 out of 100 people

don’t exhibit this property

70

60

50

40

30 300

20 200

10 100

0 0
Without manipulation With manipulation
A B
FIGURE 27-3  ■  Representing risk of common minor adverse events following manipulation. Pooled relative risk (RR) from meta-
analysis,27 RR = 1.96, or 194 events per 1000 with manipulation versus 99 per 1000 with no manipulation (control). (A) icon array
pictorially representing absolute risk; (B) bar-graph demonstrating difference between the two groups.

A B
FIGURE 27-4  ■  Representing rare risk events. (A) A circle diagram representing the absolute risk of serious adverse event following
manipulation. The grey circle represents 100 000 units, and the black dots represent the number of cases per 100 000. (B) From
prevalence data on vertebrosbasilar insufficiency (VBI)28 and diagnostic utility of a VBI test,29 this graph shows a population of 100 000
(the large grey circle), the proportion who test positive on a VBI test (16 000: the white circle), and the proportion of people who will
actually have VBI (1: the black dot).

to experience stroke following this intervention’, or cardiovascular risk’ would be more effective than ‘if
loss-frame it as ‘this treatment could cause you to you don’t exercise, you will have an increased risk of
have a stroke’. Gain-framing can be more effective if cardiovascular disease’). However, loss-framing is gener-
the aim is preventative behaviour with an outcome of ally more effective, and especially so when concerned
some certainty30 (e.g. ‘exercising more will reduce with uncertain risks.1
 27  Communicating with Patients 261

8. Ghosh AK, Ghosh K. Translating evidence based information into

BOX 27-4  Key Messages in Communicating effective risk communication: current challenges and opportunities.
Risk J Lab Clin Med 2005;145(4):171–80.
9. Moyer VA. What we don’t know can hurt our patients: physician
• Data can help our naturally poor understanding of risk innumeracy and overuse of screening tests. Ann Intern Med
• Probabilities should be considered in relation to a refer- 2012;156:392–3.
ence class 10. Edwards A. Risk communication. In: Edwards A, Elwyn G, editors.
• Gain-framing can be effective for communicating risk Shared Decision Making in Health Care: Achieving Evidence-
related to preventative behaviour which has an outcome Based Patient Choice. 2nd ed. Oxford: Oxford University Press;
2009. p. 135–42.
of at least some certainty 11. Speigelhalter DJ. Understanding uncertainty. Ann Fam Med
• Loss-frame is generally most effective, especially with 2008;6(3):196–7.
uncertain risks 12. Mason D, Prevost AT, Sutton S. Perceptions of absolute versus
• Relative risk (including odds ratios) and numbers needed relative differences between personal and comparison health risk.
to harm should be avoided in preference to pure absolute Health Psychol 2008;7(1):87–92.
risk expressions 13. should enforce transparent reporting in abstracts. Br Med J
• Natural frequencies are better understood than probabi- 2010;341:791–2.
listic interpretations of risk 14. Gordis L. Epidemiology. Philadelphia: Saunders; 2009. p. 102.
• Visual representations of risk improve understanding 15. Sainani KL. Communicating risks clearly: absolute risk and numbers
needed to treat. Am Acad Phys Med Rehabil 2012;4:220–2.
• Risk data ultimately need to be personalized and consid- 16. Akl EA, Oxman AD, Herrin J, et al. Using alternative statistical
ered in the context of uncertainty formats for presenting risks and risk reductions. Cochrane Data-
base Syst Rev 2011;(3):CD006776.
17. Fagerlin A, Zikmund-Fisher BJ, Ubel PA. Helping patients decide:
Personalizing Risk ten steps to better risk communication. J Natl Cancer Inst
2011;103:1436–43.
Edwards et al. (2000) reported that risk estimates based 18. Gigerenzer G. What are natural frequencies? Br Med J 2011;
on personal risk factors were most effective in improving 343:d6386.
patient outcomes.31 A subsequent Cochrane review 19. Eddy DM. Probabilistic reasoning in clinical medicine: problems
and opportunities. In: Kahneman D, Sloviv P, Tversky A, editors.
reported that compared to generalized numerical risk Judgement under Uncertainty: Heuristics and Biases. Cambridge
communication, personalized risk communication UK: Cambridge University Press; 1982. p. 249–67.
improved knowledge, perception and uptake of risk- 20. Cahan A, Gilon D, Manor O. Probabilistic reasoning and clinical
reducing interventions.32 Personalized risk may include decision-making: do doctors overestimate diagnostic probabilities?
attempts to identify a smaller sub-group akin to the indi- Q J Med 2003;96:763–9.
21. Ghosh AK, Ghosh K, Erwin PJ. Do medical students and physi-
vidual patient, and/or consideration of the individual’s cians understand probability? Q J Med 2004;97:53–5.
own risk factors for an event. This dimension of risk 22. Gigerenzer G, Huffage U. How to improve Bayesian reasoning
communication contextualizes population data estimates without instruction: frequency formats. Psychol Rev 1996;102:
within single patients’ risk factors, together with their 684–704.
23. Cosmides L, Tooby J. Are humans good intuitive statisticians after
values and world-view. all? Rethinking some conclusions from the literature on judgement
Ultimately, despite the data, most risk estimates are under uncertainty. Cognition 1996;58(1):1–73.
communicated in the context of uncertainty. Data help 24. Stacey D, Bennett CL, Barry MJ, et al. Decision aids for people
inform decisions, but human nature and the complexity facing health treatment or screening decisions. Cochrane Database
of the world make certainty impossible. This is an Syst Rev 2011;(1):CD001431.
25. Lipkus IM, Hollands J. The visual communication of risk. J Natl
accepted difficult stance in risk communication.33 Under- Cancer Inst 1999;25:149–63.
standing uncertainty means accepting that risk commu- 26. Lipkus IM. Numeric, verbal, and visual formats of conveying health
nication is best done knowing that responses to risk risks: suggested best practices and future recommendations. Med
depend on a patient’s characteristics, values and experi- Decis Making 2007;27(5):696–713.
27. Carlesso LC, Gross AR, Santaguida PL, et al. Adverse events asso-
ences, and sociocultural worldviews.11,33 This knowledge ciated with the use of cervical manipulation and mobilization for
should be embraced, not ignored. Box 27-4 summarizes the treatment of neck pain in adults: a systematic review. Man Ther
the key messages from this section. 2010;15(5):434–44.
28. Boyle E, Côte P, Grier AR. Examining vertebrobasilar artery stroke
REFERENCES in two Canadian provinces. J Manipulative Physiol Ther 2009;
32:S194–200.
1. Edwards A, Elwyn G, Covey J, et al. Presenting risk information–a 29. Hutting N, Verhagen AP, Vijverman V, et al. Diagnostic accuracy
review of the effects of ‘framing’ and other manipulations on of premanipulative vertebrobasilar insufficiency tests: a systematic
patient outcomes. J Health Commun 2001;6(1):61–82. review. Man Ther 2013;18(3):177–82.
2. Gigerenzer G. How innumeracy can be exploited. In: Reckoning 30. Fagerlin A, Peters E. Quantitative information. In: Fischhoff B,
with Risk – Learning to Live with Uncertainty. London: Penguin Brewer NT, Downs JS, editors. Communicating Risks and Benefits:
Press; 2002. p. 201–10. An Evidence-Based User’s Guide. Silver Spring, MD: US Depart-
3. Longman T, Turner RM, King M, et al. The effects of communi- ment of Health and Human Services, Food and Drug Administra-
cating uncertainty in quantities health risk estimates. Patient Educ tion; 2011. p. 53–64.
Cou 2012;89:252–9. 31. Edwards A, Hood K, Matthews EJ, et al. The effectiveness of one-
4. Ahmed H, Naik G, Willoughby H, et al. Communicating risk. Br to-one risk communication interventions in health care: a system-
Med J 2012;344:e3996. atic review. Med Decis Making 2000;20:290–7.
5. Gigerenzer G, Gaissmaier W, Kurz-Milcke E. Helping doctors and 32. Edwards AG, Evans R, Dundon J. Personalised risk communication
patients make sense of health statistics. Psychol Sci Publ Int for informed decision making about taking screening tests.
2007;8:53–96. Cochrane Database Syst Rev 2006;(4):CD001865.
6. Lipkus IM, Samsa G, Rimmer BK. General performance on a 33. Politi MC, Han PK, Col NF. Communicating the uncertainty of
numeracy scale among highly educated samples. Med Decis Making harms and benefits of medical interventions. Med Decis Making
2001;21:37–44. 2007;27:681–95.
7. Gigerenzer G, Galesic M. Why do single event probabilities
confuse patients. Br Med J 2012;344:e245.
 CHAPTER 28 

Pain Management Introduction

CHAPTER OUTLINE

Editor’s Introduction Ch 28.3  Physical Interventions of Pain Management

and Potential Processes  269
Ch 28.1  The Patient’s Pain Experience  262
Kathleen Sluka
Hubert Van Griensven
Ch 28.2  Educational Approaches to
Pain Management  265
James McAuley

EDITOR’S IN TRODUCTION

Pain is a multidimensional experience that has with pain, therefore, involves multiple
been defined as an unpleasant sensory and interventions that include education, exercise,
emotional experience associated with actual or manual therapy and modalities such as electrical
potential tissue damage or described in terms of and thermal agents. Along with these,
such damage (International Association for the understanding the individual patient’s pain
Study of Pain). As the definition implies, pain experience and context is critical to successful
not only involves the sensation (location, management. This chapter will address three
duration, intensity, quality) but also has an areas in the very broad field of pain
emotional component (unpleasantness). As a management by physiotherapists. The first
complex experience, pain can affect every section will discuss the patient’s experience of
dimension of a person’s life including daily pain and how this may impact on interactions
activities, work, family relationships and social with health professionals. Secondly, the current
interactions. Thus, successful treatment must evidence base for the provision of education will
use multiple approaches aimed at all dimensions be outlined and thirdly, the processes that may
of pain, including the sensory and emotional potentially underlie some commonly used
aspects. Physiotherapy management of a person physical interventions will be explored.

CHAPTER 28.1  ■  THE PATIENT’S PAIN EXPERIENCE

Hubert Van Griensven

Much of manual therapy rests on the assumption that systems and questionnaires that can help the clinician to
pain results from nociception: increases and decreases in objectify the patient’s pain experience.2 However, patients
pain in response to positions, movements and manipula- with persistent pain find it difficult to quantify their pain
tions are interpreted as indicators of the health of specific and their own descriptions do not necessarily match
musculoskeletal and neural tissues. This end-organ model formal tools for pain assessment.3 Tools used to measure
or structure–pathology model is powerful and persuasive but aspects of pain may therefore provide us with categoriza-
also has its limitations. Firstly, the central nervous system tions and outcome measures, but the wider pain assess-
modifies sensory input, for instance when there is central ment involves empathy or a sense of understanding the
sensitization, thus altering the relationship between stim- experience of another person in pain.4 A clinician needs
ulus and sensation (Chapter 2). Secondly, persistent pain to be able to actively listen to the patient’s story in order
is frequently not stimulus-dependent (Chapter 2), while to be in a position to provide information and advice that
much of the musculoskeletal examination is based on is valued by the patient.5,6
responses to stimuli. Finally, pain is ultimately an intensely This section discusses this subjective pain experi-
subjective experience, which is intimately connected with ence, drawing mostly on qualitative research (Chapter
personal meaning. 23). Although it is acknowledged that an individual’s
The subjective aspects of pain make it demand atten- pain is influenced by, for instance, age,7 ethnicity,8
tion, interfere with some activities while driving others, religion9 and gender,10 the focus here is on personal
and disrupt thought.1 There are many pain scoring experience.
262
 28  Pain Management Introduction 263

belonging to the individual.21 The battle to maintain

COMING TO TERMS WITH control therefore includes the internal battle to retain
PAIN AND DISABILITY one’s original self and body.19,21 Bodywork approaches
such as yoga, qigong, Feldenkrais or Rolfing, which aim
Most people who experience pain first try to find a reso- to adjust overall wellbeing through adjustment of the
lution.11 Unfortunately not all pain can be eliminated or body, may play a role in reintegrating a patient’s experi-
even reduced, leading people with persistent pain to visit ence of themselves.22
numerous health-care practitioners in search of a cure. A Externally, the battle for control includes a struggle to
succession of failed treatments can eventually lead to the retain work, with the fear about the future a cause of
conclusion that there is no solution. This can be difficult anxiety and distress.16,23,24 The unpredictability of pain
to accept if clinicians do not provide a clear explanation can make it difficult to comply with the requirements of
for the pain.12 Indeed, primary care research has found regular employment.16,25 As a consequence of these and
that patients only accept reassurance if it includes a posi- other changes, individuals with persistent pain are likely
tive explanation which covers all relevant factors.13 Clini- to experience a strong sense of loss, for instance of abili-
cians are therefore advised to find out what their patient’s ties, finances and identity.24 Roles within the family also
information needs are.5 Explanations should help the change, for instance when a parent is no longer able to
patient make sense of not only the nociceptive origins of pick up a child or have sex because of pain.11 Although
their pain, but also reasons for its persistence. Teaching many pain sufferers experience a loss of hope, having a
pain mechanisms and how physical, psychological and (pain) diagnosis and a supportive environment can help
circumstances may influence pain may play an important to counteract this.24
role in this.14,15 Several studies describe the development of social
People with persistent pain find it difficult to maintain isolation. Individuals with pain who recognize their low
a sense of control, because long-term pain tends to fluc- mood and tendency at lash out at those around them,
tuate unpredictably.12,16 This makes it difficult to plan may feel forced to withdraw from interaction with
activities and set goals, both in the shorter and longer others.17,19 This withdrawal may be compounded by a
term.16 It also creates fear and uncertainty about life roles, fear of being judged by others,19 a loss of physical
both in the present and in the future.17 It is therefore ability and concentration24 and feeling uneasy about
important for clinicians not to dismiss accounts of unpre- having to rely on others.17 Although many individuals
dictable and inconsistent pain patterns, but to believe with persistent pain feel a need to talk about their
their patients and listen. An understanding of the physiol- problems, this conflicts with fear that doing so will
ogy and psychology of persistent pain, combined with a turn others away.17 As a consequence, friendships and
belief in what the patient reports, can aid in the provision personal relationships are likely to change or end.24
of realistic and empathetic explanations. This can increase Visits to a familiar health-care practitioner over an
the patient’s sense of control and ability to look beyond extended period may therefore play a role in support-
pain and suffering. ing patients with persistent pain, even if the treatments
Clinicians are advised to check adherence to, and do not yield objective improvements.24,26
effectiveness of, any advice or treatment provided.
Reasons for (non-)compliance can be deeply personal.
For example, patients may not take prescribed medica-
tion because of side effects,18 but also because some indi- ADOPTING A ROLE IN THE HEALTH
viduals with pain associate it with a lack of self-respect.17 AND SOCIAL CARE SYSTEM
Non-compliance with any treatment may therefore
warrant some careful and empathetic probing, in order Individuals with persistent pain often go through numer-
to find strategies that suit the individual. ous health-care appointments with long waits in between
and repeated disappointments.24 They experience poor
communication and a lack of understanding of the
PERSONAL AND SOCIAL CHANGES patient’s position on the part of medical professionals.27
IN RESPONSE TO PAIN Pain sufferers have described how clinicians tend to lose
interest once they realize that they are unable to provide
People with long-term pain have reported turning into a an effective treatment for the pain, and may even make
different person and experiencing a loss of ‘self’.19 Inter- the patient feel as if they are to blame for their
nally this may be associated with an experience of self- condition.27
loathing, while externally it can lead to a hardening of Unsuccessful attempts at diagnosis and treatment can
attitudes towards others, a reduction in empathy and lead to individuals feeling stigmatized and written off by
lashing out at friends and relatives.19,20 These unpleasant health-care practitioners.23 In trying to get their com-
aspects of their personality can be experienced as separate plaint legitimized by the health profession, people with
from the individual’s old self.19 This duality may extend persistent pain have described how they feel under pres-
to the way the body is experienced; although the body in sure to appear unwell, but not too unwell.12,28 The result-
general is not experienced consciously to a high degree, ing juggling act can increase feelings of helplessness and
painful, numb or dysfunctional parts are.17,21 As a conse- injustice20 and may force them into a sick role.12,20,27 The
quence, these parts may be experienced as ‘not me’, while way patients present may therefore be influenced by pre-
functioning and non-painful parts are identified as still vious consultations and what they think the clinician
264 PART III  Advances in Clinical Science and Practice

needs to see and hear. Building a relationship is therefore 10. Unruh A. Pain in women. Pain Res Manage 2008;13(3):199–200.
a key component of the consultation.5 11. Nielsen M. The patient’s voice. In: van Griensven H, Strong J,
Unruh A, editors. Pain. A Textbook for Healthcare Practitioners.
Similar conflicting demands on the presentation of Edinburgh: Churchill Livingstone; 2013. p. 9–19.
pain and other symptoms are experienced when dealing 12. Osborn M, Smith J. The personal experience of chronic benign
with the social security system. People with pain who lower back pain: an interpretative phenomenological analysis. Br J
are unable to work may wish to be viewed as normal Health Psychol 1998;3:65–83.
13. Dowrick C, Ring A, Humphris G, et al. Normalisation of unex-
people by the outside world,17 but this can conflict with plained symptoms by general practitioners: a functional typology.
the need to demonstrate eligibility to receive compensa- Br J Gen Pract 2004;54:165–70.
tion or benefits.27 They are likely to feel under pressure 14. Nijs J, van Wilgen C, Van Oosterwijck J, et al. How to explain
to demonstrate that their pain is real, but this is dif- central sensitisation to patients with ‘unexplained’ chronic muscu-
ficult because pain itself is invisible and may not be loskeletal pain: practice guidelines. Man Ther 2012;16:413–18.
15. Moseley G. Unraveling the barriers to reconceptualization of the
consistent across different days.16,20,23,24,27,29–31 As a con- problem in chronic pain: the actual and perceived ability of patients
sequence they encounter disbelief about why they are and health professionals to understand the neurophysiology. J Pain
suffering, which in turn leads to frustration, anger, guilt 2003;4(4):184–9.
and despair.12,16 16. Corbett M, Foster N, Ong B. Living with low back pain – stories
of hope and despair. Soc Sci Med 2007;65:1584–94.
17. Campbell C, Cramb G. ‘Nobody likes a back bore’ – exploring lay
perspectives of chronic pain: revealing the hidden voices of nonser-
CONCLUSION vice users. Scand J Caring Sci 2008;22:383–90.
18. Smith M, Muralidharan A. Pain pharmacology and the pharmaco-
Living with, and trying to cope with, ongoing pain can logical management of pain. In: van Griensven H, Strong J, Unruh
A, editors. Pain. A Textbook for Health Professionals. Edinburgh:
have a profound effect on the individual. This has been Churchill Livingstone; 2013. p. 159–80.
described in terms of loss or suspension of self, wellness, 19. Smith J, Osborn M. Pain as an assault on the self: an interpretative
roles, employment and future.11,32 This forces people phenomenological analysis of the psychological impacto of chronic
with pain into different roles, not only in their personal benign low back pain. Psychol Health 2007;22(5):517–34.
20. McParland J, Eccleston C, Osborn M, et al. It’s not fair: an inter-
lives but also when dealing with the health-care system. pretative phenomenological analysis of discourses of justice and
An understanding of subjective aspects of living and fairness in chronic pain. Health 2010;15(5):459–74.
coping with pain can help clinicians to empathize and 21. Osborn M, Smith J. Living with a body separate from the self. The
engage with their patients, and to find effective pain- experience of the body in chronic benign low back pain: an inter-
management strategies for them as individuals. pretative phenomenological analysis. Scand J Caring Sci
2006;20:216–22.
Clinicians are advised to reflect on the fact that they 22. Maitland J. Spacious Body. Explorations in Somatic Ontology.
are likely to come across as ‘switching off’ or ‘turning Berkeley: North Atlantic Books; 1995.
away’ to patients with persistent pain, and to examine 23. Holloway I, Sofaer-Bennett B, Walker J. The stigmatisation of
how these patients make them feel. For example, they people with chronic back pain. Disabil Rehabil 2006;29(18):
1456–64.
may feel helpless and useless, under pressure to see 24. Walker J, Sofaer B, Holloway I. The experience of chronic low back
patients who are more responsive to physiotherapy, or pain: accounts of loss in those seeking help from pain clinics. Pain
angry because they are put in a position where their 2006;10:199–207.
patient’s problems do not match their expertise. Reflect- 25. Patel S, Greasley K, Watson P. Barriers to rehabilitation and return
ing on these issues can lead to an improvement in the to work for unemployed chronic pain patients: a qualitative study.
Eur J Pain 2007;11(8):831–40.
way a clinician relates to his or her patients with persis- 26. Pincus T, Vogel S, Breen A, et al. Persistent back pain – why do
tent pain. This process of introspection may be aided by physical therapy clinicians continue treatment? A mixed methods
the use of mindfulness techniques33,34 and acknowledging study of chiropractors, osteopaths and physiotherapists. Eur J Pain
one’s vulnerabilities as a health-care practitioner.35 2006;10(1):67–76.
27. Walker J, Holloway I, Sofaer B. In the system: the lived experience
of chronic back pain from the perspectives of those seeking help
REFERENCES from pain clinics. Pain 1999;80:621–8.
1. Melzack R, Casey K. Sensory, motivational, and central control 28. Toye F, Barker K. ‘Could I be imagining this?’ – the dialectic
determinants of pain. In: Kenshalo D, editor. The Skin Senses. struggles of people with persistent unexplained back pain. Disabil
Springfield, Illinois: Charles C Thomas; 1968. p. 423–43. Rehabil 2010;32(21):1722–32.
2. Strong J, van Griensven H. Assessing pain. In: van Griensven H, 29. Crowe M, Whitehead L, Gagan M, et al. Listening to the body and
Strong J, Unruh A, editors. Pain. A Textbook for Health Profes- talking to myself – the impact of chronic lower back pain: a qualita-
sionals. Edinburgh: Churchill Livingstone; 2013. p. 91–114. tive study. Int J Nurs Stud 2010;47:586–92.
3. De Souza L, Frank A. Subjective pain experience of people with 30. Vroman K, Warner R, Chamberlain K. Now let me tell you in my
chronic back pain. Physiother Res Int 2013;5(4):207–19. own words: narratives of acute and chronic low back pain. Disabil
4. Goubert L, Craig K, Vervoort T, et al. Facing others in pain: the Rehabil 2009;31(12):976–87.
effects of empathy. Pain 2005;118:285–8. 31. Werner A, Widding Isaksen L, Malterud K. ‘I’m not the kind of
5. Main CJ, Buchbinder R, Porcheret M, et al. Addressing patient woman who complains of everything’: illness stories on self and
beliefs and expectations in the consultation. Best Pract Res Clin shame in women with chronic pain. Soc Sci Med 2004;59:1035–45.
Rheumatol 2010;24(2):219–25. 32. Bunzli S, Watkins R, Smith A, et al. Lives on hold. A qualitative
6. Gask L, Usherwood T. ABC of psychological medicine. The con- synthesis exploring the experience of chronic low back pain. Clin J
sultation. Br Med J 2002;324:1567–9. Pain 2013;29(10):907–16.
7. Gagliese L. Pain and aging: the emergence of a new subfield of pain 33. Grabovac A, Lau M, Willett B. Mechanisms of mindfulness: a Bud-
research. J Pain 2009;10(4):343–53. dhist psychological model. Mindfulness 2011;2(3):154–66.
8. Edwards C, Fillingim R, Keefe F. Race, ethnicity and pain. Pain 34. Kabat-Zinn J. Full Catastrophe Living. How to Cope with Stress,
2001;94:133–7. Pain and Illness using Mindfulness Meditation. London: Piatkus;
9. Büssing A, Michalsen A, Balzat H, et al. Are spirituality and religi- 1990.
osity resources for patients with chronic pain conditions? Pain Med 35. Rowe L, Kidd M. First do no Harm. Being a Resilient Doctor in
2009;10(2):327–39. the 21st Century. Sydney: McGraw Hill; 2009.
 28  Pain Management Introduction 265

CHAPTER 28.2  ■  EDUCATIONAL APPROACHES TO PAIN

MANAGEMENT
James McAuley

Patient education is a cornerstone of contemporary

health care; it is essential to the quality of care for chronic CONTENT OF EDUCATION
diseases and is important for the care of acute health INTERVENTIONS FOR LOW BACK PAIN
conditions. Patient education improves outcomes for a
range of health conditions including diabetes, asthma, Approaches to patient education for musculoskeletal
chronic obstructive pulmonary disease, hypertension, disorders have mostly been developed for patients with
cardiac disease, rheumatic disease and cancer.1 low back pain. These approaches can be grouped into
This section reviews the evidence for patient educa- three broad categories: biomedical, biopsychosocial or
tion for musculoskeletal conditions, with a focus on low pain neurophysiology education. Biomedical approaches
back pain. The important role of patient education as the to education focus on biomechanical properties of the
first-line management of musculoskeletal pain conditions spine and information is provided on ergonomics and
is reflected in clinical practice guidelines.2,3 advice on posture.37 This type of education is most closely
Broadly, patient education involves the provision of aligned with Back Schools,38 developed in the late 1960s
information by a health-care provider to a patient. This and early 1970s, and has been incorporated into multi-
can range from advice or simple information on diagno- disciplinary or functional restoration programmes.39–41
sis, prognosis or treatment,4 through to comprehensive Biopsychosocial approaches (including brief education)
education lasting several hours and across multiple were developed in the late 1980s and early 1990s from
occasions.5 the biopsy­chosocial model of back pain.42 These educa-
The aim of patient education is to improve patient tional approaches emphasize the importance of the rela-
outcomes either as a single intervention or to add to the tionship between thoughts and feelings to low back pain/
treatment effects of any other intervention that the disability43 and advise patients to avoid bed rest44 and that
patient is receiving. The goal is to move a patient from a gradual return to activity is likely to increase the rate
a passive recipient of health care to an active partner in of their recovery.45,46 Much of the content of the biopsy-
the management of their health condition. chosocial education can be found in the Back Book.14 Pain
neurophysiology education or pain biology education47,48
was developed in the early 2000s and focuses on educat-
ing the patient about the neurophysiological mechanisms
DELIVERY OF PATIENT EDUCATION that underlie their pain.5,49 This approach attempts to
reconceptualize a patient’s understanding of their pain by
Education can be delivered verbally to individuals6–9 or emphasizing that pain does not reflect the extent of tissue
to groups of patients10–12 via written materials such as damage, but is rather a protective output produced by the
leaflets or information booklets,13–15 by material from brain when sensory information is evaluated as threaten-
the Internet including web pages,16,17 social media/ ing, dangerous or harmful.5,50
YouTube18,19 and smartphone apps,20–22 or by educational
videos.23,24 Education can also be delivered at a societal
level and mass media campaigns have been developed THE EFFECTIVENESS OF PATIENT
to educate the public about pain,25,26 most notably and EDUCATION FOR LOW BACK PAIN
successfully in Australia.27 In clinical practice the delivery
of patient education is usually verbal and/or written Much of the research on the effectiveness of patient
information provided to individual patients,28 though education for musculoskeletal conditions has been con-
information delivered through the Internet or smart- ducted on patients with low back pain. The conclusions
phone apps is becoming increasingly common and of systematic reviews of this research are summarized
important.29 below. These conclusions broadly reflect those of educa-
Education for patients with musculoskeletal pain tion for other musculoskeletal conditions such as neck
typically involves providing information on diagnosis,30–32 pain.51,52 The effectiveness of educational interventions is
prognosis33 and management34 of their condition. For usually determined by their effects on pain, disability and
a patient with a non-specific pain condition this infor- return to work. Findings and conclusions are typically
mation is intended to reassure the patient that their made from comparing the educational approach to wait-
pain is not caused by a serious disease32 and that list, placebo or usual care assessed at short term, when
increased activity and the resumption of normal activi- the effects are presumed to be largest.
ties is likely to speed up their recovery.35 For patients
with acute musculoskeletal pain, education also aims
to increase the patient’s expectations that their pain
Biomedical Education (Back Schools)
will resolve and that they will recover within a few Five reviews have systematically reviewed the evidence
weeks.2,35,36 for the effectiveness of biomedical education (Back
266 PART III  Advances in Clinical Science and Practice

Schools).10,12,53–55 Although Brox et al.53 and Heymans associated with reduced sick leave/increased return
et al.12 found conflicting evidence, Turner54 and Demou- to work.
lin et al.55 concluded that biomedical education is not
effective at reducing either pain intensity or disability for
patients with chronic low back pain. Brox et al.,53 Demou- PATIENT EDUCATION AND
lin et al.55 and Turner54 all concluded that for patients MALADAPTIVE BELIEFS
with chronic low back pain biomedical education does
not reduce work absences, though Heymans et al.10,12 Some authors have pointed out that as patient education
found conflicting evidence. The quality of the evidence is complex and aimed at changing behaviours, theoretical
for these conclusions was typically low to moderate.12 models are likely to provide a useful guide for their
development or refinement.9,60 Pain, disability and return
Biopsychosocial Education (Advice/ to work are important outcomes that reflect patients’
concerns61 and are included in the core outcomes for
Brief Education) research on low back pain.62 Psychological theories
There are four systematic reviews on the effect of bio- suggest that underlying these outcomes are patient
psychosocial education for low back pain.9,53,56,57 Advice beliefs.63 Patient beliefs can therefore be considered to
or brief education does not reduce pain intensity for be the primary targets of patient education, and changes
either acute,9,53,56 subacute9 or chronic low back pain in these beliefs are likely to lead to improved patient
patients.9 Brox et al.53 concluded that brief education is outcomes.
effective at reducing disability, whereas Engers et al.9 and Inaccurate or unhelpful beliefs about low back pain
Shaheed et al.56 concluded that it was not. Although Brox are common in the general population64–67 and are caused
et al.53 and Shaheed et al.56 concluded that brief educa- by poor or out-dated information.68 For example,
tion was effective at reducing sick leave, Henrotin et al.57 patients who have erroneous or unhelpful beliefs about
concluded a biopsychosocial booklet alone was insuffi- pain are more likely to be distressed and worried about
cient to produce effects and Engers et al.9 concluded that their condition, to report increased pain and disability
only education that lasted longer than 2.5 hours was and to seek inappropriate management.60,63 For patients
effective, although there was no effect for patients with with low back pain the presence of these beliefs is a
chronic low back pain. It should be noted that the quality marker for increased risk of poor outcome and a slow
of available evidence was ‘very low’, leading Shaheed recovery.36
et al.56 to caution against conclusions that could be used Patient beliefs have been demonstrated to be stronger
to inform clinical management. predictors of poor outcome than factors such as pain.69
These beliefs are not only predictive of poor outcome,70,71
Pain Neurophysiology/Pain but they are significant barriers to recovery.63,72 Changes
in these beliefs are associated with clinical improve-
Biology Education ments73,74 and there is evidence that they underlie the
There is one systematic review on the effect of pain development of chronic symptoms.75 The causal relation-
neurophysiology/pain biology education for chronic low ships between beliefs and poor outcomes such as
back pain58 and one of the effect of pain neurophysiology/ unhealthy behaviours, pain and disability are outlined in
pain biology education on chronic pain, with most psychological theories such as the social cognition models
included studies on low back pain.59 Clarke et al.58 and including self-efficacy,76,77 the theory of planned behav-
Louw et al.59 concluded that pain neurophysiology edu- iour,78 and the fear-avoidance model.79–81
cation was effective at reducing pain intensity for patients When providing patient education, the aim of the
with chronic low back pain or other chronic pain. Clarke health-care practitioner is to change unhelpful beliefs
et al.58 found evidence that these effects become larger by providing accurate, evidenced-based information to
over time. Louw et al.59 concluded that pain neurophysi- reduce health anxiety or worries, increase confidence
ology education decreased disability for patients with dif- and make a patient an active participant in the man-
ferent chronic pain conditions whereas Clarke et al.58 did agement of their health (a patient-centred approach).
not reach the same conclusion for patients with chronic Changing unhelpful beliefs to more adaptive beliefs
low back pain. Neither of these reviews reported on sick is presumed to lead ultimately to decreased pain and
leave/return to work. The quality of the evidence included disability.
in these reviews typically ranged from moderate- to high- Unfortunately, relatively few studies have tested
quality studies,59 providing some confidence in the whether education can effectively change maladaptive
conclusions. or unhelpful beliefs.57 Those studies that have measured
The conclusions from systematic reviews provide the effect of education on catastrophizing6,82 and fear-
conflicting evidence that biomedical and biopsychosocial avoidance beliefs83 suggest that these beliefs may be
education are effective at reducing pain and disability difficult to change even with lengthy intervention
associated with low back pain. Even when effects are (greater than 3 hours) heavily focused on psychosocial
found, the size of the effect is often small and may not factors. It is therefore not known to what extent the
be clinically important. Larger and more robust effects conflicting evidence on the effectiveness of patient
are found for patients with chronic pain who are pro- education provided by systematic reviews might be due
vided with pain neurophysiology education. Biomedical to a failure to accurately target and change patient
and biopsychosocial education are most consistently beliefs.84
 28  Pain Management Introduction 267

6. Pengel LHM, Refshauge KM, Maher CG, et al. Physiotherapist-

COMMON BELIEFS TARGETED BY directed exercise, advice, or both for subacute low back pain – A
randomized trial. Ann Intern Med 2007;146:787–96.
PATIENT EDUCATION 7. Frost H, Lamb SE, Doll HA, et al. Randomised controlled trial of
physiotherapy compared with advice for low back pain. BMJ
Education targets commonly held erroneous, faulty or 2004;329:708. doi:10.1136/bmj.38216.868808.7C.
maladaptive beliefs that patients may have about their 8. Rantonen J, Vehtari A, Karppinen J, et al. Face-to-face information
combined with a booklet versus a booklet alone for treatment of
pain and their condition. mild low-back pain: a randomized controlled trial. Scand J Work
Suitable targets for education are beliefs about pain Environ Health 2013;40:156–66. doi:10.5271/sjweh.3398.
that have been shown to be associated with poor outcome, 9. Engers A, Jellema P, Wensing M, et al. Individual patient education
including catastrophic pain beliefs (a belief that the pain for low back pain. Cochrane Database Syst Rev 2008;CD004057,
has a serious cause, that the pain will persist and the doi:10.1002/14651858.CD004057.pub3.
10. Heymans MW, van Tulder MW, Esmail R, et al. Back schools for
condition will inevitably deteriorate), fear-avoidance nonspecific low back pain: a systematic review within the frame-
beliefs (when pain is experienced physical activities work of the Cochrane Collaboration Back Review Group. Spine
should be avoided and rest should be taken) and self- 2005;30:2153–63.
efficacy beliefs (the confidence that a patient has the 11. Cohen JE, Goel V, Frank JW, et al. Group education interventions
for people with low back pain. An overview of the literature. Spine
ability to achieve outcomes that are important and 1994;19:1214–22.
desirable).60,63 12. Heymans MW, van Tulder MW, Esmail R, et al. Back schools for
Research that shows that these beliefs are associated non-specific low-back pain. Cochrane Database Syst Rev
with poor outcomes such as pain and disability70,71 was a 2004;CD000261–CD000261, doi:10.1002/14651858.CD000261.
major reason for the development of biopsychosocial pub2.
13. Udermann BE, Spratt KF, Donelson RG, et al. Can a patient
education.42 Pain neurophysiology education focuses on educational book change behavior and reduce pain in chronic low
identifying and changing a belief that hurt equals harm.49,85 back pain patients? Spine J 2004;4:425–35. doi:10.1016/j.spinee.
A strong belief that the presence of pain is always associ- 2004.01.016.
ated with tissue damage is regarded by this approach as 14. Roland M, Dixon M. Randomized controlled trial of an educational
booklet for patients presenting with back pain in general practice.
underpinning other maladaptive beliefs such as cata- J R Coll Gen Pract 1989;39:244–6.
strophic and fear-avoidant beliefs.48 15. Burton AK, Waddell G, Tillotson KM, et al. Information and
advice to patients with back pain can have a positive effect. A ran-
domized controlled trial of a novel educational booklet in primary
PAIN NEUROPHYSIOLOGY EDUCATION care. Spine 1999;24:2484–91.
16. Hendrick PA, Ahmed OH, Bankier SS, et al. Manual therapy. Man
Ther 2012;17:318–24. doi:10.1016/j.math.2012.02.019.
In contrast to biomedical and biopsychosocial education 17. Washington TA, Fanciullo GJ, Sorensen JA, et al. Quality of
there is evidence that pain neurophysiology education chronic pain websites. Pain Med 2008;9:994–1000. doi:10.1111/
effectively targets and changes patients’ beliefs. In par- j.1526-4637.2008.00419.x.
18. Fischer J, Geurts J, Valderrabano V, et al. Educational quality of
ticular, pain neurophysiology has been found to decrease youtube videos on knee arthrocentesis. JCR. J Clin Rheumatol
pain-related catastrophizing in people with chronic or 2013;19:373–6. doi:10.1097/RHU.0b013e3182a69fb2.
subacute pain.47,86,87 A simple book using pain metaphors 19. Stephen K, Cumming GP. Searching for pelvic floor muscle exer-
based on principles of the neurophysiology of pain has cises on YouTube: what individuals may find and where this might
also been found to decrease catastrophizing in patients fit with health service programmes to promote continence. Meno-
pause Int 2012;18:110–15. doi:10.1258/mi.2012.012007.
with chronic low back pain,88 although written material 20. Wallace LS, Dhingra LK. A systematic review of smartphone appli-
provided to patients with fibromyalgia did not.89 Investi- cations for chronic pain available for download in the United States.
gations are underway to determine whether pain neuro- J Opioid Manag 2014;10:63–8. doi:10.5055/jom.2014.0193.
physiology effectively targets and changes catastrophizing 21. Reynoldson C, Stones C, Allsop M, et al. Assessing the quality and
usability of smartphone apps for pain self-management. Pain Med
and self-efficacy in patients with acute low back pain and 2014;15:898–909. doi:10.1111/pme.12327.
whether these effects are associated with pain and dis- 22. Rosser BA, Eccleston C. Smartphone applications for pain manage-
ability outcomes.90 ment. J Telemed Telecare 2011;17:308–12. doi:10.1258/jtt.2011.
101102.
23. Oliveira AA, Gevirtz RR, Hubbard DD. A psycho-educational
REFERENCES video used in the emergency department provides effective treat-
1. Lagger G, Pataky Z, Golay A. Efficacy of therapeutic patient educa- ment for whiplash injuries. CORD Conf Proc 2006;31:1652–7.
tion in chronic diseases and obesity. Patient Educ Couns doi:10.1097/01.brs.0000224172.45828.e3.
2010;79:283–6. doi:10.1016/j.pec.2010.03.015. 24. Pozo-Cruz B, Parraca J, Pozo-Cruz J, et al. An occupational,
2. Koes BW, van Tulder M, Lin C-WC, et al. An updated overview internet-based intervention to prevent chronicity in subacute lower
of clinical guidelines for the management of non-specific low back back pain: a randomised controlled trial. J Rehabil Med
pain in primary care. Eur Spine J 2010;19:2075–94. doi:10.1007/ 2012;44:581–7. doi:10.2340/16501977-0988.
s00586-010-1502-y. 25. Gross DP, Russell AS, Ferrari R, et al. Evaluation of a Canadian
3. Dagenais S, Tricco AC, Haldeman S. Synthesis of recommenda- back pain mass media campaign. Spine 2010;35:906–13. doi:10.1097/
tions for the assessment and management of low back pain from BRS.0b013e3181c91140.
recent clinical practice guidelines. Spine J 2010;10:514–28. 26. Waddell G, O’Connor M, Boorman S, et al. Working Backs Scot-
doi:10.1016/j.spinee.2010.03.032. land: a public and professional health education campaign for back
4. Henrotin YE, Cedraschi C, Duplan B, et al. Information and low pain. Spine 2007;32:2139–43. doi:10.1097/BRS.0b013e31814541bc.
back pain management: a systematic review. Spine 2006;31:E326– 27. Buchbinder R, Jolley D, Wyatt M. 2001 Volvo Award Winner in
34. doi:10.1097/01.brs.0000217620.85893.32. Clinical Studies: effects of a media campaign on back pain beliefs
5. Nijs J, van Wilgen CP, Van Oosterwijck J, et al. How to explain and its potential influence on management of low back pain in
central sensitization to patients with ‘unexplained’ chronic muscu- general practice. Spine 2001;26:2535–42.
loskeletal pain: practice guidelines. Man Ther 2011;16:413–18. 28. Dupeyron A, Ribinik P, Gélis A, et al. Education in the manage-
doi:10.1016/j.math.2011.04.005. ment of low back pain. Literature review and recall of key
268 PART III  Advances in Clinical Science and Practice

recommendations for practice. Ann Phys Rehabil Med 2011;54:319– low back pain. Spine J 2008;8:948–58. doi:10.1016/j.spinee.2007.
35. doi:10.1016/j.rehab.2011.06.001. 07.389.
29. Pellisé F, Sell P, EuroSpine Patient Line Task Force. Patient infor- 54. Turner JA. Educational and behavioral interventions for back pain
mation and education with modern media: the Spine Society of in primary care. Spine 1996;21:2851–7, discussion 2858–9.
Europe Patient Line. Eur Spine J 2009;18(Suppl. 3):395–401. 55. Demoulin C, Marty M, Genevay S, et al. Effectiveness of preven-
doi:10.1007/s00586-009-0973-1. tive back educational interventions for low back pain: a critical
30. Hancock MJ, Maher CG, Latimer J, et al. Systematic review of tests review of randomized controlled clinical trials. Eur Spine J
to identify the disc, SIJ or facet joint as the source of low back pain. 2012;21:2520–30. doi:10.1007/s00586-012-2445-2.
Eur Spine J 2007;16:1539–50. doi:10.1007/s00586-007-0391-1. 56. Shaheed CA, Maher CG, Williams KA, et al. Critical Review.
31. Henschke N, Maher CG, Refshauge KM. A systematic review YJPAI 2014;15:2–15. doi:10.1016/j.jpain.2013.09.016.
identifies five ‘red flags’ to screen for vertebral fracture in patients 57. Henrotin YE, Cedraschi C, Duplan B, et al. Information and low
with low back pain. J Clin Epidemiol 2008;61:110–18. doi:10.1016/j. back pain management: a systematic review. Spine 2006;31:E326.
jclinepi.2007.04.013. 58. Clarke CL, Ryan CG, Martin DJ. Pain neurophysiology education
32. Henschke N, Maher CG, Refshauge KM, et al. Prevalence of and for the management of individuals with chronic low back pain: a
screening for serious spinal pathology in patients presenting to systematic review and meta-analysis. Man Ther 2011;16:544–9.
primary care settings with acute low back pain. Arthritis Rheum doi:10.1016/j.math.2011.05.003.
2009;60:3072–80. doi:10.1002/art.24853. 59. Louw A, Diener I, Butler DS, et al. The effect of neuroscience
33. da C Menezes Costa L, Maher CG, Hancock MJ, et al. The prog- education on pain, disability, anxiety, and stress in chronic muscu-
nosis of acute and persistent low-back pain: a meta-analysis. Can loskeletal pain. Arch Phys Med Rehabil 2011;92:2041–56.
Med Assoc J 2012;184:E613–24. doi:10.1503/cmaj.111271. doi:10.1016/j.apmr.2011.07.198.
34. Koes BW, van Tulder MW, Thomas S. Diagnosis and treatment of 60. Pincus T, McCracken LM. Psychological factors and treatment
low back pain. BMJ 2006;332:1430–4. doi:10.1136/bmj.332.7555. opportunities in low back pain. Best Pract Res Clin Rheumatol
1430. 2013;27:625–35. doi:10.1016/j.berh.2013.09.010.
35. Hasenbring MI, Pincus T. Effective reassurance in primary care of 61. Hush JM, Refshauge K, Sullivan G, et al. Recovery: what does this
low back pain. Clin J Pain 2014. doi:10.1097/AJP.0000000000000097; mean to patients with low back pain? Arthritis Rheum 2009;61:124–
[Epub ahead of print]. 31. doi:10.1002/art.24162.
36. Henschke N, Maher CG, Refshauge KM, et al. Prognosis in 62. Dworkin RH, Turk DC, Farrar JT, et al. Core outcome measures
patients with recent onset low back pain in Australian primary care: for chronic pain clinical trials: IMMPACT recommendations. Pain
inception cohort study. BMJ 2008;337:a171. doi:10.1136/bmj.a171. 2005;113:9–19. doi:10.1016/j.pain.2004.09.012.
37. Martin L. Back basics: general information for back school partici- 63. Main CJ, Foster N, Buchbinder R. How important are back pain
pants. Occup Med 1992;7:9–16. beliefs and expectations for satisfactory recovery from back pain?
38. Forssell MZ. The Swedish Back School. Physiotherapy 1980; Best Pract Res Clin Rheumatol 2010;24:205–17. doi:10.1016/j.
66:112–14. berh.2009.12.012.
39. Bendix T, Bendix AF, Busch E, et al. Functional restoration in 64. Bostick GP, Schopflocher D, Gross DP. Validity evidence for the
chronic low back pain. Scand J Med Sci Sports 1996;6:88–97. back beliefs questionnaire in the general population. Eur J Pain
40. Bendix T, Bendix A, Labriola M, et al. Functional restoration 2013;17:1074–81. doi:10.1002/j.1532-2149.2012.00275.x.
versus outpatient physical training in chronic low back pain: a 65. Buer N, Linton SJ. Fear-avoidance beliefs and catastrophizing:
randomized comparative study. Spine 2000;25:2494–500. occurrence and risk factor in back pain and ADL in the general
41. Poiraudeau S, Rannou F, Revel M. Functional restoration programs population. Pain 2002;99:485–91.
for low back pain: a systematic review. Ann Readapt Med Phys 66. Leeuw M, Houben RMA, Severeijns R, et al. Pain-related fear in
2007;50:425–9, 419–24. doi:10.1016/j.annrmp.2007.04.009. low back pain: a prospective study in the general population. Eur J
42. Waddell G. Biopsychosocial analysis of low back pain. Baillieres Pain 2012;11:256–66. doi:10.1016/j.ejpain.2006.02.009.
Clin Rheumatol 1992;6:523–57. 67. Ihlebæk C, Eriksen H. Are the ‘myths’ of low back pain alive in the
43. Waddell G, Main CJ, Morris EW, et al. Chronic low-back pain, general Norwegian population? Scand J Public Health 2003;31:395–
psychologic distress, and illness behavior. Spine 1984;9:209–13. 8. doi:10.1080/14034940210165163.
44. Hagen KB, Jamtvedt G, Hilde G, et al. The updated cochrane 68. Gross DP, Ferrari R, Russell AS, et al. A population-based survey
review of bed rest for low back pain and sciatica. Spine 2005; of back pain beliefs in Canada. Spine 2006;31:2142–5.
30:542–6. doi:10.1097/01.brs.0000231771.14965.e4.
45. Dahm KT, Brurberg KG, Jamtvedt G, et al. Advice to rest in 69. Crombez G, Vlaeyen JW, Heuts PH, et al. Pain-related fear is
bed versus advice to stay active for acute low-back pain and more disabling than pain itself: evidence on the role of pain-related
sciatica (Review). Cochrane Database of Systematic Reviews 2010. fear in chronic back pain disability. Pain 1999;80:329–39.
doi:10.1002/14651858.CD007612.pub2. 70. Wertli MM, Eugster R, Held U, et al. Catastrophizing-a prognos-
46. Hagen EM, Eriksen HR, Ursin H. Does early intervention with a tic factor for outcome in patients with low back pain: a systematic
light mobilization program reduce long-term sick leave for low review. Spine J 2014;14(11):2639–57. pii: S1529-9430(14)00243-5.
back pain? Spine 2000;25:1973–6. doi:10.1016/j.spinee.2014.03.003.
47. Moseley GL, Nicholas MK, Hodges PW. A randomized controlled 71. Wertli MM, Rasmussen-Barr E, Weiser S, et al. The role of fear
trial of intensive neurophysiology education in chronic low back avoidance beliefs as a prognostic factor for outcome in patients with
pain. Clin J Pain 2004;20:324–30. nonspecific low back pain: a systematic review. Spine J 2014;14:816–
48. Moseley L. Unraveling the barriers to reconceptualization of the 36.e4. doi:10.1016/j.spinee.2013.09.036.
problem in chronic pain: the actual and perceived ability of patients 72. Pincus T, Vogel S, Burton AK, et  al. Fear avoidance and prog-
and health professionals to understand the neurophysiology. J Pain nosis in back pain: a systematic review and synthesis of current
2003;4:184–9. doi:10.1016/S1526-5900(03)00488-7. evidence. Arthritis Rheum 2006;54:3999–4010. doi:10.1002/
49. Butler DS, Moseley GL. Explain Pain, 2nd Edition. 2013. Noigroup art.22273.
Publications; Adelaide, pp. 133. 73. Jensen MP, Turner JA, Romano JM. Changes in beliefs, catastroph-
50. Moseley GL. A pain neuromatrix approach to patients with chronic izing, and coping are associated with improvement in multidisci-
pain. Man Ther 2003;8:130–40. plinary pain treatment. J Consult Clin Psychol 2001;69:655–62.
51. Haines T, Gross AR, Burnie S, et al. A Cochrane review of patient doi:10.1037//0022-006X.69.4.655.
education for neck pain. Spine J 2009;9:859–71. doi:10.1016/j. 74. Mansell G, Kamper SJ, Kent P. Why and how back pain interven-
spinee.2009.04.019. tions work: what can we do to find out? Best Pract Res Clin Rheu-
52. Yu H, Côté P, Southerst D, et al. Does structured patient education matol 2013;27:685–97. doi:10.1016/j.berh.2013.10.001.
improve the recovery and clinical outcomes of patients with neck 75. Costa LDCM, Maher CG, McAuley JH, et al. Self-efficacy is more
pain? A systematic review from the Ontario Protocol for Traffic important than fear of movement in mediating the relationship
Injury Management (OPTIMa) Collaboration. Spine J 2014. pii: between pain and disability in chronic low back pain. Eur J Pain
S1529-9430(14)00347-7. doi:10.1016/j.spinee.2014.03.039. 2011;15:213–19. doi:10.1016/j.ejpain.2010.06.014.
53. Brox JI, Storheim K, Grotle M, et al. Systematic review of back 76. Bandura A. Human agency in social cognitive theory. Am Psychol
schools, brief education, and fear-avoidance training for chronic 1989;44:1175.
 28  Pain Management Introduction 269

77. Bandura A. Social cognitive theory of self-regulation. Organ Behav 85. Moseley GL. Reconceptualising pain according to modern pain
Hum Decis Process 1991;50:248–87. science. Phys Ther Rev 2007;12:169–78. doi:10.1179/108331907
78. Armitage CJ, Conner M. Efficacy of the Theory of Planned Behav- X223010.
iour: a meta-analytic review. Br J Soc Psychol 2001;40:471–99. 86. Ryan CG, Gray HG, Newton M, et al. Pain biology education and
79. Leeuw M, Goossens MEJB, Linton SJ, et al. The fear-avoidance exercise classes compared to pain biology education alone for indi-
model of musculoskeletal pain: current state of scientific evidence. viduals with chronic low back pain: a pilot randomised controlled
J Behav Med 2006;30:77–94. doi:10.1007/s10865-006-9085-0. trial. Man Ther 2010;15:382–7. doi:10.1016/j.math.2010.03.003.
80. Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences 87. Meeus M, Nijs J, Van Oosterwijck J, et al. Pain physiology educa-
in chronic musculoskeletal pain: a state of the art. Pain tion improves pain beliefs in patients with chronic fatigue syndrome
2000;85:317–32. compared with pacing and self-management education: a double-
81. Vlaeyen JWS, Linton SJ. Fear-avoidance model of chronic muscu- blind randomized controlled trial. Arch Phys Med Rehabil
loskeletal pain: 12 years on. Pain 2012;153:1144–7. doi:10.1016/j. 2010;91:1153–9. doi:10.1016/j.apmr.2010.04.020.
pain.2011.12.009. 88. Gallagher L, McAuley J, Moseley GL. A randomized-controlled
82. Jellema P, van der Windt DAWM, van der Horst HE, et al. Should trial of using a book of metaphors to reconceptualize pain and
treatment of (sub)acute low back pain be aimed at psychosocial decrease catastrophizing in people with chronic pain. Clin J Pain
prognostic factors? Cluster randomised clinical trial in general 2013;29:20–5. doi:10.1097/AJP.0b013e3182465cf7.
practice. BMJ 2005;331:84. doi:10.1136/bmj.38495.686736.E0. 89. van Ittersum MW, van Wilgen CP, Groothoff JW, et al. Is apprecia-
83. Hay E, Mullis R, Lewis M, et al. Comparison of physical treat- tion of written education about pain neurophysiology related to
ments versus a brief pain-management programme for back pain in changes in illness perceptions and health status in patients with
primary care: a randomised clinical trial in physiotherapy practice. fibromyalgia? Patient Educ Couns 2010;85(2):269–74. doi:10.1016/j.
Lancet 2005;365:2024–30. doi:10.1016/S0140-6736(05)66696-2. pec.2010.09.006.
84. Jellema P, van der Windt DAWM, van der Horst HE, et al. Why 90. Traeger AC, Moseley GL, Hübscher M, et al. Pain education to
is a treatment aimed at psychosocial factors not effective in patients prevent chronic low back pain: a study protocol for a randomised
with (sub)acute low back pain? Pain 2005;118:350–9. doi:10.1016/j. controlled trial. BMJ Open 2014;4:e005505. doi:10.1136/
pain.2005.09.002. bmjopen-2014-005505.

CHAPTER 28.3  ■  PHYSICAL INTERVENTIONS OF PAIN

MANAGEMENT AND POTENTIAL
PROCESSES
Kathleen Sluka

EXERCISE Dosing
Exercise is a mainstay of physiotherapy interventions. Despite the strong evidence that exercise is effective,
For pain management, nearly all subjects will be pre- there are insufficient data to make recommendations
scribed an exercise programme to increase physical activ- regarding the frequency, duration and intensity of an
ity, increase strength and restore normal motion. There effective exercise programme. Thus, future experiments
are numerous forms of exercise including stretching, need to determine optimal dosing parameters for devel-
strengthening, motor control, coordination, endurance opment of an effective exercise programme. However,
and aerobic. Physiotherapists use a combination of dif- the type of exercise has been tested in a variety of
ferent forms of exercise to individualize a programme to pain conditions. In most instances for those with chronic
the person with pain. pain, both strengthening and aerobic conditioning exer-
cises are equally effective.5,16,17 For example, in people
with low back pain equivalent reductions in pain and
disability and improvements in function and quality of
Clinical Studies life occurred when motor control exercises were com-
Numerous studies show the effectiveness of exercise for pared with graded activity, or when motor control
a variety of pain conditions (Cochrane reviews) including exercises were compared with general aerobic exercise.5,18
chronic low back pain, neck pain, tendonitis, osteoarthri- Similarly, in fibromyalgia comparing muscle strengthen-
tis, rheumatoid arthritis, fibromyalgia, myofascial pain ing exercises to an aerobic exercise training programme
and neuropathic pain.1–12 Further exercise can reduce the produced similar reductions in pain and improvements
number of recurrences of low back pain,13 suggesting in quality of life,17 and in those with osteoarthritis
that regular exercise can reduce the chronicity of pain. aerobic exercise, strengthening exercises and aquatic
Lastly, using a large-population database those who are exercises all reduce pain and improve function.16 Addi-
regularly physically active are less likely to develop tionally, complementary and alternative therapies that
chronic musculoskeletal pain conditions than those who include exercise, such as yoga and tai chi, as well as
are sedentary.14,15 Thus exercise and physical activity can lifestyle physical activity are also effective in people
reduce pain and disability, and improve function in with a variety of pain conditions.6,19–21 Thus, the type
people with a variety of painful conditions, can prevent of exercise given for someone with chronic pain should
the recurrence of pain and can prevent the development be targeted towards patient preference and factors that
of chronic pain. improve compliance.
270 PART III  Advances in Clinical Science and Practice

Basic Mechanisms for both low- (T-; LVA) and high-voltage activated acti-
vated calcium currents (N-, P/Q-, L-; HVA) in dorsal
Although a significant amount of clinical literature sup- root ganglia neurons,37 which is indicative of enhanced
ports the effectiveness of exercise for pain, few studies nociceptor activity. Aerobic exercise running reduced the
have addressed the underlying mechanisms. Early studies enhanced current densities of HVA and LVA calcium
examined mechanisms in uninjured animals and humans. channels, suggesting reductions in nociceptor activity
In animals, increases in withdrawal thresholds are and thus it is possible that regular exercise reduces pain
observed in rats allowed free access to running wheels,22 hypersensitivity by normalization of enhanced ion
mice bred for high running wheel activity,23 acute or channel activity of nociceptors.
long-term swimming24,25 and after a strength training Regular aerobic exercise in mice with muscle pain
programme.26 leads to increased expression of neurotrophin-3 mRNA
and protein in the muscle tissue and follows the same
time course as the analgesia.41 Neurotrophin-3 is analge-
Central Mechanisms
sic when injected or overexpressed in muscle,42 and thus
Endogenous opioids are produced in a wide range of these data suggest exercise could increase NT-3 in muscle
tissue types, including the midbrain periaqueductal grey to reduce nociceptive activity and produce analgesia.
(PAG), rostral ventromedial medulla (RVM), spinal cord
and muscle,27,28 and are key players in exercise-induced Additional Mechanisms
analgesia. Further, serotonin is a major neurotransmitter
found in endogenous inhibitory pathways including the A recent study showed that the reduction of pain behav-
PAG, RVM and spinal cord and plays a significant role iours in an animal model of neuropathic pain was blocked
in analgesia. In healthy human subjects there are increased by inhibition of adenosine receptors and enhanced
serum levels of β-endorphin in response to aerobic by inhibition of adenosine degradation systemically,39
exercise.29–31 In animals without tissue injury, blockade of and thus adenosine, either peripherally or centrally,
opioid receptors reduces analgesia produced by chronic could play a role in the analgesia produced by regular
running wheel activity and by strength training injury,23,24 exercise.
there is also reduced effectiveness of µ- and κ-opioid
agonists in the PAG in the midbrain after chronic
running wheel activity.22,32–35 In animal models of pain,
blockade of opioid receptors, systemically and in the TENS
brainstem, prevents the analgesia produced by regular
aerobic exercise in neuropathic pain, chronic muscle pain Transcutaneous electrical nerve stimulation (TENS) is
and acetic-acid-induced pain.24,36–39 In addition, there is the application of electrical stimulation to the skin for
an increased release of endogenous opioids in the PAG pain relief. TENS is generally applied at low frequencies
and RVM in response to aerobic exercise in animals with (<10 Hz) or high frequencies (>50 Hz), at varying inten-
neuropathic pain.36 On the other hand, blockade of sities. These intensities include sensory threshold, strong
peripheral opioid receptors has no effect on exercise- sensory intensity, or intensities that produce motor con-
induced analgesia in animals with neuropathic pain.36 In traction. Recent studies show that low and high frequen-
animals without tissue injury, aerobic exercise-induced cies produce analgesia through different mechanisms43
analgesia is prevented by prior depletion of serotonin and that greater intensities produce greater analgesia.44
with p-chlorophenylalanine.24 Thus these data support Electrodes can be placed to surround the site of pain,
that exercise activates our central inhibitory pathways to over a nerve or segmentally – not much research has been
produce analgesia through opioid and serotonergic done to examine optimum electrode placement sites.
mechanisms. TENS is a safe, non-invasive treatment with relatively
Central pathways not only inhibit pain, but can also few contraindications that can be either self-administered
facilitate and enhance pain behaviours. The RVM is a key or administered by a therapist. TENS is typically used as
nucleus in pain facilitation, and glutamate receptors an additional pain-management technique in a physical
mediate the facilitation. In animals, after induction of therapy management programme that includes education
chronic muscle pain or exercise-induced pain, there is and exercise.
enhanced phosphorylation of the NR1 subunit of the
NMDA receptor in the RVM,40 suggestive of enhanced
neuron activity in pain facilitation pathways. These
Clinical Studies
increases in p-NR1 in the RVM are prevented by regular The clinical literature on TENS is controversial and
physical activity,40 suggesting that regular exercise reduces recent reviews discuss potential reasons for this con-
central neuron sensitivity. troversy related to design and quality of trials.44,45 These
reviews suggest that sub-optimal dosing, inappropriate
outcome assessments and inadequate timing of outcomes
Peripheral Mechanisms
assessments contribute to negative effects. Systematic
It is also possible that exercise has effects peripherally, reviews show significant reductions in pain in individu-
reducing nociceptor activity or enhancing endogenous als post-operatively, those with osteoarthritis and those
inhibitory neuromodulators. In animals with diabetic with peripheral neuropathy.46–48 However, other system-
neuropathy, there is enhanced calcium current density atic reviews similarly show TENS is ineffective or
 28  Pain Management Introduction 271

inconclusive for a variety of painful conditions includ- used clinically, TENS activates large-diameter afferent
ing acute pain, osteoarthritis, low back pain and post- fibres.72,73 This afferent input is sent to the central nervous
operative pain;49–55 this effect may be dependent on system to activate the descending inhibitory system to
dosing of TENS.46,47 reduce hyperalgesia. Specifically, blockade of neuronal
TENS has also been shown in individuals with post- activity in the PAG, RVM and spinal cord inhibits the
operative pain, osteoarthritis and fibromyalgia to reduce analgesic effects of TENS.74–76
pain with movement, but not pain at rest,56–58 suggesting In animals without tissue injury, both low- and high-
that TENS is more effective for movement-related pain. frequency TENS reduce dorsal horn neuron activity.77–81
TENS may be effective for other evoked pain like hyper- In animals with peripheral inflammation or neuropathic
algesia and allodynia, in addition to movement pain. pain, enhanced activity of dorsal horn neurons (i.e. central
Indeed TENS reduces hyperalgesia in those with osteo- sensitization) to both noxious and innocuous stimuli is
arthritis and fibromyalgia, and allodynia in those with reduced by either high- or low-frequency TENS.82–85 In
neuropathic pain.56,59,60 parallel there is a reduction in both primary and second-
TENS produces its analgesic effect by activating ary hyperalgesia by either low- or high-frequency
opioid receptors (see Basic Science Mechanisms section TENS.82–84,86–90
for details) and as such it is important to understand In human subjects high-frequency TENS increases the
potential pharmaceutical interactions. Low-frequency concentration of β-endorphins in the bloodstream and
TENS activates mu-opioid receptors whereas high- cerebrospinal fluid, and methionine-enkephalin in the
frequency TENS activates delta-opioid receptors.43 As cerebrospinal fluid.91,92 The reduction in hyperalgesia
opioids can produce analgesic tolerance, repeated daily by high-frequency TENS is prevented by blockade of
use of TENS at the same frequency and intensity (dose) δ-opioid receptors in the RVM or spinal cord, or syn-
in healthy controls can also induce analgesic tolerance.61 aptic transmission in the ventrolateral PAG.75,76,93 The
In addition, low-frequency TENS is less effective than reduction in hyperalgesia produced by high-frequency
high-frequency TENS in both people and animals that TENS is prevented by blockade of muscarinic receptors
are opioid-tolerant.62,63 Alternating frequencies between (M1, M3) in the spinal cord94 – muscarinic receptors
low and high, or increasing intensity daily delays anal- are implicated in opioid analgesia in the spinal cord.
gesic tolerance in animal studies.64,65 Thus, understand- High-frequency TENS also enhances release of the
ing mechanisms may assist in improving efficacy of inhibitory neurotransmitter GABA in the spinal cord
treatment. dorsal horn and the TENS antihyperalgesia is reduced
On the other hand, a cumulative effect of TENS by blockade of GABAA receptors in the spinal cord.95
(delivered two to five times per week) has been shown in However, blockade of serotonin or noradrenergic recep-
individuals with chronic low back pain, osteoarthritis and tors in the spinal cord has no effect on the reversal of
neuropathic pain.60,66–68 The reasons for this cumulative hyperalgesia produced by high-frequency TENS.96 Thus
effect are not clear but may be secondary to increasing high-frequency TENS produces analgesia by activating
activity levels as a result of reduced movement pain. endogenous inhibitory mechanisms in the central
Alternatively, TENS could normalize pain physiology nervous system involving opioid, GABA and muscarinic
(i.e. reduce central sensitization or increase central inhi- receptors.
bition). In support a recent study in individuals with High-frequency TENS also reduces central neuron
fibromyalgia showed that TENS delivered to the neck or sensitization,85 and release of the excitatory neurotrans-
back increased pain thresholds outside the site of stimula- mitters glutamate and substance P in the spinal cord
tion (leg) and increased central inhibition (central pain dorsal horn in animals with inflammation.97,98 The reduc-
modulation).56 tion in glutamate is prevented by blockade of δ-opioid
receptors. Thus, one consequence of activation of inhibi-
tory pathways by TENS is to reduce excitation and con-
Dosing sequent neuron sensitization in the spinal cord.
It has become increasingly clear in the last decade that Peripherally, substance P, which is normally increased
intensity of TENS is critically important to obtain a posi- in injured animals, is reduced in dorsal root ganglia
tive effect. Specifically, stimulation amplitude must be of neurons by high-frequency TENS in animals injected
sufficient strength to produce an analgesic response.47,57,69,70 with the inflammatory irritant, formalin.97 In α-2a-
In healthy subjects, TENS delivered at a strong but com- adrenergic knockout mice, analgesia by high-frequency
fortable intensity provided a significant analgesic effect, TENS does not occur.99 Blockade of peripheral, but not
whereas TENS delivered at or below sensory threshold spinal or supraspinal, α-2a receptors prevents the analge-
was ineffective.69–71 Similarly, systematic reviews that sia produced by TENS,99 suggesting a role for peripheral
consider dosing show that high intensities are associated α-2a-adrenergic in analgesia produced by TENS. Thus,
with significant reductions in both post-operative and some of the analgesic effects of TENS are mediated
osteoarthritis pain while lower intensities are not through actions on primary afferent fibres.
effective.46,47 Low-frequency TENS reduces hyperalgesia after joint
inflammation and this reduction is prevented by blockade
of µ-opioid receptors in the spinal cord or the RVM, or
Basic Science Mechanisms synaptic transmission in the ventrolateral PAG.93 The
TENS activates a complex neuronal network to result analgesia produced by low-frequency TENS is also
in a reduction in pain. At frequencies and intensities reduced by blockade of GABAA, serotonin 5-HT2A and
272 PART III  Advances in Clinical Science and Practice

5-HT3 and muscarinic M1 and M3 receptors in the peripherally at the site of application and in the central
spinal cord.94–96 Serotonin is released during low- nervous system. Manipulation and mobilization clearly
frequency TENS in animals with joint inflammation.100 increase pain thresholds in healthy controls and increase
Low-frequency TENS also reduces dorsal horn neuron pain-free range of motion of the upper limb tension
sensitization in animals with inflammation.85 Thus, these test.126–129 Peripherally, in healthy human subjects, manip-
studies show that low-frequency TENS uses classical ulation produces a short-lived (10–30 seconds) decrease
descending inhibitory pathways involving the PAG– in motoneuron excitability.130,131 However, these effects
RVM pathway activating opioid, GABA, serotonin and are longer lasting in people with low back pain – spinal
muscarinic receptors to reduce dorsal horn neuron activ- manipulation increases the activity of the oblique abdom-
ity and the consequent pain. inal muscle for several minutes and there is no effect in
Low-frequency TENS also has effects on the periph- normal healthy controls.132 In an animal model, a lumbar
eral nervous systems. Blockade of peripheral opioid spinal thrust reduces activity of muscle spindle afferent
receptors with naloxone at the site of application prevents fibres for several seconds133 and decreases electromyo-
the analgesic effects of low-frequency but not high- graphic activity in the paraspinal muscles for minutes.134
frequency TENS in an animal model of inflammatory In addition, evidence suggests that joint mobilization
pain.101 The reduction in cold allodynia by low-frequency activates central inhibitory mechanisms to reduce central
TENS is reduced by administration of systemic phentol- excitability and have a more widespread effect. In healthy
amine to block α-adrenergic receptors.83 In parallel, the controls there is a decrease in temporal summation,
antihyperalgesia produced by low-frequency TENS in which is a measure of central excitability, following spinal
animals with joint inflammation is reduced in α2a- manipulation, suggesting central mechanisms may play a
noradrenergic receptor knockout mice, and prevented by role.135,136 In people with lateral epicondylalgia, joint
peripheral blockade of α2-noradrenergic receptors (but mobilization of the cervical spine (grade III lateral glide
not by spinal or supraspinal blockade).99 Increases in of C5/6) increases pressure pain thresholds, pain-free
blood flow occur with stronger low-frequency TENS at range of motion for the upper limb tension test and pain-
intensities that produce motor contraction (intensity free grip force,128 and in people with knee osteoarthritis
greater than 25% above motor threshold).102–106 Thus, application of joint mobilization to the knee increases
peripheral effects of TENS may involve opioid receptors pressure pain thresholds at the knee (i.e. primary hyper-
and changes in sympathetic activity utilizing local α2a- algesia) and the heel (i.e. secondary hyperalgesia).137
noradrenergic receptors. Similarly, in animal models of inflammatory pain,
grade III mobilizations of the knee joint reduce hyperal-
gesia associated with inflammation of the knee or the
MANUAL THERAPY ankle.137–139 Further ankle joint mobilization in an animal
model of neuropathic pain reduces the enhanced glial cell
Manual therapy techniques may include traditional activity in the spinal cord,146 further suggesting a reduc-
massage, soft tissue mobilization, joint mobilizations and tion in central excitability. Thus, these data show that
manipulations, nerve or ‘neural’ mobilization procedures, joint mobilizations not only have local effects but that the
joint stabilization exercises and self-mobilization exer- effects can be widespread, indicating reductions in central
cises. Clinical evidence supports the use of massage and excitability.
manipulations for a variety of pain conditions.107–122 Pharmacological studies in humans and animals have
started to decipher potential mechanisms in the central
nervous system underlying the analgesia produced by
Basic Science Mechanisms joint manipulation. The analgesia produced by joint
The basic science mechanisms underlying massage have manipulation and mobilization is not reversed by the
included evidence aimed at deciphering which central opioid antagonist, naloxone, in human subjects.140–142 or
pathways are activated. In an animal model, 10 minutes in an animal model of mobilization-induced analgesia.138
of massage to the abdomen increases pain thresholds in However, in an animal model of post-operative pain,
a cumulative manner.123 Following massage in this model blockade of opioids locally prevents the analgesia pro-
there is an increase in the neuropeptide oxytocin in the duced by mobilization.143 The analgesia produced using
plasma and PAG in response.123 Blockade of oxytocin grade III mobilization of the knee joint, in an animal
receptors, either systemically or in the PAG, reduces the model of ankle inflammation or post-operative pain, is
analgesic effect of massage.124 After delayed onset muscle prevented by spinal blockade of serotonin 5-HT1A and
soreness (DOMS) induced in otherwise healthy male α-2 noradrenergic receptors.138,144 However, blockade of
subjects, 10 minutes of massage reduced excitatory sig- GABA or opioid receptors spinally has no effect on the
nally at the level of the muscle (decreases in cytokines, analgesia produced by mobilization.138 In a post-operative
heat shock protein phosphorylation and NFκB) and pain animal model, blockade of adenosine-A1 and can-
increased signalling proteins involved in tissue repair and nabinoid receptors CB1 and CB2 in the spinal cord
metabolic control (MAP kinases, PGC-1).125 Thus prevents the effects of ankle joint mobilization.144,145
massage likely has local peripheral effects, as well as more These data suggest that joint mobilizations reduce pain
systemic and central nervous system effects that either through effects in the central nervous system by activat-
directly or indirectly reduce pain. ing descending inhibitory pathways from the RVM and
Joint manipulation and mobilization use similar mul- dorsolateral pontine tegmentum (DLPT) that are
tiple mechanisms to reduce pain that include effects non-opioid.
 28  Pain Management Introduction 273

in male and female rats. Pharmacol Biochem Behav 1998;61:

REFERENCES 19–27.
1. Bement MK. Exercise-induced hypoalgesia: an evidence-based 23. Li G, Rhodes JS, Girard I, et al. Opioid-mediated pain sensitivity
review. In: Sluka KA, editor. Mechanisms and Management of in mice bred for high voluntary wheel running. Physiol Behav
Pain for the Physical Therapist. Seattle: IASP Press; 2009. 2004;83:515–24.
p. 143–66. 24. Mazzardo-Martins L, Martins DF, Marcon R, et al. High-intensity
2. Busch AJ, Barber KA, Overend TJ, et al. Exercise for treating extended swimming exercise reduces pain-related behavior in
fibromyalgia syndrome. Cochrane Database Syst Rev 2007; mice: involvement of endogenous opioids and the serotonergic
CD003786. system. J Pain 2010;11:1393.
3. Chou R, Huffman LH. Nonpharmacologic therapies for acute and 25. Blustein JE, McLaughlin M, Hoffman JR. Exercise effects stress-
chronic low back pain: a review of the evidence for an American induced analgesia and spatial learning in rats. Physiol Behav
Pain Society/American College of Physicians clinical practice 2006;89:582–6.
guideline. Ann Intern Med 2007;147:492–504. 26. Galdino GS, Duarte ID, Perez AC. Participation of endogenous
4. Edmonds M, McGuire H, Price J. Exercise therapy for chronic opioids in the antinociception induced by resistance exercise in
fatigue syndrome. Cochrane Database Syst Rev 2004;CD003200. rats. Braz J Med Biol Res 2010;43:906–9.
5. Ferreira ML, Ferreira PH, Latimer J, et al. Comparison of general 27. Denning GM, Ackermann LW, Barna TJ, et al. Proenkephalin
exercise, motor control exercise and spinal manipulative therapy expression and enkephalin release are widely observed in non-
for chronic low back pain: a randomized trial. Pain 2007;131 neuronal tissues. Peptides 2008;29:83–92.
:31–7. 28. Sluka KA. Central mechanisms involved in pain processing. In:
6. Fontaine KR, Conn L, Clauw DJ. Effects of lifestyle physical Sluka KA, editor. Pain Mechanisms and Management for the
activity on perceived symptoms and physical function in adults Physical Therapist. Seattle: IASP Press; 2009. p. 41–72.
with fibromyalgia: results of a randomized trial. Arthritis Res Ther 29. Colt EW, Wardlaw SL, Frantz AG. The effect of running on
2010;12:R55. plasma beta-endorphin. Life Sci 1981;28:1637–40.
7. Fransen M, McConnell S, Bell M. Therapeutic exercise for people 30. Rahkila P, Hakala E, Alen M, et al. Beta-endorphin and cortico-
with osteoarthritis of the hip or knee. A systematic review. J Rheu- tropin release is dependent on a threshold intensity of running
matol 2002;29:1737–45. exercise in male endurance athletes. Life Sci 1988;43:551–8.
8. Hayden JA, van Tulder MW, Malmivaara A, et al. Exercise therapy 31. Rahkila P, Hakala E, Salminen K, et al. Response of plasma endor-
for treatment of non-specific low back pain. Cochrane Database phins to running exercises in male and female endurance athletes.
Syst Rev 2005;CD000335. Med Sci Sports Exerc 1987;19:451–5.
9. Kluding PM, Pasnoor M, Singh R, et al. The effect of exercise on 32. Smith MA, Yancey DL. Sensitivity to the effects of opioids in rats
neuropathic symptoms, nerve function, and cutaneous innervation with free access to exercise wheels: mu-opioid tolerance and physi-
in people with diabetic peripheral neuropathy. J Diabetes Com- cal dependence. Psychopharmacology (Berl) 2003;168:426–34.
plications 2012;26:424–8. 33. D’Anci KE, Gerstein AV, Kanarek RB. Long-term voluntary
10. Lluch E, Arguisuelas MD, Coloma PS, et al. Effects of deep cervi- access to running wheels decreases kappa-opioid antinociception.
cal flexor training on pressure pain thresholds over myofascial Pharmacol Biochem Behav 2000;66:343–6.
trigger points in patients with chronic neck pain. J Manipulative 34. Mathes WF, Kanarek RB. Chronic running wheel activity attenu-
Physiol Ther 2013;36:604–11. ates the antinociceptive actions of morphine and morphine-6-
11. Munneke M, de JZ, Zwinderman AH, et al. Effect of a high- glucouronide administration into the periaqueductal gray in rats.
intensity weight-bearing exercise program on radiologic damage Pharmacol Biochem Behav 2006;83:578–84.
progression of the large joints in subgroups of patients with rheu- 35. Mathes WF, Kanarek RB. Wheel running attenuates the antino-
matoid arthritis. Arthritis Rheum 2005;53:410–17. ciceptive properties of morphine and its metabolite, morphine-6-
12. Stegner AJ, Shields MR, Meyer JD, et al. Effects of acute and glucuronide, in rats. Physiol Behav 2001;74:245–51.
chronic physical activity on chronic pain conditions. In: Ekkekakis 36. Stagg NJ, Mata HP, Ibrahim MM, et al. Regular exercise reverses
P, editor. Routledge Handbook of Physical Activity and Mental sensory hypersensitivity in a rat neuropathic pain model: role of
Health. London: Routledge; 2013. p. 387–99. endogenous opioids. Anesthesiol 2011;114:940–8.
13. Choi BK, Verbeek JH, Tam WW, et al. Exercises for prevention 37. Shankarappa SA, Piedras-Renteria ES, Stubbs EB Jr. Forced-
of recurrences of low-back pain. Cochrane Database Syst Rev exercise delays neuropathic pain in experimental diabetes: effects
2010;CD006555. on voltage-activated calcium channels. J Neurochem 2011;
14. Landmark T, Romundstad PR, Borchgrevink PC, et al. Longitu- 118:224–36.
dinal associations between exercise and pain in the general 38. Bement MK, Sluka KA. Low-intensity exercise reverses chronic
population–the HUNT pain study. PLoS ONE 2013;8:e65279. muscle pain in the rat in a naloxone-dependent manner. Arch Phys
15. Landmark T, Romundstad P, Borchgrevink PC, et al. Associations Med Rehabil 2005;86:1736–40.
between recreational exercise and chronic pain in the general 39. Martins DF, Mazzardo-Martins L, Soldi F, et al. High-intensity
population: evidence from the HUNT 3 study. Pain 2011; swimming exercise reduces neuropathic pain in an animal model
152:2241–7. of complex regional pain syndrome type I: evidence for a role of
16. Uthman OA, van der Windt DA, Jordan JL, et  al. Exercise for the adenosinergic system. Neuroscience 2013;234:69–76.
lower limb osteoarthritis: systematic review incorporating trial 40. Sluka KA, O’Donnell JM, Danielson J, et al. Regular physical
sequential analysis and network meta-analysis. BMJ 2013;347: activity prevents development of chronic pain and activation of
f5555. central neurons. J Appl Physiol 2013;114:725–33.
17. Bircan C, Karasel SA, Akgun B, et al. Effects of muscle strength- 41. Sharma NK, Ryals JM, Gajewski BJ, et al. Aerobic exercise alters
ening versus aerobic exercise program in fibromyalgia. Rheumatol analgesia and neurotrophin-3 synthesis in an animal model of
Int 2008;28:527–32. chronic widespread pain. Phys Ther 2010;90:714–25.
18. Macedo LG, Latimer J, Maher CG, et al. Effect of motor control 42. Gandhi R, Ryals JM, Wright DE. Neurotrophin-3 reverses
exercises versus graded activity in patients with chronic nonspe- chronic mechanical hyperalgesia induced by intramuscular acid
cific low back pain: a randomized controlled trial. Phys Ther injection. J Neurosci 2004;24:9405–13.
2012;92:363–77. 43. Sluka KA, Walsh DM. Transcutaneous electrical nerve stimulation
19. Busch AJ, Webber SC, Brachaniec M, et al. Exercise therapy for and interferential current. In: Sluka KA, editor. Mechanisms adn
fibromyalgia. Curr Pain Headache Rep 2011;15:358–67. Management of Pain for the Physical Therapist. Seattle: IASP
20. Lauche R, Langhorst J, Dobos G, et al. A systematic review and Press; 2009. p. 167–90.
meta-analysis of Tai Chi for osteoarthritis of the knee. Comple- 44. Sluka KA, Marchand S, Bjordal JM, et al. What makes TENS
ment Ther Med 2013;21:396–406. work? Making sense of the clinical literature. Phys Ther 2013;
21. Holtzman S, Beggs RT. Yoga for chronic low back pain: a meta- 93:1397–402.
analysis of randomized controlled trials. Pain Res Manag 45. Bennett MI, Hughes N, Johnson MI. Methodological quality in
2013;18:267–72. randomised controlled trials of transcutaneous electric nerve
22. Kanarek RB, Gerstein AV, Wildman RP, et al. Chronic running- stimulation for pain: low fidelity may explain negative findings.
wheel activity decreases sensitivity to morphine-induced analgesia Pain 2011;152:1226–32.
274 PART III  Advances in Clinical Science and Practice

46. Bjordal JM, Johnson MI, Lopes-Martins RA, et al. Short-term 70. Moran F, Leonard T, Hawthorne S, et al. Hypoalgesia in response
efficacy of physical interventions in osteoarthritic knee pain. A to Transcutaneous Electrical Nerve Stimulation (TENS) depends
systematic review and meta-analysis of randomised placebo- on stimulation intensity. J Pain 2011;12:929–35.
controlled trials. BMC Musculoskelet Disord 2007;8:51. 71. Aarskog R, Johnson MI, Demmink JH, et al. Is mechanical pain
47. Bjordal JM, Johnson MI, Ljunggreen AE. Transcutaneous electri- threshold after transcutaneous electrical nerve stimulation
cal nerve stimulation (TENS) can reduce postoperative analgesic (TENS) increased locally and unilaterally? A randomized placebo-
consumption. A meta-analysis with assessment of optimal treat- controlled trial in healthy subjects. Physiother Res Int 2007;12:
ment parameters for postoperative pain. Eur J Pain 2003;7: 251–63.
181–8. 72. Levin MF, Hui-Chan CW. Conventional and acupuncture-like
48. Jin DM, Xu Y, Geng DF, et al. Effect of transcutaneous electrical transcutaneous electrical nerve stimulation excite similar afferent
nerve stimulation on symptomatic diabetic peripehral neuropathy: fibers. Arch Phys Med Rehabil 1993;74:54–60.
a meta-analysis of randomized controlled trials. Diabetes Res Clin 73. Radhakrishnan R, Sluka KA. Deep tissue afferents, but not cutane-
Practice 2010;89:10–15. ous afferents, mediate TENS-induced antihyperalgesia. J Pain
49. Hurlow A, Bennett MI, Robb KA, et al. Transcutaneous electric 2005;6:673–80.
nerve stimulation (TENS) for cancer pain in adults. Cochrane 74. Desantana JM, Sluka KA. Blockade of the ventrolateral PAG pre-
Database Syst Rev 2012;(3):CD006276. vents the effects of TENS. Neuroscience 2009;163:1233–41.
50. Khadilkar A, Odebiyi DO, Brosseau L, et al. Transcutaneous elec- 75. Kalra A, Urban MO, Sluka KA. Blockade of opioid receptors in
trical nerve stimulation (TENS) versus placebo for chronic low- rostral ventral medulla prevents antihyperalgesia produced by
back pain. Cochrane Database Syst Rev 2008;CD003008. transcutaneous electrical nerve stimulation (TENS). J Pharmacol
51. Kroeling P, Gross A, Goldsmith CH, et al. Electrotherapy for Exp Ther 2001;298:257–63.
neck pain. Cochrane Database Syst Rev 2009;CD004251. 76. Sluka KA, Deacon M, Stibal A, et al. Spinal blockade of opioid
52. Nnoaham KE, Kumbang J. Transcutaneous electrical nerve stimu- receptors prevents the analgesia produced by TENS in arthritic
lation (TENS) for chronic pain. Cochrane Database Syst Rev rats. J Pharmacol Exp Ther 1999;289:840–6.
2008;CD003222. 77. Lee KH, Chung JM, Willis WD. Inhibition of primate spinotha-
53. Rutjes AW, Nuesch E, Sterchi R, et al. Transcutaneous electro- lamic tract cells by TENS. J Neurosurg 1985;62:276–87.
stimulation for osteoarthritis of the knee. Cochrane Database Syst 78. Sjolund BH. Peripheral nerve stimulation suppression of C-fiber
Rev 2009;CD002823. evoked flexion reflex in rats. Part 1: Parameters of continuous
54. Walsh DM, Howe TE, Johnson MI, et al. Transcutaneous electri- stimulation. J Neurosurg 1985;63:612–16.
cal nerve stimulation for acute pain (review). Cochrane Database 79. Sjolund BH. Peripheral nerve stimulation suppression of C-fiber
Syst Rev 2009;CD006142. evoked flexion reflex in rats. Part 2. Parameters of low rat train
55. Dowswell T, Bedwell C, Lavender T, et al. Transcutaneous elec- stimulation of skin and muscle afferent nerves. J Neurosurg
trical nerve stimulation (TENS) for pain relief in labour. Cochrane 1988;68:279–83.
Database Syst Rev 2009;CD007214. 80. Garrison DW, Foreman RD. Decreased activity of spontaneous
56. Dailey DL, Vance CGT, Liebano RE, et al. Transcutaneous Elec- and noxiously evoked dorsal horn cells during transcutaneous
trical Nerve Stimulation (TENS) reduces and improves function electrical nerve stimulation (TENS). Pain 1994;58:309–15.
in people with fibromyalgia. J Pain 2012;12:23. 81. Garrison DW, Foreman RD. Effects of prolonged transcutaneous
57. Rakel B, Frantz R. Effectiveness of transcutaneous electrical nerve electrical nerve stimulation (TENS) and variation of stimulation
stimulation on postoperative pain with movement. J Pain variables on dorsal horn cell activity. Europ J Phys Med Rehabil
2003;4:455–64. 1997;6:87–94.
58. Law PPW, Cheing GLY, Tsui AYY. Does transcutaneous electrical 82. Somers DL, Clemente FR. High-frequency transcutaneous elec-
nerve stimulation improve the physical performance of people with trical nerve stimulation alters thermal but not mechanical allo-
knee osteoarthritis? J Clin Rheumatol 2004;10:295–9. dynia following chronic constriction injury of the rat sciatic nerve.
59. Vance CG, Rakel BA, Blodgett NP, et al. Effects of transcutaneous Arch Phys Med Rehabil 1998;79:1370–6.
electrical nerve stimulation on pain, pain sensitivity, and function 83. Nam TS, Choi Y, Yeon DS, et al. Differential antinocicptive effect
in people with knee osteoarthritis: a randomized controlled trial. of transcutaneous electrical stimulation on pain behavior sensitive
Phys Ther 2012. or insensitive to phentolamine in neuropathic rats. Neurosci Lett
60. Cheing GL, Luk ML. Transcutaneous electrical nerve stimulation 2001;301:17–20.
for neuropathic pain. J Hand Surg [Br] 2005;30:50–5. 84. Leem JW, Park ES, Paik KS. Electrophysiological evidence
61. Liebano R, Rakel B, Vance C, et al. An investigation of the devel- for the antinociceptive effect of transcutaneous electrical nerve
opment of analgesic tolerance to Transcutaneous Electrical Nerve stimulation on mechanically evoked responsiveness of dorsal
Stimulation (TENS) in humans. Pain 2011;152:335–42. horn neurons in neuropathic rats. Neurosci Lett 1995;192:
62. Leonard G, Courtier C, Marchand S. Reduced analgesic effect of 197–200.
acupuncture-like TENS but not conventional TENS in opioid- 85. Ma YT, Sluka KA. Reduction in inflammation-induced sensitiza-
treated patients. J Pain 2011;12:929–35. tion of dorsal horn neurons by transcutaneous electrical nerve
63. Chandran P, Sluka KA. Development of opioid tolerance with stimulation in anesthetized rats. Exp Brain Res 2001;137:
repeated transcutaneous electrical nerve stimulation administra- 94–102.
tion. Pain 2003;102:195–201. 86. Sluka KA, Bailey K, Bogush J, et al. Treatment with either high
64. Sato KL, Sanada LS, Rakel BA, et al. Increasing intensity of TENS or low frequency TENS reduces the secondary hyperalgesia
prevents analgesic tolerance in rats. J Pain 2012;13:884–90. observed after injection of kaolin and carrageenan into the knee
65. DeSantana JM, Santana-Filho VJ, Sluka KA. Modulation between joint. Pain 1998;77:97–102.
high- and low-frequency transcutaneous electric nerve stimulation 87. Vance CG, Radhakrishnan R, Skyba DA, et al. Transcutaneous
delays the development of analgesic tolerance in arthritic rats. electrical nerve stimulation at both high and low frequencies
Arch Phys Med Rehabil 2008;89:754–80. reduces primary hyperalgesia in rats with joint inflammation in a
66. Facci LM, Nowotny JP, Tormen F, et al. Effects of transcutaneous time-dependent manner. Phys Ther 2007;87(1):44–51.
electrical nerve stimulation (TENS) and interferential currents 88. Ainsworth L, Budelier K, Clinesmith M, et al. Transcutaneous
(IFC) in patients with nonspecific chronic low back pain: random- electrical nerve stimulation (TENS) reduces chronic hyperalgesia
ized clinical trial. Sao Paulo Med J 2011;129:206–16. induced by muscle inflammation. Pain 2006;120:182–7.
67. Marchand S, Charest J, Li J, et al. Is TENS purely a placebo 89. Gopalkrishnan P, Sluka KA. Effect of varying frequency, intensity
effect? A controlled study on chronic low back pain. Pain and pulse duration of TENS on primary hyperalgesia in inflamed
1993;54:99–106. rats. Arch Phys Med Rehabil 2000;81:984–90.
68. Law PP, Cheing GL. Optimal stimulation frequency of transcu- 90. Resende MA, Sabino GG, Candido CRM, et al. Transcutaneous
taneous electrical nerve stimulation on people with knee osteoar- electrical stimulation (TENS) effects in experimental inflamma-
thritis. J Rehabil Med 2004;36:220–5. tory edema and pain. Eur J Pharmacol 2004;504:217–22.
69. Rakel B, Cooper N, Adams HJ, et al. A new transient sham TENS 91. Salar G, Job I, Mingrino S, et al. Effect of transcutaneous electro-
device allows for investigator blinding while delivering a true therapy on CSF β-endorphin content in patients without pain
placebo treatment. J Pain 2010;11:230–8. problems. Pain 1981;10:169–72.
 28  Pain Management Introduction 275

92. Han JS, Chen XH, Sun SL, et al. Effect of low and high frequency 115. Delitto A, George SZ, Van Dillen LR, et al. Low back pain.
TENS on met-enkephalin-arg-phe and dynorphin A immunore- J Orthop Sports Phys Ther 2012;42:A1–57.
activity in human lumbar CSF. Pain 1991;47:295–8. 116. Childs JD, Cleland JA, Elliott JM, et al. Neck pain: clinical prac-
93. DeSantana JM, da Silva LF, De Resende MA, et al. Transcutane- tice guidelines linked to the International Classification of Func-
ous electrical nerve stimulation at both high and low frequencies tioning, Disability, and Health from the Orthopedic Section of
activates ventrolateral periaqueductal grey to decrease mechanical the American Physical Therapy Association. J Orthop Sports Phys
hyperalgesia in arthritic rats. N S 2009;163:1233–41. Ther 2008;38:A1–34.
94. Radhakrishnan R, Sluka KA. Spinal muscarinic receptors are acti- 117. Kelley MJ, Shaffer MA, Kuhn JE, et al. Shoulder pain and mobil-
vated during low or high frequency TENS-induced antihyperal- ity deficits: adhesive capsulitis. J Orthop Sports Phys Ther
gesia in rats. Neuropharm 2003;45:1111–19. 2013;43:A1–31.
95. Maeda Y, Lisi TL, Vance CG, et al. Releaes of GABA and activa- 118. Carcia CR, Martin RL, Houck J, et al. Achilles pain, stiffness, and
tion of GABAA receptors in the spinal cord mediates the effects of muscle power deficits: achilles tendinitis. J Orthop Sports Phys
TENS in rats. Brain Res 2007;1136:43–50. Ther 2010;40:A1–26.
96. Radhakrishnan R, King EW, Dickman J, et  al. Blockade of 119. McPoil TG, Martin RL, Cornwall MW, et al. Heel pain–plantar
spinal 5-HT receptor subtypes prevents low, but not high, fasciitis: clinical practice guildelines linked to the international
frequency TENS-induced antihyperalgesia in rats. Pain 2003;105: classification of function, disability, and health from the orthopae-
205–13. dic section of the American Physical Therapy Association.
97. Rokugo T, Takeuchi T, Ito H. A histochemical study of substance J Orthop Sports Phys Ther 2008;38:A1–18.
P in the rat spinal cord: effect of transcutaneous electrical nerve 120. Moss P, Sluka KA, Wright A. The initial effects of knee joint
stimulation. J Nippon Med Sch 2002;69:428–33. mobilisation on osteoarthritic hyperalgesia. Man Ther 2006;
98. Sluka KA, Vance CGT, Lisi TL. High-frequency, but not low- 12:109–18.
frequency, transcutaneous electrical nerve stimulation reduces 121. Vicenzino B, Collins D, Wright A. The initial effects of a cervical
aspartate and glutamate release in the spinal cord dorsal horn. spine manipulative physiotherapy treatment on the pain and dys-
J Neurochem 2005;95:1794–801. function of lateral epicondylalgia. Pain 1996;68:69–74.
99. King EW, Audette K, Athman GA, et al. Transcutaneous electrical 122. Vicenzino B, Paungmali A, Buratowski S, et  al. Specific manipu-
nerve stimulation activates peripherally located alpha-2A adrener- lative therapy treatment for chronic lateral epicondylalgia pro-
gic receptors. Pain 2005;115:364–73. duces uniquely characteristic hypoalgesia. Man Ther 2001;6:
100. Sluka KA, Lisi TL, Westlund KN. Increased release of serotonin 205–12.
in the spinal cord during low, but not high, frequency TENS in 123. Lund I, Ge Y, Yu LC, et al. Repeated massage-like stimulation
rats with joint inflammation. Arch Phys Med Rehab 2006;87: induces long-term effects on nociception: contribution of oxyto-
1137–40. cinergic mechanisms. Eur J Neurosci 2002;16:330–8.
101. Sabino GS, Santos CM, Francischi JN, et al. Release of endoge- 124. Agren G, Lundeberg T, Uvnas-Moberg K, et  al. The oxy-
nous opioids following transcutaneous electric nerve stimulation tocin antagonist 1-deamino-2-D-Tyr-(Oet)-4-Thr-8-Orn-oxyto-
in an experimental model of acute inflammatory pain. J Pain cin reverses the increase in the withdrawal response latency
2008;9:157–63. to thermal, but not mechanical nociceptive stimuli following
102. Sherry JE, Oehrlein KM, Hegge KS, et al. Effect of burst-mode oxytocin administration or massage-like stroking in rats. Neu-
transcutaneous electrical nerve stimulation on peripheral vascular rosci Lett 1995;187:49–52.
resistence. Phys Ther 2001;81:1183–91. 125. Crane JD, Ogborn DI, Cupido C, et al. Massage therapy attenu-
103. Cramp FL, McCullough GR, Lowe AS, et al. Transcutaneous ates inflammatory signaling after exercise-induced muscle damage.
electric nerve stimulation: the effect of intensity on local and distal Sci Transl Med 2012;4:119ra13.
cutaneous blood flow and skin temperature in healthy subjects. 126. George SZ, Bishop MD, Bialosky JE, et al. Immediate effects of
Arch Phys Med Rehabil 2002;83:5–9. spinal manipulation on thermal pain sensitivity: an experimental
104. Cramp AF, Gilsenan C, Lowe AS, et al. The effect of high- and study. BMC Musculoskelet Disord 2006;7:68.
low-frequency transcutaneous electrical nerve stimulation upon 127. Bialosky JE, Bishop MD, Robinson ME, et al. The influence of
cutaneous blood flow and skin temperature in healthy subjects. expectation on spinal manipulation induced hypoalgesia: an exper-
Clin Physiol 2000;20:150–7. imental study in normal subjects. BMC Musculoskelet Disord
105. Chen CC, Johnson MI, McDonough S, et al. The effect of trans- 2008;9:19.
cutaneous electrical nerve stimulation on local and distal cutane- 128. Vicenzino B, Gutschlag F, Collins D, et al. An investigation of the
ous blood flow following a prolonged heat stimulus in healthy effects of spinal manual therapy on forequarter pressure and
subjects. Clin Physiol Funct Imaging 2007;27:154–61. thermal pain thresholds and sympathetic nervous system activity
106. Sandberg ML, Sandberg MK, Dahl J. Blood flow changes in the in asymptomatic subjects In: Shacklock M (ed). Moving in on
trapezius muscle and overlying skin following transcutaneous elec- Pain, Butterworth Heinemann, Adelaide 1995.
trical nerve stimulation. Phys Ther 2007;87:1047–55. 129. Wright A, Vicenzino B. Cervical mobilisation techniques, sympa-
107. Patel KC, Gross A, Graham N, et al. Massage for mechanical neck thetic nervous system effects and their relationship to analgesia.
disorders. Cochrane Database Syst Rev 2012;(9):CD004871. In: Schacklock M, editor. Moving in on Pain. Adelaide: Butter-
108. Furlan AD, Imamura M, Dryden T, et al. Massage for low-back worth Heinneman; 1995. p. 164–73.
pain. Cochrane Database Syst Rev 2008;CD001928. 130. Bulbulian R, Burke J, Dishman JD. Spinal reflex excitability
109. Furlan AD, Yazdi F, Tsertsvadze A, et al. A systematic review and changes after lumbar spine passive flexion mobilization. J Manipu-
meta-analysis of efficacy, cost-effectiveness, and safety of selected lative Physiol Ther 2002;25:526–32.
complementary and alternative medicine for neck and low-back 131. Dishman JD, Bulbulian R. Spinal reflex attenuation associated
pain. Evid Based Complement Alternat Med 2012;2012:953139. with spinal manipulation. Spine 2000;25:2519–24.
110. Plews-Ogan M, Owens JE, Goodman M, et al. A pilot study 132. Ferreira ML, Ferreira PH, Latimer J, et al. Comparison of general
evaluating mindfulness-based stress reduction and massage for the exercise, motor control exercise and spinal manipulative therapy
management of chronic pain. J Gen Intern Med 2005;20: for chronic low back pain: a randomized trial. Pain 2007;131:31–7.
1136–8. 133. Sung PS, Kang YM, Pickar JG. Effect of spinal manipulation
111. Gross A, Miller J, D’Sylva J, et al. Manipulation or mobilisation duration on low threshold mechanoreceptors in lumbar paraspinal
for neck pain. Cochrane Database Syst Rev 2010;CD004249. muscles – A preliminary report. Spine 2005;30:115–22.
112. Rubinstein SM, Terwee CB, Assendelft WJ, et al. Spinal manipu- 134. Pickar JG. Neurophysiological effects of spinal manipulation.
lative therapy for acute low-back pain. Cochrane Database Syst Spine J 2002;2:357–71.
Rev 2012;(9):CD008880. 135. George SZ, Bishop MD, Bialosky JE, et al. Immediate effects of
113. Rubinstein SM, van MM, Assendelft WJ, et al. Spinal manipula- spinal manipulation on thermal pain sensitivity: an experimental
tive therapy for chronic low-back pain. Cochrane Database Syst study. BMC Musculoskelet Disord 2006;7:68.
Rev 2011;CD008112. 136. Bialosky JE, Bishop MD, Robinson ME, et al. The influence of
114. Rubinstein SM, van MM, Assendelft WJ, et al. Spinal manipula- expectation on spinal manipulation induced hypoalgesia: an exper-
tive therapy for chronic low-back pain. Cochrane Database Syst imental study in normal subjects. BMC Musculoskelet Disord
Rev 2011;CD008112. 2008;9:19.
276 PART III  Advances in Clinical Science and Practice

137. Moss P, Sluka KA, Wright A. The initial effects of knee joint lateral epicondylalgia. J Manipulative Physiol Ther 2004;27:
mobilisation on osteoarthritic hyperalgesia. Man Ther 2006; 180–5.
12:109–18. 143. Martins DF, Bobinski F, Mazzardo-Martins L, et al. Ankle joint
138. Skyba DA, Radhakrishnan R, Rohlwing JJ, et al. Joint manipula- mobilization decreases hypersensitivity by activation of peripheral
tion reduces hyperalgesia by activation of monoamine receptors opioid receptors in a mouse model of postoperative pain. Pain
but not opioid or GABA receptors in the spinal cord. Pain Med 2012;13:1049–58.
2003;106:159–68. 144. Martins DF, Mazzardo-Martins L, Cidral-Filho FJ, et al. Ankle
139. Sluka KA, Wright A. Knee joint mobilization reduces secondary joint mobilization affects postoperative pain through peripheral
mechanical hyperalgesia induced by capsaicin injection into the and central adenosine A1 receptors. Phys Ther 2013;93:401–12.
ankle joint. Europ J Pain 2001;5:81–7. 145. Martins DF, Mazzardo-Martins L, Cidral-Filho FJ, et al. Periph-
140. Zusman M, Edwards BC, Donaghy A. Investigation of a proposed eral and spinal activation of cannabinoid receptors by joint mobi-
mechanism for the relief of spinal pain with passive joitn move- lization alleviates postoperative pain in mice. N S 2013;
ment. J Manual Med 1989;4:58–61. 255:110–21.
141. Vicenzino B, O’Callahan J, Kermode F, et al. No influence of 146. Martins DF, Mazzardo-Martins L, Gadotti VM, et al. Ankle joint
naloxone on the initial hypoalgesic effect of spinal manual therapy. mobilization reduces axonotmesis-induced neuropathic pain and
In: Devor M, Rowbotham MC, Wiesenfeld-Hallin Z, editors. glial activation in the spinal cord and enhances nerve regeneration
Proceedings from the 9th World Congress on Pain. Seattle: IASP in rats. Pain 2011;152(11):2653–61.
Press; 2000. p. 1039–44.
142. Paungmali A, O’Leary S, Souvlis T, et al. Naloxone fails to antag-
onize initial hypoalgesic effect of a manual therapy treatment for
 CHAPTER 29 

Spinal Manipulation
Christopher McCarthy  •  Joel Bialosky  •  Darren Rivett

slightly beyond the patient’s physiological range of

INTRODUCTION movement’.6,7
A commonly cited definition would take the form of
Spinal manipulation (SM) is a modality ubiquitous to ‘a forced, passive movement of vertebral segments, car-
most cultures, and possesses an evidence base that sup- rying the elements of articulation beyond the usual range
ports its use in contemporary musculoskeletal practice.1 of movement to the limit of anatomic range’.8 Clearly this
However, there are a number of issues regarding this form of definition details the mechanism of how one
ancient and modern practice that lead some health-care might apply a technique to the vertebral column but does
practitioners to take an adamant stance against the use not define what the technique is. This is not the typical
of these techniques.2,3 The debate regarding the use of format one expects when defining a therapeutic proce-
manipulation in the modern musculoskeletal manage- dure. For example, another specific form of manual
ment of spinal dysfunction is fuelled by some crucial therapy, the Elpey manoeuvre,9 is defined as ‘a canalith
issues regarding the objectives of and evidence for SM. repositioning manoeuvre to reposition otolithic debris
It may be that uncertainty regarding both the mecha- from the semicircular ducts, to the utricle in benign par-
nisms and effectiveness of SM, coupled with uncertainty oxysmal positional vertigo’. It is not defined as ‘four
regarding the terminology being used to define SM are sequential movements of the neck performed in sitting
hampering the understanding of this approach to spinal and lying in paroxysmal positional vertigo’. An adequate
dysfunction. It would appear that there is lack of clarity definition carries some information regarding the objec-
in the evidence base, resulting in differences in the rela- tives and mechanisms of the treatment, in the context of
tive importance placed on the techniques by differing the dysfunction it is being utilized in. In light of the
manipulative professions. For example, British chiroprac- mechanisms discussed in this chapter we will offer a new
tors will manipulate cervical spine patients 20 times more definition of SM for the reader’s consideration.
frequently than Irish physiotherapists.4,5 If the under- One method of developing a definition would be to
standing of the mechanisms, effectiveness and objectives undertake a review of SM techniques to identifying simi-
of the technique were defined, presumably we would not larities and disparities in approach and thus define the
see such marked professional differences in the utilization key components of SM. A review of multidisciplinary
of SM techniques. textbooks,10–13 reveal two common approaches to SM,
This chapter will endeavour to address these issues in which one might term ‘direct contact gapping’ and ‘posi-
three sections. The first section will consider some of the tional gapping’. Direct contact gapping techniques
proposed aims and objectives of SM and suggest a defini- involve direct application of operator force on two adja-
tion of SM that reflects the biomechanical, neurophysi- cent vertebral segments, with force application in a direc-
ological and psychosocial mechanisms that will be tion that produces segmental motion leading to joint
discussed in the second section. In light of the evidence surface separation. The example in Figure 29-1 shows the
for clinical effectiveness, a discussion of some of the risks right side of T5 is directed in a posterior–anterior and
of SM and methods we may use to reduce risk will be cephalad direction while the left side of T6 is simul­
discussed in Section 3 of this chapter. taneously directed in a posterior–anterior and caudad
direction.
In contrast, positional gapping is commonly applied in
regions of the vertebral column, where it is difficult to
DEFINING SPINAL MANIPULATION directly contact both vertebrae and move them in the
opposing directions simultaneously. For example, in the
When one considers the amount of scientific and lay mid-lumbar and mid-cervical spines vertebral segments
literature on spinal manipulation, it is perhaps surprising are positioned in starting positions that do not follow the
to find no absolute consensus on the definition of manip- normal coupled movements of the region (see Fig. 29-1).
ulation. Typically the definition will make reference to In these positions one segment can be stabilized while
some form of passive handling of the spine6 or some the other is moved away from it in a direction the patient
reference to a low-amplitude highly accelerative thrust- cannot easily induce themselves.14–16 Many authors6,16,17
ing movement applied to the passive patient.7 In addition, have suggested that the direction of motion produced
there may be some reference to the point in passive range results in separation of joint surfaces, in contrast to the
of movement where a technique is applied, varying from typical translatory motions invoked by mobilization tech-
being at ‘a restriction in range’ to ‘a range that extends niques that are aimed along facet joint planes (i.e. Nags
277
278 PART III  Advances in Clinical Science and Practice

A B

FIGURE 29-1  ■  (A) The direct gapping of T5 and T6 with little spinal position required but direct contact on adjacent vertebral seg-
ments and movement directed posterior–anteriorly (not along the plane of the facet joint). (B) The positioning of the vertebral seg-
ments in small degrees of extension, right lateral flexion and left rotation (not the natural coupling of these movements) with
movement being induced at a plane perpendicular to the plane of the right zygapophyseal joint, unlike mobilizations following the
facet joint surface plane.

and Snags).18 Thus motion that results in joint surface moved under extreme capsular tension.6 Spinal manipula-
separation or gapping could be considered to be a defin- tion techniques, applied with this objective tend to
ing feature of manipulation, distinguishing the technique involve low-amplitude, high-velocity and high-force
from segmental mobilizations that do not aim to produce thrusts, in order to overcome the tension induced by the
surface separation. end-of-range positioning.19,20
The neurophysiological mechanisms for why this phe- In light of the viscoelastic properties of collagenous
nomenon might contribute to pain relief and return to tissue there is a natural rebound to rapidly applied forces,
function will be discussed in depth in Section 2 (Neuro- meaning that at higher speeds more force is required to
physiological effects); however, there are a number of produce elongation than when forces are applied at slow
theoretical perspectives on the effects of manipulation speeds.21 Thus while the objective of this type of approach
that may have led to some of the disparity in perceived to SM is lengthening of tissue, one is left to consider if
objectives of SM. With differing anticipated effects of a this is an optimal method of stretching the vertebral
technique, come differing approaches to application of columns of patients in pain. It is proposed that the surface
SM. An SM technique in the hands of one clinician could separation, induced by SM, could break microscopic,
appear very gentle and comfortable whereas a clinician intra-articular adhesions evident in immobilized facet
with a differing objective could undertake an SM tech- joints;17 however, these adhesions are not currently visible
nique that may appear to be a vigorous, end-of-range in vivo when imaged with the highest resolution MRI
stretch. Both clinicians would define their intervention as scanners, and thus we have no evidence to support the
an SM technique; however, the objective, application and theory. Of course it is equally feasible that mobilization,
therefore effect of the technique could be very disparate. not just SM, could break these adhesions. Thus, as the
When evaluating the effect of SM, researchers need to link between SM and lengthening tissue is not clear we
be aware that while a group of intervening clinician may will not include it within our definition of SM.
be undertaking SM techniques, not all clinicians will
perform the techniques in the same manner and percep- Inducing Cavitation Within the Joint?
tions of the objectives of SM may differ.
Cavitation phenomenon is the formation and collapse of
bubbles (cavities) within the synovial fluid of spinal joints
OBJECTIVES OF SPINAL and has been observed during SM.22-24 Surface separation,
resulting in an increase in intra-articular volume, will
MANIPULATION (BIOMECHANICAL) drop intra-articular pressure. If pressures fall to a thresh-
Stretching/Tearing Tissue? old level, ‘vapour pressure’ micro-clouds of bubbles will
form within the synovial fluid.15 The subsequent gaseous/
One commonly perceived objective of SM is the produc- fluid mix results in a transient period, where less force is
tion of a tensile stress sufficient to cause lengthening of required to induce movement.25,26 This minor, transient
tissue, or even ‘tearing of adhesions’.19 With this objec- effect lasts approximately 20–60 minutes.22,24
tive in mind, manipulation is typically undertaken towards Cavitation phenomenon is well described in engineer-
the end of passive range and has the objective of produc- ing fields as a phenomenon that is damaging to engines
ing movement that extends to the anatomical integrity of (associated with the rapid changes in fluid pressure in
tissue. However, if one accepts that one of the key defin- pistons) and this has led some authors to consider whether
ing features of SM is to gap the joint surfaces it would cavitation phenomenon is in itself damaging to the artic-
seem unlikely that this objective will be met if the joint ular cartilage of the synovial joint.27,28 However, cohort
capsule has been tightened to the limit of extensibility. If studies of metacarpophalangeal ‘knuckle crackers’ have
anything you could argue that the joint surfaces are in a revealed no increase in the odds of developing osteoar-
position where they are least likely to separate when thritis in these joints.29,30 One might extrapolate these
 29  Spinal Manipulation 279

data to the spine (recorded frequency characteristics of significantly different to those of mobilization we will not
the sound of cavitation in spinal and MCP joints are include muscular responses as an objective of SM, within
similar31) and suggest that occasional SM techniques, a definition.
resulting in cavitation, are unlikely to be damaging the
joints of our patients.
While cavitation may not be harmful, the clinical rel-
evance of this phenomenon in the treatment of spinal OBJECTIVES OF SPINAL
pain is not clear. A number of authors have shown that MANIPULATION
SM techniques can lead to cavitation being observed spe- (NEUROPHYSIOLOGICAL)
cifically at the targeted joint as well as in the contralateral
joint, and indeed at a number of levels away from the Limitations of the Biomechanical Model
targeted joint.22,23,32 The operator undertaking an SM will
not necessarily hear an audible pop with every patient SM is commonly defined by its mechanical parameters50
they treat.33,34 A number of authors have shown equivocal and the treatment effect at times attributed to a potential
short-term pain relief35 and autonomic nervous system mechanical mechanism.51,52 For example, SM is theorized
responses36,37 with SM techniques with or without an to alter spinal pain conditions through the release of
audible pop. Cavitation can occur with passive movement entrapped synovial tissue, tearing of articular lesions, or
applied with high- or low-velocity movement16,38,39 and unbuckling of spinal motion segments.51 Clinically, the
while similar biomechanical effects on joint mobility use of SM is often driven by a mechanical emphasis53,54
have been observed,18,20 alteration in electromyographic as clinicians attempt to restore position or movement to
responses during slow-velocity movement have not.40 In specific vertebral segments identified as malaligned or
contrast to the evidence suggesting the audible pop may hypomobile during the examination process. Positive
not be relevant to clinical effectiveness, there have been clinical outcomes accompany the mechanically based
some initial data to suggest an audible pop has been implementation of SM; however, the literature does not
associated with small reductions in inflammatory cyto- support a specific mechanical mechanism. Firstly, clinical
kines and in a small reduction in pain sensitivity.41,42 assessment of malaligned or hypomobile vertebral seg-
We are still to establish the relative importance of the ments are notoriously unreliable55–57 and the validity of
operator and/or the patient hearing the audible pop, these assessments is questionable.58–60 For example, poor
commonly observed in the majority, but not all SM tech- agreement is present between manually assessed and
niques. In Section 2 (Neurophysiological effects) we will magnetic resonance imaging-quantified vertebral mobil-
discuss the interaction of the mechanisms of SM, but it ity,59 and pain with passive vertebral mobility assessment
is clear that expectation of effect does have a bearing on does not correspond to magnetic resonance imaging-
outcome.43 A number of authors has demonstrated that quantified vertebral motion.58 A specific mechanical
the outcome of an SM will be strongly influenced by the mechanism of SM necessitates the ability to reliably iden-
positive or negative expectations of the technique43,44 and tify a mechanical fault and the literature suggests current
thus if the patient deems an audible pop to be the marker clinical assessment approaches are lacking in these prop-
of a successful technique the clinician may wish to con- erties. Secondly, forces accompanying SM are not specific
sider this in their choice of technique and in the method to a vertebral segment. For example, the forces transmit-
in which SM is undertaken. As an audible pop is not ted by SM are dispersed beyond the targeted segment61
universal, not necessarily localized to the targeted joint resulting in mechanical effects at multiple segments.62
and its effect on pain is equivocal it may not be sensible In fact the cavitation, considered a hallmark of SM,50
to consider the audible pop as the pre-eminent objective frequently occurs several vertebral levels away from the
of the SM. Consequently, we will not include the objec- targeted joint.23,63 Subsequently, the mechanical isolation
tive of invoking an audible pop as part of our definition of SM to a targeted vertebral level does not appear
of SM but will suggest that intra-articular cavitation is possible.
commonly produced during the technique. Thirdly, while movement accompanies SM,62 changes
in spinal alignment are transient. For example, Tullberg
et al.,64 using roentgen stereophotogrammetric analysis,
Reducing Muscle Hypertonicity/Stiffness observed no changes in the alignment of the sacrum and
There is some preliminary evidence to suggest that fol- the ilium following SM to the sacroiliac joint in partici-
lowing SM there is a short-term reduction in local spinal pants with low back pain. This study does not support a
muscle electromyographic activity in muscles that are mechanical mechanism of SM related to reducing a
hypertonic16,45 and a short-term reduction in motoneuron malaligned vertebral segment. Finally, clinical outcomes
pool activity.40,46,47 This might go some way to explaining are independent of the specific mechanical parameters of
the small increases in motion observed following SM.22,48 the SM. For example, similar outcomes were observed in
There appears to be some selective electromyographic response to two different types of SM (but not to a non-
stretch responses to rapidly applied (thrust/impulse) thrust mobilization) in individuals meeting a clinical pre-
techniques (duration 0.1 to 0.2 seconds) that are not diction rule suggesting a likely positive clinical response
evoked with passive movements of a longer duration.40 to SM.65 Furthermore, results are similar in studies allow-
However, long-term effects on muscle function do not ing clinicians to choose the manual therapy intervention
appear to differ between the techniques.49 Thus as long- as compared to those in which the intervention is prede-
term muscle responses to SM do not appear to be termined.66 Collectively, this body of literature suggests
280 PART III  Advances in Clinical Science and Practice

the clinical outcomes corresponding to SM likely result Potential Peripheral Mechanisms

from a general response to the interventions rather than
successfully targeting a vertebral level or the specific SM is associated with a reduction of blood and serum
mechanical parameters of the technique. level cytokines beyond that observed in response to a
sham intervention or control group in healthy partici-
pants.42 Additionally, SM is associated with differing
Neurophysiological Mechanisms levels of circulatory pain biomarkers in individuals with
low back pain68 and circulatory cannabinoids in healthy
of Spinal Manipulation individuals.69 Subsequently, SM may inhibit pain through
A comprehensive model has been developed to describe a peripheral effect upon inflammatory mediators.
the mechanisms through which manual therapies such
as SM inhibit pain.67 The model (Fig. 29-2) suggests
the mechanical force of an SM results in a cascade of Potential Spinal Cord Mediated
neurophysiological responses mediated by the peripheral
nervous system, the spinal cord and/or the supraspinal
Mechanisms
structures. Animal studies allow visualization of the SM is associated with attenuation of temporal summation
nervous system in response to an intervention providing in healthy individuals35,70 and those with low back pain.71
direct evidence for a specific mechanism. Such approaches Furthermore, lessening of temporal summation in
are not possible in humans necessitating the dependence response to SM exceeds that corresponding to the expec-
upon behavioural measures as indirect support for a tation of receiving an SM.72 Temporal summation is char-
particular mechanism in most manual therapy mecha- acterized by increased pain sensitivity in response to a
nistic studies. Although suggestive of a specific mecha- painful stimulus of unchanging magnitude provided at an
nism, the reader should be aware of the limitations of interpulse interval frequency of <3 seconds.73 Studies in
this approach. anaesthetized animals confirm the wind-up of neurons in

Placebo
Non-specific
responses
Expectation
Pain Modulatory
Pain-related Circuitry
PAIN brain circuitry ACC Endocrine response
Amygdala • B-endorphins
PAG • Opioid response
RVN
Rating
Autonomic response
Imaging • Skin temperature
• Skin conduction
• Cortisol levels
• Heart rate

Neuromuscular responses
Mechanical • Motor neuron pool
Tissue Spinal cord
stimulus • Afferent discharge
• Muscle activity

Temporal summation
Decrease spasm
Increase range of motion Imaging

The model suggests a transient, mechanical stimulus to the tissue produces a chain of
neurophysiological effects. Solid arrows denote a direct mediating effect. Broken arrows denote an
associative relationship which may include:
= an association between a construct and its measure
= an association between a neural and a psychological construct
Bold boxes indicate the measurement of a construct

ACC = anterior cingular cortex; PAG = periaqueductal grey; RVM = rostral ventromedial medulla
FIGURE 29-2  ■  Model of the neurophysiological mechanisms of spinal manipulation. ACC, Anterior cingular cortex; PAG, Periaque-
ductal grey; RVM, Rostral ventromedial medulla.
 29  Spinal Manipulation 281

the dorsal horn of the spinal cord with a temporal mechanisms are likely influential in the response to SM.94
summation protocol.74,75 Subsequently, SM-related atten- While not studied extensively in SM, placebo mecha-
uation of temporal summation suggests a mechanism cor- nisms are influential in other types of complementary and
responding to modification of dorsal horn excitability. alternative medicine. For example, Kalauokalani et al.,95
A reflex link exists between the lumbar joint capsule randomly assigned 135 individuals with chronic LBP to
and the paraspinal musculature.76,77 The mechanical force receive either acupuncture or massage. Group differences
from SM may stimulate this neuromuscular reflex were not observed in clinical outcomes; however, partici-
response resulting in pain inhibition related to counter pants with greater expectation for acupuncture and
irritation78 or proprioceptive input to the central nervous receiving acupuncture had significantly better outcomes
system.79 Stimulation of this link is suggested by studies than those with higher expectation for massage who
demonstrating afferent discharge in response to SM. For received acupuncture and vice versa. Specific to SM,
example, positive action potentials at the S1 nerve root baseline expectations for improvement and to benefit
have been recorded in response to SM in anaesthetized from SM were associated with better clinical outcomes at
subjects undergoing spinal surgery.80,81 4 weeks in participants with neck pain receiving SM to
A lessening of the spinal motoneuron pool excitability the thoracic spine.44 Additionally, attenuation of temporal
is associated with SM. The Hoffman Reflex (H-reflex) is summation in response to SM as has been observed in
comparable to a monosynaptic stretch reflex; however, it several studies35,70–72 may be negated if participants expect
utilizes electrical stimulation as the stimulus. A decrease more pain following the SM.43
in H-reflex has been observed following SM in the
lumbar40,82 and cervical spine.83 Collectively, these find-
ings suggest a brief inhibition of motoneuron pool
excitability speculated to result from Ia afferents.84 The
SAFETY AND PRACTICAL ISSUES
characteristic hypoalgesia and decrease in muscle spasm ASSOCIATED WITH SPINAL
frequently accompanying SM in the clinical setting may MANIPULATION
result from the related diminished afferent input to the
spinal cord. A number of systematic reviews of the randomized con-
trolled trial literature have concluded that SM is effective
Potential Supraspinally Mediated in the reduction of spinal pain and is cost-effective96–98
Despite this, there has been much controversy over many
Mechanisms years regarding the risk of adverse events following the
SM may directly influence the supraspinal structures to application of spinal manipulation, in particular cervical
impart its clinical effect. Hypoalgesia accompanying SM spine manipulation.99 Risk estimates have focused on dis-
is characterized by similar features as that observed in section injury to the vertebral artery leading to stroke, but
animal studies of direct stimulation of the periaqueductal vary widely from 1 in 163 000100 manipulations to about
grey leading to speculation of similar mechanisms.85 1 in 5 000 000.101 Most estimates are inherently flawed as
More recently, changes in cortical excitability have been they have usually relied on retrospective methodologies,
observed in response to SM in individuals with recurring usually surveys of practitioners or searches of insurance
neck pain as indicated by somatosensory evoked or medical records. Recall bias, incomplete records and
potentials86,87 and transcranial magnetic stimulation.88,89 legal restrictions may limit the accuracy of the data relat-
Changes in cortical excitability as indicated by transcra- ing to the number of adverse events, while the number of
nial magnetic stimulation have also been observed in actual manipulations performed (the denominator) is
response to SM applied to the lumbar spine in healthy generally an estimate extrapolated from a limited sample
individuals.90 Collectively, these studies suggest a supra- of practitioners. At best we can state that the risk of stroke
spinally mediated effect of SM on nervous system excit- following neck manipulation is unknown but that the
ability with potential implications for clinical outcomes. actual incidence is likely very rare.102 It is this rareness
Imaging modalities are improving and offer the potential that makes it very difficult to conduct any sort of mean-
for more direct visualization of nervous system responses ingful prospective study of serious complications, such as
to SM. A recent study used functional magnetic reso- craniocervical arterial dissection and consequent stroke.
nance imaging to visualize changes in pain processing A recent systematic review102 of adverse events related
following SM. Ten healthy participants were imaged to manual therapy (including manipulation) reported that
during a painful task prior to and immediately following nearly half of all patients undergoing manual therapy will
SM directed to the thoracic spine. Changes in cerebral experience transient and minor adverse effects, typically
blood flow corresponding to changes in pain ratings were increased pain and most commonly after the first treat-
observed following the SM.88 ment. No serious adverse events were found and it was
Placebo is a psychological and biologically active concluded that the risk of such events was lower than
process associated with a robust analgesic effect91 and from taking medication for the same condition.
reflective of descending inhibitory mechanisms of pain
inhibition.92 Subsequently, placebo effects represent Minimizing Risk in Applying
a supraspinally mediated mechanism of SM. Placebo
mechanisms play a role in all interventions for pain.
Manipulation
For example, pain medication is significantly more To help avoid adverse events, manipulation should be
effective when patients are aware they are receiving it applied using the same principles as for passive joint
than treatment that is concealed.93 Similarly, placebo mobilization of the spine. That is, manipulation should
282 PART III  Advances in Clinical Science and Practice

be viewed simply as an extension or progression of mobi- practitioner.104 With patients for whom spinal manipula-
lization, as Maitland et al.103 and other clinical authorities tion is contemplated, it is critically important that the
have long advocated. Mobilization should be applied patient history is used to establish and test reasoning
initially and its effects evaluated over the time period hypotheses related to the potential for adverse events.
between consecutive treatment sessions. Manipulation The practitioner should aim during the patient history to
should generally only be applied when mobilization has make the best judgement on the likelihood of the pres-
been progressed in vigour or grade, and when its effects ence of serious pathology and contraindications to spinal
are no longer satisfactory. manipulation based on available information.
Further recommendations to promote the safe appli- Contraindications to spinal manipulation include the
cation of spinal manipulation are as follows.104–107 following:109
• Minimal force should be applied to any spinal struc- • upper motoneuron lesion
ture. Low-amplitude and short lever thrust tech- • spinal cord compromise
niques are preferable. • multi-level spinal nerve/nerve root compromise
• Spinal manipulation techniques should at all times (cervical spine)
feel comfortable to the patient. In applying cervical • deteriorating neurological status
spine manipulation, placing the patient’s head on a • intense, unremitting, non-mechanical pain
pillow in supine lying is often more comfortable to • constant night pain (stopping patient from falling
the patient than alternative positions. This position asleep)
also allows the practitioner to better monitor the • recent trauma to relevant region, especially the head
patient’s facial expression and for any nystagmus. and neck
• Neck manipulation techniques should not be per- • craniovertebral ligament instability
formed at the end of range of overall cervical spine • vertebrobasilar insufficiency or internal carotid
physiological movement, especially for extension artery pathology.
and rotation. The head and cervical spine segments The clinician should also exercise caution before apply-
not included in the manipulation can be used to ing manipulation in the presence of the following:109
direct loads to the targeted segment, thus minimiz- • cervical spine anatomical anomaly
ing stress on the rest of the neck.9 • congenital collagenous condition (e.g. Down
• Positioning and briefly holding the patient in the syndrome)
pre-manipulative test position is advisable prior to • connective tissue disease
thrusting to evaluate patient comfort and to feel for • currently or recently active cancer
any protective muscle spasm or other concerning • first episode of spinal pain before age 18 or after 55
end-feel. In neck manipulation, enquiry should spe- • hypermobility syndrome
cifically be made about any dizziness in the pre- • inflammatory joint disease (e.g. rheumatoid arthri-
manipulative test position which may be indicative tis, ankylosing spondylitis)
of vertebrobasilar insufficiency leading to cerebral • local infection
ischaemia. • osteoporosis
• Repeated manipulation within the same session or • prolonged use of steroid medication
over a number of consecutive sessions should be • recent or frequent manipulation
avoided, owing to potential dangers of frequent, • systemic illness
repeated manipulations and a lack of longer-term • throat infection (cervical spine).
benefit. It is important that the clinician is aware that craniocervi-
The use of manipulation in the upper cervical spine cal arterial dissection may mimic musculoskeletal dys-
is losing favour in manipulative physiotherapy because function in the early stage of its pathological progression
of the perceived increased risk in this region. In a as headache or neck pain may be the presenting
survey of member organizations of the International symptom.104,110,111 Indeed a patient experiencing pain
Federation of Orthopaedic Manipulative Physical Thera- from a dissecting artery may well seek manipulative
pists (IFOMPT) undertaken by Carlesso and Rivett in therapy for the relief of their pain.13 A high index of
2007,108 eight member organizations (40%) reported suspicion is particularly advisable in cases of severe,
that their members had decreased the use of manipula- acute-onset neck or head pain described as ‘unlike any
tion in the upper cervical spine over the last decade. other’.111,112 To this end, it is therefore also important to
Thirteen member organizations (65%) further indicated recognize potential risk factors for arterial dissection
that upper cervical spine manipulation techniques taught because unless there are explicit signs or symptoms of
to practitioners in post-professional courses had been neurovascular compromise (e.g. hemianopia, dysarthria)
changed to limit the amount of rotation. evident in the recent history or on examination, no indi-
vidual or isolated clinical feature or clinical test has ade-
quate clinical utility to detect the patient who will stroke
Clinical Reasoning and Patient Selection following cervical spine manipulation.
Clinical reasoning refers to the thinking skills underpin- The following factors have been proposed to increase
ning clinical practice. It is clear from the literature that the risk of craniocervical arterial pathology:110–113
many documented adverse events following the applica- • anticoagulant medication
tion of spinal manipulation could have been easily avoided • blood clotting disorders or changes in blood prop-
if better clinical reasoning had been exercised by the erties such as hyperhomocysteinaemia
 29  Spinal Manipulation 283

• cardiovascular disease, especially a previous cere- Interestingly, recent research into blood flow to the brain
brovascular accident or transient ischaemic attack with two contrasting types of cervical spine manipulative
• diabetes mellitus technique found no significant differences with either
• history of smoking technique, suggesting the type of manipulation employed
• hypercholesterolaemia may be less important than careful patient selection.118
• hyperlipidaemia There are also substantial jurisdictional differences
• hypertension in educational standards in spinal manipulation, as well
• immediately post-partum as in regulatory restrictions to practice manipulation.
• migraine-type headache To help address this, the IFOMPT member organi­
• past history of trauma to the cervical spine or head, zations have collectively endorsed an ‘International
or craniocervical arteries Framework for Examination of the Cervical Region for
• recent infection. Potential of Cervical Arterial Dysfunction Prior to
The physical examination generally provides minimal Orthopaedic Manual Therapy Intervention’.109 The
additional information related to the safe application of framework is designed to provide guidance to practitio-
manipulation as most clinical tests have limited validity. ners in the assessment of the cervical spine region for
Clearly if the physical examination elicits signs that are the potential of cervical artery dysfunction in advance
consistent with a mechanical joint presentation, then of planned manual therapy interventions, particularly
manual therapy (including manipulation) may be indi- neck manipulation.
cated in the absence of any contraindications or precau-
tions ascertained in the patient interview or detected on
testing. CONCLUSION – DEFINITION
Provocative positional testing for vertebrobasilar OF SPINAL MANIPULATION
insufficiency has long been recommended in practice
prior to cervical spine manipulation. Such testing is In light of the material we have presented in this chapter,
intended to provide a challenge to the vascular supply to we have proposed a definition of spinal manipulation that
the brain, and the provocation of signs or symptoms of reflects our current understanding of the technique. It
cerebrovascular ischaemia during or immediately after accepts the limitations of the evidence base in the field
testing is interpreted as a positive test result. Sustained and thus our incomplete understanding of SM’s mecha-
end-range rotation has been advocated and has been pro- nisms. It reflects our understanding of the mechanical,
posed as the most provocative and valid test.114,115 The neurophysiological and psychological effects of SM.
sustained pre-manipulative test position has also been
advocated.115 However, the predictive ability of any of Spinal manipulation is the application of rapid movement
these positional tests to identify patients at risk of manip- to vertebral segments producing joint surface separation,
ulative stroke is questionable and at best they can be transient sensory afferent input and reduction in
considered a test of the adequacy of the collateral circula- perception of pain. Joint surface separation will commonly
tion in the presence of compromised contralateral verte- result in intra-articular cavitation that, in turn, is
bral artery flow.116 commonly accompanied with an audible pop. Post-
More recently, Kerry and Taylor117 have advocated manipulation reductions in pain perception are influenced
that a raft of physical tests of the cardiovascular status of by supraspinal mechanisms including expectation of
an individual be undertaken pre-manipulatively, includ- benefit.
ing blood pressure measurement, palpation of the carotid
artery and examination of the cranial nerves. Biologically
it is plausible that some of these tests may assist in detect- REFERENCES
ing a patient presenting with a dissection in progress. 1. Livingston MC. The mystery and history of spinal manipulation.
However, there are no data demonstrating an ability of Can Fam Physician 1981;27(2):300–2.
2. Ernst E. Spinal manipulation: its safety is uncertain. CMAJ
any of these cardiovascular tests, either individually or in 2002;166(1):40–1.
combination, to predict the patient at risk of a craniocer- 3. Ernst E. Spinal manipulation: are the benefits worth the risks?
vical arterial dissection subsequent to neck manipulation. Expert Rev Neurother 2007;7(11):1451–2.
In fact, hypertension and most other general cardiovas- 4. Hurley L, Yardley K, Gross AR, et al. A survey to examine atti-
cular risk factors (such as smoking) have been shown as tudes and patterns of practice of physiotherapists who perform
cervical spine manipulation. Man Ther 2002;7(1):10–18.
unlikely to be significant risk factors for craniocervical 5. Thiel H, Bolton J. Estimate of the number of treatment visits
arterial dissection.112 involving cervical spine manipulation by members of the British
It is important that the clinician refer the patient for and Scottish Chiropractic association over a one year period. Clin
immediate medical investigation when their clinical sus- Chiro 2004;7:163–7.
6. Evans DW. Why do spinal manipulation techniques take the form
picion of progressive arterial dissection or other serious they do? Towards a general model of spinal manipulation. Man
pathology is supported by reasoned historical features Ther 2010;15(3):212–19.
and clinical examination findings. 7. Moore A. Systematic review of spinal manipulation: including
different techniques. J R Soc Med 2006;99(6):278–9.
8. Mosby’s Medical Dictionary. 8th ed. Edinburgh: Elsevier; 2009.
International Context 9. Syed I, Ahmed W, Selvadurai D. Dix-Hallpike and Epley manoeu-
vres. Br J Hosp Med (Lond) 2012;73(10):C149–51.
There are many different types of manipulative tech- 10. Hartman L. Handbook of Osteopathic Technique. 3rd ed.
nique utilized across the world and between professions. London: Cengage Learning; 1996.
284 PART III  Advances in Clinical Science and Practice

11. Gibbons P, Tehan P. Manipulation of the Spine, Thorax and system: a randomized clinical trial. J Man Manip Ther 2010;
Pelvis: An Osteopathic Perspective. 3rd ed. Elsevier Health Sci- 18(4):181–90.
ences; 2009. 37. Sillevis R, Cleland J. Immediate effects of the audible pop from a
12. Bergmann TF, Peterson D. Chiropractic Technique: Principles thoracic spine thrust manipulation on the autonomic nervous
and Procedures. 3rd ed. New York: Elsevier Health Sciences; system and pain: a secondary analysis of a randomized clinical trial.
2010. J Manipulative Physiol Ther 2011;34(1):37–45.
13. McCarthy CJ. Combined Movement Theory; Rational Mobilisa- 38. Herzog W. The physics of spinal manipulation: work-energy and
tion and Manipulation of the Vertebral Column. Edinburgh: Else- impulse-momentum principles. J Manipulative Physiol Ther
vier Health Sciences; 2010. 1993;16(1):51–4.
14. Haas M. The physics of spinal manipulation. Part III. Some char- 39. Reggars JW. Recording techniques and analysis of the articular
acteristics of adjusting that facilitate joint distraction. J Manipula- crack. A critical review of the literature. Australas Chiropr Oste-
tive Physiol Ther 1990;13(6):305–8. opathy 1996;5(3):86–92.
15. Haas M. The physics of spinal manipulation. Part IV. A theoretical 40. Dishman JD, Weber KA, Corbin RL, et al. Understanding inhibi-
consideration of the physician impact force and energy require- tory mechanisms of lumbar spinal manipulation using H-reflex
ments needed to produce synovial joint cavitation. J Manipulative and F-wave responses: a methodological approach. J Neurosci
Physiol Ther 1990;13(7):378–83. Methods 2012;210(2):169–77.
16. Herzog W. The biomechanics of spinal manipulation. J Bodyw 41. Bialosky JE, Bishop MD, Robinson ME, et al. The relationship
Mov Ther 2010;14(3):280–6. of the audible pop to hypoalgesia associated with high-velocity,
17. Cramer GD, Cambron J, Cantu JA, et al. Magnetic resonance low-amplitude thrust manipulation: a secondary analysis of an
imaging zygapophyseal joint space changes (gapping) in low back experimental study in pain-free participants. J Manipulative
pain patients following spinal manipulation and side-posture posi- Physiol Ther 2010;33(2):117–24.
tioning: a randomized controlled mechanisms trial with blinding. 42. Teodorczyk-Injeyan JA, Injeyan HS, Ruegg R. Spinal manipula-
J Manipulative Physiol Ther 2013;36(4):203–17. tive therapy reduces inflammatory cytokines but not substance P
18. Exelby L. The Mulligan concept: its application in the manage- production in normal subjects. J Manipulative Physiol Ther
ment of spinal conditions. Man Ther 2002;7(2):64–70. 2006;29(1):14–21.
19. Forand D, Drover J, Suleman Z, et al. The forces applied by 43. Bialosky JE, Bishop MD, Robinson ME, et al. The influence of
female and male chiropractors during thoracic spinal manipula- expectation on spinal manipulation induced hypoalgesia: an exper-
tion. J Manipulative Physiol Ther 2004;27(1):49–56. imental study in normal subjects. BMC Musculoskelet Disord
20. Herzog W. The physics of spinal manipulation. J Manipulative 2008;9:19.
Physiol Ther 1992;15(6):402–5. 44. Bishop MD, Mintken PE, Bialosky JE, et  al. Patient expectations
21. Lopez-Garcia MD, Beebe DJ, Crone WC. Young’s modulus of of benefit from interventions for neck pain and resulting
collagen at slow displacement rates. Biomed Mater Eng 2010; influence on outcomes. J Orthop Sports Phys Ther 2013;43(7):
20(6):361–9. 457–65.
22. Cramer GD, Ross K, Pocius J, et al. Evaluating the relationship 45. Suter E, McMorland G, Herzog W. Short-term effects of spinal
among cavitation, zygapophyseal joint gapping, and spinal manip- manipulation on H-reflex amplitude in healthy and symptomatic
ulation: an exploratory case series. J Manipulative Physiol Ther subjects. J Manipulative Physiol Ther 2005;28(9):667–72.
2011;34(1):2–14. 46. Dishman JD, Dougherty PE, Burke JR. Evaluation of the effect
23. Ross JK, Bereznick DE, McGill SM. Determining cavitation of postural perturbation on motoneuronal activity following
location during lumbar and thoracic spinal manipulation: is various methods of lumbar spinal manipulation. Spine J 2005;
spinal manipulation accurate and specific? Spine 2004;29(13): 5(6):650–9.
1452–7. 47. Dishman JD, Greco DS, Burke JR. Motor-evoked potentials
24. Evans DW, Breen AC. A biomechanical model for mechanically recorded from lumbar erector spinae muscles: a study of cortico-
efficient cavitation production during spinal manipulation: pre- spinal excitability changes associated with spinal manipulation.
thrust position and the neutral zone. J Manipulative Physiol Ther J Manipulative Physiol Ther 2008;31(4):258–70.
2006;29(1):72–82. 48. Snodgrass SJ, Rhodes HR. Cervical spine posteroanterior stiffness
25. Miller T, Smiley JT. Cavitation sounds during spinal manipulative differs with neck position. J Electromyogr Kinesiol 2012;22(6):
treatments. J Manipulative Physiol Ther 1994;17(4):268–70. 829–34.
26. Reggars JW. The therapeutic benefit of the audible release associ- 49. Dishman JD, Bulbulian R. Comparison of effects of spinal manip-
ated with spinal manipulative therapy. A critical review of the ulation and massage on motoneuron excitability. Electromyogr
literature. Australas Chiropr Osteopathy 1998;7(2):80–5. Clin Neurophysiol 2001;41(2):97–106.
27. Ernst E. Does spinal manipulation have specific treatment effects? 50. Evans DW, Lucas N. What is ‘manipulation’? A reappraisal. Man
Fam Pract 2000;17(6):554–6. Ther 2010;15(3):286–91.
28. Ernst E. Adverse effects of spinal manipulation: a systematic 51. Evans DW. Mechanisms and effects of spinal high-velocity, low-
review. J R Soc Med 2007;100(7):330–8. amplitude thrust manipulation: previous theories. J Manipulative
29. Castellanos J, Axelrod D. Effect of habitual knuckle cracking on Physiol Ther 2002;25(4):251–62.
hand function. Ann Rheum Dis 1990;49(5):308–9. 52. Triano JJ. Biomechanics of spinal manipulative therapy. Spine J
30. Deweber K, Olszewski M, Ortolano R. Knuckle cracking and 2001;1(2):121–9.
hand osteoarthritis. J Am Board Fam Med 2011;24(2):169–74. 53. Abbott JH, Flynn TW, Fritz JM, et al. Manual physical assessment
31. Reggars JW. The manipulative crack. Frequency analysis. Austra- of spinal segmental motion: intent and validity. Man Ther
las Chiropr Osteopathy 1996;5(2):39–44. 2009;14(1):36–44.
32. Dunning J, Mourad F, Barbero M, et al. Bilateral and multiple 54. van Trijffel E, Oostendorp RA, Lindeboom R, et al. Perceptions
cavitation sounds during upper cervical thrust manipulation. BMC and use of passive intervertebral motion assessment of the spine:
Musculoskelet Disord 2013;14:24. a survey among physiotherapists specializing in manual therapy.
33. Flynn T, Fritz J, Whitman J, et al. A clinical prediction rule for Man Ther 2009;14(3):243–51.
classifying patients with low back pain who demonstrate short- 55. van Trijffel E, Anderegg Q, Bossuyt PM, et al. Inter-examiner
term improvement with spinal manipulation. Spine 2002;27(24): reliability of passive assessment of intervertebral motion in the
2835–43. cervical and lumbar spine: a systematic review. Man Ther 2005;
34. Cleland JA, Flynn TW, Childs JD, et al. The audible pop from 10(4):256–69.
thoracic spine thrust manipulation and its relation to short-term 56. Hollerwoger D. Methodological quality and outcomes of studies
outcomes in patients with neck pain. J Man Manip Ther 2007; addressing manual cervical spine examinations: a review. Man
15(3):143–54. Ther 2006;11(2):93–8.
35. Bishop MD, Beneciuk JM, George SZ. Immediate reduction in 57. Seffinger MA, Najm WI, Mishra SI, et al. Reliability of spinal
temporal sensory summation after thoracic spinal manipulation. palpation for diagnosis of back and neck pain: a systematic review
Spine J 2011;11(5):440–6. of the literature. Spine 2004;29(19):E413–25.
36. Sillevis R, Cleland J, Hellman M, et al. Immediate effects of a 58. Beneck GJ, Kulig K, Landel RF, et al. The relationship between
thoracic spine thrust manipulation on the autonomic nervous lumbar segmental motion and pain response produced by a
 29  Spinal Manipulation 285

posterior-to-anterior force in persons with nonspecific low back 81. Colloca CJ, Keller TS, Gunzburg R, et al. Neurophysiologic
pain. J Orthop Sports Phys Ther 2005;35(4):203–9. response to intraoperative lumbosacral spinal manipulation.
59. Landel R, Kulig K, Fredericson M, et al. Intertester reliability and J Manipulative Physiol Ther 2000;23(7):447–57.
validity of motion assessments during lumbar spine accessory 82. Dishman JD, Bulbulian R. Spinal reflex attenuation associated
motion testing. Phys Ther 2008;88(1):43–9. with spinal manipulation. Spine 2000;25(19):2519–24.
60. Haas M, Groupp E, Panzer D, et al. Efficacy of cervical endplay 83. Dishman JD, Burke J. Spinal reflex excitability changes after cervi-
assessment as an indicator for spinal manipulation. Spine 2003; cal and lumbar spinal manipulation: a comparative study. Spine J
28(11):1091–6. 2003;3(3):204–12.
61. Herzog W, Kats M, Symons B. The effective forces transmitted 84. Dishman JD, Cunningham BM, Burke J. Comparison of tibial
by high-speed, low-amplitude thoracic manipulation. Spine nerve H-reflex excitability after cervical and lumbar spine manipu-
2001;26(19):2105–10. lation. J Manipulative Physiol Ther 2002;25(5):318–25.
62. Gal J, Herzog W, Kawchuk G, et al. Movements of vertebrae 85. Wright A. Hypoalgesia post-manipulative therapy: a review of a
during manipulative thrusts to unembalmed human cadavers. potential neurophysiological mechanism. Man Ther 1995;1(1):
J Manipulative Physiol Ther 1997;20(1):30–40. 11–16.
63. Cramer GD, Ross JK, Raju PK, et al. Distribution of cavitations 86. Taylor HH, Murphy B. Altered central integration of dual somato-
as identified with accelerometry during lumbar spinal manipula- sensory input after cervical spine manipulation. J Manipulative
tion. J Manipulative Physiol Ther 2011;34(9):572–83. Physiol Ther 2010;33(3):178–88.
64. Tullberg T, Blomberg S, Branth B, et al. Manipulation does not 87. Haavik-Taylor H, Murphy B. Cervical spine manipulation alters
alter the position of the sacroiliac joint. A roentgen stereophoto- sensorimotor integration: a somatosensory evoked potential study.
grammetric analysis. Spine 1998;23(10):1124–8. Clin Neurophysiol 2007;118(2):391–402.
65. Cleland JA, Fritz JM, Kulig K, et al. Comparison of the effec­ 88. Daligadu J, Haavik H, Yielder PC, et al. Alterations in cortical and
tiveness of three manual physical therapy techniques in a sub­ cerebellar motor processing in subclinical neck pain patients fol-
group of patients with low back pain who satisfy a clinical lowing spinal manipulation. J Manipulative Physiol Ther 2013;
prediction rule: a randomized clinical trial. Spine 2009;34(25): 36(8):527–37.
2720–9. 89. Taylor HH, Murphy B. Altered sensorimotor integration with
66. Kent P, Marks D, Pearson W, et al. Does clinician treatment cervical spine manipulation. J Manipulative Physiol Ther 2008;
choice improve the outcomes of manual therapy for nonspecific 31(2):115–26.
low back pain? A metaanalysis. J Manipulative Physiol Ther 90. Fryer G, Pearce AJ. The effect of lumbosacral manipulation on
2005;28(5):312–22. corticospinal and spinal reflex excitability on asymptomatic par-
67. Bialosky JE, Bishop MD, Price DD, et al. The mechanisms of ticipants. J Manipulative Physiol Ther 2012;35(2):86–93.
manual therapy in the treatment of musculoskeletal pain: a com- 91. Vase L, Petersen GL, Riley JL III, et al. Factors contributing to
prehensive model. Man Ther 2009;14:531–8. large analgesic effects in placebo mechanism studies conducted
68. Degenhardt BF, Darmani NA, Johnson JC, et al. Role of osteo- between 2002 and 2007. Pain 2009;145(1–2):36–44.
pathic manipulative treatment in altering pain biomarkers: a pilot 92. Price DD, Craggs J, Verne GN, et al. Placebo analgesia is accom-
study. J Am Osteopath Assoc 2007;107(9):387–400. panied by large reductions in pain-related brain activity in irritable
69. McPartland JM, Giuffrida A, King J, et al. Cannabimimetic effects bowel syndrome patients. Pain 2007;127(1–2):63–72.
of osteopathic manipulative treatment. J Am Osteopath Assoc 93. Colloca L, Lopiano L, Lanotte M, et al. Overt versus covert treat-
2005;105(6):283–91. ment for pain, anxiety, and Parkinson’s disease. Lancet Neurol
70. George SZ, Bishop MD, Bialosky JE, et al. Immediate effects of 2004;3(11):679–84.
spinal manipulation on thermal pain sensitivity: an experimental 94. Bialosky JE, Bishop MD, George SZ, et al. Placebo response to
study. BMC Musculoskelet Disord 2006;7:68. manual therapy: something out of nothing? J Man Manip Ther
71. Bialosky JE, Bishop MD, Robinson ME, et al. Spinal manipulative 2011;19(1):11–19.
therapy has an immediate effect on thermal pain sensitivity in 95. Kalauokalani D, Cherkin DC, Sherman KJ, et al. Lessons from a
people with low back pain: a randomized controlled trial. Phys trial of acupuncture and massage for low back pain: patient expec-
Ther 2009;89(12):1292–303. tations and treatment effects. Spine 2001;26(13):1418–24.
72. Bialosky JE, George SZ, Horn ME, et al. Spinal manipulative 96. Michaleff ZA, Lin CW, Maher CG, et al. Spinal manipulation
therapy specific changes in pain sensitivity in individuals with low epidemiology: systematic review of cost effectiveness studies.
back pain. J Pain 2014;15(2):136–48. J Electromyogr Kinesiol 2012;22(5):655–62.
73. Price DD, Staud R, Robinson ME, et al. Enhanced temporal sum- 97. Carroll LJ, Cassidy JD, Peloso PM, et al. Methods for the best
mation of second pain and its central modulation in fibromyalgia evidence synthesis on neck pain and its associated disorders: the
patients. Pain 2002;99(1–2):49–59. Bone and Joint Decade 2000–2010 Task Force on Neck Pain and
74. Cuellar JM, Dutton RC, Antognini JF, et al. Differential Its Associated Disorders. J Manipulative Physiol Ther 2009;
effects of halothane and isoflurane on lumbar dorsal horn 32(2 Suppl.):S39–45.
neuronal windup and excitability. Br J Anaesth 2005;94(5): 98. Scholten-Peeters GG, Thoomes E, Konings S, et al. Is manipula-
617–25. tive therapy more effective than sham manipulation in adults: a
75. Guan Y, Borzan J, Meyer RA, et al. Windup in dorsal horn systematic review and meta-analysis. Chiropr Man Therap
neurons is modulated by endogenous spinal mu-opioid mecha- 2013;21(1):34.
nisms. J Neurosci 2006;26(16):4298–307. 99. Wand BM, Heine PJ, O’Connell NE. Should we abandon cervical
76. Licciardone JC, Kearns CM, Hodge LM, et al. Associations of spine manipulation for mechanical neck pain? Yes. Br Med J
cytokine concentrations with key osteopathic lesions and clinical 2012;344:e3679.
outcomes in patients with nonspecific chronic low back pain: 100. Rivett DA, Reid D. Risk of stroke for cervical spine manipulation
results from the OSTEOPATHIC Trial. J Am Osteopath Assoc in New Zealand. N Z J Physiother 1998;26(2):14–17.
2012;112(9):596–605. 101. Hurwitz EL, Aker PD, Adams AH, et al. Manipulation and mobi-
77. Solomonow M, Zhou BH, Harris M, et al. The ligamento- lization of the cervical spine. A systematic review of the literature.
muscular stabilizing system of the spine. Spine 1998;23(23): Spine 1996;21:1746–59.
2552–62. 102. Carnes D, Mars TS, Mullinger B, et al. Adverse events and
78. Boal RW, Gillette RG. Central neuronal plasticity, low back pain manual therapy: a systematic review. Man Ther 2010;15(4):
and spinal manipulative therapy. J Manipulative Physiol Ther 355–63.
2004;27(5):314–26. 103. Maitland GD, Hengeveld E, Banks K, et al. Maitland’s Vertebral
79. Pickar JG, Wheeler JD. Response of muscle proprioceptors to Manipulation. 6th ed. London: Butterworths; 2000.
spinal manipulative-like loads in the anesthetized cat. J Manipula- 104. Rivett DA. Adverse effects of cervical manipulative therapy. In:
tive Physiol Ther 2001;24(1):2–11. Boyling JD, Jull GA, editors. Grieve’s Modern Manual Therapy
80. Colloca CJ, Keller TS, Gunzburg R. Neuromechanical character- of the Vertebral Column. 3rd ed. Edinburgh: Churchill Living-
ization of in vivo lumbar spinal manipulation. Part II. Neurophysi- stone; 2004. p. 533–49.
ological response. J Manipulative Physiol Ther 2003;26(9): 105. Childs JD, Flynn TW, Fritz JM, et al. Screening for vertebrobasi-
579–91. lar insufficiency in patients with neck pain: manual therapy
286 PART III  Advances in Clinical Science and Practice

decision-making in the presence of uncertainty. J Orthop Sports 113. Arnold M, Bousser MG. Carotid and vertebral dissection. Practi-
Phys Ther 2005;35(5):300–6. cal Neurology 2005;5:100–9.
106. Rushton A, Rivett D, Flynn T, et al. International framework for 114. Mitchell J, Keene D, Dyson C, et al. Is cervical spine rotation, as
examination of the cervical region for potential of Cervical Arte- used in the standard vertebrobasilar insufficiency test, associated
rial Dysfunction prior to Orthopaedic Manual Therapy interven- with a measureable change in intracranial vertebral artery blood
tion. Man Ther 2014;19(3):222–8. flow? Man Ther 2004;9(4):220–7.
107. Hing WA, Reid DA, Monaghan M. Manipulation of the cervical 115. Rivett DA, Shirley D, Magarey M, et al. Clinical Guidelines for
spine. Man Ther 2003;8(1):2–9. Assessing Vertebrobasilar Insufficiency in the Management of
108. Carlesso L, Rivett D. Manipulative practice in the cervical spine: Cervical Spine Disorders. Melbourne: Australian Physiotherapy
a survey of IFOMPT member countries. JMMT 2011;19(2): Association; 2006.
66–70. 116. McLeod LR, Thomas L, Osmotherly P, et al. The effect of end-
109. Rushton A, Rivett D, Carlesso L, et al. International Framework range cervical rotation on vertebral and internal carotid arterial
for Examination of the Cervical Region for Potential of Cervical blood flow and cerebral inflow. Man Ther 2014 Nov 29. pii:
Arterial Dysfunction Prior to Orthopaedic Manual Therapy Inter- S1356-689X(14)00233-1. doi: 10.1016/j.math.2014.11.012. [Epub
vention. Auckland: International Federation of Orthopaedic ahead of print].
Manipulative Physical Therapists; 2012. 117. Kerry R, Taylor AJ. Cervical arterial dysfunction assessment and
110. Kerry R, Taylor AJ, Mitchell JM, et al. Cervical arterial dysfunc- manual therapy. Man Ther 2006;11(4):243–53.
tion and manual therapy: a critical literature review to inform 118. Thomas L, Rivett D, Levi C. The effect of selected manual
professional practice. Man Ther 2008;13(4):278–88. therapy interventions for mechanical neck pain on vertebral and
111. Taylor AJ, Kerry R. A ‘system based’ approach to risk assessment internal carotid arterial blood flow and cerebral inflow. Phys Ther
of the cervical spine prior to manual therapy. Int J Ost Med 2013;93(11):1563–74.
2010;13:85–93.
112. Thomas LC, Rivett DA, Attia JR, et al. Risk factors and clinical
features of craniocervical arterial dissection. Man Ther 2011;
16(4):351–6.
 CHAPTER 30 

Neurodynamic Management of the

Peripheral Nervous System
Michel Coppieters  •  Robert Nee

The spread of biomechanical effects along the nerve pro-

INTRODUCTION vides a credible explanation for why moving a distant
body part can change sensory responses provoked at the
Recent surveys among musculoskeletal physiotherapists end of a neurodynamic test. Experimental pain induced
reveal that neurodynamic techniques are frequently part by injecting hypertonic saline into the thenar or calf
of a multimodal treatment approach to patients with muscles is not changed by applying structural differentia-
compression neuropathies, such as cervical radiculopa- tion manoeuvres associated with the median nerve,
thy1,2 and carpal tunnel syndrome (CTS).3 To our knowl- straight leg raise (SLR), or slump tests, respectively.16,17
edge, no survey datum exists that documents practice This indicates that neurodynamic tests can potentially be
patterns for other compression neuropathies, such as used to distinguish pain related to muscle irritation from
cubital or tarsal tunnel syndrome, or sural nerve pathol- pain related to increased nerve mechanosensitivity.9
ogy. In this chapter we will discuss the use of neurody- Most asymptomatic individuals (≥80%) report sensory
namic tests as diagnostic tests, different neurodynamic responses at the end of range of neurodynamic tests that
treatment options and some clinical reasoning consider- change with structural differentiation.9,18–20 Common
ations behind their application, what pathophysiological descriptors include stretching, aching, pain, burning and
processes may be influenced with treatment and an over- tingling.9,18–20 These data suggest that asymptomatic indi-
view of the evidence from clinical studies. We will end viduals have a certain level of nerve mechanosensitivity.
this chapter with some final considerations regarding The variety of sensory responses reported by asymptom-
neurodynamics. atic individuals means it is important to specify the type
of sensory response that qualifies as a ‘positive’ neurody-
namic test in symptomatic populations. To be confident
NEURODYNAMIC TESTS that a neurodynamic test is most likely identifying a
patient with increased nerve mechanosensitivity, the test
Neurodynamic tests try to determine whether a patient’s needs to reproduce at least part of the patient’s symptoms
symptoms are related to increased nerve mechanosen- and the symptoms should change with structural
sitivity by using specific combinations of spine and differentiation.9
limb movements that apply mechanical forces to a part Resistance to movement and range of motion (ROM)
of the nervous system (Fig. 30-1).4–6 Biomechanical data have also been proposed as criteria to define a ‘positive’
show that joint movements involved in neurodynamic neurodynamic test.4,5 Inter-examiner reliability for mea-
tests increase nerve strain, sliding and compression.7–12 suring elbow extension at the onset of resistance during
Neurodynamic tests also apply mechanical forces to the neurodynamic test for the median nerve is low.9
non-neural tissues.4,5 When central pain mechanisms Studies on detecting the onset of resistance during the
are not the primary reason for a patient’s pain experi- SLR and slump tests have only reported intra-examiner
ence, a positive neurodynamic test response could be reliability.21,22 Poor inter-examiner reliability suggests
related to neural or non-neural tissue sensitivity. A that the onset of resistance is unlikely to be sensitive
neurodynamic test response is thought to be related enough to be a useful criterion for defining a ‘positive’
to neural tissue sensitivity when it changes with move- neurodynamic test.9
ment of a distant body part that further loads or unloads Neurodynamic test ROM can be quantified by mea-
the nervous system (e.g. releasing neck flexion reduces suring the joint angle at pain onset or pain tolerance (e.g.
a sensory response in the posterior thigh during the elbow extension for the median nerve neurodynamic test,
slump test). Analysing a neurodynamic test response knee extension for the slump test). Neurodynamic test
by moving a distant body part is termed structural ROM is highly variable in asymptomatic and symptom-
differentiation.4,5,13 atic individuals.9,22–25 There is also considerable overlap
Using structural differentiation to analyse neural in neurodynamic test ROM between asymptomatic and
tissue responses is supported by biomechanical and symptomatic individuals, and between the involved and
experimental pain model data. When a joint movement uninvolved limbs of symptomatic individuals.9,23 Neuro-
is performed at the end of a neurodynamic test, the bio- dynamic test ROM variability and overlap make it unlikely
mechanical effects spread along the entire nerve.9,14,15 that an absolute ROM cut-off can be found that
287
288 PART III  Advances in Clinical Science and Practice

7 8 peripheral neuropathic pain will bias the estimates of the

diagnostic performance of neurodynamic tests.38
Studies investigating the ability of the SLR and slump
6 tests to detect lumbar radicular pain have used electrodi-
agnostic testing, or surgical or imaging evidence of
3
1 lumbar disc herniation as the reference standard. When
using these reference standards, the diagnostic perfor-
mance of the SLR is relatively poor.39,40 Positive responses
to a crossed SLR (a relatively uncommon clinical finding)
4 or the slump test may help confirm the presence of
5 2 lumbar radicular pain related to lumbar disc hernia-
tion.39,41 Again, potential limitations in the reference
standards require caution when interpreting these results.
FIGURE 30-1  ■  End position of the base neurodynamic test for A surgical reference standard limits the generalizability
the median nerve. The components and sequence for this base of diagnostic performance findings because it narrows the
test are: 1–2, shoulder abduction to ~90–100°, while shoulder spectrum of patients who can be included in the study
girdle elevation is prevented; 3, wrist extension; 4, forearm
supination; 5, shoulder external rotation; and 6, elbow exten- and may alter the prevalence of the target condition.39,42
sion. Ipsilateral (7) or contralateral (8) lateroflexion of the mid Lastly, there is not necessarily a strong correlation
and lower cervical spine are common manoeuvres to assist in between imaging findings and the presence or absence of
structural differentiation if a patient’s symptoms are (at least lumbar radicular pain.40,43 Therefore, similar to electro-
partially) reproduced in the distal upper quadrant. Wrist move-
ments are commonly used to structurally differentiate if symp-
diagnostic reference standards, imaging reference stan-
toms are elicited in the proximal upper quadrant. Base dards may misclassify patients and bias estimates of the
neurodynamic tests can be modified to suit individual patients. diagnostic performance of neurodynamic tests.38
The upper limb neurodynamic tests for the median, ulnar and The difficulty in investigating the diagnostic perfor-
radial nerve, the slump and side-lying slump (femoral nerve) mance of neurodynamic tests is that there is no agreed
test and straight leg raise test are considered base neurody-
namic tests. upon reference standard for establishing that an indi-
vidual patient has increased nerve mechanosensitivity.44
This means there is a mismatch between the intent of
neurodynamic tests (identifying increased nerve mecha-
accurately discriminates symptomatic from asymptom- nosensitivity) and the various reference standards that
atic individuals. have been used in published research. Until a reference
Looking for a certain deficit in neurodynamic test standard for increased nerve mechanosensitivity can be
ROM in the involved limb compared to the uninvolved agreed upon, using neurodynamic tests for diagnostic
limb (limb asymmetry) is another method for using ROM purposes is primarily based on lower evidence from bio-
to define a ‘positive’ neurodynamic test. Asymptomatic mechanical and experimental pain model data described
individuals typically show a 5–10° difference between previously.
limbs in ROM for the median nerve26–29 and SLR25 tests. Another issue related to neurodynamic testing is the
However, we are not aware of any data showing that a concept of sequencing. Standardized sequences for apply-
certain amount of limb asymmetry in neurodynamic test ing the movements involved in different neurodynamic
ROM can discriminate symptomatic from asymptomatic tests have been described, yet clinicians have always been
individuals. Consequently, at this stage it is unlikely that encouraged to change the order of movement to match
ROM can be a useful criterion for defining a ‘positive’ an individual patient’s presentation.4,5,45 Neurodynamic
neurodynamic test.9 Based on information available at test sequencing is partly based on the belief that different
this time, a ‘positive’ neurodynamic test should at least orders of movement can apply different levels of strain
partly reproduce the patient’s symptoms and the symp- to a particular nerve segment at the end of a neurody-
toms should change with structural differentiation.9 This namic test.5 However, cadaveric data have shown that,
definition of a ‘positive’ neurodynamic test is reliable when joints are moved through similar ranges of motion,
when applied to symptomatic populations.23,30,31 nerve strain at the end of the test does not change with
When electrodiagnostic tests are used as the reference different orders of movement.10,46 However, when differ-
standard to determine the diagnostic accuracy of neuro- ent neurodynamic test sequences are applied clinically,
dynamic tests, data suggest that the neurodynamic test joints likely move through different ranges of motion.
for the median nerve can help diagnose cervical radicu- Potential differences between sequences in ranges of
lopathy,32 but not CTS.33–35 However, care is required joint motion may be more likely to affect nerve biome-
when interpreting these findings because of the limita- chanics at the end of a neurodynamic test than any spe-
tions of using electrodiagnostic tests as the reference cific effects from the order of movement.46
standard. Increased nerve mechanosensitivity can be We are not aware of any published or recent studies
present in cervical radiculopathy and CTS even when that have explored whether different sequences can
standard electrodiagnostic tests are normal.36,37 This improve the diagnostic performance of a neurodynamic
means that patients with peripheral neuropathic pain who test. Regardless of any potential impact on diagnostic
have increased nerve mechanosensitivity rather than con- performance, neurodynamic test sequencing may still
duction loss will often be incorrectly classified by the have value clinically. A joint movement is not likely to
reference standard as not having peripheral neuropathic reach a full ROM when performed in the later stages of
pain. Potential misclassification of patients who have a neurodynamic test.47 This knowledge can help the
 30  Neurodynamic Management of the Peripheral Nervous System 289

clinician modify a neurodynamic test when examining a increases in nerve strain.5 These clinical assumptions
patient with a sensitive or stiff body part. Using a patient were confirmed in a series of cadaveric48,50 and in vivo
with a highly sensitive or stiff shoulder as an example, the studies51 in the upper quarter (Fig. 30-2). When the same
best approach to neurodynamic testing for the median joints were moved through the same ranges of motion,
nerve might be to use a distal-to-proximal sequence with comparable start and end positions, the strain was
where shoulder abduction would be the last movement. substantially lower and the excursion of the nerve relative
This sequence would apply less mechanical load to the to surrounding structures was approximately 2.548,50 to 551
non-neural tissues in the shoulder but would still apply times larger for a sliding technique (Fig. 30-2). In con-
adequate nerve strain and nerve compression to provoke trast, a study in the lower limb reported much smaller
sensitized neural tissues. Different neurodynamic test differences.52 Although the sliding technique still resulted
sequences may also help with structural differentiation. in a significantly larger excursion of the sciatic nerve, it
For example, in a patient who has plantar heel pain, it is questionable whether the observed mean difference of
may be useful to modify the SLR so that ankle dorsiflex- 0.6 mm is clinically meaningful. Because start and end
ion and eversion are performed before hip flexion. Ankle positions varied significantly in this study,52 we believe
dorsiflexion and eversion apply strain to the plantar fascia the results should be interpreted cautiously, especially
and tibial and plantar nerves simultaneously.14 Subse- because another in vivo study for the sciatic nerve that
quent hip flexion does not change strain on the plantar used identical start and end positions revealed large dif-
fascia but increases strain on the tibial and plantar ferences in excursion between the sliding and tensioning
nerves.14 This modified test sequence could make it easier techniques (Fig. 30-3).53
for the clinician to determine whether there is a nerve- Although sliding and tensioning techniques result in
related component to the patient’s plantar heel pain. very different biomechanical effects on the nervous
system, it is important to emphasize that one type of
technique is not always superior to the other.48 Sliding
NEURODYNAMIC MANAGEMENT techniques are less vigorous and may be more appropri-
ate in more irritable conditions; tensioning techniques
Neurodynamic techniques can be categorized as tech- may have a place in the later stages or in more sport-
niques that aim to either mobilize the nervous system specific rehabilitation. To date, there is virtually no com-
itself, or mobilize the structures that surround it. Sliding parative clinical research to guide technique choices.
and tensioning techniques mobilize the nervous system,5,48 Sound clinical reasoning, and perhaps erring on the side
whereas a cervical contralateral lateral glide technique49 of caution, remains of cardinal importance.
is an example of a common technique that mobilizes the
structures surrounding the nervous system. Whether it is
indicated to mobilize the nervous system or its surround-
Mobilization of Surrounding Structures
ing structures will depend on many factors, such as which The cervical contralateral lateral glide technique (Fig.
pain mechanisms are in operation, the history, severity 30-4) was first described by Elvey as a treatment tech-
and ‘irritability’ of the condition, stages of tissue healing, nique for neuropathic disorders.49 The immediate effects
associated pathologies, signs and symptoms and results of the technique have been investigated in several condi-
from technical investigations. tions, including nerve-related neck and/or arm pain54,55
and musculoskeletal conditions, such as lateral epicon-
dylalgia56 and chronic whiplash-associated disorders.57 To
Sliding and Tensioning Techniques our knowledge, the technique has invariably demon-
When clinicians first conceptualized the idea of mobiliz- strated positive immediate effects across different
ing the nervous system as a treatment approach, tech- conditions.54–57 The equivalent technique for the lumbar
niques were implemented that resembled neurodynamic spine – a segmental lumbar lateral flexion contralateral
tests or parts thereof. These days, these techniques are to the painful side – has also shown positive effects
referred to as tensioning techniques. Nerve gliding is when administered to patients with peripheral nerve
obtained by moving one or several joints in such a manner sensitization.58
that the nerve bed is elongated and, as a consequence,
strain in the nervous system increases. Adjacent or more
remote joints may also be positioned to further increase
Treating the Neural Container
the load on the nervous system. Although very few Unhealthy neighbouring tissues or postural changes are
adverse events were reported in the literature, clinicians likely important contributing factors in the development
quickly realized that these techniques were sometimes and maintenance of peripheral neuropathic pain states,
too aggressive. Clinicians therefore developed the concept and may require attention. Although important, this is
of sliding techniques. beyond the scope of this chapter.
In a sliding technique, at least two joints are moved
simultaneously, either actively or passively, in such a
manner that one movement counterbalances the increase INDICATIONS AND
in nerve strain caused by another movement.5 The CONTRAINDICATIONS
clinical assumption is that – compared to tensioning tech-
niques – sliding techniques are associated with much Elvey4 proposed a set of specific signs that should be
larger excursions of the nervous system relative to sur- present, in addition to a patient interview suggestive of
rounding structures, but without the potentially large peripheral neuropathic pain, to support the hypothesis of
290 PART III  Advances in Clinical Science and Practice

1
Strain in median nerve at wrist Median
+6% nerve
excursion
2 +4%
at wrist
+2%
Strain in reference position
–2%
180

Elbow
150
120
90
60 4.7

Wrist
30 mm
$ Tensioning technique 0

+6%
2 +4%
+2%
Strain in reference position
–2%
180
Elbow 150
120
90
60 12.4
Wrist

30 mm
% Sliding technique 0

1 Median nerve excursion 1

2 in upper arm 2

10.2
1.8 mm

& Tensioning technique ' Sliding technique

FIGURE 30-2  ■  Example of a tensioning technique and corresponding sliding technique for the median nerve at the wrist (A,B)47,49
and the upper arm (C,D).50 For the tensioning techniques, both depicted movements (1 and 2) increase the length of the nerve
bedding. For the sliding techniques, the movement that elongates the length of the nerve bedding (2) is counterbalanced by another
movement that reduces the length of the nerve bedding (1). The waveform diagrams in (A) and (B) represent the strain in the median
nerve at the wrist (top waveform), and the range of motion of the elbow (middle waveform) and wrist (lower waveform) for two
consecutive repetitions of the technique. For the elbow, 180° represents full extension. Clear differences in peak strain can be seen.
The bar diagrams (A–D) demonstrate the large differences in excursion of the median nerve (in mm) relative to surrounding struc-
tures between the sliding and tensioning techniques.

a ‘neurogenic disorder’ for which physiotherapy manage- has never been investigated directly, the criteria have
ment could be considered. These criteria were: (a) an been used as inclusion criteria in several clinical trials.54,58,59
active movement dysfunction that is related to non- Furthermore, research has now identified which ele-
compliance of a specific nerve; (b) a passive movement ments of the patient interview may be suggestive of
dysfunction that correlates with the active dysfunction; neuropathic pain.60,61 Various questionnaires may yield
(c) a positive neurodynamic test; (d) an abnormal response valuable information as well in this respect (e.g.
to nerve palpation; (e) signs of a musculoskeletal dysfunc- S-LANNS,62 DN463). Several papers have investigated
tion that would indicate that the cause of the neurogenic nerve palpation.31,44,64,65 However, considering our current
disorder would be responsive to physiotherapy; and (f) a understanding of pathophysiological processes, if the
protective posture that shortens the anatomical course of entrapment site cannot be palpated directly or indirectly,
the affected nerve. Although the value of these criteria we do not know whether abnormal responses to palpation
 30  Neurodynamic Management of the Peripheral Nervous System 291

can routinely be elicited at other points along the affected systemic diseases for which neurodynamic exercises are
peripheral nerve. A protective posture may also not either contraindicated or for which we currently have no
always be present, especially if the neuropathy is associ- evidence. The criteria may have merit because they
ated with minimal pain. The criterion regarding the pres- remind clinicians of potentially useful items to look out
ence of a musculoskeletal disorder is a good reminder for before implementing neurodynamic techniques.
that many of these criteria and neuropathic pain can be
present following sinister space-occupying lesions or
INFLUENCES ON PATHOBIOLOGICAL
PROCESSES
Until recently,48 we could only largely speculate on what
pathophysiological changes could potentially be influ-
enced with neurodynamics. Although there is still much
to discover and much is still speculative, there are now at
least some preliminary data on possible working mecha-
nisms of neurodynamic techniques. Most of these studies
have either been conducted in patients with CTS or in
animal models. Because of the high prevalence of CTS
in the general population (3.8%),66 CTS is often used as
1 a possible model for compression neuropathies in general.

1.0 mm 17.0 1
2
Normalization of Impaired
2 mm
Nerve Movement
A Tensioning technique B Sliding technique The majority of investigations demonstrated that patients
FIGURE 30-3  ■  Example of a tensioning technique and corre- with a compression neuropathy, such as CTS, have
sponding sliding technique for the sciatic and tibial nerve.  reduced longitudinal67–69 and transverse70–72 nerve move-
(A) For the tensioning technique, both hip flexion (1) and knee ment compared to healthy controls. Due to the cross-
extension (2) increase the length of the nerve bedding. (B) For
the sliding technique, knee extension (2) which elongates the sectional nature of these studies, it is still unclear
nerve bedding is counterbalanced by hip extension (1) which whether altered nerve biomechanics is a consequence of
reduces the length of the nerve bedding. The bar diagrams the pathophysiological processes of a neuropathy, or pos-
demonstrate the large difference in excursion of the sciatic sibly a predisposing factor for the development of a
nerve (in mm) in the posterior thigh between the two tech-
niques.53 The location of the measurements is indicated with the
neuropathy. Recent unpublished work revealed that
ultrasound transducer. experimentally increasing carpal tunnel pressure to

Head

C1 C1

C2 C2

C3 C3

C4 C4

C5 C5

C6 C6

C7 C7
$ % &

FIGURE 30-4  ■  A cervical contralateral lateral glide technique for (for example) the C5–C6 segment (i.e. to mobilize the structures that
surround the C6 spinal nerve), can be performed in various ways. (A) The patient’s head rests in neutral on the plinth while the
therapist aims to translate C5 relative to C6, away from the affected side. (B) Because the technique is typically performed without
fixation of adjacent spinal levels, the translation will also occur at neighbouring segments. (C) Alternatively, all spinal levels superior
to the C6 nerve root can be translated together to the contralateral side. The patient’s head then rests against the abdomen of the
therapist, who shifts his/her trunk slightly to the contralateral side (not shown). When possible, the techniques are typically per-
formed with the affected arm in a position that preloads the affected peripheral nerve.
292 PART III  Advances in Clinical Science and Practice

similar and even higher levels than typically observed in splinting is unlikely to have. Some of these issues are
patients with CTS did not influence longitudinal or discussed elsewhere in this chapter.
transverse nerve movement.73 Also, longitudinal excur-
sion of the median nerve does not change following Reduction of Extraneural
carpal tunnel release surgery.74,75 These findings indicate
that an acute increase or decrease in pressure does not
Oedema and Pressure
alter nerve excursion. If a prolonged increase in pressure Carpal tunnel pressure is elevated in patients with CTS,
would, however, result in alterations in connective tissues, and this elevated pressure is considered an important
perhaps there is a place for interventions that aim to mechanism in CTS.85,86 There is only preliminary evi-
normalize nerve movement and restore the homoeostasis dence from a small randomized trial that suggests that
in and around the neuropathy. To the authors’ knowl- neurodynamic exercises can reduce carpal tunnel pres-
edge, there are no studies yet to support this. sure in a subgroup (around 50%) of patients with CTS.87
It has also been suggested that early mobilization may Considering the invasive nature of carpal tunnel pressure
limit adhesions and scar formation following surgical measurements,88 only a small sample of patients and only
release in patients with neuropathies.76 A recent Cochrane immediate effects have been studied. If neurodynamic
review, however, indicated that there is currently no evi- exercises are capable of reducing extraneural pressure
dence available for or against post-operative rehabilita- affecting a nerve and its functions, this reduction in pres-
tion following CTS surgery.77 Two studies investigated sure may also have a positive impact on intraneural blood
the effect of early mobilization following ulnar nerve flow and axonal transport. These two processes are con-
transposition for cubital tunnel syndrome.78,79 Early sidered vital for the integrity of the peripheral nervous
mobilization resulted in substantially less contractures system.81,83,89,90
(4% versus 52%)78 and a quicker return to work (1 month
versus 2.75 months79 or in half the time78). Dispersal of Inflammatory Mediators
In a key paper, Dilley et al.90 demonstrated that an
Evacuation of Intraneural Oedema inflamed nerve becomes extremely sensitive to mild com-
Following nerve compression, impaired intraneural blood pression or elongation, whereas the conduction velocity
flow can lead to localized hypoxia, oedema, inflammation through the inflamed region may remain largely unaf-
and fibrosis.80 In many circumstances, symptoms such as fected. Ectopic action potentials were generated mid-
paraesthesia or even numbness caused by reduced blood axon at the inflamed nerve region following mild
supply to a peripheral nerve due to temporary compres- mechanical provocation. At the demyelinated and
sion are easily reversible with movement or a change in inflamed nerve site, ion channel up-regulation and pro-
posture. If pressure cannot be alleviated and hypoxia per- liferation occurred resulting in the establishment of an
sists, the endothelial cells of the capillaries inside the abnormal or ectopic impulse-generating site, which can
peripheral nerve may break down, resulting in intraneu- be triggered by elements of the inflammatory soup.91
ral oedema.81 Considering the absence of a lymphatic Song et al.92 delivered inflammatory mediators around
drainage system within the bundles of axons in a periph- the L5 dorsal root ganglion in rodents to create a neuro-
eral nerve,82 evacuation of this oedema is more difficult, pathic pain state and investigated the effect of spinal
potentially resulting in an increase in intraneural pressure mobilization. When compared to no intervention, mobi-
and possibly a mini-compartment syndrome within the lization resulted in reduced hyperexcitability of the dorsal
nerve fascicles.82 This is an ideal environment for fibro- root ganglion neurons, along with a reduction in severity
blasts to proliferate and form scar tissue, resulting in the and duration of thermal and mechanical hyperalgesia.92
fibrotic stage.83 A recent MRI study revealed a reduction The authors concluded that mobilization resulted in
in intraneural oedema following neurodynamic exercises faster elimination of the inflammation and excitability of
in patients with CTS, compared to a wait-and-see the inflamed dorsal root ganglion neurons by improving
approach.84 It is worthwhile noting that although the blood supply and nutrition to the affected dorsal root
nerve was inflamed and swollen, mobilization exercises ganglion.
for the median nerve did not aggravate symptoms, sug-
gesting that when applied skilfully, neurodynamic exer-
cises can be performed safely, without significant adverse Influence on the Neuro-Immune
events. In fact, the reduction in nerve swelling was associ-
ated with an improvement in symptoms and function.84
Response
Perhaps movement-based interventions, such as neuro- Besides local inflammation and demyelination at the
dynamics, can play an important role in this oedematous compression site,83 animal models of (severe) nerve
stage, helping to prevent progression to the less revers- lesions revealed immune inflammatory responses in the
ible stage of nerve fibrosis. Also worthwhile noting is that corresponding ipsilateral dorsal root ganglia and dorsal
splinting resulted in a similar reduction in intraneural horn of the spinal cord, but also in higher centres in the
oedema.84 Although we believe there might be a place for central nervous system, and even in the dorsal horn and
the use of a splint in CTS and perhaps partial immobili- dorsal root ganglia contralateral to the side of the nerve
zation in other neuropathies (if limited in time and as part lesion.93 These might be important mechanisms for the
of a broader biologically plausible management approach), development of widespread pain and mirror pains that
movement is likely to have additional benefits that occur like mirror images on both sides of the body.94,95
 30  Neurodynamic Management of the Peripheral Nervous System 293

Less severe nerve compression models, resulting in sub- ‘moderate’ (≥0.6 but <1.2) to ‘large’ (≥1.2 but <2.0)
stantially less axonal loss at the compression site, also treatment effects.109 In contrast to these favourable
revealed inflammatory changes and glia cell activation in results for non-operative management of lumbar radicu-
the dorsal root ganglia and spinal cord.96 Santos et al.97 lar pain, one clinical trial suggests that neurodynamic
investigated the effect of neural mobilization in rats with treatment may not be helpful after lumbar surgery.110
a sciatic nerve lesion. Compared to rats with a nerve Patients who have cervical radicular pain do better
lesion but no intervention, non-operated rats and sham- with neurodynamic treatment than advice to remain
operated rats, the group that received neurodynamic active.111 Cervical radicular pain was defined as reproduc-
mobilizations demonstrated a substantial decrease in tion of symptoms with median nerve neurodynamic
nerve growth factor concentration and in glia cell activa- testing and less than two abnormal neurological signs at
tion in the corresponding dorsal root ganglia and spinal the same nerve root level. Neurodynamic treatment
cord. Both nerve growth factor and glia cell activation are involved brief education, manual therapy with contralat-
considered important players in neuropathic pain.91,98,99 eral cervical lateral glide and shoulder girdle oscillation
These changes were associated with pain reversal (hyper- techniques, and a home programme of nerve gliding
algesia, allodynia and thermal sensitivity).97 Further exercises for the cervical nerve roots and median
research is certainly required, but these findings suggest nerve.49,112 Standardized mean differences for pain (0.7–
that movement-based interventions like neurodynamics 0.9) and self-reported function (0.6–0.9) showed ‘moder-
may have positive effects on the neuro-inflammatory ate’ treatment effects favouring neurodynamic treatment
responses associated with the occurrence of widespread at a 3- to 4-week follow-up.111 A previous clinical trial
pain. reported similar effect sizes that were not statistically
significant because of a relatively small sample size.59,113
According to the published trials, neurodynamic treat-
Facilitation of Descending Modulation ment effects are less favourable for patients who have
The initial analgesic effects following various forms of peripheral neuropathic pain conditions affecting the
manual therapy have frequently been linked to the activa- upper or lower limb. Although neurodynamic treatment
tion of the descending pain inhibitory system projecting appears to be better than no treatment for patients with
from the periaqueductal grey region in the mid-brain to CTS, it is not superior to other interventions (e.g. carpal
the spinal cord.100–103 Temporal summation is considered bone mobilization, splinting).114 Furthermore, adding
a measure of dorsal horn excitability. Compared to a neurodynamic techniques to other interventions such as
sham intervention, neurodynamic techniques resulted in splinting and tendon gliding exercises does not improve
a reduction of temporal summation in patients with CTS, outcomes.114 These findings are consistent regardless of
suggesting reduced dorsal horn excitability, possibly due whether neurodynamic techniques involve the entire
to activation of the descending inhibitory system.104 An upper limb or focus on moving only the wrist and hand.
animal study revealed that neurodynamic techniques fol- Despite these findings, it has been suggested that addi-
lowing a sciatic nerve injury modulate the expression of tional high-quality research on the efficacy of conserva-
endogenous opioids in the periaqueductal grey region.105 tive interventions for CTS such as neurodynamic
Furthermore, the injured animals that received neurody- treatment is needed.114 This additional research should
namic mobilizations showed improved locomotion and blind participants to interventions where possible, blind
muscle force compared to injured animals that did not outcome assessors and measure short-term and long-
receive treatment. These data support the view that neu- term outcomes, including the need for surgery.114
rodynamic exercises facilitate pain relief via endogenous Based on the available evidence, neurodynamic treat-
analgesic modulation. ment may not be beneficial for patients who have cubital
tunnel syndrome. One randomized clinical trial showed
that adding nerve gliding exercises to education on the
CLINICAL TRIAL EVIDENCE pathomechanics of cubital tunnel syndrome and advice
to avoid aggravating activities did not improve 6-month
Relatively few clinical trials have measured neurodynamic outcomes in patients who had mild to moderate symp-
treatment effects. Lumbar and cervical radicular pain, toms.115 However, nearly 30% of participants were lost
CTS, cubital tunnel syndrome and tarsal tunnel syn- to follow-up and were not included in the statistical anal-
drome have been the peripheral neuropathic pain condi- ysis, which may have impacted the results.
tions studied in these trials. It also appears from one small clinical trial that adding
Patients with lumbar radicular pain do better when neurodynamic treatment to conservative management of
SLR or slump ‘tensioning’ techniques are added to a tarsal tunnel syndrome may not be very helpful.116 Con-
programme of lumbar mobilization and exercise.106–108 servative management involved ice, gastrocnemius
Lumbar radicular pain was defined as reproduction of stretching, lower extremity strengthening, shoe inserts
symptoms with SLR or slump testing, no neurological for patients who had low medial arches or pronation
signs and no centralization of symptoms with repeated deformities, and bandaging for patients who had ankle
movements. Standardized mean differences (reported oedema. Neurodynamic treatment involved a slump ‘ten-
or calculated from reported data) for pain (0.65–1.42) sioning’ technique. Significantly fewer participants who
and self-reported disability (0.75–1.96) after a 3-week received neurodynamic treatment still had a positive
intervention (six visits) favoured neurodynamic treat- Tinel sign at the tibial nerve below the medial malleolus
ment. These standardized mean differences represent after the 6-week intervention (risk difference calculated
294 PART III  Advances in Clinical Science and Practice

from reported data = 0.54, 95% confidence interval 0.31– previously that for the same syndrome (e.g. CTS), the
0.93). However, there were no differences between dominant pathomechanism may be very different in dif-
groups in pain, combined talocrural and subtalar joint ferent patients.127 In some it may be localized at the
ROM, foot muscle strength or the number of participants entrapment site, but in others the dominant pain mecha-
whose symptoms were provoked with the ankle dorsiflex- nism may be located in the dorsal root ganglia, spinal
ion and eversion test for the tibial nerve. cord or brain. It is then to be expected that patients with
Researchers have consistently been encouraged to the same syndrome but different pathomechanisms may
identify characteristics that predict whether patients will respond differently in clinical trials to a more or less set
respond to an intervention.117,118 Schäfer et al.58 and Nee intervention, be it neurodynamics, other forms of con-
et al.119 provided preliminary data on characteristics that servative management, or surgery. This may also explain
may help identify patients with lumbar or cervical radicu- the discrepancy that sometimes seems to exist between
lar pain who are likely to improve with neurodynamic more physiological research findings with smaller and
treatment. Patients who have physical signs of increased perhaps more uniform samples of patients in more con-
nerve mechanosensitivity (e.g. reproduction of symptoms trolled environments (this certainly also applies to animal
with neurodynamic testing and a change in these symp- studies), compared to large-scale clinical trials with long-
toms with structural differentiation, increased sensitivity term follow-up. In clinical practice, we want every patient
to nerve palpation), no neurological signs and an absence to improve, but numbers needed to treat are rarely close
of neuropathic pain qualities (i.e. clinician-administered to one. Identification of responders and non-responders
or self-report version of the Leeds Assessment of Neu- remains important.
ropathic Symptoms and Signs score <12) are likely to Discussing the potential effects of various interven-
improve with neurodynamic treatment.58,119 For patients tions should not overshadow the importance of the
who have cervical radicular pain, older age and smaller quality of the patient–clinician relationship. Data suggest
deficits in median nerve neurodynamic test ROM in the that a stronger therapeutic alliance between the patient
involved limb relative to the uninvolved limb are also and clinician is associated with better outcomes for
associated with improvement.119 Further research is patients who have musculoskeletal128,129 or peripheral
needed to determine whether these characteristics iden- neuropathic pain.130,131 Understanding the patient’s per-
tify patients who do well regardless of the intervention spective about the pain experience and the impact of any
(prognostic factors) or patients who respond better to associated psychosocial issues, providing clear explana-
neurodynamic treatment than to alternative treatments tions to the patient (including a diagnosis where appro-
(treatment effect modifiers).120,121 priate), and involving the patient in the decision-making
process are examples of factors that can strengthen the
patient–clinician relationship.132,133
FINAL CONSIDERATIONS There is an increased awareness of the role of the
central nervous system in persistent pain states.91,98,134,135
The number of studies investigating various aspects Patient perspectives have undoubtedly improved thanks
of neurodynamics has grown substantially over recent to this. On the other hand, recent findings from respected
decades. There remain concerns however about the low research groups have reminded us that abnormal primary
quality of evidence due to the small number of clinical afferent input may also remain critical for maintaining
trials and/or relatively high risk of bias of studies. The pain in peripheral neuropathies136 and phantom limb
interventions that are evaluated in clinical trials are often pain,137 and that addressing this abnormal input can lead
poorly described,122 and this also applies to trials in neu- to drastic improvements.137 As pointed out in this chapter,
rodynamics. These factors make it difficult to provide perhaps neurodynamics (and other movement-based
strong recommendations for the management of periph- interventions) can contribute to address both peripheral
eral neuropathic pain. More high-quality research is and central mechanisms in patients with persistent neu-
required. ropathic pain states.
Clinical research in neurodynamics, and neuropathies
in general, is hampered by the absence of a gold standard
or universally accepted criteria to diagnose any REFERENCES
neuropathy.123–125 Our understanding of the pathophysi- 1. Coppieters M, Nee RJ, Jull G, et al. How do you and your col-
ology of compression neuropathies evolves rapidly. leagues treat cervical radiculopathy? A nationwide survey of MPA
members. In APA Conference New Moves. Melbourne, Australia:
Unfortunately, taking nerve biopsies is rarely possible 2013.
and the most commonly used animal models create more 2. Coppieters MW. The body and the brain. Current concepts in
severe nerve lesions with much more damage126 than the rehabilitation of neuropathic pain. 4th International Congress on
neuropathies we typically encounter in physiotherapy Neuropathic Pain. IASP NeuPSIG; Toronto, Canada; 2013.
3. Coppieters M, Soon BT. Non-invasive management of carpal
practices. tunnel syndrome. A national practice survey among Australian
It is good to be aware that we treat many syndromes hand therapists. In: APA Physiotherapy Conference, Brisbane,
with neurodynamic techniques (e.g. carpal, cubital and Australia; 2011.
tarsal tunnel syndrome, thoracic outlet syndrome, supinator 4. Elvey RL. Physical evaluation of the peripheral nervous system in
and pronator teres syndrome). Most of these syndromes disorders of pain and dysfunction. J Hand Ther 1997;10(2):122–9.
5. Butler DS. The Sensitive Nervous System. 1st ed. Unley, S. Aust.:
are still heavily debated, even CTS. Syndromes describe Noigroup Publications; 2000.
a collection of signs and symptoms that may not have 6. Smart K, Blake C, Staines A, et al. Clinical indicators of
a single identifiable pathogenesis. We have argued ‘nociceptive’, ‘peripheral neuropathic’ and ‘central’ mechanisms of
 30  Neurodynamic Management of the Peripheral Nervous System 295

musculoskeletal pain. A Delphi survey of expert clinicians. Man 30. Philip K, Lew P, Matyas T. The inter-therapist reliability of the
Ther 2010;15:80–7. slump test. Aust J Physiother 1989;35:89–94.
7. Breig A, Troup J. Biomechanical considerations in the straight- 31. Schmid AB, Brunner F, Luomajoki H, et al. Reliability of clinical
leg-raising test: cadaveric and clinical studies of the effects of tests to evaluate nerve function and mechanosensitivity of the
medial hip rotation. Spine 1979;4(3):242–50. upper limb peripheral nervous system. BMC Musculoskelet
8. Gilbert K, Brismee J, Collins D, et al. 2006 Young Investigator Disord 2009;10:11.
Award Winner: lumbosacral nerve root displacement and strain. 32. Wainner R, Fritz J, Irrgang J, et al. Reliability and diagnostic
Part 2. A comparison of 2 straight leg conditions in unembalmed accuracy of the clinical examination and patient self-report mea-
cadavers. Spine 2007;32(14):1521–5. sures for cervical radiculopathy. Spine 2003;28(1):52–62.
9. Nee RJ, Jull GA, Vicenzino B, et al. The validity of upper-limb 33. Wainner R, Fritz J, Irrgang J, et al. Development of a clinical
neurodynamic tests for detecting peripheral neuropathic pain. prediction rule for the diagnosis of carpal tunnel syndrome. Arch
J Orthop Sports Phys Ther 2012;42(5):413–24. Phys Med Rehabil 2005;86:609–18.
10. Boyd BS, Topp KS, Coppieters MW. Impact of movement 34. Vanti C, Bonfiglioli R, Calabrese M, et al. Upper limb neurody-
sequencing on sciatic and tibial nerve strain and excursion during namic test 1 and symptoms reproduction in carpal tunnel syn-
the straight leg raise test in embalmed cadavers. J Orthop Sports drome. A validity study. Man Ther 2011;16:258–63.
Phys Ther 2013;43(6):398–403. 35. Vanti C, Bonfiglioli R, Calabrese M, et al. Relationship between
11. Rade M, Kononen M, Vanninen R, et al. 2014 Young Investigator interpretation and accuracy of the upper limb neurodynamic test
Award Winner: in vivo magnetic resonance imaging measurement 1 in carpal tunnel syndrome. J Manipulative Physiol Ther 2012;
of spinal cord displacement in the thoracolumbar region of asymp- 35:54–63.
tomatic subjects. Part 1: straight leg raise test. Spine 2014; 36. Slipman C, Plastaras C, Palmitier R, et al. Symptom provocation
39(16):1288–93. of fluoroscopically guided cervical nerve root stimulation: are
12. Ridehalgh C, Moore A, Hough A. Normative sciatic nerve excur- dynatomal maps identical to dermatomal maps? Spine 1998;
sion during a modified straight leg raise test. Man Ther 2014;19: 23(20):2235–42.
59–64. 37. Witt J, Hentz J, Stevens J. Carpal tunnel syndrome with normal
13. Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and nerve conduction studies. Muscle Nerve 2004;29:515–22.
treatment. Man Ther 1999;4(2):63–73. 38. Reitsma J, Rutjes A, Khan K, et al. A review of solutions for
14. Coppieters MW, Alshami AM, Babri AS, et al. Strain and excur- diagnostic accuracy studies with an imperfect or missing reference
sion of the sciatic, tibial, and plantar nerves during a modified standard. J Clin Epidemiol 2009;62:797–806.
straight leg raising test. J Orthop Res 2006;24(9):1883–9. 39. van der Windt D, Simons E, Riphagen I, et al. Physical examina-
15. Alshami AM, Babri AS, Souvlis T, et al. Strain in the tibial and tion for lumbar radiculopathy due to disc herniation in patients
plantar nerves with foot and ankle movements and the influence with low back pain. Cochrane Database Syst Rev 2010;(2):
of adjacent joint positions. J Appl Biomech 2008;24(4):368–76. CD007430.
16. Coppieters MW, Kurz K, Mortensen TE, et al. The impact of 40. Scaia V, Baxter D, Cook C. The pain provocation-based straight
neurodynamic testing on the perception of experimentally induced leg raise test for diagnosis of lumbar disc herniation, lumbar
muscle pain. Man Ther 2005;10(1):52–60. radiculopathy, and/or sciatica: a systematic review of clinical
17. Coppieters MW, Alshami AM, Hodges PW. An experimental pain utility. J Back Musculoskeletal Rehabil 2012;25:215–23.
model to investigate the specificity of the neurodynamic test for 41. Majlesi J, Togay H, Unalan H, et al. The sensitivity and specificity
the median nerve in the differential diagnosis of hand symptoms. of the slump and the straight leg raising tests in patients with
Arch Phys Med Rehabil 2006;87(10):1412–17. lumbar disc herniation. J Clin Rheumatol 2008;14:87–91.
18. Walsh J, Flatley M, Johnston N, et al. Slump test: sensory 42. Fritz J, Wainner R. Examining diagnostic tests: an evidence-based
responses in asymptomatic subjects. J Man Manipulative Ther perspective. Phys Ther 2001;81(9):1546–64.
2007;15(4):231–8. 43. Beith I, Kemp A, Kenyon J, et al. Identifying neuropathic
19. Lai W, Shih Y, Lin P, et al. Normal neurodynamic responses to back and leg pain: a cross-sectional study. Pain 2011;152:
the femoral slump test. Man Ther 2012;17:126–32. 1511–16.
20. Martinez M, Cubas C, Girbes E. Ulnar nerve neurodynamic test: 44. Walsh J, Hall T. Reliability, validity and diagnostic accuracy of
study of the normal sensory response in asymptomatic individuals. palpation of the sciatic, tibial and common peroneal nerves in the
J Orthop Sports Phys Ther 2014;44:450–6. examination of low back related leg pain. Man Ther 2009;
21. Hall T, Zusman M, Elvey R. Adverse mechanical tension in the 14(6):623–9.
nervous system? Analysis of straight leg raise. Man Ther 1998; 45. Maitland G. Negative disc exploration: positive canal signs. Aust
3(3):140–6. J Physiother 1979;25(3):129–34.
22. Herrington L, Bendix K, Cornwell C, et al. What is the normal 46. Nee RJ, Yang CH, Liang CC, et al. Impact of order of movement
response to structural differentiation within the slump and straight on nerve strain and longitudinal excursion: a biomechanical study
leg raise tests? Man Ther 2008;13(4):289–94. with implications for neurodynamic test sequencing. Man Ther
23. Walsh J, Hall T. Agreement and correlation between the straight 2010;15(4):376–81.
leg raise and slump tests in subjects with leg pain. J Manipulative 47. Coppieters MW, Van de Velde M, Stappaerts KH. Positioning in
Physiol Ther 2009;32:184–92. anesthesiology: toward a better understanding of stretch-induced
24. Johnson E, Chiarello C. The slump test: the effects of head and perioperative neuropathies. Anesthesiology 2002;97(1):75–81.
lower extremity position on knee extension. J Orthop Sports Phys 48. Coppieters MW, Butler DS. Do ‘sliders’ slide and ‘tensioners’
Ther 1997;26(6):310–17. tension? An analysis of neurodynamic techniques and consid-
25. Boyd B, Villa P. Normal inter-limb differences during the straight erations regarding their application. Man Ther 2008;13(3):
leg raise neurodynamic test: a cross sectional study. BMC Muscu- 213–21.
loskelet Disord 2012;13:245. 49. Elvey R. Treatment of arm pain associated with abnormal brachial
26. Covill L, Petersen S. Upper extremity neurodynamic tests: range plexus tension. Aust J Physiother 1986;32:225–30.
of motion asymmetry may not indicate impairment. Physiother 50. Coppieters MW, Alshami AM. Longitudinal excursion and strain
Theory Pract 2011;28:535–41. in the median nerve during novel nerve gliding exercises for carpal
27. Boyd B. Common interlimb asymmetries and neurogenic tunnel syndrome. J Orthop Res 2007;25(7):972–80.
responses during upper limb neurodynamic testing: implications 51. Coppieters MW, Hough AD, Dilley A. Different nerve-gliding
for test interpretation. J Hand Ther 2012;25:56–64. exercises induce different magnitudes of median nerve longitudi-
28. Van Hoof T, Vangestel C, Shacklock M, et al. Asymmetry of nal excursion: an in vivo study using dynamic ultrasound imaging.
ULNT1 elbow extension range-of-motion in a healthy popula- J Orthop Sports Phys Ther 2009;39(3):164–71.
tion: consequences for clinical practice and research. Phys Ther 52. Ellis RF, Hing WA, McNair PJ. Comparison of longitudinal
Sport 2012;13:141–9. sciatic nerve movement with different mobilization exercises: an
29. Stalioraitis V, Robinson K, Hall T. Side-to-side range of move- in vivo study utilizing ultrasound imaging. J Orthop Sports Phys
ment variability in variants of the median and radial neurodynamic Ther 2012;42(8):667–75.
test sequences in asymptomatic people. Man Ther 2014;19: 53. Coppieters MW, Andersen LS, Johansen R, et al. Excursion of the
338–42. sciatic nerve during nerve mobilization exercises. An in vivo
296 PART III  Advances in Clinical Science and Practice

cross-sectional study using dynamic ultrasound imaging. J Orthop 75. Tuzuner S, Ozkaynak S, Acikbas C, et al. Median nerve excursion
Sports Phys Ther (in press). during endoscopic carpal tunnel release. Neurosurgery
54. Coppieters MW, Stappaerts KH, Wouters LL, et al. The immedi- 2004;54(5):1155–60, discussion 1160–1.
ate effects of a cervical lateral glide treatment technique in patients 76. Millesi H, Zoch G, Reihsner R. Mechanical properties of periph-
with neurogenic cervicobrachial pain. J Orthop Sports Phys Ther eral nerves. Clin Orthop Relat Res 1995;314:76–83.
2003;33(7):369–78. 77. Peters S, Page MJ, Coppieters MW, et al. Rehabilitation following
55. Coppieters MW, Stappaerts KH, Wouters LL, et al. Aberrant carpal tunnel release. Cochrane Database Syst Rev 2013;(6):
protective force generation during neural provocation testing and CD004158.
the effect of treatment in patients with neurogenic cervicobrachial 78. Warwick L, Seradge H. Early versus late range of motion follow-
pain. J Manipulative Physiol Ther 2003;26(2):99–106. ing cubital tunnel surgery. J Hand Ther 1995;8(4):245–8.
56. Vicenzino B, Collins D, Wright A. The initial effects of 79. Weirich SD, Gelberman RH, Best SA, et al. Rehabilitation after
a cervical spine manipulative physiotherapy treatment on the subcutaneous transposition of the ulnar nerve: immediate versus
pain and dysfunction of lateral epicondylalgia. Pain 1996;68(1): delayed mobilization. J Shoulder Elbow Surg 1998;7(3):244–9.
69–74. 80. Sunderland S. The nerve lesion in the carpal tunnel syndrome.
57. Sterling M, Pedler A, Chan C, et al. Cervical lateral glide increases J Neurol Neurosurg Psychiatry 1976;39(7):615–26.
nociceptive flexion reflex threshold but not pressure or thermal 81. Rempel DM, Diao E. Entrapment neuropathies: pathophysiology
pain thresholds in chronic whiplash associated disorders: a pilot and pathogenesis. J Electromyogr Kinesiol 2004;14(1):71–5.
randomised controlled trial. Man Ther 2010;15(2):149–53. 82. Lundborg G, Myers R, Powell H. Nerve compression injury
58. Schäfer A, Hall T, Muller G, et al. Outcomes differ between and increased endoneurial fluid pressure: a ‘miniature compart-
subgroups of patients with low back and leg pain following neural ment syndrome’. J Neurol Neurosurg Psychiatry 1983;46(12):
manual therapy: a prospective cohort study. Eur Spine J 2011; 1119–24.
20:482–90. 83. Mackinnon SE. Pathophysiology of nerve compression. Hand
59. Allison GT, Nagy BM, Hall T. A randomized clinical trial of Clin 2002;18(2):231–41.
manual therapy for cervico-brachial pain syndrome – a pilot study. 84. Schmid AB, Elliott JM, Strudwick MW, et al. Effect of splinting
Man Ther 2002;7(2):95–102. and exercise on intraneural edema of the median nerve in carpal
60. Smart KM, Blake C, Staines A, et al. The discriminative validity tunnel syndrome – an MRI study to reveal therapeutic mecha-
of ‘nociceptive,’ ‘peripheral neuropathic,’ and ‘central sensitiza- nisms. J Orthop Res 2012;30(8):1343–50.
tion’ as mechanisms-based classifications of musculoskeletal pain. 85. Chen SJ, Lin HS, Hsieh CH. Carpal tunnel pressure is correlated
Clin J Pain 2011;27(8):655–63. with electrophysiological parameters but not the 3 month surgical
61. Smart KM, Blake C, Staines A, et al. Mechanisms-based classifica- outcome. J Clin Neurosci 2013;20(2):272–7.
tions of musculoskeletal pain: part 2 of 3: symptoms and signs of 86. Diao E, Shao F, Liebenberg E, et al. Carpal tunnel pressure alters
peripheral neuropathic pain in patients with low back (+/− leg) median nerve function in a dose-dependent manner: a rabbit
pain. Man Ther 2012;17(4):345–51. model for carpal tunnel syndrome. J Orthop Res 2005;23(1):
62. Bennett MI, Smith BH, Torrance N, et  al. The S-LANSS score 218–23.
for identifying pain of predominantly neuropathic origin: valida- 87. Coppieters MW. Physiotherapy management of nerve-related
tion for use in clinical and postal research. J Pain 2005;6(3): neck and arm pain. In: Second Brazilian conference of manipula-
149–58. tive and musculoskeletal physiotherapy (II COBRAFIMM). Sao
63. Bouhassira D, Attal N, Alchaar H, et al. Comparison of pain Paulo, Brazil: 2012.
syndromes associated with nervous or somatic lesions and devel- 88. Coppieters MW, Schmid AB, Kubler PA, et al. Description, reli-
opment of a new neuropathic pain diagnostic questionnaire ability and validity of a novel method to measure carpal tunnel
(DN4). Pain 2005;114(1–2):29–36. pressure in patients with carpal tunnel syndrome. Man Ther
64. Fernandez-de-Las-Penas C, Coppieters MW, Cuadrado ML, 2012;17(6):589–92.
et al. Patients with chronic tension-type headache demonstrate 89. Bisby MA. Functions of retrograde axonal transport. Fed Proc
increased mechano-sensitivity of the supra-orbital nerve. Head- 1982;41(7):2307–11.
ache 2008;48(4):570–7. 90. Dilley A, Bove GM. Disruption of axoplasmic transport induces
65. Hall T, Quintner J. Responses to mechanical stimulation of the mechanical sensitivity in intact rat C-fibre nociceptor axons.
upper limb in painful cervical radiculopathy. Aust J Physiother J Physiol 2008;586(2):593–604.
1996;42(4):277–85. 91. Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive
66. Atroshi I, Gummesson C, Johnsson R, et al. Prevalence of carpal response of the nervous system to damage. Annu Rev Neurosci
tunnel syndrome in a general population. JAMA 1999;282(2): 2009;32:1–32.
153–8. 92. Song XJ, Gan Q, Cao JL, et al. Spinal manipulation reduces pain
67. Hough AD, Moore AP, Jones MP. Reduced longitudinal excursion and hyperalgesia after lumbar intervertebral foramen inflamma-
of the median nerve in carpal tunnel syndrome. Arch Phys Med tion in the rat. J Manipulative Physiol Ther 2006;29(1):5–13.
Rehabil 2007;88(5):569–76. 93. Cheng CF, Cheng JK, Chen CY, et al. Mirror-image pain is medi-
68. Korstanje JW, Scheltens-De Boer M, Blok JH, et al. Ultrasono- ated by nerve growth factor produced from tumor necrosis factor
graphic assessment of longitudinal median nerve and hand flexor alpha-activated satellite glia after peripheral nerve injury. Pain
tendon dynamics in carpal tunnel syndrome. Muscle Nerve 2014;155(5):906–20.
2012;45(5):721–9. 94. Milligan ED, Twining C, Chacur M, et al. Spinal glia and proin-
69. Valls-Sole J, Alvarez R, Nunez M. Limited longitudinal sliding of flammatory cytokines mediate mirror-image neuropathic pain in
the median nerve in patients with carpal tunnel syndrome. Muscle rats. J Neurosci 2003;23(3):1026–40.
Nerve 1995;18(7):761–7. 95. Konopka KH, Harbers M, Houghton A, et al. Bilateral sensory
70. Allmann KH, Horch R, Uhl M, et al. MR imaging of the carpal abnormalities in patients with unilateral neuropathic pain; a quan-
tunnel. Eur J Radiol 1997;25(2):141–5. titative sensory testing (QST) study. PLoS ONE 2012;7(5):e37524.
71. Erel E, Dilley A, Greening J, et al. Longitudinal sliding of the 96. Schmid AB, Coppieters MW, Ruitenberg MJ, et al. Local and
median nerve in patients with carpal tunnel syndrome. J Hand remote immune-mediated inflammation after mild peripheral
Surg [Br] 2003;28(5):439–43. nerve compression in rats. J Neuropathol Exp Neurol 2013;72(7):
72. Nakamichi K, Tachibana S. Restricted motion of the median nerve 662–80.
in carpal tunnel syndrome. J Hand Surg [Br] 1995;20(4):460–4. 97. Santos FM, Silva JT, Giardini AC, et al. Neural mobilization
73. Coppieters MW. Physiotherapy management of nerve-related reverses behavioral and cellular changes that characterize neuro-
neck and arm pain. In: Second Brazilian Conference of Manipula- pathic pain in rats. Mol Pain 2012;8:57.
tive and Musculoskeletal Physiotherapy (II COBRAFIMM) 2012. 98. Latremoliere A, Woolf CJ. Central sensitization: a generator of
Sao Paulo, Brazil. pain hypersensitivity by central neural plasticity. J Pain 2009;
74. Tuzuner S, Inceoglu S, Bilen FE. Median nerve excursion in 10(9):895–926.
response to wrist movement after endoscopic and open carpal 99. Smith K. Neuroscience: settling the great glia debate. Nature
tunnel release. J Hand Surg [Am] 2008;33(7):1063–8. 2010;468(7321):160–2.
 30  Neurodynamic Management of the Peripheral Nervous System 297

100. Wright A. Hypoalgesia post-manipulative therapy: a review of a 118. Goldstein M, Scalzitti D, Craik R, et al. The revised research
potential neurophysiological mechanism. Man Ther 1995; agenda for physical therapy. Phys Ther 2011;91:165–74.
1(1):11–16. 119. Nee R, Vicenzino B, Jull G, et al. Baseline characteristics of
101. Sterling M, Jull G, Wright A. Cervical mobilisation: concurrent patients with nerve-related neck and arm pain predict the likely
effects on pain, sympathetic nervous system activity and motor response to neural tissue management. J Orthop Sports Phys Ther
activity. Man Ther 2001;6(2):72–81. 2013;43(6):379–91.
102. Vicenzino B, Collins D, Benson H, et al. An investigation of the 120. Hancock M, Herbert R, Maher C. A guide to interpretation of
interrelationship between manipulative therapy-induced hypoal- studies investigating subgroups of responders to physical therapy
gesia and sympathoexcitation. J Manipulative Physiol Ther interventions. Phys Ther 2009;89(7):698–704.
1998;21(7):448–53. 121. Kent P, Keating J, Leboeuf-Yde C. Research methods for sub-
103. O’Leary S, Falla D, Hodges PW, et al. Specific therapeutic exer- grouping low back pain. BMC Med Res Methodol 2010;10:62.
cise of the neck induces immediate local hypoalgesia. J Pain 122. Hoffmann TC, Glasziou PP, Boutron I, et al. Better reporting of
2007;8(11):832–9. interventions: template for intervention description and replica-
104. Bialosky JE, Bishop MD, Price DD, et al. A randomized sham- tion (TIDieR) checklist and guide. BMJ 2014;348:g1687.
controlled trial of a neurodynamic technique in the treatment of 123. Thoomes EJ, Scholten-Peeters GG, de Boer AJ, et al. Lack of
carpal tunnel syndrome. J Orthop Sports Phys Ther 2009;39(10): uniform diagnostic criteria for cervical radiculopathy in conserva-
709–23. tive intervention studies: a systematic review. Eur Spine J 2012;
105. Santos FM, Grecco LH, Pereira MG, et al. The neural mobiliza- 21(8):1459–70.
tion technique modulates the expression of endogenous opioids in 124. Genevay S, Atlas SJ, Katz JN. Variation in eligibility criteria from
the periaqueductal gray and improves muscle strength and mobil- studies of radiculopathy due to a herniated disc and of neurogenic
ity in rats with neuropathic pain. Behav Brain Funct 2014;10:19. claudication due to lumbar spinal stenosis: a structured literature
106. Adel S. Efficacy of neural mobilization in treatment of low back review. Spine (Phila Pa 1976) 2010;35(7):803–11.
dysfunctions. J Am Sci 2011;7(4):566–73. 125. Bland JD. Carpal tunnel syndrome. Curr Opin Neurol 2005;
107. Cleland J, Childs J, Palmer J, et al. Slump stretching in the man- 18(5):581–5.
agement of non-radicular low back pain: a pilot clinical trial. Man 126. Hu P, Bembrick AL, Keay KA, et al. Immune cell involvement in
Ther 2006;11(4):279–86. dorsal root ganglia and spinal cord after chronic constriction or
108. Nagrale A, Patil S, Gandhi R, et al. Effect of slump stretching transection of the rat sciatic nerve. Brain Behav Immun 2007;
versus lumbar mobilization with exercise in subjects with non- 21(5):599–616.
radicular low back pain: a randomized clinical trial. J Man Manip- 127. Schmid AB, Nee RJ, Coppieters MW. Reappraising entrapment
ulative Ther 2012;20:35–42. neuropathies–mechanisms, diagnosis and management. Man Ther
109. Hopkins W. A new view of statistics. 2011 Available from: <http:// 2013;18(6):449–57.
www.sportsci.org/resource/stats/index.html>; [cited 2011 Decem- 128. Hall A, Ferreira P, Maher C, et al. The influence of the therapist-
ber 7]. patient relationship on treatment outcome in physical rehabilita-
110. Scrimshaw S, Maher C. Randomized controlled trial of neural tion: a systematic review. Phys Ther 2010;90:1099–110.
mobilization after spinal surgery. Spine 2001;26(24):2647–52. 129. Ferreira P, Ferreira M, Maher C, et al. The therapeutic alliance
111. Nee R, Vicenzino B, Jull G, et al. Neural tissue management between clinicians and patients predicts outcome in chronic low
provides immediate clinically relevant benefits without harmful back pain. Phys Ther 2013;93:470–8.
effects for patients with nerve-related neck and arm pain: a ran- 130. Ong B, Konstantinou K, Corbett M, et al. Patients’ own accounts
domised trial. J Physiother 2012;58:23–30. of sciatica. Spine 2011;36:1251–6.
112. Nee R, Vicenzino B, Jull G, et al. A novel protocol to develop a 131. Hopayian K, Notley C. A systematic review of low back pain and
prediction model that identifies patients with nerve-related neck sciatica patients’ expectations and experiences of health care. Spine
and arm pain who benefit from the early introduction of neural J 2014;doi:10.1016/j.spinee.2014.02.029; (in press).
tissue management. Contemp Clin Trials 2011;32:760–70. 132. Pinto R, Ferreira M, Oliveira V, et al. Patient-centred communi-
113. Gross A, Hoving J, Haines T, et al. A Cochrane review of manipu- cation is associated with positive therapeutic alliance: a systematic
lation and mobilization for mechanical neck disorders. Spine review. J Physiother 2012;58:77–87.
2004;29(14):1541–8. 133. Peersman W, Rooms T, Bracke N, et al. Patients’ priorities
114. Page M, O’Connor D, Pitt V, et al. Exercise and mobilisation regarding outpatient physiotherapy care: a qualitative and quanti-
interventions for carpal tunnel syndrome (Review). Cochrane tative study. Man Ther 2013;18:155–64.
Database Syst Rev 2012;(6):Art. No.:CD009899. 134. Keefe FJ, Porter L, Somers T, et al. Psychosocial interventions for
115. Svernlov B, Larrson M, Rehn K, et al. Conservative treatment of managing pain in older adults: outcomes and clinical implications.
the cubital tunnel syndrome. J Hand Surg 2009;34E:201–7. Br J Anaesth 2013;111(1):89–94.
116. Kavlak Y, Uygur F. Effects of nerve mobilization exercise as an 135. Lee MC, Tracey I. Imaging pain: a potent means for investigating
adjunct to the conservative treatment for patients with tarsal pain mechanisms in patients. Br J Anaesth 2013;111(1):64–72.
tunnel syndrome. J Manipulative Physiol Ther 2011;34:441–8. 136. Haroutounian S, Nikolajsen L, Bendtsen TF, et al. Primary affer-
117. Foster N, Dziedzic K, van der Windt D, et al. Research priorities ent input critical for maintaining spontaneous pain in peripheral
for non-pharmacological therapies for common musculoskeletal neuropathy. Pain 2014;155(7):1272–9.
problems: nationally and internationally agreed recommenda- 137. Vaso A, Adahan HM, Gjika A, et al. Peripheral nervous system
tions. BMC Musculoskelet Disord 2009;10:3. origin of phantom limb pain. Pain 2014;155(7):1384–91.
 CHAPTER 31 

Therapeutic Exercise
Deborah Falla  •  Rod Whiteley  •  Marco Cardinale  •  Paul Hodges

INTRODUCTION Indications for Exercise

There is undoubtedly a link between pain and altered
This chapter aims to provide a framework to design motor control. Disturbed motor control ultimately con-
exercise-based interventions to reach desired rehabilita- tributes to impaired motor output, which may include
tion goals, be they improvements in neuromuscular poor control/coordination, reduced strength, impaired
control (muscle activation, movement strategy, endurance, diminished force steadiness or smoothness of
alignment/posture and movement quality), strength, movement, all of which are well documented in people
endurance, or some combination of these. This chapter with musculoskeletal pain (for a review see Chapter 6).
focuses on motor control training and resistance train- The association between pain and motor control impair-
ing, but notes that exercise for other features may be ment is supported by the abundance of literature describ-
relevant for a patient’s presentation including range of ing neuromuscular dysfunction in people across a range
motion, muscle length, sensory function and postural of musculoskeletal pain conditions, in addition to the
alignment. numerous experimental pain studies confirming that pain
may have an immediate and profound effect on motor
control.1–3 It is hypothesized that impaired motor func-
tion may contribute to the recurrence of musculoskeletal
PRINCIPLES OF MANAGEMENT pain, further emphasizing the importance of early and
Clinical Prescription of Exercise effective exercise interventions. This has been particu-
larly the case for spinal pain, where continuous motor
When working with an otherwise healthy patient, the impairments have been documented despite recovery
physiotherapist must first conduct a needs analysis to from an acute episode and return to normal activity.4–8
define the desired exercise goal, prescribe the appropri- Ongoing deficits in motor control could lead to poor
ate training parameters to achieve the goals and use control of movement, abnormal loading, repeated micro-
validated measures to assess progress (Fig. 31-1). This trauma and eventually pain. Moreover, actual pain may
chapter is arbitrarily divided into sections according to not necessarily have to be present for motor control
the desired outcomes of exercise, but it is necessary to changes to persist. Factors such as fear of pain may have
remember that these outcomes are not mutually exclu- similar effects and may explain altered motor control in
sive. Situations will often arise where multiple goals are patients with pain when they are in remission.9,10 Although
important. For instance a person may initially require there is no clear consensus on the cause–effect relation-
improvements in control of a movement, and once this ship between altered motor control and pain/injury, it is
is established move on to strength/endurance adaptation. evident that pain/injury is associated with impaired motor
A clear understanding of the parameters associated with function and thus training can be considered relevant in
exercise prescription will aid in this process. Accurate this context.
exercise prescription requires an understanding of an The importance of training as a component of reha-
individual’s existing function, along with a needs analysis bilitation is also supported by studies that show that a
regarding the functional requirements of his/her work/ reduction in pain with treatment which excludes exercise
sport/daily activity (Fig. 31-1). It is then important to (e.g. manipulative therapy as a sole treatment) is insuffi-
conduct an appropriate assessment to guide exercise cient to enhance neuromuscular control in patients with
prescription. Once this information is gathered, it is musculoskeletal pain.11–13 Guidance of an exercise pro-
possible to define the training methodology, the specific gramme depends on identifying features of motor output
means and exercises used, and the details of the pro- that are compromised in the patient, particularly those
gramme in terms of its volume, intensity and progres- which underlie the deficit in performance of the patient’s
sion. Finally, the continuous assessments to monitor identified goal.
progress and to ascertain the effectiveness of the thera-
peutic exercise programme to change the target features, Assessment to Guide
represent fundamental milestones in the training pro-
gramme in order to introduce adjustments and/or reca-
Exercise Prescription
librate the training contents to ensure the objectives Guidance of exercise relies on assessment of a range of
are met. potential targets including the quality of movement,
298
 31  Therapeutic Exercise 299

Performance Define the Develop the

needs/needs training training
analysis methodology programme

Assess the Define the Control and

patient’s training means review
level and specific adaptations
exercises

FIGURE 31-1  ■  A simple framework to develop an evidence-based approach to exercise prescription.

motor control, strength and endurance, and sensory Although there is some indication that tests of
function. The battery of tests used will depend on the movement quality may provide information relevant for
patient’s condition and the identified treatment goal. The guidance of exercise prescription, the ability of such
following section outlines some of the general consider- assessments to identify injury risk remains questionable.19
ations when planning a patient’s assessment to guide Thus, it is important to keep in mind that the use of many
exercise prescription. assessments of movement quality is best restricted to
guidance of exercise prescription.
Assessment of Movement Quality
Assessment of Motor Control
Movement quality refers to the kinematics of the perfor-
mance of a movement, that is, the actual joint angles, Pain and injury are commonly associated with changes
velocities and variability associated with single bouts and in motor control and many clinical assessments have been
repetitions of this movement pattern. Physiotherapists developed to evaluate specific features of the control and
often consider that poor ‘quality’ of movement perfor- coordination of muscle activation, posture and move-
mance is related to excessive tissue loading and an indi- ment. The basic assumption is that features of the strat-
vidual’s likelihood of injury (both past and present). egy of muscle activation, posture and movement may
Individuals generally present with some features of move- abnormally load the tissues and be responsible for at
ment impairment (related to a function or a specific least part of the patient’s symptoms. The specific assess-
physiological movement direction), which is related to ments that are used depend on the clinical condition,
their presenting problem. Although a reference database the target task and the features of performance of the
of normative data may not be available for a complex task that the clinician considers are a priority. In back
functional task for comparison of an individual’s perfor- and neck pain, specific assessments of muscle activation
mance, the physiotherapist will often examine a set of strategy, postures and movements have been developed.
standardized movements such as shoulder abduction and Methods such as observation, palpation and specific
flexion (for the upper limb) and a single leg squat, or devices (e.g. air-filled cuff to quantify the quality of upper
walking (for the lower limb), and then extrapolate from cervical flexion to assess the deep cervical flexor muscles;
the perceived quality of these movements to a clinical ultrasound imaging to measure the pattern of abdominal
inference of the ‘movement quality’ in function. There is and back extensor muscle activation; photography to
some evidence for the accuracy of this approach. For measure alignment of specific anatomical sites) are used
instance, in low back pain the quality (timing and ampli- to evaluate performance. Tests of motor control are
tude) of pelvic motion during hip rotation provides reli- diverse and the degree to which the validity and reliability
able and meaningful information that guides exercise have been assessed varies, with some tests evaluated
prescription.14,15 Unfortunately, in many conditions such extensively (e.g. voluntary activation of deep lumbar20
reliability is not evident. As an example, in assessment of and neck muscles21–24; dissociation of hip from spine
the shoulder disorders, visual estimation of the quality of motion15) and others not.
scapular movement associated with arm movements is
considered clinically important. However, the accuracy Assessment of Muscle Structure
of this visual estimation has poor inter-rater reliability
and poor correlation to ‘gold standard’ examination of Adequate muscle structure is essential to meet demands
the tracking of implanted bone pins.16 Acceptable reli- of motor output. Comprehensive assessment using imag-
ability has been documented when the estimation is ing methods such us ultrasound/computed tomography/
limited to classification as ‘normal’ versus either ‘subtle’ magnetic resonance imaging scans can provide the clini-
or ‘obvious’ dysfunction.17 Similarly, clinical examination cian with relevant information about muscle mass (cross-
of the quality of a single leg squat is difficult, with good sectional area), structure, fatty infiltration and injury.
reliability only achieved for panel rating of video perfor- These parameters will likely influence the motor output
mance when ranked as ‘good’, ‘fair’, or ‘poor’.18 and have been identified as relevant for a range of
300 PART III  Advances in Clinical Science and Practice

conditions (e.g. muscle atrophy and fatty infiltration in prescription. Conventional assessment paradigms using
back,25 neck26 and shoulder27 pain). isokinetic dynamometry provide limited validity for
assessment of fatigue as the common algorithms simply
consider performance decline from the first to last (typi-
Assessment of Strength Parameters
cally five) repetition.30 A better approach may be to derive
Comprehensive assessment of strength may consider a the linear slope of the decline in work across the entire
range of features including; peak force, rate of force exercise test. Although a promising approach, this is
development and rate of force relaxation. The use of unlikely to be implemented in clinical practice until this
instrumented devices to estimate muscle strength has becomes a standard feature of the reporting software.31
gained increasing popularity over the last decade, espe- Alternative measures of fatigue/endurance for clinical
cially with a more widespread clinical adoption of hand- practice range from simple measures of time to task
held dynamometers. Typically, these devices only provide failure in standardized tasks (e.g. Biering Sorensen test
the peak force recorded by the load cell during a specific to assess back extensor endurance), to comprehensive
task, whereas more sophisticated dynamometers (such as measurement of decline in median frequency of an elec-
isokinetic dynamometers or linear encoders, accelerom- tromyography recording using advanced clinical electro-
eters and other isoinertial dynamometers) can calculate/ myography systems that provide this measure as an
measure the force (or torque when angular rotation is output. For a clinician it is important to consider which
performed with an isokinetic dynamometer) produced at muscle/muscle group requires assessment and then deter-
all angles of the range of motion, during different con- mine from their available measurement tools how best
tractile activities (isometric, concentric or eccentric) and to assess endurance to identify whether the feature should
different velocities of contraction. Often, the maximum be targeted in the exercise programme.
force generated in a specific task provides sufficient infor-
mation for the clinician to detect differences between Summary of Assessment
healthy and injured sides of an individual, or to screen
for differences from normative data (as in the case of Assessment of the range of features of motor perfor-
hamstrings to quadriceps28 and shoulder internal to exter- mance that the clinician considers to be relevant for the
nal rotation29 strength ratios). In the context of a recover- presentation of the patient (including motor control,
ing injury, tracking progress on such force measures is a endurance, strength/power capabilities) is of paramount
useful means of documenting response to treatment and importance to establish an optimal training programme,
the course of recovery. It is important to know that the and is fundamental to assess progress of a patient. All
information generated during such assessments is specific relevant features of motor output need to be assessed to
to the movement pattern used and the speed and modal- decide on the most appropriate intervention.
ity of contraction. In the case of isometric actions, the
value derived for a maximal voluntary contraction can
only be extrapolated to a limited range of motion outside
Specificity and Selectivity of Exercise
the angle used for testing. Assessment of strength param- Clinical trials of patients with a range of musculoskeletal
eters are used to identify the deficits to target with reha- pain conditions report significant and clinically mean-
bilitation, to define the variables of a training intervention ingful reductions in pain and disability for training
and to guide exercise intensity such as establishing the programmes, including low-intensity training (often
external load (as a percentage of maximum) to use in the focused on precision and control) and high-intensity
rehabilitation programme. For instance, if the maximum training (focused on strength and endurance effects).
force generated during elbow flexion is 120 N, this means Thus, various training approaches require consideration
the maximum load a patient can tolerate in that position for the individual patient and may be appropriate for
is 12 kg. A 9.6 kg-load could be selected if the target the management of the patient’s symptoms and pre-
intensity is 80% of the patient’s maximal voluntary sentation. An important consideration is that the neu-
contraction. romuscular and functional changes induced by the
training paradigm are specific to the mode of exercise
performed.32,33 Depending on the training paradigm,
Assessment of Muscle Fatigue
the adaptations that transpire may involve distinct struc-
Muscle fatigue/endurance is important to consider clini- tural and functional changes in the periphery (e.g.
cally. The inability of a muscle to sustain force output enhanced muscle mass) and across the regions of the
will have consequences for maintenance of a function and nervous system from the spinal cord to the motor cortex
could lead to poor control of movement. Traditionally, and other supraspinal centres.32,34 Given that people
fatigue is quantified as time to task failure (when impos- with musculoskeletal pain present with an array of defi-
sible to maintain a target force). Alternative measures can cits of motor output ranging from subtle changes in
be used to quantify the processes that occur as the capac- coordination between muscles through to reduced
ity of the muscle declines before task failure is reached maximal force capacity for a given muscle or muscle
(e.g. electromyography measures such as median fre- group (see Chapter 6), this knowledge implies that dif-
quency: see Chapter 17). Assessment of the fatigability of ferent forms of exercise will need to be considered and
a muscle group could provide valuable information should be prescribed according to the neuromuscular
(if it is considered to be a relevant feature of the impairments that are revealed by the clinical assessment
priority goal) when interpreting the target for exercise of the patient.
 31  Therapeutic Exercise 301

The need for specificity in therapeutic exercise has also serve to prevent changes in muscle structural proper-
been supported by a number of exercise trials in patients ties that have been documented in patients with chronic
with musculoskeletal pain. For example, low-load motor musculoskeletal pain (e.g. atrophy of selected muscles,4,52
control training, but not high-load resistance training of preferential atrophy of slow-twitch oxidative type-I
the neck/back, has been shown to be effective to enhance fibres,53,54 and fatty infiltration of muscle tissue26,55). For
the activation of the deep cervical flexor muscles35 or instance, the presence of fatty tissue infiltration of the
abdominal muscles,36 restore the coordination between neck extensor muscles, which is present in patients with
the deep and superficial flexors,35,37 enhance the speed of moderate to severe pain following a whiplash injury, is
deep muscle activation when challenged by a postural not detected until 3 months after the injury56 and changes
perturbation35,36 and improve the patient’s ability to in muscle fibre type in multifidus is not present until 6
maintain an upright posture of the cervical spine during months.54 These observations suggest some of the struc-
prolonged sitting.38 In contrast, resistance training of the tural changes may, at least in part, represent a secondary
neck muscles led to superior gains in cervical muscle adaptation to altered motor control and may be poten-
strength, endurance and resistance to fatigue compared tially prevented by specific training interventions. In
to a low-load motor control programme.39,40 Likewise, addition, it is hypothesized that early and effective train-
resistance training targeted at atrophied muscles was ing of motor control may help to prevent transition to
required to ameliorate the long-standing atrophy and chronicity and reduce the recurrence of symptoms.57
fatty infiltration in patients with chronic low back pain.41 Future studies are clearly warranted to confirm these
It is therefore established that in the presence of pain hypotheses.
and/or dysfunction, specificity of training is an important
concept to consider in the prescription of an exercise
programme. Specificity of training should also be consid-
Variability in Response to Exercise
ered relative to the velocity of exercise, the position of A multitude of neuromuscular adaptations have been
the patient (joint angle) and the movement pattern during documented in people with musculoskeletal pain with
exercise.42 Thus, if specific aspects of motor control are large variability noted between individual patients (see
identified to be important features in a patient’s presenta- Chapter 6 for a review). Such variability in patient pre-
tion then it is likely that a ‘specific’ and targeted approach sentation may partly explain the variable symptomatic
is required to achieve meaningful change. benefit experienced by patients from standardized exer-
Another issue that requires consideration is the poten- cise programmes; responses range from an excellent
tial for interaction between treatments in combined exer- outcome to minimal benefit. An important determinant
cise approaches. Several studies have suggested that of symptomatic response to exercise is the degree of neu-
combining large volumes of endurance training with romuscular impairment before training. For example, in
resistance exercise might impair the effectiveness of each patients with low back pain, baseline transversus abdomi-
modality. It is thought that endurance training has posi- nis activation predicts those who respond best to specific
tive effects on endurance, but to the detriment of strength motor control training.13,58 Likewise, specific motor
and power outcomes (and the reverse for strength train- control exercise for the deep cervical flexor muscles is
ing at the expense of endurance outcomes). Although the most effective at relieving pain in people with neck pain
exact nature of this relationship is still debated with that demonstrate the poorest control of their deep
respect to its magnitude and the interaction for specific muscles at baseline.59 These findings further indicate that
muscle groups of interest,43,44 a strong molecular basis can treatment outcome will likely be best when exercise is
explain why this might occur.45 selected and tailored based on a precise assessment of a
patients’ neuromuscular control.
Timing of Exercise
Changes in neuromuscular control appear early after the
FORMS OF EXERCISE COMMONLY
initial onset of pain or injury.7,46 In addition, experimental APPLIED TO MANAGE
pain studies confirm that pain has an immediate and MUSCULOSKELETAL PAIN
profound effect on motor behaviour.47,48 On this basis it
has been suggested that exercise to address impairment A key aim of exercise programmes is to induce long-
of motor behaviour is commenced early within the reha- lasting changes in motor behaviour, either to restore
bilitation programme.49,50 Gentle and specific exercises correct motor patterns or to enhance other aspects of
have also been shown to provide immediate pain motor performance.60 Optimization of motor output can
relief,12,36,51 which further supports early inclusion of spe- be achieved with practice, reflecting the ability of the
cific training for the management of musculoskeletal motor system to adapt and refine motor output towards
pain. Generally, it is considered important to address higher efficiency. Numerous studies have confirmed that
issues of motor control before loading the muscle to both muscle tissue and the neural control of muscle
induce change in strength, endurance and structure.41 adapts in response to a variety of motor experiences,
Thus higher load resistance training typically follows including motor control, strength and endurance train-
later in the rehabilitation programme.26,27 ing.32,34,61–63 Moreover, these adaptations may persist
Although the benefit of early rehabilitation of motor despite the absence of continued training, which suggests
deficits has not been fully examined in clinical trials, it is the motor system is able to maintain these adaptations.64
assumed that early rehabilitation of motor function may The following sections present two common forms of
302 PART III  Advances in Clinical Science and Practice

training applied for the rehabilitation of musculoskeletal A critical issue for exercise prescription is that numer-
conditions; namely motor control training and resistance ous studies have confirmed that many of the alterations
(strength, endurance) training. The neuromuscular adap- in motor control of the spine cannot be ameliorated by
tations that occur with each form of training are reviewed strength or endurance training, or by general physical
and the general principles of each training approach activity.13,35–37 Thus, training approaches targeted at cor-
presented. rection of the motor control faults and re-establishing
normal motor strategies are an important aspect of the
treatment of musculoskeletal pain.76 The benefit of such
Motor Control Training training has been well documented for both low back
Individuals with musculoskeletal pain present with defi- pain and neck pain, and for some conditions of the limbs
cits in motor control (e.g. coordination of muscles, (e.g. training focused on rehabilitation of motor control
posture and movement; reviewed in Chapter 6), which of the knee in patellofemoral pain).77 As a general recom-
not only affect tissue loading, but also contribute to defi- mendation it appears logical and consistent with many
cits in general features of motor output such as poor contemporary exercise approaches (e.g. Hodges et al.50)
endurance and strength. Examples of motor control defi- to correct aberrant features of motor control before
cits that are commonly targeted with exercise are the loading the muscles to induce change in strength, endur-
compromised control of the deep spinal muscles that are ance and muscle structure. Thus, the initial emphasis in
frequently observed in people with back and neck pain. prescription of an exercise programme should generally
Among other features, compromised activation is char- involve optimization of control, coordination and preci-
acterized by delayed activation when the spine is per- sion of movement.
turbed (e.g. rapid arm movements are accompanied by Several training approaches that target restoration of
delayed transversus abdominis and multifidus activation features of motor control have been described, especially
in back pain65,66 and delayed longus colli and capitis67 for the management of low back and neck pain.49,50,78–81
activation in neck pain), and reduced amplitude of activa- Generally the objective is to address features of posture/
tion across a range of functions.68–73 Patients with mus- alignment, movement and muscle activation strategies to
culoskeletal pain may also present with functional changes achieve the goal of optimization of tissue loading and
(reorganization) of the neuronal properties in the senso- movement quality followed by progression into increas-
rimotor system. Exercise also targets neuroplastic changes ingly challenging situations towards full function50 (Fig.
in the nervous system. For instance, topography of the 31-2). Most motor control training approaches encour-
primary motor cortex representations of transversus age prescription of exercise that is tailored to the motor
abdominis74 and the lumbar paraspinal75 muscles, mea- control deficits and functional demands that are identi-
sured using transcranial magnetic stimulation, is modi- fied for the individual patient based on findings of com-
fied in patients with recurrent episodes of low back pain. prehensive assessment. Just like other forms of exercise
This is indicative of cortical reorganization and is related management, motor control training cannot be applied
to behaviour features such as the activation of the muscle in a uniform manner. Detailed assessment is essential to
in association with arm movement.74 identify the features of motor control that are likely to

Beliefs and
attitudes
Correction of motor control ‘faults’
Posture
Movement General fitness
Muscle activation

Strength and
endurance
Optimization of motor control Optimization of motor control

Static progression Dynamic progression Sensorimotor

function
Static control of joint Dynamic control of joint (e.g. balance,
orientation/alignment orientation/alignment and proprioception)
movement
Adjacent
regions
Functional re-education
Specific to patient goals
Other issues
(e.g. breathing,
continence)

FIGURE 31-2  ■  Integrated model of motor control intervention for musculoskeletal pain disorders: An overview of the basic progres-
sion from initial goal of correction of faults in muscle activation, posture and movement to functional re-education and the interven-
ing steps through static and dynamic training. On the right are additional issues that may be necessary to consider. (Adapted with
permission from Hodges et al.50)
 31  Therapeutic Exercise 303

be related to the patient’s symptoms and the intervention considered that short sessions of high-quality practice are
is targeted to those features. As alluded to above, this better than long sessions with deteriorating quality of
must include assessment and subsequent intervention performance. Rapid changes in cortical excitability are
targeted at muscle activation, posture/alignment and already apparent following short (10–15 minutes) inter-
movement. vals of motor control training88 and extended within-
In terms of muscle activation in spinal pain, consider- session task repetitions may not facilitate additional gains
able attention has been focused on evaluation and in overall motor performance91 or could be detrimental
rehabilitation of the function of the deeper muscles of if performance quality is diminished. Cognitive effort
the lumbar and cervical spines.16,17,21,27,28,81–83 Although is also known to significantly contribute to the extent
changes in activation of the more superficial muscles of cortical neuroplastic changes associated with novel
must also be addressed, changes in activation of deeper motor-skill acquisition,92,93 thus the complexity of train-
muscles are commonly identified and often included as a ing should be slowly increased to encourage continued
component of the exercise programme. Considerable cognitive effort. The quality of training is critical to con-
work has established that deficits in coordination of the sider. For instance, improvements in the behaviour of
deeper trunk muscles can be addressed by first encourag- activation of the transversus abdominis muscle in low
ing the patient to learn the skill of voluntary activation back pain patients have been correlated to the quality of
of the muscles, repeated practice of this contraction, and training and are associated with improvements in self-
then incorporation of the activation into dynamic and reported pain and function.37
static functions.35–38,49,50,79,84 In a similar manner, specific As transfer to function is likely to be optimal when
features of activation of superficial muscles, posture/ practice is performed as close to the function as possi-
alignment and movement are addressed by first using a ble,94 progression to functional exercise is critical.50 For
range of clinical strategies to correct the ‘fault’ in motor instance, isolated motor control training of the deep cer-
control (e.g. feedback, instruction, manual guidance, vical flexor muscles in people with chronic neck pain
etc.), followed by repetition and integration into func- enhanced the activation of these muscles and reduced the
tion. Although less investigated, a similar motor control necessary contribution of the superficial flexor muscles
approach has/can be applied to other musculoskeletal during performance of craniocervical flexion, but this did
conditions (e.g. lateral hip pain,85 shoulder pain82,86). not transfer to reduced superficial neck muscle activity
The rationale for this approach is based on the prin- during a functional activity.95 This highlights that train-
ciple of novel motor-skill training, which places emphasis ing should be progressed to include specific training of
on improved performance of selected (sub-optimal) com- problematic functional activities in order to optimize
ponents of function rather than the simple execution of motor control in the tasks that the patient identifies as
a sequence of movements. This approach is consistent the priority functional goal.
with accepted methods for training motor skills that
involve initial cognitive attention to performance of task Neuromuscular Adaptations
components, followed by repetition within changing
environments and contexts to achieve more automatic A key premise of motor control training is that the fea-
activation.87 It follows that this approach requires detailed tures of motor control that are targeted with the exercise
assessment of motor deficits and then application of approach are changed by the intervention and related to
motor learning principles that are targeted to accurate recovery. Besides a positive effect on pain and disability,
modification of the relevant features of motor behav- specific motor control training has been shown to restore
iour.49,50 These include principles such as ‘segmentation’ or reverse specific motor control impairments patients
(practice of individual components of a task before prac- with in musculoskeletal pain. For instance, a single
tice of the whole task), ‘simplification’ (practice with session of cognitive activation of transversus abdominis
reduced demand to enable better-quality performance) improves the timing of activation of this muscle during
and use of ‘augmented feedback’.50 The ability to target postural perturbations,36 and this is further improved and
a specific component of movement requires greater skill maintained by repeated training.63 Likewise, specific acti-
and increased levels of attention and precision than con- vation of deep cervical flexor muscles increases their acti-
traction of all muscles (e.g. strength training) and several vation during an isometric task,35 improves the activation
studies have shown that skill training achieves greater time when challenged by postural perturbations35,59 and
change in motor behaviour and motor cortex organiza- restores the directional specificity of neck muscle activity
tion than these other types of muscle activation.36,37,83 (which is normally observed in healthy individuals, but
lost in many people with neck pain) during isometric
contractions across a range of directions.84 Activity of
Training Principles of Motor Control Training
superficial trunk and neck muscles can also be reduced
Motor control training is typically commenced early with specific motor control training,35,37 even after a
within the rehabilitation programme. Ideally training single session.37,96 Interventions targeted at specific motor
should be performed in a pain-free manner in order to features also change posture,38 movement97 and sensory
optimize success, since pain and the distraction associated function.98 Furthermore, motor cortex organization can
with pain might interfere with the neuroplastic changes be restored in association with improved pain and
that would otherwise occur with motor-skill training.88–90 improved coordination of muscle activation in low back
Task repetitions should also be limited to ensure that pain.99 However, it should be noted that the specific fea-
factors such as fatigue are minimized. It is generally tures that need to be trained are individual-specific and
304 PART III  Advances in Clinical Science and Practice

treatment must be targeted to the changes identified in mitochondrial density and increases the use of lipids as a
the individual patient. substrate.120,122 These adaptations are accompanied by
Parameters of the muscle activation strategy at base- increased maximal oxygen uptake capacity.122 Endurance
line are related to the responsiveness of an individual training also leads to decreased motor unit interspike
patient to a motor control intervention13,58,59 and the interval variability,123 lower motor unit discharge rates62
degree of change in muscle activation is related to clinical and a slower decline of motor unit conduction velocity
improvement.13,58,59,100 The weight of physiological evi- during sustained contractions.61
dence and evidence from high-quality clinical trials sup- Several studies have evaluated the effect of resistance
ports the relevance of exercise for motor control based training in patients with musculoskeletal complaints.
on precise assessment to identify which features, if any, Most show clinical benefit. A recent systematic review124
of posture/movement/muscle activation are considered confirmed that resistance training can increase muscle
relevant for the patient’s presentation.50 strength, reduce pain and improve functional ability in
patients suffering from chronic low back pain, knee
osteoarthritis, chronic tendinopathy and those under
Resistance Training recovery after hip replacement surgery, especially for
As highlighted earlier, musculoskeletal conditions are individuals presenting with loss of muscle strength and
often accompanied by deficits in strength and endurance. functional ability.
Thus resistance training forms an important component
of many rehabilitation programmes. Depending on the Intensity of Resistance Training
evaluation of the patient’s capacity and their functional
requirements, the intensity, frequency and duration of Force generation, or the peak force generated during a
exercises are manipulated to optimize improvements in simple movement (e.g. knee extension, shoulder external
strength and/or endurance. rotation), has been well documented as an indicator for
Strength training enhances maximum force produc- the strength abilities of a group of muscles in a given task.
tion and maximal rate of force development,101 which is Such evaluation requires use of a dynamometer. It will
accompanied by increased muscle cross-sectional area likely be limited to an isometric task for a hand-held or
and fibre pennation angle.102–104 Type II (phasic) muscle fixed dynamometer, or through a single plane of move-
fibres preferentially hypertrophy with heavy resistance ment for an isokinetic dynamometer with limited possi-
exercise.105 Such structural alterations typically take bilities also achievable with isoinertial dynamometers. In
several weeks to occur.106 Changes in the myosin heavy practice, information from more complex multijoint
chain isoforms,103,107 Na+–K+ pump activity108 and Ca2+ movements is often of interest. In the occupational and
sensitivity107,109 occur earlier than changes in the whole sports setting this could be a lifting task that can be rep-
muscle morphology. Neural adaptations have also been licated using free weights. The maximum amount of
observed following strength training which explain the weight able to be lifted by an individual for one repetition
disproportionate increase in muscle force compared to of a given exercise (but not two repetitions) is termed the
muscle size during the initial stages of training.110 Early ‘one repetition maximum’ (1 RM) for that person, for
gains in strength have been attributed to a variety of that exercise, on that day. In the field of weight training,
mechanisms, including increased maximal motor unit this has become a commonly employed benchmark to
discharge rates,62,111 increased incidence of brief inter- estimate ‘strength’ of an individual for a given exercise.
spike intervals (doublets)112 and decreased interspike In a clinical setting, this is a useful technique to more
interval variability.113 Strength training also increases the accurately estimate the intensity of a given exercise for
tensile strength of tendons, ligaments and connective an individual.
tissue in muscle.114,115 This form of training usually Prescription of the intensity of the exercise is typically
involves lifting weights and/or using external resistances undertaken as a percentage of an individual’s 1 RM. At
of moderate to high intensity. Prolonged programmes of the beginning of an exercise programme the percentage
resistance exercise produce muscle hypertrophy. Recent necessary to achieve training-induced adaptations in
work also suggests that lifting relatively low-intensity strength is low (30–40%) for sedentary, untrained indi-
loads to the point of task failure116 or using blood flow viduals or very high (80–95%) for those already highly
restriction with low load117 can induce a similar degree trained.42 A typical training intensity would be between
of hypertrophy to that obtained with heavy resistance 60% and 70% of an RM for healthy but untrained
exercise. adults.42,125
Endurance training programmes improve resistance In practice, a patient may also perform a single exer-
to fatigue and are associated with reduced muscle cise set to fatigue with the number of repetitions per-
fibre cross-sectional area, mitochondrial biogenesis and formed determined by the intensity. That is, if an
angiogenesis.118–120 Transformation of muscle fibres from individual performs a given exercise until fatigue, and
type IIB to type IIA is common with endurance train- completes 25 repetitions, then by definition this was a
ing.121 As observed for strength training, it has been relatively low-intensity exercise (in spite of the fact that
shown that changes in the myosin heavy chain iso- the individual will be fatigued at the end of the exercise).
forms,103,107 Na+–K+ pump activity108 and Ca2+ sensitiv- As the response to exercise is considered to be related to
ity107,109 occur earlier than changes in the whole the intensity, it is useful to consult a table or formula to
muscle morphology following a period of endurance estimate the 1 RM from a fatiguing exercise and plan the
training. Metabolically, endurance training increases appropriate resistance level for subsequent sessions.
 31  Therapeutic Exercise 305

Although regression equations are available that purport are no firm rules, it is generally recommended that exer-
to predict the 1 RM of an individual from a submaximal cise can be performed more frequently (e.g. daily or even
test, the predictive abilities of such equations have vari- two to three times per day) in the early stages of training
able accuracy and depend on the population and the when the volume of exercise is relatively low.42 As train-
exercise chosen with an error that ranges from <1% error ing progresses and the intensity and volume increase, the
(bench press) to 9–14% error (deadlift).126 For clinical frequency of exercise is reduced.
purposes, no single equation is clearly superior to another, The duration of training will also vary depending on
and the differences in the predicted values could be rela- the goals of exercise. For example, strength increase can
tively large if very low external loads are used (i.e. loads occur with as little as 2 weeks of resistance training, but,
permitting more than ten repetitions) (as an example, see: if the aim is to increase muscle cross-sectional area then
Eston and Evans127). training must continue with high volume for at least 6–8
weeks.
Volume of Resistance Training
Clinical Prescription of Resistance Training
There has been substantial debate concerning the appro-
priate operational definition of training volume within When the aim of a training programme is to enhance
the resistance exercise literature, making this parameter strength, high loads are prescribed for a low number of
difficult to evaluate and replicate in research and/or repetitions, whereas a large number of repetitions at low
provide practical guidelines for exercise prescription. intensity are used to enhance endurance. A key principle
One of the most widely accepted definitions for this vari- in resistance training is that of overload.125,129 This prin-
able is volume load, which takes into account the total ciple states that a greater than normal stress or load on
number of repetitions performed and weight (kg) lifted the body is required to induce training adaptation. As
(i.e. [repetitions (no.) × external load (kg)]. Through the performance improves with training, the intensity or
use of volume load assignment, it is possible to manipu- volume of exercise must increase to constantly place
late the dosage of an exercise programme by altering (a) demand on the muscle/s. For endurance training, typi-
the number of sets performed per exercise, (b) the total cally the duration of the contractions or the number of
number of exercises performed and/or (c) the loading repetitions of the exercise are increased, whereas for
parameters of exercise (i.e. the absolute intensity or the strength training the amount of resistance is increased
actual load lifted). The volume of exercise varies widely progressively.42 Performance of too little exercise will fail
across training interventions depending on the main to induce positive training adaptation, whereas prescrip-
focus of the training prescription. For instance, several tion of excessive exercise can result in overtraining with
studies have demonstrated significant improvements in associated decrements in performance, and possibly
neck muscle strength in patients with chronic neck pain injury.130 Regular, careful standardized assessment of
with application of different protocols and exercise capacity and adjustment of the exercise parameters is
volume. In the study by Falla et al.39 patients with chronic fundamental to optimal prescription of an individualized
neck pain trained using a head lift exercise and performed programme (Fig. 31-1).
12–15 repetitions with a weight that they could lift 12 Although systematic reviews confirm the efficacy of
times on the first training session (12 RM) and progressed strength training in various musculoskeletal pain condi-
to 15 repetitions over a 4-week period. For a further 2 tions, optimal exercise parameters have not been estab-
weeks the patients performed three sets of 15 repetitions lished.124,131–133 For example, a recent systematic review
of the initial 12 RM load once per day. A significant examined the effects of resistance training for lateral
improvement in neck muscle strength was also observed epicondylosis/epicondylalgia.131 Twelve studies were
by Ylinen et al.,128 yet this 12-day programme used Ther- included (nine reporting on isotonic exercise, two iso-
aband® to train the neck flexor muscles and a single series metric exercise and one isokinetic exercise). Exercise pro-
of 15 repetitions directly forward, obliquely towards right gramme duration ranged from 4 to 52 weeks, and exercises
and left, and directly backward were performed. The aim were prescribed one to six times per day, with an average
with this programme was to maintain the level of resis- duration of 15 minutes per session, and three to 50 rep-
tance at 80% of the participant’s maximum isometric etitions (average: 15), with one to four sets per session.
strength recorded at each visit. Rather than relying on a Despite the variation in exercise dose and type, all studies
predefined volume of training, the volume of exercise reported substantial reduction in pain and improvement
should be determined based on the intended aim of train- in grip strength. Thus, optimal exercise design and dosing
ing (e.g. a greater number of repetitions is more likely to is not defined. Research is necessary with systematic
enhance endurance than strength) and status of the manipulation of intensity, volume, frequency and dura-
patient so that the patient can perform the exercise tion of exercise to determine the ‘optimal dose’ to enhance
without causing discomfort or reproduction of their motor output and manage symptoms in patients with
symptoms. various musculoskeletal disorders.
A clearer understanding of dosage is available for
design of a programme that is focused solely on strength
Frequency and Duration of
gain. A meta-analysis134 of dose–response relations in
Resistance Training
strength training (177 studies presenting 1803 effect
The frequency of exercise to enhance strength and endur- sizes) suggested the response to exercise is dose-specific,
ance also varies across training protocols. Although there non-linear and related to the baseline training status of
306 PART III  Advances in Clinical Science and Practice

the individual – higher gains are available for less absolute 9. Moseley G, Nicholas M, Hodges P. Does anticipation of back pain
work in less trained individuals. For untrained individu- predispose to back trouble? Brain 2004;127:2339–47.
10. Tucker K, Larsson AK, Oknelid S, et al. Similar alteration of
als, maximal strength gains are elicited at a mean training motor unit recruitment strategies during the anticipation and
intensity of 60% of 1 RM, 3 days per week, and with a experience of pain. Pain 2012;153:636–43.
mean training volume of four sets per muscle group. 11. Jull G, Trott P, Potter H, et al. A randomized controlled trial of
Recreationally trained non-athletes exhibit maximal exercise and manipulative therapy for cervicogenic headache.
Spine 2002;27(17):1835–43.
strength gains with a mean training intensity of 80% of 12. Lluch E, Schomacher J, Gizzi L, et al. Immediate effects of active
1 RM, 2 days per week, and a mean volume of four sets. cranio-cervical flexion exercise versus passive mobilisation of the
For athlete populations, maximal strength gains are elic- upper cervical spine on pain and performance on the cranio-
ited at a mean training intensity of 85% of 1 RM, 2 days cervical flexion test. Man Ther 2014;19(1):25–31.
per week, and with a mean training volume of eight sets 13. Ferreira P, Ferreira M, Maher C, et al. Changes in recruitment of
transversus abdominis correlate with disability in people with
per muscle group.134 Thus for an untrained individual a chronic low back pain. Br J Sports Med 2009;55:153–69.
large effect (effect size >2) could be achieved using 65% 14. Hoffman SL, Johnson MB, Zou D, et al. Effect of classification-
(of 1 RM) intensity, performed three times per week, specific treatment on lumbopelvic motion during hip rotation in
three or four sets per session, whereas the same training people with low back pain. Man Ther 2011;16:344–50.
15. Scholtes SA, Gombatto SP, Van Dillen LR. Differences in lum-
parameters on an athlete will result in much smaller bopelvic motion between people with and people without low
(effect size <0.5) gains. Thus, when setting goals for resis- back pain during two lower limb movement tests. Clin Biomech
tance training, not only the dose, but the training history 2009;24:7–12.
of the individual must be considered to optimize the 16. Bourne DA, Choo AM, Regan WD, et al. The placement of skin
outcome. surface markers for non-invasive measurement of scapular kine-
matics affects accuracy and reliability. Ann Biomed Eng 2011;39:
777–85.
17. Myers JB, Oyama S, Hibberd EE. Scapular dysfunction in high
SUMMARY AND CONCLUSION school baseball players sustaining throwing-related upper extrem-
ity injury: a prospective study. J Shoulder Elbow Surg 2013;22:
1154–9.
Exercise has therapeutic effects for various musculosk- 18. Crossley KM, Zhang WJ, Schache AG, et al. Performance on the
eletal conditions. Evidence is accruing to support the single-leg squat task indicates hip abductor muscle function. Am
role of exercise programmes that target motor control J Sports Med 2011;39:866–73.
training and resistance training for their beneficial and 19. Teyhen D, Bergeron MF, Deuster P, et al. Consortium for health
profound effects on the neuromuscular system. The and military performance and American College of Sports Medi-
cine Summit: utility of functional movement assessment in iden-
effectiveness of every exercise programme resides in the tifying musculoskeletal injury risk. Curr Sports Med Rep
ability of the clinician to assess the status of the patient 2014;13:52–63.
and prescribe the most appropriate exercise interventions 20. Pinto RZ, Ferreira PH, Ferreira M, et al. Reliability and discrimi-
to address the specific features of their presentation to natory capacity of a clinical scale for assessing abdominal muscle
coordination. J Manipulative Physiol Ther 2012;34:562–9.
achieve significant and durable improvements in clinical 21. Falla D, Campbell C, Fagan A, et al. Relationship between cranio-
outcomes. Exercise is medicine, and as such it is important cervical flexion range of motion and pressure change during the
that the clinician develops and controls the effectiveness cranio-cervical flexion test. Man Ther 2003;8(2):92–6.
of the ‘dosage’ of its prescriptions (in terms of volume, 22. Juul T, Langberg H, Enoch F, et al. The intra- and inter-rater
intensity and exercise modalities). It is hoped that the reliability of five clinical muscle performance tests in patients with
and without neck pain. BMC Musculoskelet Disord 2013;14:339.
framework provided in this chapter can be a guide to 23. O’Leary S, Falla D, Jull G. The relationship between superficial
develop safe and effective exercise programmes. muscle activity during the cranio-cervical flexion test and clinical
features in patients with chronic neck pain. Man Ther 2011;
16:452–5.
REFERENCES 24. James G, Doe T. The craniocervical flexion test: intra-tester reli-
1. Hodges PW, Tucker K. Moving differently in pain: a new theory ability in asymptomatic subjects. Physiother Res Int 2010;15:
to explain the adaptation to pain. Pain 2011;152:S90–8. 144–9.
2. Falla D, Farina D. Neural and muscular factors associated with 25. Hides JA, Stokes MJ, Saide M, et al. Evidence of lumbar multifi-
motor impairment in neck pain. Curr Rheumatol Rep 2007; dus muscle wasting ipsilateral to symptoms in patients with acute/
9:497–502. subacute low back pain. Spine 1994;19(2):165–72.
3. Graven-Nielsen T, Arendt-Nielsen L. Impact of clinical and 26. Elliott J, Jull G, Noteboom JT, et al. Fatty infiltration in the cervi-
experimental pain on muscle strength and activity. Curr Rheuma- cal extensor muscles in persistent whiplash-associated disorders: a
tol Rep 2008;10:475–81. magnetic resonance imaging analysis. Spine 2006;31(22):847–55.
4. Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is 27. Beeler S, Ek ET, Gerber C. A comparative analysis of fatty infiltra-
not automatic after resolution of acute, first-episode low back tion and muscle atrophy in patients with chronic rotator cuff tears
pain. Spine 1996;21(23):2763–9. and suprascapular neuropathy. J Shoulder Elbow Surg 2013;22:
5. Falla D, Jull G, Edwards S, et al. Neuromuscular efficiency of the 1537–46.
sternocleidomastoid and anterior scalene muscles in patients with 28. Croisier JL. Factors associated with recurrent hamstring injuries.
chronic neck pain. Disabil Rehabil 2004;26(12):712–17. Sports Med 2004;34:681–95.
6. Sterling M, Jull G, Vicenzino B, et al. Development of motor 29. Byram IR, Bushnell BD, Dugger K, et  al. Preseason shoulder
dysfunction following whiplash injury. Pain 2003;103:65–73. strength measurements in professional baseball pitchers: identify-
7. Butler HL, Hubley-Kozey CL, Kozey JW. Changes in electro- ing players at risk for injury. Am J Sports Med 2010;38:
myographic activity of trunk muscles within the sub-acute phase 1375–82.
for individuals deemed recovered from a low back injury. J Elec- 30. Pincivero DM, Lephart SM, Karunakara RA. Reliability and pre-
tromyogr Kinesiol 2013;23(2):369–77. cision of isokinetic strength and muscular endurance for the quad-
8. Moreside JM, Quirk DA, Hubley-Kozey CL. Temporal patterns riceps and hamstrings. Int J Sports Med 1997;18:113–17.
of the trunk muscles remain altered in a low back-injured popula- 31. Maffiuletti NA, Bizzini M, Desbrosses K, et al. Reliability of knee
tion despite subjective reports of recovery. Arch Phys Med Rehabil extension and flexion measurements using the Con-Trex isokinetic
2014;95:686–98. dynamometer. Clin Physiol Funct Imaging 2007;27:346–53.
 31  Therapeutic Exercise 307

32. Adkins D, Boychuk J, Remple M, et al. Motor training induces 56. Elliott J, Pedler A, Kenardy J, et al. The temporal development
experience-specific patterns of plasticity across motor cortex and of fatty infiltrates in the neck muscles following whiplash injury:
spinal cord. J Appl Physiol 2006;101:1776–82. an association with pain and posttraumatic stress. PLoS ONE
33. Fluck M. Functional, structural and molecular plasticity of mam- 2011;6(6):e21194.
malian skeletal muscle in response to exercise stimuli. J Exp Biol 57. Hides JA, Jull GA, Richardson CA. Long-term effects of specific
2006;209:2239–48. stabilizing exercises for first-episode low back pain. Spine
34. Duchateau J, Semmler JG, Enoka RM. Training adaptations in 2001;26:243–8.
the behavior of human motor units. J Appl Physiol 2006;101: 58. Unsgaard-Tøndel M, Lund Nilsen TI, Magnussen J, et al. Is
1766–75. activation of transversus abdominis and obliquus internus abdomi-
35. Jull G, Falla D, Vicenzino B, et al. The effect of therapeutic nis associated with long-term changes in chronic low back pain?
exercise on activation of the deep cervical flexor muscles in people A prospective study with 1-year follow-up. Br J Sports Med
with chronic neck pain. Man Ther 2009;14:696–701. 2012;46:729–34.
36. Tsao H, Hodges PW. Immediate changes in feedforward postural 59. Falla D, O’Leary S, Farina D, et al. The change in deep cervical
adjustments following voluntary motor training. Exp Brain Res flexor activity after training is associated with the degree of pain
2007;181:537–46. reduction in patients with chronic neck pain. Clin J Pain
37. Tsao H, Druitt TR, Schollum TM, et al. Motor training of the 2012;28(7):628–34.
lumbar paraspinal muscles induces immediate changes in motor 60. Nielsen JB, Cohen LG. The Olympic brain. Does corticospinal
coordination in patients with recurrent low back pain. J Pain plasticity play a role in acquisition of skills required for high-
2010;11(11):1120–8. performance sports? J Physiol 2008;586:65–70.
38. Falla D, Jull G, Russell T, et al. Effect of neck exercise on sitting 61. Vila-Chã C, Falla D, Correia MV, et al. Adjustments in motor unit
posture in patients with chronic neck pain. Phys Ther 2007;87(4): properties during fatiguing contractions after training. Med Sci
408–17. Sports Exerc 2012;44:616–24.
39. Falla D, Jull G, Hodges P, et al. An endurance-strength training 62. Vila-Chã C, Falla D, Farina D. Motor unit behavior during sub-
regime is effective in reducing myoelectric manifestations of cervi- maximal contractions following six weeks of either endurance or
cal flexor muscle fatigue in females with chronic neck pain. Clin strength training. J Appl Physiol (1985) 2010;109:1455–66.
Neurophysiol 2006;117:828–37. 63. Tsao H, Hodges PW. Persistence of improvements in postural
40. O’Leary S, Jull G, Kim M, et al. Training mode-dependent strategies following motor control training in people with recur-
changes in motor performance in neck pain. Arch Phys Med rent low back pain. J Electromyogr Kinesiol 2008;18:559–67.
Rehabil 2012;93(7):1225–33. 64. Bawa P. Neural control of motor output: can training change it?
41. Danneels LA, Vanderstraeten GG, Cambier DC, et al. Effects of Exerc Sport Sci Rev 2002;30:59–63.
three different training modalities on the cross sectional area of 65. Hodges PW, Richardson CA. Inefficient muscular stabilization of
the lumbar multifidus muscle in patients with chronic low back the lumbar spine associated with low back pain. A motor control
pain. Br J Sports Med 2001;35:186–91. evaluation of transversus abdominis. Spine 1996;21(22):2640–50.
42. Kisner C, Colby LA. Therapeutic Exercise: Foundations and 66. MacDonald D, Moseley GL, Hodges PW. Why do some patients
Techniques. Philadelphia, USA: F.A. Davis Company; 2012. keep hurting their back? Evidence of ongoing back muscle dys-
43. Häkkinen K, Alen M, Kraemer WJ, et al. Neuromuscular adapta- function during remission from recurrent back pain. Pain
tions during concurrent strength and endurance training versus 2009;142:183–8.
strength training. Eur J Appl Physiol 2003;89:42–52. 67. Falla D, Jull G, Hodges PW. Feedforward activity of the cervical
44. Karavirta L, Häkkinen A, Sillanpää E, et al. Effects of combined flexor muscles during voluntary arm movements is delayed in
endurance and strength training on muscle strength, power and chronic neck pain. Exp Brain Res 2004;157:43–8.
hypertrophy in 40–67-year-old men. Scand J Med Sci Sports 68. Falla D, Jull G, Hodges PW. Patients with neck pain demonstrate
2011;21:402–11. reduced electromyographic activity of the deep cervical flexor
45. Hawley JA. Molecular responses to strength and endurance train- muscles during performance of the craniocervical flexion test.
ing: are they incompatible? Appl Physiol Nutr Metab Spine 2004;29(19):2108–14.
2009;34:355–61. 69. Schomacher J, Boudreau S, Petzke F, et al. Localized pressure pain
46. Sterling M, Jull G, Vicenzino B, et al. Physical and psychological sensitivity is associated with lower activation of the semispinalis
factors predict outcome following whiplash injury. Pain 2005;114: cervicis muscle in patients with chronic neck pain. Clin J Pain
141–8. 2013;29:898–906.
47. Falla D, Arendt-Nielsen L, Farina D. Gender-specific adaptations 70. Schomacher J, Farina D, Lindstroem R, et al. Chronic trauma-
of upper trapezius muscle activity to acute nociceptive stimulation. induced neck pain impairs the neural control of the deep semispi-
Pain 2008;138:217–25. nalis cervicis muscle. Clin Neurophysiol 2012;123(7):1403–8.
48. Muceli S, Falla D, Farina D. Reorganization of muscle 71. MacDonald D, Moseley G, Hodges P. People with recurrent low
synergies during multidirectional reaching in the horizontal back pain respond differently to trunk loading despite remission
plane with experimental muscle pain. J Neurophysiol 2014;111: from symptoms. Spine (Phila Pa 1976) 2010;35(7):818–24.
1615–30. 72. Ferreira PH, Ferreira ML, Hodges PW. Changes in recruitment
49. Jull G, Sterling M, Falla D, et al. Whiplash, Headache and Neck of the abdominal muscles in people with low back pain: ultrasound
Pain: Research Based Directions for Physical Therapies. Edin- measurement of muscle activity. Spine (Phila Pa 1976) 2004;
burgh: Elsevier, Churchill Livingstone; 2008. 29:2560–6.
50. Hodges P, Cholewicki J, van Dieen J. Spinal Control: The Reha- 73. O’Leary S, Cagnie B, Reeve A, et al. Is there altered activity of
bilitation of Back Pain. State of the Art and Science. Churchill the extensor muscles in chronic mechanical neck pain? A func-
Livingstone, Elsevier; 2013. tional magnetic resonance imaging study. Arch Phys Med Rehabil
51. O’Leary S, Falla D, Hodges P, et al. Specific therapeutic exercise 2011;92(6):929–34.
of the neck induces immediate local hypoalgesia. J Pain 2007;8: 74. Tsao H, Galea MP, Hodges PW. Reorganization of the motor
832–9. cortex is associated with postural control deficits in recurrent low
52. Jull G, Amiri M, Bullock-Saxton J, et al. Cervical musculoskeletal back pain. Brain 2008;131:2161–71.
impairment in frequent intermittent headache. Part 1: Subjects 75. Tsao H, Danneels L, Hodges PW. Smudging the motor brain in
with single headaches. Cephalalgia 2007;27:793–802. young adults with recurrent low back pain. Spine 2011;
53. Uhlig Y, Weber BR, Grob D, et al. Fiber composition and fiber 36:1721–7.
transformations in neck muscles of patients with dysfunction of 76. Boudreau SA, Farina D, Falla D. The role of motor learning and
the cervical spine. J Orthop Res 1995;13(2):240–9. neuroplasticity in designing rehabilitation approaches for muscu-
54. Hodges PW, James G, Blomster L, et al. Can pro-inflammatory loskeletal pain disorders. Man Ther 2010;15(5):410–14.
cytokine gene expression explain multifidus muscle fiber changes 77. Crossley KM, Bennell K, Green S, et al. Physical therapy for
after an intervertebral disc lesion? Spine 2014;In Press. patellofemoral pain: a randomized, double-blinded, placebo-
55. Alaranta H, Tallroth K, Soukka A, et al. Fat content of lumbar controlled trial. Am J Sports Med 2002;30:857–65.
extensor muscles and low back disability: a radiographic and clini- 78. Sahrmann S. Diagnosis and Treatment of Movement Impairment
cal comparison. J Spinal Disord 1993;6:137–40. Syndromes. St Louis, MO: Mosby; 2002.
308 PART III  Advances in Clinical Science and Practice

79. Richardson C, Hodges PW, Hides J. Therapeutic Exercise for response to strength training: changes in muscle architecture.
Lumbopelvic Stabilization: A Motor Control Approach for the J Physiol 2001;534:613–23.
Treatment and Prevention of Low Back Pain. 2nd ed. Edinburgh: 103. Fitts RH. Effects of regular exercise training on skeletal muscle
Churchill Livingstone; 2004. contractile function. Am J Phys Med Rehabil 2003;82:320–31.
80. McGill SM. Low Back Disorders: Evidence Based Prevention and 104. Seynnes OR, de Boer M, Narici MV. Early skeletal muscle hyper-
Rehabilitation. Champaign, IL.: Human Kinetics; 2007. trophy and architectural changes in response to high-intensity
81. O’Sullivan PB. Diagnosis and classification of chronic low back resistance training. J Appl Physiol 2007;102:368–73.
pain disorders: maladaptive movement and motor control impair- 105. Kraemer WJ, Volek JS, Fleck SJ. Chronic musculoskeletal adapta-
ments as underlying mechanism. Man Ther 2005;10:242–55. tions to resistance training. In: Roitman JL, editor. ACSM’s
82. Worsley P, Warner M, Mottram S, et al. Motor control retraining Resource Manual for Guidelines for Exercise Testing and Pre-
exercises for shoulder impingement: effects on function, muscle scription. 4th ed. Philadelphia: Lippincott Williams & Wilkins;
activation, and biomechanics in young adults. J Shoulder Elbow 2001. p. 176.
Surg 2013;22:e11–19. 106. Folland JP, Williams AG. The adaptations to strength training:
83. Hall L, Tsao H, MacDonald D, et al. Immediate effects of morphological and neurological contributions to increased
co-contraction training on motor control of the trunk muscles in strength. Sports Med 2007;37:145–68.
people with recurrent low back pain. J Electromyogr Kinesiol 107. Fluck M, Hoppeler H. Molecular basis of skeletal muscle
2009;19:763–73. plasticity – from gene to form and function. Rev Physiol Biochem
84. Falla D, Lindstrøm R, Rechter L, et al. Effectiveness of an 8-week Pharmacol 2003;146:159–216.
exercise programme on pain and specificity of neck muscle activity 108. Green HJ, Barr DJ, Fowles JR, et al. Malleability of human skel-
in patients with chronic neck pain: a randomized controlled study. etal muscle Na(+)-K(+)-ATPase pump with short-term training.
Eur J Pain 2013;17:1517–28. J Appl Physiol 2004;97:143–8.
85. Grimaldi A. Assessing lateral stability of the hip and pelvis. Man 109. Green HJ, Ballantyne CS, MacDougall JD, et al. Adaptations in
Ther 2011;16:26–31. human muscle sarcoplasmic reticulum to prolonged submaximal
86. Christiansen DH, Falla D, Frost P, et al. Physiotherapy after Sub- training. J Appl Physiol 2003;94:2034–42.
acromial Decompression Surgery: Development of An Exercise 110. Moritani T, deVries HA. Neural factors versus hypertrophy in the
Intervention Submitted for Publication. 2014. time course of muscle strength gain. Am J Phys Med 1979;
87. Fitts PM, Posner MI. Human Performance. USA: Wadsworth; 58:115–30.
1967. 111. Patten C, Kamen G, Rowland DM. Adaptations in maximal motor
88. Boudreau S, Romaniello A, Wang K, et al. The effects of intra- unit discharge rate to strength training in young and older adults.
oral pain on motor cortex neuroplasticity associated with short- Muscle Nerve 2001;24:542–50.
term novel tongue-protrusion training in humans. Pain 112. Van Cutsem M, Duchateau J, Hainaut K. Changes in single motor
2007;132:169–78. unit behaviour contribute to the increase in contraction speed
89. Ferguson AR, Crown ED, Grau JW. Nociceptive plasticity inhib- after dynamic training in humans. J Physiol 1998;513:295–305.
its adaptive learning in the spinal cord. Neuroscience 2006;141: 113. Griffin L, Painter PE, Wadhwa A, et al. Motor unit firing vari-
421–31. ability and synchronization during short-term light-load training
90. Ingham D, Tucker KJ, Tsao H, et al. The effect of pain on in older adults. Exp Brain Res 2009;197:337–45.
training-induced plasticity of the corticomotor system. Eur J Pain 114. Stone MH. Implications for connective tissue and bone alterations
2011;15:1028–34. resulting from resistance exercise training. Med Sci Sports Exerc
91. Svensson P, Romaniello A, Arendt-Nielsen L, et al. Plasticity in 1988;20:51–62.
corticomotor control of the human tongue musculature induced 115. Conroy BP, Earle RW, Beachle TR. Bone, muscle and connective
by tongue-task training. Exp Brain Res 2003;152:42–51. tissue adaptations to physical activity. In: Essentials of Strength
92. Pascual-Leone A, Nguyet D, Cohen LG, et al. Modulation of Training and Conditioning. Champaign, IL: Human Kinetics;
muscle responses evoked by transcranial magnetic stimulation 1994.
during the acquisition of new fine motor skills. J Neurophysiol 116. Mitchell CJ, Churchward-Venne TA, West DW, et al. Resistance
1995;74:1037–45. exercise load does not determine training-mediated hypertrophic
93. Kleim JA, Barbay S, Cooper NR, et al. Motor learning-dependent gains in young men. J Appl Physiol 2012;113:71–7.
synaptogenesis is localized to functionally reorganized motor 117. Abe T, Loenneke JP, Fahs CA, et al. Exercise intensity and muscle
cortex. Neurobiol Learn Memory 2002;77:63–77. hypertrophy in blood flow-restricted limbs and non-restricted
94. Shumway-Cook A, Woollacott M. Motor Control: Translating muscles: a brief review. Clin Physiol Funct Imaging 2012;
Research into Clinical Practice. Philadelphia, PA: Lippincott Wil- 32:247–52.
liams & Wilkins; 2006. 118. Baldwin KM, Haddad F. Effects of different activity and inactivity
95. Falla D, Jull G, Hodges P. Training the cervical muscles with paradigms on myosin heavy chain gene expression in striated
prescribed motor tasks does not change muscle activation during muscle. J Appl Physiol 2001;90:345–57.
a functional activity. Man Ther 2008;13:507–12. 119. Gibala MJ, Little JP, van Essen M, et al. Short-term sprint interval
96. Lluch E, Schomacher J, Gizzi L, et al. Immediate effects of active versus traditional endurance training: similar initial adaptations in
cranio-cervical flexion exercise versus passive mobilisation of the human skeletal muscle and exercise performance. J Physiol
upper cervical spine on pain and performance on the cranio- 2006;575:901–11.
cervical flexion test. Man Ther 2014;19:25–31. 120. Hoppeler H, Fluck M. Plasticity of skeletal muscle mitochondria:
97. Scholtes SA, Norton BJ, Lang CE, et al. The effect of within- structure and function. Med Sci Sports Exerc 2003;35:95–104.
session instruction on lumbopelvic motion during a lower limb 121. Scott W, Stevens J, Binder-Macleod SA. Human skeletal muscle
movement in people with and people without low back pain. Man fiber type classifications. Phys Ther 2001;81:1810–16.
Ther 2010;15:496–501. 122. Wilmore JH, Costill DL, Kenney WL. Physiology Of Sport And
98. Jull G, Falla D, Treleaven J, et al. Retraining cervical joint posi- Exercise. United Kingdom: Human Kinetics; 2008.
tion sense: The effect of two exercise regimes. J Orthop Res 2007; 123. Cracraft JD. Effects of Exercise on Firing Patterns of Single
25(3):404–12. Motor Units. Med Sci Sports Exerc 1975;7:86.
99. Tsao H, Galea MP, Hodges PW. Driving plasticity in the motor 124. Kristensen J, Franklyn-Miller A. Resistance training in musculo-
cortex in recurrent low back pain. Euro J Pain 2010;14:832–9. skeletal rehabilitation: a systematic review. Br J Sports Med
100. Vasseljen O, Fladmark AM. Abdominal muscle contraction thick- 2012;46:719–26.
ness and function after specific and general exercises: a random- 125. Medicine ACoS. Position stand: progression models in resistance
ized controlled trial in chronic low back pain patients. Man Ther training for healthy adults. Med Sci Sports Exerc 2002;34:
2010;15:482–9. 364–80.
101. Aagaard P. Training-induced changes in neural function. Exerc 126. LeSuer DA, McCormick JH, Mayhew JL, et al. The accuracy of
Sport Sci Rev 2003;31:61–7. prediction equations for estimating 1-RM performance in the
102. Aagaard P, Andersen JL, Dyhre-Poulsen P, et al. A mechanism bench press, squat, and deadlift. J Strength Cond Res 2007;
for increased contractile strength of human pennate muscle in 11:211–13.
 31  Therapeutic Exercise 309

127. Eston R, Evans HJ. The validity of submaximal ratings of per- 131. Raman J, MacDermid JC, Grewal R. Effectiveness of different
ceived exertion to predict one repetition maximum. J Sports Sci methods of resistance exercises in lateral epicondylosis – a system-
Med 2009;8:567–73. atic review. J Hand Ther 2012;25:5–25.
128. Ylinen J, Takala EP, Nykanen M, et al. Active neck muscle training 132. Lange AK, Vanwanseele B, Fiatarone Singh MA. Strength train-
in the treatment of chronic neck pain in women: a randomized ing for treatment of osteoarthritis of the knee: a systematic review.
controlled trial. JAMA 2003;289(19):2509–16. Arthritis Rheum 2008;59:1488–94.
129. Hellebrandt F, Houtz SJ. Mechanisms of muscle training in man: 133. Taylor NF, Dodd KJ, Damiano DL. Progressive resistance exer-
experimental demonstration of the overload principle. Phys Ther cise in physical therapy: a summary of systematic reviews. Phys
Rev 1956;36:371. Ther 2005;85:1208–23.
130. Fry AC. The role of training intensity in resistance exercise, over- 134. Peterson MD, Rhea MR, Alvar BA. Applications of the dose-
training and overreaching. In: Kreider R, Fry A, O’Toole M, response for muscular strength development: a review of meta-
editors. Overtraining in Sport. Champaign, IL: Human Kinetics; analytic efficacy and reliability for designing training prescription.
1998. J Strength Cond Res 2005;19:950–8.
 CHAPTER 32 

Management of the
Sensorimotor System
CHAPTER OUTLINE

Ch 32.1  The Cervical Region  310 Ch 32.3  The Lower Limb  319
Ulrik Röijezon • Julia Treleaven Nicholas Clark • Scott Lephart
Ch 32.2  Sensorimotor Control of Lumbar Spine
Alignment  315
Jaap van Dieën • Idsart Kingma • Nienke Willigenburg
• Henri Kiers

CHAPTER 32.1  ■  THE CERVICAL REGION

Ulrik Röijezon Julia Treleaven
●

The sensory and motor systems of the neck are vital for position and movement sense of the shoulder,17,18 elbow17
the perception, movement and stability of the head rela- and hand,19 as well as reduced pointing acuity to a visual
tive to the trunk, for eye and arm–hand functioning and target.20
for postural control. This section focuses on the somato- Oculomotor impairments include decreased smooth
sensory system of the cervical spine (i.e. cervical proprio- pursuit velocity gain, especially when the neck is in
ception). The cervical proprioceptors are essential for the torsion, and altered velocity and latency of saccadic eye
position and movement sense of the head and have abun- movements.21–29 Moreover, changes in the activation of
dant neurophysiological connections to the visual and neck muscles during eye movements have been reported.30
vestibular organs and subsequent input to the sensorimo- Postural control is also known to be disturbed in
tor control system. This has implications for head and people with neck pain. Several studies have reported
eye movement control and postural control, as well as increased sway in quite stance,31–41 but impairments in
symptoms such as dizziness and visual complaints in more functional tasks (e.g. walking with head turns) have
people with neck pain disorders. also been reported.42
Variations, however, are large between individuals
with neck pain. While impairments have been reported
REPORTED COMPLAINTS AND in both non-traumatic (idiopathic) and trauma-induced
IMPAIRMENTS neck pain disorders, some studies have reported no or
only minor impairments. Several studies have reported
A large variety of complaints and motor control impair- more pronounced impairments in people following a
ments presumed to be related to disturbed cervical whiplash injury and in individuals with dizziness.3,9,26,32,40
somatosensory information and/or processing of this The suggested pathophysiology underlying such impair-
information have been reported in neck pain disorders, ments is illustrated in Figure 32-1.
including cervical and upper extremity control as well as
oculomotor and postural control.
Dizziness/unsteadiness and or light-headedness are OVERALL MANAGEMENT APPROACH
common symptoms associated with neck pain, especially
in those with chronic whiplash-associated disorder.1–3 Assessment and treatment of altered cervical propriocep-
Loss of balance and actual falls occur but are less tion in the management of neck pain is as important as
common.3 In addition, light sensitivity, needing to con- considering lower limb proprioceptive training following
centrate to read and visual fatigue are the most prevalent an ankle or knee injury. Sensorimotor disturbances in
visual complaints associated with neck pain.4 neck pain disorders are largely heterogeneous, and treat-
Impaired cervical movement control in neck pain ment therefore needs to be individually tailored and based
includes reduced cervical position1,3,5–7 and movement on the patient’s history and physical activities of daily
sense,8–10 as well as reduced cervical force steadiness,11 living as well as findings from the clinical assessment.
movement smoothness,6,12,13 speed14,15 and conjunct Management should preferably include local neck
motions.14,16 Impairments of upper limb kinematics docu- treatment in combination with tailored sensorimotor
mented in people with neck pain include reduced exercises.43 This combined approach will address the
310
 32  Management of the Sensorimotor System 311

Impact of somatosensory dysfunction in the cervical spine

Sensorimotor control
disturbances
Altered afferent integration
and tuning

CNS
Representation cortex
Somatic reorganization
Cortical reweighting
Visual Vestibular
system system Altered
descending
Altered reflex
Altered
responses
descending
Increased
Altered cervical sensitivity
somatosensory input FIGURE 32-2  ■  Retraining cervical movement sense using a laser
mounted on a headband. The patient traces patterns such as a
Pain
zigzag placed 1 m from the laser.
Inflammation

Altered
mechanoreceptors TAILORED SENSORIMOTOR EXERCISE
Direct damage APPROACH BASED ON IMPAIRMENTS
Functional impairment
Morphological changes The greatest deficits in sensorimotor tests have been
Muscle spindle sensitivity
measured in patients with whiplash complaining of diz-
ziness,3,27,40 but these deficits can be present in non-dizzy
Trauma SNS activation
patients with idiopathic neck pain.5,26,32 Although the
causes of the disturbances are similar, an individual
patient may present with dysfunction in either one or
Stress
several aspects of sensorimotor control.49
FIGURE 32-1  ■  The suggested pathophysiology of sensorimotor
impairments associated with neck disorders. CNS, central
nervous system; SNS, sympathetic nervous system.
Head Position and Movement Control
A low-cost method of mounting a laser pointer on a
headband and directing the laser beam at a target, can be
used to monitor both cervical position and movement
local causes disturbing cervical afferent input and con- sense.
sider the important links between the cervical, vestibular
and ocular systems and any secondary adaptive changes
Cervical Joint Position Error
in sensorimotor control.
The patient is seated and a target is placed to indicate the
starting laser point (90 cm from wall). The patient, with
TAILORED LOCAL TREATMENT eyes closed, performs at least three repetitions of an
active neck movement and is asked to accurately return
Pain reduction, normalized range of motion and neuro- to the starting position. Errors, as little as 4.5° (equivalent
muscular control, as well as adequate strength and endur- to 7.1 cm with the patient seated 90 cm from the target)
ance of the cervical spine, need to be addressed in neck between the start and end position, can indicate a deficit
pain disorders. This can be directed using traditional in proprioception.50,51 Joint position error can be retrained
local treatment such as acupuncture, manual therapy and by practising relocating the head to a neutral position
various training regimens. Specific traditional local treat- (guided by the laser beam).
ments to the neck such as acupuncture, manual therapy
and craniocervical flexion training have been shown to
Cervical Movement Sense
improve symptoms and dysfunctions related to disturbed
cervical somatosensory information, including cervical A laser mounted on a headband can also be used to allow
position sense, dizziness and/or standing balance in the patient to trace patterns such as a zigzag (20 × 14 cm)
patients with neck pain.44–48 However, management of placed 1 m from the laser (Fig. 32-2). Recently, pilot
patients not responding sufficiently to traditional inter- normative values (less than 25 seconds and seven times
ventions should also include exercise regimens specifi- outside of a 5-mm radius) were suggested.52 Cervical
cally targeting cervical proprioception and its relation to movement sense can be improved by practice of accu-
eye movement and postural control. rately tracing patterns using the laser. More sophisticated
312 PART III  Advances in Clinical Science and Practice

computerized assessment and treatment methods are

commercially available9 and a virtual reality device has
been developed to measure and train velocity and accu-
racy of head movement.15 Cervical movement acuity can
also be trained using an unstable dynamic system such as
controlling the movement of a ball on a plate mounted
on the head.53

Oculomotor Control
Gaze Stability
In this test, the patient is requested to keep their eyes
focused on a target while they actively move their head
in rotation and flexion/extension. Inability to maintain
focus, reduced or awkward cervical motion (less than
45°), reproduction of dizziness, blurring of vision or
nausea are abnormal responses. Gaze stability can be
practised by the patient by moving their head into direc-
tions of difficulty maintaining optimal movement and
range of motion while fixating their gaze on the focus
point.54 Focusing on a point in a mirror may help initially.
The patient or therapist can also passively move the trunk
whilst the patient maintains focus.

Smooth Pursuit
The patient is requested to keep their head still while
FIGURE 32-3  ■  Smooth pursuit eye movement practised by fol-
following, with the eyes, a moving target (20°/s through lowing a laser pointer, moved backwards and forwards on a
a visual angle of 40°). The test is repeated with the neck wall by the patient’s hand. The patient follows the laser with
in torsion (head still but trunk rotated 45° to each side). their eyes as accurately as they can, while keeping the head still.
Any decline in the smoothness of eye follow or an inabil- Here the patient is positioned in a neck torsion position to the
ity to keep up with the target with quick, catch-up eye left (head still while the trunk is rotated 45° to the right).
movements, particularly when the target is crossing the
midline, or symptom reproduction, in torsion compared Postural Control
to neutral is noted.28 Smooth pursuit can be practised by
following a laser pointer, moved backwards and forwards Inability to maintain stance for 30 seconds, large increases
on a wall by the patient’s hand (Fig. 32-3). in sway, slower responses to correct or rigidity are con-
sidered abnormal responses in comfortable and narrow
stance either on a firm or a soft foam surface with eyes
EYE–HEAD–TRUNK COORDINATION open and closed. In younger patients, the same perfor-
Eye–Head Coordination mance features can be evaluated in tandem and with
single leg stance on a firm surface. Comparison of per-
The patient moves the eyes first to a target which is then formance when the head is still and trunk rotated under
followed by head movement, ensuring that the eyes are the stationary head (biasing cervical proprioception)
kept focused on the target. The test is performed with might be useful.57 Dynamic tests such as the step test and
movement in right and left rotation and flexion and the timed 10-m walk with head turns42,58 can be used for
extension of the neck. Often patients with neck pain are elderly patients with neck pain and patients with neck
unable to keep the head still while the eyes move or they pain complaining of dizziness, unsteadiness or loss of
lose focus during the head movements.54,55 Eye–head balance. The starting level for balance retraining will
coordination can be practised with attention to correctly depend on which tests the patient failed or had difficulty
isolating eye and head movement. with. Patients practise the exercise, gradually increasing
stability time to 30 seconds.
Trunk–Head Coordination
General Recommendations,
The test is performed with the patient standing by asking
them to hold the head still, eyes open, while rotating their
Progression of Treatment
trunk to the left and right. Patients with neck pain often It is recommended that exercises for each aspect of sen-
have difficulty keeping their head still when their trunk sorimotor control should be performed two to five times
is moving.56 This can be practised with the patient using per day. Temporary reproduction of dizziness or visual
a mirror or laser to provide feedback for keeping the head disturbances is acceptable; however, exacerbation of neck
stationary while turning the trunk (Fig. 32-4). pain or headache is not. Decreasing the number
 32  Management of the Sensorimotor System 313

of repetitions or altering the patient position to a more

supported position such as supine lying should prevent
this. Progression can be achieved by increasing the dura-
tion, repetitions and the degree of difficulty of the task
and by performing activities such as an oculomotor task
simultaneously with a balance task. Exercises should be
performed at a speed and range of movement and posi-
tion that allows the patient to perform the task with
precision and continuous correction. Exercises should
also be performed in functional positions and contexts.
Table 32-1 outlines some suggested exercises for each
impairment and Table 32-2 outlines different ways to
progress these exercises.

CONCLUSION
Assessment and management of altered cervical proprio-
ception in people with neck pain is as important as con-
sidering lower limb proprioceptive retraining following
a lower limb injury. Afferent information from the cervi-
cal receptors can be altered via a number of mechanisms
and the findings of the assessment should direct and tailor
the most appropriate management to the individual
patient with a neck disorder. Management should include
both local treatment to the neck in combination with
tailored exercises to improve any deficits in cervical posi-
tion and movement control, oculomotor control, eye–
FIGURE 32-4  ■  Trunk head coordination practised with the patient
using a laser pointer to provide feedback for keeping the head
head–trunk coordination and postural control. This
stationary while turning the trunk. combined approach will address the local causes of altered

TABLE 32-1  Examples of Exercises to Improve Sensorimotor Control in Neck Pain Disorders
Activity Task
Cervical joint position error Relocate head back to neutral, eyes closed, laser on headband, check with eyes open
Relocate trunk back to neutral, keep head still
Relocate to predetermined positions in range (dots along wall), laser on headband, eyes
closed, check eyes open
Cervical movement sense Practice tracing intricate patterns on the wall with laser on headband and eyes open – increase
speed, increase complexity of pattern
Balance Eyes open then closed, firm then soft surface
Different stances – comfortable, narrow, tandem, single leg
Walking with head movements – rotation, flexion and extension of the neck whilst maintaining
direction and velocity of gait
Performing oculomotor or JPE, movement sense exercises whilst balance training
Eye follow Eyes follow laser light moving backwards and forwards across a wall whilst sitting in a neutral
neck position, then with the neck in torsion (move laser light with hand in lap), gradually
increase speed and range of motion
Gaze stability Maintain gaze as therapist moves the trunk or neck passively
Maintain gaze as the patient actively moves their trunk or neck in all directions
Change the focus point – e.g. spot to few words, business card
Fix gaze, close eyes, move head and open eyes to check that they have maintained gaze
(imaginary gaze)
Change the background of the target – plain, stripes, checks
Eye–head coordination Move eyes to focus on a point and then move head in the same direction. Return to neutral
Move eyes to focus on a point in one direction and then move the head in the opposite
direction
Actively move head and eyes together
Move head and eyes together whilst peripheral vision restricted (blackened sides of goggles)
Move hand, arm, head and trunk following with the eyes with or without vision restricted
Trunk–head coordination Passively hold head and actively move trunk left and right, and vice versa
Keep head still, use focus point or laser for feedback, rotate trunk left and right
Increase range and speed of movement

JPE, Joint position error

314 PART III  Advances in Clinical Science and Practice

TABLE 32-2  Variables That Can be Adjusted for Progression of Exercises

Variable Start Progression Further Progression Applicable Exercise Task
Focus point Dot Word Business card Gaze stability, eye–head coordination
Background to focus Plain Stripes Checkerboard pattern Gaze stability, eye–head coordination
point
Patient position Supine Sitting Standing/walking Gaze stability, JPE, eye follow
Neck position Neutral Torsion 30° Torsion 45° Eye follow, JPE, movement sense
Speed of movement Slow Medium Fast Eye follow, trunk–head coordination
Vision Unrestricted Peripheral restricted Eyes closed Gaze stability, eye–head
coordination, balance
Range of motion Small Medium Large All
Duration of exercise 30 seconds 1–2 minutes 3–5 minutes All
Frequency of exercise 2× day 3× day 5× day All

JPE, Joint position error.

cervical afferent input and consider the important links 16. Woodhouse A, Vasseljen O. Altered motor control patterns in
between the cervical, vestibular and ocular systems and whiplash and chronic neck pain. BMC Musculoskelet Disord
any secondary adaptive changes. 2008;9.
17. Knox JJ, Beilstein DJ, Charles SD, et al. Changes in head and neck
position have a greater effect on elbow joint position sense in people
REFERENCES with whiplash-associated disorders. Clin J Pain 2006;22(6):512–18.
1. Heikkila HV, Wenngren B-I. Cervicocephalic kinesthetic sensibil- 18. Sandlund J, Djupsjöbacka M, Ryhed B, et al. Predictive and dis-
ity, active range of cervical motion, and oculomotor function in criminative value of shoulder proprioception tests for patients with
patients with whiplash injury. Arch Phys Med Rehabil 1998;799:1089. whiplash-associated disorders. J Rehabil Med 2006;38(1):44–9.
2. Humphreys BK, Bolton J, Peterson C, et al. A cross-sectional study 19. Huysmans MA, Hoozemans MJ, van der Beek AJ, et al. Position
of the association between pain and disability in neck pain patients sense acuity of the upper extremity and tracking performance in
with dizziness of suspected cervical origin. J Whiplash Relat Disord subjects with non-specific neck and upper extremity pain and
2003;1(2):63–73. healthy controls. J Rehabil Med 2010;42(9):876–83.
3. Treleaven J, Jull G, Sterling M. Dizziness and unsteadiness follow- 20. Sandlund J, Röijezon U, Björklund M, et al. Acuity of goal-directed
ing whiplash injury: characteristic features and relationship with arm movements to visible targets in chronic neck pain. J Rehabil
cervical joint position error. J Rehabil Med 2003;35(1):36–43. Med 2008;40(5):366–74.
4. Treleaven J, Takahashi H. Characteristics of visual disturbances 21. Gimse R, Tjell C, Bjorgen IA, et al. Disturbed eye movements after
reported by individuals with neck pain. Man Ther 2014; in press. whiplash due to injuries to the posture control system. J Clin Exp
<http://dx.doi.org/10.1016/j.math.2014.01.005>. Neuropsychol 1996;18(2):178–86.
5. Kristjansson E, Dall’Alba P, Jull G. A study of five cervicocephalic 22. Hildingsson C, Wenngren B, Bring G, et al. Oculomotor problems
relocation tests in three different subject groups. Clin Rehabil after cervical spine injury. Acta Orthop Scand 1989;60(5):513–16.
2003;17(7):768–74. 23. Kelders WPA, Kleinrensink GJ, Van der Geest JN, et al. The
6. Sjölander P, Michaelson P, Jaric S, et al. Sensorimotor disturbances cervico-ocular reflex is increased in whiplash injury patients. J Neu-
in chronic neck pain – Range of motion, peak velocity, smoothness of rotrauma 2005;22(1):133–7.
movement, and repositioning acuity. Man Ther 2008;13(2):122–31. 24. Montfoort I, Kelders WPA, van der Geest JN, et al. Interaction
7. Chen X, Treleaven J. The effect of neck torsion on joint position between ocular stabilization reflexes in patients with whiplash
error in subjects with chronic neck pain. Man Ther 2013. injury. Invest Ophthalmol Vis Sci 2006;47(7):2881–4.
8. Kristjansson E, Hardardottir L, Asmundardottir M, et al. A new 25. Storaci R, Manelli A, Schiavone N, et al. Whiplash injury and
clinical test for cervicocephalic kinesthetic sensibility: ‘The fly’. oculomotor dysfunctions: clinical-posturographic correlations. Eur
Arch Phys Med Rehabil 2004;85(3):490–5. Spine J 2006;15(12):1811–16.
9. Kristjansson E, Oddsdottir GL. ‘The Fly’: a new clinical assessment 26. Tjell C, Rosenhall U. Smooth pursuit neck torsion test: a specific
and treatment method for deficits of movement control in the cervi- test for cervical dizziness. Am J Otol 1998;19(1):76–81.
cal spine reliability and validity. Spine 2010;35(23):E1298–305. 27. Tjell C, Tenenbaum A, Sandström S. Smooth pursuit neck torsion
10. Woodhouse A, Liljeback P, Vasseljen O. Reduced head steadiness test – A specific test for whiplash associated disorders? J Whiplash
in whiplash compared with non-traumatic neck pain. J Rehabil Med Relat Disord 2003;1(2):9–24.
2010;42(1):35–41. 28. Treleaven J, Jull G, LowChoy N. Smooth pursuit neck torsion test
11. Woodhouse A, Stavdahl O, Vasseljen O. Irregular head movement in whiplash-associated disorders: relationship to self-reports of
patterns in whiplash patients during a trajectory task. Exp Brain Res neck pain and disability, dizziness and anxiety. J Rehabil Med
2010;201(2):261–70. 2005;37(4):219–23.
12. Grip H, Sundelin G, Gerdle B, et al. Cervical helical axis charac- 29. Wenngren B, Pettersson K, Lowenhielm G, et al. Eye motiliy and
teristics and its center of rotation during active head and upper arm auditory brainstem response dysfunction after whiplash injury. Acta
movements-comparisons of whiplash-associated disorders, non- Orthop Scand 2002;122(3):276–83.
specific neck pain and asymptomatic individuals. J Biomech 30. Bexander CSM, Hodges PW. Cervico-ocular coordination during
2008;41(13):2799–805. neck rotation is distorted in people with whiplash-associated disor-
13. Sarig-Bahat H, Weiss PL, Laufer Y. The effect of neck pain on ders. Exp Brain Res 2012;217(1):67–77.
cervical kinematics, as assessed in a virtual environment. Arch Phys 31. Alund M, Ledin T, Odkvist L, et al. Dynamic posturography
Med Rehabil 2010;91(12):1884–90. among patients with common neck disorders. A study of 15 cases
14. Röijezon U, Djupsjöbacka M, Björklund M, et al. Kinematics of with suspected cervical vertigo. J Vestib Res 1993;3(4):383–9.
fast cervical rotations in persons with chronic neck pain: a cross- 32. Field S, Treleaven J, Jull G. Standing balance: a comparison
sectional and reliability study. BMC Musculoskelet Disord 2010;11. between idiopathic and whiplash-induced neck pain. Man Ther
15. Sarig Bahat H, Weiss PL, Laufer Y. The effect of neck pain on 2008;13(3):183–91.
cervical kinematics, as assessed in a virtual environment. Arch Phys 33. Karlberg M, Magnusson M, Malmstrom EM, et al. Postural and
Med Rehabil 2010;91(12):1884–90. symptomatic improvement after physiotherapy in patients with
 32  Management of the Sensorimotor System 315

dizziness of suspected cervical origin. Arch Phys Med Rehabil 46. Palmgren PJ, Sandström PJ, Lundqvist FJ, et al. Improvement after
1996;779:874–82. chiropractic care in cervicocephalic kinesthetic sensibility and sub-
34. Karlberg M, Persson L, Magnusson M. Impaired postural control jective pain intensity in patients with nontraumatic chronic neck
in patients with cervico-brachial pain. Acta Otolaryngol Suppl pain. J Manipulative Physiol Ther 2006;29(2):100–6.
1995;440–2. 47. Reid S, Rivett D, Katekar M, et al. Sustained natural apophyseal
35. Madeleine P, Prietzel H, Svarrer H, et al. Quantitative posturog- glides (SNAGs) are an effective treatment for cervicogenic dizzi-
raphy in altered sensory conditions: a way to assess balance instabil- ness. Man Ther 2008;13:357–66.
ity in patients with chronic whiplash injury. Arch Phys Med Rehabil 48. Jull G, Falla D, Treleaven J, et al. Retraining cervical joint position
2004;85(3):432–8. sense: the effect of two exercise regimes. J Orthop Res 2007;
36. Michaelson P, Michaelson M, Jaric S, et al. Vertical posture and 25(3):404–12.
head stability in patients with chronic neck. J Rehabil Med 49. Treleaven J, Jull G, LowChoy N. The relationship of cervical joint
2003;35(5):229–35. position error to balance and eye movement disturbances in persis-
37. Poole E, Treleaven J, Jull G. The influence of neck pain on balance tent whiplash. Man Ther 2006;11(2):99–106.
and gait parameters in community dwelling elders. Man Ther 50. Revel M, Andre-Deshays C, Minguet M. Cervicocephalic kines-
2008;13:317–24. thetic sensibility in patients with cervical pain. Arch Phys Med
38. Röijezon U, Björklund M, Djupsjöbacka M. The slow and fast Rehabil 1991;72:288–91.
components of postural sway in chronic neck pain. Man Ther 51. Roren A, Mayoux-Benhamou M, Fayad F, et al. Comparison of
2011;16(3):273–8. visual and ultrasound based techniques to measure head reposition-
39. Sjöström HJ, Allum J, Carpenter MG, et al. Trunk sway measures ing in healthy and neck-pain subjects. Man Ther 2008;14(3):270–7.
of postural stability during clinical balance tests in patients with 52. Pereira M, Beaudin C, Gurbans G, et al. Cervical movement sense:
chronic whiplash injury symptoms. Spine 2003;28(15):1725–34. a proposed clinical tool. J Eval Clin Pract, Under Review.
40. Treleaven J, Jull G, Low Choy N. Standing balance in persistent 53. Röijezon U, Björklund M, Bergenheim M, et al. A novel method
WAD – Comparison between subjects with and without dizziness. for neck coordination exercise – a pilot study on persons with
J Rehabil Med 2005;37(4):224–9. chronic non-specific neck pain. J Neuroengineering Rehabil
41. Treleaven J, Jull G, Murison R, et al. Is the method of signal analy- 2008;5:doi:10.1186/743-0003-5-36.
sis and test selection important for measuring standing balance in 54. Treleaven J, Jull G, Grip H. Head eye co-ordination and gaze
chronic whiplash? Gait Posture 2005;21(4):395–402. stability in subjects with persistent whiplash associated disorders.
42. Stokell R, Lui A, Williams K, et al. Dynamic and functional balance Man Ther 2011;16(3):252–7.
tasks in those with persistent whiplash. Man Ther 2011;16:394–8. 55. Grip H, Jull G, Treleaven J. Head Eye Co-Ordination Using simul-
43. Jull G, Sterling M, Falla D, et al. Whiplash, Headache and Neck taneous measurement of eye in head and head in space movements:
Pain. London: Elsevier; 2008. potential for use in subjects with a whiplash injury. J Clin Monit
44. Fattori B, Borsari C, Vannucci G, et al. Acupuncture treatment for Comput 2009;23(1):31–40.
balance disorders following whiplash injury. Acupunct Electrother 56. Treleaven J, Takasaki H, Grip H, editors. Trunk Had Co-Ordination
Res 1996;21(3–4):207–17. in Neck Pain. Quebec Canada: IFOMPT IFOMPT; 2012.
45. Heikkila H, Johansson M, Wenngren BI. Effects of acupuncture, 57. Yu LJ, Stokell R, Treleaven J. The effect of neck torsion on postural
cervical manipulation and NSAID therapy on dizziness and stability in subjects with persistent whiplash. Man Ther 2011;
impaired head repositioning of suspected cervical origin: a pilot 16(4):339–43.
study. Man Ther 2000;5(3):151–7. 58. Herdman S. Vestibular Rehabilitation. Philadelphia Davis; 2000.

CHAPTER 32.2  ■  SENSORIMOTOR CONTROL OF

LUMBAR SPINE ALIGNMENT
Jaap van Dieën Idsart Kingma Nienke Willigenburg Henri Kiers
● ● ●

MOTOR CONTROL AND LOW BACK PAIN reflects a cause or a consequence of LBP, impaired control
might contribute to recurrence or persistence of LBP.
Clinical guidelines advocate exercise to prevent chronic Overall, the literature on changes in motor behaviour
or recurrent low back pain (LBP)1 and motor control with LBP is rather inconsistent. Evidence for both
training specifically appears to be a mainstay of treat- increased and decreased muscle activity has been pre-
ment. The rationale for this is that inadequate motor sented,22 and for spinal alignment both hyper- and hypo-
control contributes to causation, recurrence and/or per- lordosis have been reported.23–25 In addition, studies have
sistence of LBP. Inadequate motor control could indeed reported increased variability in trunk movement,26,27 but
contribute to LBP, since the lumbar spine is inherently also reduced variability.26,28 Part of this inconsistency
unstable2 and, consequently, loss of control over spinal could be due to competing effects of pain and associated
alignment might cause noxious tissue loading.3,4 If this impairments on one hand and secondary adaptations on
occurs repeatedly, it may cause ‘wear-and-tear’ of tissues, the other hand. More specifically, decreased muscle activ-
injury and inflammation. Conditions such as decreased ity and increased variability could be associated with
segmental stiffness3–6 due to injury or degeneration,7,8 pain-related inhibition and nociceptive interference with
respiratory challenges,9,10 dual tasking,11 ligament creep the control, while increased muscle activity and reduced
after sustained trunk bending12 and trunk muscle variability could be consequences of so-called guarding
fatigue14–17 increase the probability of a loss of control behaviour. Guarding behaviour refers to a strategy of
over lumbar alignment. stiffening the spine by adapted muscle recruitment, pos-
Athletes with reduced control over spinal motion after sibly to compensate for a lack of control over spinal
sudden perturbations have a higher chance of developing motion.29 Such behaviour might prevent loss of control
LBP.17 Similarly, individuals with LBP from the general and consequent tissue irritation. However, in spite of the
population display impaired control.18–21 Whether this relatively low increase in muscle activation involved, this
316 PART III  Advances in Clinical Science and Practice

may come at the cost of increased muscle fatigue30 and in a particular direction. This difference in drift disap-
increased compression on the spine,31–33 while reduced pears when subjects frequently observe an indication of
motor variability may cause more stereotypical loading their trunk orientation on a computer screen,43 indicat-
patterns. The low variance in motor behaviour could also ing that it is not a motor problem causing the reduced
hamper behavioural flexibility and re-learning of trunk precision in maintaining a static trunk posture with LBP,
control.34 Guarding behaviour, while primarily adaptive, but rather, a sensory problem – a problem in detecting
might therefore in the long term contribute to persis- slow drift. Basic neurophysiological studies have shown
tence of pain.22,35–37 that pain may negatively affect proprioceptive informa-
While a role of motor control impairments in causa- tion from muscle spindles44 and the slow drift in thorax
tion and recurrence of LBP is plausible, current therapies orientation observed was reminiscent of that seen in
aimed at enhancing motor control show only limited healthy subjects during stimulation of paraspinal muscle
effect sizes.38 This may indicate that motor control spindles.39 Furthermore, in spite of inconsistent evi-
impairments are not the main problem in all patients with dence,45–51 proprioception appears affected at least in
LBP, such that only a subgroup of patients will benefit some patients with LBP.52–62
from motor control training, or that the content of these Combined, the above observations suggest that
interventions is sub-optimal. Therefore, more insight in impaired sensorimotor control in patients with LBP may
to the nature of motor control impairments in LBP is be due to a proprioceptive impairment. If so, the differ-
needed. To this end, recent studies have focused on ence between patients and controls would be expected to
sensory feedback in spinal control and the implications decrease when muscle vibration is applied, since it would
of these studies will be discussed in the subsequent have more of an effect in controls than in patients.
paragraphs. Although vibration negatively affects the precision of
trunk control in both patients and controls, without such
an interaction effect43 a stronger response to paraverte-
SENSORIMOTOR CONTROL OF bral muscle vibration was observed in patients compared
THE LUMBAR SPINE to controls when visual information was removed.42
Further evidence for a proprioceptive impairment in
The lumbar spine is controlled by means of intrinsic LBP was found when subjects were asked to perform a
stiffness and damping resulting from spinal passive tissues task which challenges control over lumbar spine move-
and active trunk musculature. Intrinsic stiffness and ments.63 When asked to make slow, spiral-like thorax
damping can be enhanced by increasing co-activation of movements tracking a target moving in the frontal and
agonistic and antagonistic muscles. In addition, several sagittal planes, subjects with LBP were less precise in
feedback mechanisms contribute to spinal control. tracking the target. When paravertebral muscle vibration
The effect of visual feedback appears limited, both in was applied, performance of the healthy controls
the anteroposterior direction39 and the mediolateral decreased to the level of the patients, while performance
direction.69 However, effects of visual manipulations on in patients was unaffected. Taken together, these results
spinal control40 and of closing the eyes when balancing indicate that a proprioceptive impairment is present in
on an unstable surface41 indicate that, depending on the LBP, which negatively affects trunk control when insuf-
context, the contribution of visual feedback can be more ficiently compensated by other sensory modalities.
pronounced. Vestibular feedback strongly affects spinal Proprioceptive impairments in spinal control may
control, both in the anteroposterior39 and in the medio- have effects on balance control. This could be relevant
lateral direction40 and has an even greater effect in seated for recurrence and persistence of LBP, since recovery
balancing on an unstable chair.69 Tactile information, reactions after balance loss are associated with high trunk
through contact with a stationary object with minimal loading.64,65
force involved, whether at the hand or the trunk, reduces To assess whether proprioceptive impairments in LBP
trunk sway39 and contact with a moving object increases affect balance control, LBP patients and controls were
trunk sway.69 Finally, proprioceptive feedback, specifi- tested while sitting as still as possible on a chair mounted
cally from muscle spindles in the paravertebral muscula- on a hemisphere, requiring the participants to use trunk
ture, strongly affects trunk posture. This has been movements to maintain balance. Muscle vibration
demonstrated by exciting muscle spindles through induced a slight but similar deterioration of balance
mechanical vibration, with bilateral stimulation leading performance in both groups, whilst closing the eyes led
to an illusion of trunk movement and compensatory to a large but again similar deterioration of balance
responses in the anteroposterior direction39,42 and unilat- performance in both groups.41 Finally, the effects of LBP
eral stimulation leading to responses in the mediolateral were small and inconsistent.41,66–68 Effects of LBP and
direction.69 vibration in this task are thus quite subtle. In retrospect,
this finding may not be that surprising. The main chal-
lenge in the task is to maintain a vertical orientation.
SENSORIMOTOR CONTROL Given the nature of this task, proprioceptive feedback
IN LOW BACK PAIN does not provide information on the orientation relative
to gravity – with the seat tilted one way and the thorax
When sitting in a relaxed upright posture, individuals the other way a vertical orientation may still be present.
with LBP drift more from their starting position than In line with this, an experiment on healthy subjects
healthy controls,43 without a general preference for drift showed that the effect of paravertebral muscle
 32  Management of the Sensorimotor System 317

stimulation is substantially reduced when sitting on an expensive instrumentation. A promising approach, which
unstable versus a stable chair, while the effects of visual needs further research, would be to test vibration effects
and vestibular manipulations are strongly increased.69 on trunk control as described above.
While these data suggest that the proprioceptive
impairments in LBP do not substantially affect the
ability to control balance through trunk movement, MANAGEMENT OF SENSORIMOTOR
LBP has been associated with adverse changes in balance CONTROL IN LBP
control. LBP patients tend to make less use of trunk
movements in control of standing balance, which renders The results described above raise the question whether
them less effective in challenging conditions,70,71 placing trunk proprioception can be improved via intervention.
them at increased risk of falling.72,73 Most likely this Spinal mobilization appears to have a small positive effect
is a consequence of guarding behaviour that stiffens in this respect.75 Balancing exercises, such as those using
the spine.70,71 a ‘Swiss ball’, are popular and are often referred to as
Studies on trunk control reviewed above assessed per- proprioceptive training. However, given the findings
formance mostly in terms of thorax orientation. Visual, regarding sensory manipulations in balancing described
vestibular and tactile compensations for proprioceptive above, it would seem that this is not appropriate. Perhaps
impairments are not likely to be as effective for control- these exercises teach patients to use vestibular and/or
ling lumbar alignment as they are for thorax orientation, visual information more effectively, to enhance trunk
since lumbar alignment is only observable by means of control by compensating for a proprioceptive impair-
proprioceptive information. Therefore, proprioceptive ment. For cervical disorders, training repositioning, first
impairments may be even more important in relation to under visual, augmented feedback, later without feed-
LBP than suggested by these measurements. back, has been used with positive effects on propriocep-
In conclusion, precision of trunk control in relatively tion.76 In clinical practice, manually guided lumbar
simple, low-intensity tasks may be reduced in individuals movement appears to be used to the same end. In addi-
with LBP. This appears to be due to a proprioceptive tion, exposure to whole-body vibration did yield a short-
impairment rather than a motor impairment. Impaired term effect on trunk repositioning in healthy subjects.77
proprioceptive feedback might also cause patients with However, these approaches have not been investigated
LBP to adopt habitual sitting and standing postures in LBP. Other training modalities, such as those that
towards either extreme of the range of motion. Adaptive, focus on precise control like the tracking task described
guarding behaviour may compensate for sensorimotor above, on isolated control of single trunk muscles78,79
impairments. This may be positive, because of its initial or on sensory discrimination80,81 may have positive effects
benefits, or negative because of its long-term costs. on proprioception.
Finally, the benefit of improving proprioception or the
use of proprioceptive feedback on prevention of persis-
ASSESSMENT OF SENSORIMOTOR tence and recurrence of LBP remains to be proven.
CONTROL IN LOW BACK PAIN
The effect of impaired proprioception on the quality
of trunk control is context-dependent. Reduced preci- REFERENCES
sion of trunk control in LBP patients is not necessarily 1. Pillastrini P, Gardenghi I, Bonetti F, et al. An updated overview of
reflected in tasks that do not require maximum preci- clinical guidelines for chronic low back pain management in
primary care. Joint Bone Spine 2012;79:176–85.
sion. In contrast, guarding behaviour may result in 2. Crisco JJ, Panjabi MM. Euler stability of the human ligamentous
decreased movement variability compared to that in spine. Part II Experiment. Clin Biomech (Bristol, Avon) 1992;7:
healthy controls. These are important considerations 27–32.
when diagnosing sensorimotor control impairment in 3. Panjabi MM. The stabilizing system of the spine. Part I. Function,
dysfunction, adaptation, and enhancement. J Spinal Disord 1992;
LBP patients. 5:383–9, discussion 97.
There is no accepted clinical test to assess lumbar 4. Panjabi MM. The stabilizing system of the spine. Part II.
proprioception. In research, it is usually measured by Neutral zone and instability hypothesis. J Spinal Disord 1992;5:
repositioning (i.e. the subject moves from neutral to a 390–7.
given pelvis or thorax inclination, moves back to neutral 5. Cholewicki J, Panjabi MM, Khachatryan A. Stabilizing function of
trunk flexor-extensor muscles around a neutral spine posture. Spine
and subsequently is asked to move back again to what he 1997;22:2207–12.
or she assumes is the same posture).45,47–50,52–56,58–61 Differ- 6. van Dieën JH, Kingma I. Spine function and low back pain: interac-
ences between this posture and the target posture are tions of passive and active tissues. In: Hodges PW, Cholewicki J,
measured. Such a test requires minimal instrumentation, van Dieën JH, editors. Spinal Control: The Rehabilitation of Back
Pain State of the Art and Science. 1st ed. Edinburgh: Churchill
(e.g. an inclinometer or goniometer). The reliability of Livingstone; 2013. p. 41–58.
these measurements appears to be sufficient for individ- 7. Quint U, Wilke HJ. Grading of degenerative disk disease and
ual assessment, provided that errors are averaged over six functional impairment: imaging versus patho-anatomical findings.
or more repeated trials.60,74 However, the effects of Eur Spine J 2008;17:1705–13.
memory and the fact that a conscious perception is tested 8. Zhao FD, Pollintine P, Hole BD, et al. Discogenic origins of spinal
instability. Spine 2005;30:2621–30.
could threaten the validity of this test. Moreover, norma- 9. McGill SM, Sharratt MT, Seguin JP. Loads on spinal tissues during
tive data are not available. Alternatively, movement simultaneous lifting and ventilatory challenge. Appl Ergon 1995;
detection tests have been used,46,57,62 but these require 38:1772–92.
318 PART III  Advances in Clinical Science and Practice

10. Hodges PW, Heijnen I, Gandevia SC. Postural activity of the 34. Moseley GL, Hodges PW. Reduced variability of postural strategy
diaphragm is reduced in humans when respiratory demand prevents normalization of motor changes induced by back pain: a
increases. J Physiol 2001;37:99–1008. risk factor for chronic trouble? Behav Neurosci 2006;120:474–6.
11. Brereton LC, McGill SM. Effects of physical fatigue and cognitive 35. van Dieën JH, Moseley GL, Hodges PW. Motor control changes
challenges on the potential for low back injury. Hum Mov Sci and low back pain: cause or effect? In: Hodges PW, Cholewicki J,
1999;18:839–57. van Dieën JH, editors. Spinal Control: The Rehabilitation of Back
12. Sanchez-Zuriaga D, Adams MA, Dolan P. Is activation of the back Pain State of the Art and Science. 1st ed. Edinburgh: Churchill
muscles impaired by creep or muscle fatigue? Spine 2010;35: Livingstone; 2013. p. 207–18.
517–25. 36. van Dieën JH. Low-back pain and motor behavior: contingent
13. van Dieen JH. Asymmetry of erector spinae muscle activity in adaptations, a common goal. In: 6th Interdisciplinary World Con-
twisted postures and consistency of muscle activation patterns gress on Low Back and Pelvic Pain. Barcelona: 2007.
across subjects. Spine (Phila Pa 1976) 1996;21:2651–61. 37. Hodges PW, Tucker K. Moving differently in pain: a new theory
14. van Dieen JH, Luger T, van der Eb J. Effects of fatigue on to explain the adaptation to pain. Pain 2011;152:S90–8.
trunk stability in elite gymnasts. Eur J Appl Physiol 2012;112: 38. Macedo LG, Maher CG, Latimer J, et al. Motor control exercise
1307–13. for persistent, nonspecific low back pain: a systematic review. Phys
15. van Dieen JH, van der Burg P, Raaijmakers TA, et al. Effects of Ther 2009;89:9–25.
repetitive lifting on kinematics: inadequate anticipatory control or 39. Maaswinkel E, Veeger HEJ, van Dieen JH. Interactions of touch
adaptive changes? J Mot Behav 1998;30:20–32. feedback with muscle vibration and galvanic vestibular stimulation
16. Granata KP, Gottipati P. Fatigue influences the dynamic stability in the control of trunk posture. Gait Posture 2013.
of the torso. Appl Ergon 2008;51:1258–71. 40. Goodworth AD, Peterka RJ. Contribution of sensorimotor integra-
17. Cholewicki J, Silfies SP, Shah RA, et al. Delayed trunk muscle reflex tion to spinal stabilization in humans. J Neurophysiol 2009;
responses increase the risk of low back injuries. Spine 2005; 102:496–512.
30:2614–20. 41. Willigenburg NW, Kingma I, van Dieen JH. Center of pressure
18. Alexiev AR. Some differences of the electromyographic erector trajectories, trunk kinematics and trunk muscle activation during
spinae activity between normal subjects and low back pain patients unstable sitting in low back pain patients. Gait Posture 2013;
during the generation of isometric trunk torque. Electromyogr 38:625–30.
Clin Neurophysiol 1994;34:495–9. 42. Claeys K, Brumagne S, Dankaerts W, et al. Decreased variability
19. Magnusson ML, Aleksiev AR, Wilder DG, et al. Unexpected load in postural control strategies in young people with non-specific low
and asymmetric posture as etiologic factors in low back pain. Eur back pain is associated with altered proprioceptive reweighting. Eur
Spine J 1996;5:23–35. J Appl Physiol 2011;111:115–23.
20. Radebold A, Cholewicki J, Panjabi MM, et al. Muscle response 43. Willigenburg NW, Kingma I, van Dieen JH. Precision control of
pattern to sudden trunk loading in healthy individuals and in an upright trunk posture in low back pain patients. Clin Biomech
patients with chronic low back pain. Spine 2000;25:947–54. (Bristol, Avon) 2012;27:866–71.
21. Reeves NP, Cholewicki J, Milner TE. Muscle reflex classification 44. Thunberg J, Ljubisavljevic M, Djupsjöbacka M, et al. Effects on
of low-back pain. J Electromyogr Kinesiol 2005;15:53–60. the fusimotor-muscle spindle system induced by intramuscular
22. van Dieen JH, Selen LP, Cholewicki J. Trunk muscle activation in injections of hypertonic saline. Exp Brain Res 2002;142:319–26.
low-back pain patients, an analysis of the literature. J Electromyogr 45. Asell M, Sjölander P, Kerschbaumer H, et al. Are lumbar reposi-
Kinesiol 2003;13:333–51. tioning errors larger among patients with chronic low back pain
23. Evcik D, Yucel A. Lumbar lordosis in acute and chronic low back compared with asymptomatic subjects? Arch Phys Med Rehabil
pain patients. Rheumatol Int 2003;23:163–5. 2006;87:1170–6.
24. Harrison DD, Cailliet R, Janik TJ, et al. Elliptical modeling of the 46. Silfies SP, Cholewicki J, Reeves NP, et al. Lumbar position sense
sagittal lumbar lordosis and segmental rotation angles as a method and the risk of low back injuries in college athletes: a prospective
to discriminate between normal and low back pain subjects. J Spinal cohort study. BMC Musculoskelet Disord 2007;8.
Disord 1998;11:430–9. 47. Descarreaux M, Blouin JS, Teasdale N. Repositioning accuracy and
25. Dankaerts W, O’Sullivan P, Burnett A, et  al. Differences in movement parameters in low back pain subjects and healthy control
sitting postures are associated with nonspecific chronic low back subjects. Eur Spine J 2005;14:185–91.
pain disorders when patients are subclassified. Spine 2006;31: 48. Koumantakis GA, Winstanley J, Oldham JA. Thoracolumbar pro-
698–704. prioception in individuals with and without low back pain: intra-
26. Lamoth CJ, Meijer OG, Daffertshofer A, et al. Effects of chronic tester reliability, clinical applicability, and validity. J Orthop Sports
low back pain on trunk coordination and back muscle activity Phys Ther 2002;32:327–35.
during walking: changes in motor control. Eur Spine J 2006; 49. Lam SSK, Jull G, Treleaven J. Lumbar spine kinesthesia in patients
15:23–40. with low back pain. J Orthop Sports Phys Ther 1999;29:294–9.
27. Vogt L, Pfeifer K, Portscher M, et al. Influences of nonspecific low 50. Newcomer K, Laskowski ER, Yu B, et al. Repositioning error in
back pain on three-dimensional lumbar spine kinematics in loco- low back pain. Comparing trunk repositioning error in subjects
motion. Spine 2001;26:1910–19. with chronic low back pain and control subjects. Spine 2000;
28. van den Hoorn W, Bruijn SM, Meijer OG, et al. Mechanical cou- 25:245–50.
pling between transverse plane pelvis and thorax rotations during 51. Hobbs AJ, Adams RD, Shirley D, et al. Comparison of lumbar
gait is higher in people with low back pain. J Biomech 2012; proprioception as measured in unrestrained standing in individuals
45:342–7. with disc replacement, with low back pain and without low back
29. van Dieen JH, Cholewicki J, Radebold A. Trunk muscle recruit- pain. J Orthop Sports Phys Ther 2010;40:439–46.
ment patterns in patients with low back pain enhance the stability 52. Brumagne S, Lysens R, Spaepen A. Lumbosacral position sense
of the lumbar spine. Spine (Phila Pa 1976) 2003;28:834–41. during pelvic tilting in men and women without low back pain: test
30. van Dieen JH, Westebring-van der Putten EP, Kingma I, et al. development and reliability assessment. J Orthop Sports Phys Ther
Low-level activity of the trunk extensor muscles causes electromyo- 1999;29:345–51.
graphic manifestations of fatigue in absence of decreased oxygen- 53. Brumagne S, Cordo P, Lysens R, et al. The role of paraspinal muscle
ation. J Electromyogr Kinesiol 2009;19:398–406. spindles in lumbosacral position sense in individuals with and
31. Marras WS, Davis KG, Ferguson SA, et al. Spine loading charac- without low back pain. Spine (Phila Pa 1976) 2000;25:989–94.
teristics of patients with low back pain compared with asymptom- 54. Newcomer KL, Laskowski ER, Yu B, et al. Differences in reposi-
atic individuals. Spine 2001;26:2566–74. tioning error among patients with low back pain compared with
32. Marras WS, Ferguson SA, Burr D, et al. Spine loading in patients control subjects. Spine 2000;25:2488–93.
with low back pain during asymmetric lifting exertions. Spine J 55. O’Sullivan PB, Burnett A, Floyd AN, et al. Lumbar repositioning
2004;4:64–75. deficit in a specific low back pain population. Spine 2003;
33. Healey EL, Fowler NE, Burden AM, et al. Raised paraspinal 28:1074–9.
muscle activity reduces rate of stature recovery after loaded exercise 56. Gill KP, Callaghan MJ. The measurement of lumbar propriocep-
in individuals with chronic low back pain. Arch Phys Med Rehabil tion in individuals with and without low back pain. Spine
2005;86:710–15. 1998;23:371–7.
 32  Management of the Sensorimotor System 319

57. Lee AS, Cholewicki J, Reeves NP, et al. Comparison of trunk pro- 70. Mok NW, Brauer SG, Hodges PW. Hip strategy for balance
prioception between patients with low back pain and healthy con- control in quiet standing is reduced in people with low back pain.
trols. Arch Phys Med Rehabil 2010;91:1327–31. Spine (Phila Pa 1976) 2004;29:E107–12.
58. Georgy E. Lumbar repositioning accuracy as a measure of proprio- 71. Mok NW, Brauer SG, Hodges PW. Changes in lumbar movement
ception in patients with back dysfunction and healthy controls. in people with low back pain are related to compromised balance.
Asian Spine J 2011;5:201–7. Spine (Phila Pa 1976) 2011;36:E45–52.
59. Astfalck RG, O’Sullivan PB, Smith AJ, et al. Lumbar spine reposi- 72. Lee WK, Kong KA, Park H. Effect of preexisting musculoskeletal
tioning sense in adolescents with and without non-specific chronic diseases on the 1-year incidence of fall-related injuries. J Prev Med
low back pain – an analysis based on sub-classification and spinal Public Health 2012;45:283–90.
regions. Man Ther 2013;18:410–17. 73. Muraki S, Akune T, Oka H, et al. Prevalence of falls and the asso-
60. Hidalgo B, Gobert F, Bragard D, et al. Effects of proprioceptive ciation with knee osteoarthritis and lumbar spondylosis as well as
disruption on lumbar spine repositioning error in a trunk forward knee and lower back pain in Japanese men and women. Arthritis
bending task. J Back Musculoskelet Rehabil 2013;26:381–7. Care Res 2011;63:1425–31.
61. Olivier B, Stewart AV, McKinon W. Injury and lumbar reposition 74. Allison GT, Fukushima S. Estimating three-dimensional spinal
sense in cricket pace bowlers in neutral and pace bowling specific repositioning error: the impact of range, posture, and number of
body positions. Spine J 2013. trials. Spine 2003;28:2510–16.
62. Taimela S, Kankaanpaa M, Luoto S. The effect of lumbar fatigue 75. Learman KE, Myers JB, Lephart SM, et al. Effects of spinal manip-
on the ability to sense a change in lumbar position – A controlled ulation on trunk proprioception in subjects with chronic low back
study. Spine 1999;24:1322–7. pain during symptom remission. J Manipulative Physiol Ther
63. Willigenburg NW, Kingma I, Hoozemans MJ. van Dieen JH. Pre- 2009;32:118–26.
cision control of trunk movement in low back pain patients. Hum 76. Jull G, Falla D, Treleaven J, et al. Retraining cervical joint position
Mov Sci 2013;32:228–39. sense: the effect of two exercise regimes. J Orthop Res
64. van der Burg JC, Pijnappels M, van Dieen JH. Out-of-plane trunk 2007;25:404–12.
movements and trunk muscle activity after a trip during walking. 77. Fontana TL, Richardson CA, Stanton WR. The effect of weight-
Exp Brain Res 2005;165:407–12. bearing exercise with low frequency, whole body vibration on lum-
65. Oddsson LIE, Persson T, Cresswell AG, et al. Interaction between bosacral proprioception: a pilot study on normal subjects. Aust J
voluntary and postural motor commands during perturbed lifting. Physiother 2005;51:259–63.
Spine 1999;24:545–52. 78. Tsao H, Hodges PW. Immediate changes in feedforward postural
66. Radebold A, Cholewicki J, Polzhofer GK, et al. Impaired postural adjustments following voluntary motor training. Exp Brain Res
control of the lumbar spine is associated with delayed muscle 2007;181:537–46.
response times in patients with chronic idiopathic low back pain. 79. Tsao H, Hodges PW. Persistence of improvements in postural
Spine 2001;26:724–30. strategies following motor control training in people with recurrent
67. van Dieen JH, Koppes LL, Twisk JW. Low back pain history and low back pain. J Electromyogr Kinesiol 2008;18:559–67.
postural sway in unstable sitting. Spine (Phila Pa 1976) 2010;35: 80. Wand BM, Abbaszadeh S, Smith AJ, et al. Acupuncture applied as
812–17. a sensory discrimination training tool decreases movement-related
68. Van Daele U, Hagman F, Truijen S, et al. Decrease in postural sway pain in patients with chronic low back pain more than acupuncture
and trunk stiffness during cognitive dual-task in nonspecific chronic alone: a randomised cross-over experiment. Br J Sports Med
low back pain patients, performance compared to healthy control 2013;47:1085–9.
subjects. Spine (Phila Pa 1976) 2010;35:583–9. 81. Luomajoki H, Moseley GL. Tactile acuity and lumbopelvic motor
69. Andreopoulou G, Maaswinkel E, Cofre Lizama LE, et al. Effects control in patients with back pain and healthy controls. Br J Sports
of support surface stability on feedback control of trunk posture. Med 2011;45:437–40.
Exp Brain Res 2015;doi:10.1007/s00221-014-4185-5.

CHAPTER 32.3  ■  THE LOWER LIMB

Nicholas Clark Scott Lephart
●

cartilage, ligament, nerve) from potentially injurious

INTRODUCTION tensile, compressive and torsional forces. In order to
develop effective clinical management strategies for the
Normal human movement depends on effective senso- sensorimotor system it is necessary to review the senso-
rimotor control. Sensorimotor control refers to central rimotor system and consider how it is affected by mus-
nervous system (CNS) regulation of joint stability, posture culoskeletal injury. Findings from research will be
and movement,1,2 operating on a ‘sensory motor’ basis presented and translated to the clinical context in a way
where sensory input to the CNS is first required in order that provides a sound scientific foundation for rational
to generate effective motor output from the CNS.3,4 Sen- clinical interventions that beneficially affect lower limb
sorimotor control is achieved by the sensorimotor system sensorimotor control.
which includes all components involved in the acquisition
of a sensory stimulus and its transmission to the CNS,
the processing of that sensory stimulus within the CNS, BRIEF REVIEW OF THE
and the resulting motor output from the CNS.5 From a SENSORIMOTOR SYSTEM
lower limb injury prevention and rehabilitation perspec-
tive, the sensorimotor system is predominantly employed The sensorimotor system is composed of sensory,
for optimizing joint stability.6–8 Joint stability refers to the processing (CNS), and motor components.1,5 The
ability of a joint to remain in or promptly return to sensory component refers to afferent pathways that
proper alignment and functional position.1 The primary include the sensory nerve ending, the sensory nerve
role of sensorimotor control of joint stability is to activate fibre, the afferent synapses and interneurons and the
muscle to stress-shield non-contractile tissues (bone, ascending tracts; the processing component refers to
320 PART III  Advances in Clinical Science and Practice

all elements within the CNS (spinal cord, brain stem interventions can then be selected for each component of
and cerebral cortex); the motor component refers to the sensorimotor system. Lower limb joint injury fre-
efferent pathways that include an upper motor neuron, quently results in destruction of mechanoreceptors.24,25
the efferent synapses and interneurons, the descending Loss of capsuloligamentous mechanoreceptors is consis-
tracts, the lower motor neuron and the motor end tently associated with impaired proprioception26–29 and
plates.1,5 The components of the sensorimotor system altered processing and organization of the somatosensory
are integrated to control coordinated activation of the cortex.30–32 Unilateral joint injury can manifest with an
skeletal muscles (dynamic restraints) to optimize joint inability to fully activate peri-articular musculature.33–35
stability.1,5 Appropriate sensorimotor control of joint Altered ipsilateral muscle activation patterns local to the
stability and coordination of the dynamic restraints injury site36,37 and remote from the injury site38 can be
ultimately manifests with normal postural stability, evident. Unilateral joint injury can manifest bilateral pro-
kinematics and kinetics during human movement. prioceptive deficits39,40 and inability to fully activate
Understanding the individual components of the sen- muscles contralateral to the injured side.35,41,42 Pain can
sorimotor system, and the way in which the compo- result in impaired proprioception,43,44 muscle inhibi-
nents are configured and integrated, allows the clinician tion,45,46 altered inter-muscular firing patterns47,48 and
to plan interventions that are targeted at one or more reduced muscle strength.45,49 Joint effusion is also associ-
components of the system. ated with impaired proprioception50 and muscle inhibi-
tion.14,51,52 Since musculoskeletal injury affects all
components of the sensorimotor system, it is not surpris-
THE SENSORY COMPONENT OF THE ing that lower limb musculoskeletal injury, pain and effu-
SENSORIMOTOR SYSTEM sion manifest with altered postural stability53–55 and
altered kinematics and kinetics during functional
The sensory component of the sensorimotor system tasks.51,56–58 Lower limb joint injury is not limited to the
includes the visual, vestibular, tactile, thermal, nocicep- musculoskeletal system and, therefore, should also be
tive and proprioceptive systems.1 Of these, the proprio- considered a neurological problem. Unilateral joint
ceptive system is most important with regard to joint injury can manifest ipsilateral motor dysfunction remote
stability, posture and movement.1,3 Proprioception is from the injury site. Furthermore, unilateral joint injury
composed of the senses of joint position (joint position does not limit its effects to one side of the body but also
sense), joint motion (kinaesthesia) and force (force extends its influence to the contralateral side. Because of
sense).1,9 Proprioception results from mechanoreceptor the potentially widespread effects of apparently isolated
stimulation in the musculoskeletal tissues.10,11 A mecha- joint injury, clinicians should extend management of the
noreceptor is a specialized sensory nerve ending stimu- sensorimotor system beyond the local site and side of
lated by mechanical deformation: mechanical deformation injury.
is converted into electrical signals that are transmitted to
the CNS.9,12 Mechanoreceptors in the non-contractile
tissues of joints include Ruffini, Pacinian and Golgi
endings.13–20 Joint tissues, therefore, fulfil neurological as MANUAL THERAPY AND THE
well as mechanical functions.12,14 Mechanoreceptors in SENSORIMOTOR SYSTEM
skeletal muscles include muscle spindles and Golgi
tendon organs.4,21,22 Different musculoskeletal tissues are This section will focus on lower limb joint manual therapy
thus innervated with different mechanoreceptor nerve in the form of mobilizations and manipulations. Mobili-
endings. Joint and muscle mechanoreceptors have differ- zations and manipulations are passive movements of a
ent functional properties due to different stimulus thresh- patient’s joint, performed by the clinician, and primarily
olds and adaptation characteristics and, consequently, used to improve joint mobility by reducing pain, mobiliz-
different stimulation (intervention) techniques are needed ing intracapsular fluid, and stretching capsuloligamen-
(Table 32-3). Joint and muscle tissues can be targeted tous tissues.59–62 Pain neurons and proprioceptor neurons
with a variety of manual and exercise therapy techniques synapse in the dorsal horn of the spinal cord with shared
to deliberately induce mechanoreceptor stimulation and ascending tracts that convey sensory information to
proprioceptive feedback to the CNS. The clinician can, supraspinal levels.63 Stimulation of mechanoreceptor
therefore, use specific intervention techniques to access neurons activates an inhibitory interneuron that blocks
the sensorimotor system to beneficially affect senso­ the transmission of nociceptor impulses to higher CNS
rimotor control of joint stability, posture and human nuclei: this is the pain gate mechanism.63,64 Manual
movement. therapy can use capsuloligamentous mechanoreceptor
stimulation to block the inhibitory effects of pain on the
sensorimotor system. Specific joint mobilization tech-
EFFECTS OF INJURY ON THE niques are reported effective for immediately reducing
SENSORIMOTOR SYSTEM knee and ankle pain.65,66 Passive movement of peripheral
joints causes intrasynovial fluid movement67 and increased
To administer effective interventions for the sensorimo- lymphatic drainage,68,69 and both are desirable to decrease
tor system it is important to know how the system can be joint effusions. Manual therapy can be administered to
affected by musculoskeletal injury. When the effects facilitate clearance of excessive intrasynovial fluid, reverse
of musculoskeletal injury are recognized, effective effusion-induced inhibition of the sensorimotor system,


TABLE 32-3  Example Intervention Techniques to Stimulate Mechanoreceptors in Different Lower Limb Musculoskeletal
and Cutaneous Tissues
Joint Manual Taping/Bracing Active Examples
Mechanoreceptor Predominant Stimulation Adaptation Proprioception Therapy Technique Technique Therapy Mode
Tissue Nerve Ending Stimulation Type Threshold Characteristic Sub-Modality Examples Exercise Examples
Capsule Ruffini ending Tension Low Slow JPS/kinaesthesia Sustained – Dynamic > static
mobilization exercises
Golgi ending Tension High Slow Kinaesthesia Intermittent – Dynamic
mobilizations exercises
Ligament Ruffini ending Tension Low Slow JPS/kinaesthesia Sustained – Dynamic > static
mobilization exercises
Pacinian ending Tension/ Low Fast Kinaesthesia Intermittent – Dynamic
compression mobilizations exercises
Golgi ending Tension High Slow Kinaesthesia Intermittent – Dynamic
mobilizations exercises
Meniscus/ Ruffini ending Tension Low Slow JPS/kinaesthesia Sustained – Dynamic > static
Labrum mobilization exercises
Pacinian ending Tension/ Low Fast Kinaesthesia Intermittent – Dynamic
compression mobilizations exercises
Golgi ending Tension High Slow Kinaesthesia Intermittent – Dynamic
mobilizations exercises
Fat pad Pacinian ending Tension/ Low Fast Kinaesthesia – Fat pad taping Dynamic
compression exercises
Fascia Pacinian ending Tension/ Low Fast Kinaesthesia – Fascial taping Dynamic
compression exercises
Skin Hair follicle Flutter, stroking Low Fast – – EB/NS/Taping –
receptor
Merkel disc Pressure/ High Slow Kinaesthesia – EB/NS –
indentation
Meissner Flutter, stroking Low Fast Kinaesthesia – EB/NS –
corpuscle
Ruffini ending Skin tension Low Slow JPS/kinaesthesia – Taping Dynamic
exercises
Pacinian ending Vibration Low Fast Kinaesthesia – – Dynamic
exercises
Muscle Spindle primary Velocity of active Low Fast Kinaesthesia Intermittent – Dynamic > static
length change mobilizations exercises
Spindle Active length Low Fast JPS/kinaesthesia Intermittent – Dynamic > static
secondary mobilizations exercises
Golgi Tendon Active tension High Slow JPS/kinaesthesia/FS – – Dynamic/static
Organ exercises
32  Management of the Sensorimotor System

Mechanoreceptor information from references: 13–15, 18–20, 23.

JPS, Joint position sense; FS, force sense; EB, elastic bandage; NS, neoprene sleeve.
321
322 PART III  Advances in Clinical Science and Practice

and promote reacquisition of normal lower limb

biomechanics.
Capsuloligamentous tissue contains mechanoreceptor
nerve endings and familiarity with sensorimotor system
circuitry is useful for planning interventions to enhance
proprioception. Feline knee studies have reported that
low tensile forces in ligaments strongly stimulate gamma
motor neurons and increase the sensitivity of the muscle
spindle.70–73 More recent studies in humans have described
how tensile loads applied to the ankle ligaments elicit
increased muscle spindle discharge in uninjured and
injured athletes.74 The range of forces applied by manual
therapists during mobilizations and manipulations
include the forces reported capable of stimulating
ligament–muscle spindle circuitry.75–77 Direct stimulation
of capsuloligamentous mechanoreceptors and indirect
stimulation of muscle spindles provides a pathway by
which joint manual therapy can have an effect on pro- FIGURE 32-5  ■  Example of a knee accessory mobilization tech-
nique. (From Kaltenborn 1999.60)
prioceptive feedback to the CNS. Authors have reported
that lower quadrant joint mobilizations and manipula-
tions are able to immediately enhance post-intervention
proprioception.78–80 circuits results in long-term learning due to adaptation
Proprioceptive information is transmitted to higher of neuron structure, increased effectiveness of synaptic
CNS centres by the ascending tracts in the spinal cord.5,81 transmission and modification of CNS somatotopic
Stimulation of the knee ligaments and menisci results maps.96,97
in increased electrical activity in the cerebral cortex.82,83 Joint manual therapy has the potential to affect all
This verifies the human brain can be directly accessed components of the sensorimotor system. Because all
via sensory nerve endings in the periphery and, therefore, components of the sensorimotor system can be affected
joint manual therapy can be used with the intent of by joint mobilizations and manipulations, there is the
stimulating the cerebral cortex. Interventions that stimu- potential for joint manual therapy to have an immediate
late the cerebral cortex are of importance because sensory effect on the performance of functional tasks. Specific
information from cortical sensory nuclei is transmitted lower limb joint mobilizations have been shown to yield
to the premotor and primary motor centres via trans- an immediate positive effect on postural stability and
cortical axons and is important in modifying feedforward dynamic balance98–100 and the kinematics of walking gait
motor programmes and the learning of movement and drop-landing tasks.101,102
patterns.84 Joint manual therapy is capable of reducing pain and
The components of the sensorimotor system are inte- effusion, and positively affecting all components of the
grated to coordinate activation of skeletal muscle to opti- lower limb sensorimotor system. Because joint manual
mize joint stability.5 This requires reflex and voluntary therapy can affect all components of the sensorimotor
activation of extrafusal muscle fibres.1,85 A reflex is a ste- system, it is able to manifest an immediate beneficial
reotyped involuntary muscle response to a sensory stimu- effect in the performance of functional tasks. Joint manual
lus.10 Studies have described reflex activation of the therapy is, therefore, a clinically effective intervention
hamstrings in response to mechanical stimulation of that can be used to help patients prepare for more active
the anterior cruciate ligament,86–88 reflex activation of the rehabilitation in the form of exercise therapy sessions and
medial hamstrings and medial quadriceps in response to the performance of functional movement patterns.
mechanical stimulation of the medial collateral liga-
ment,89,90 and reflex activation of the hamstrings in
response to stimulation of the meniscus.83 These studies TAPING AND BRACING AND THE
indicate specific joint–muscle sensory-motor circuitry is SENSORIMOTOR SYSTEM
hardwired into the human CNS. Sensory-motor circuitry
mediates feedback activation of skeletal muscle to stress- This section will discuss the clinical use of athletic tape,
shield non-contractile tissues: activation is specifically elastic bandages and neoprene sleeves. The skin possesses
directed at muscles that are antagonists to the direction three types of sensory nerve endings: thermoreceptors,
of joint motion and loading perceived by the CNS. nociceptors and mechanoreceptors.9 Superficial cutane-
In the short term, lower quadrant joint mobilization ous mechanoreceptors include hair follicle receptors,
and manipulation techniques have been shown to be Merkel discs and Meissner corpuscles, while deeper sub-
capable of facilitating extrafusal muscle fibre activation cutaneous tissue mechanoreceptors include Pacinian cor-
and increasing muscle strength.91–95 In the long term, puscles and Ruffini endings.4,9,23 Proprioception is
stimulation of sensory-motor neurocircuitry via intermit- predominantly the result of muscle and joint mechano-
tent joint mobilizations (Fig. 32-5) is useful for benefi- receptor stimulation, although cutaneous mechanorecep-
cially affecting sensorimotor control of joint stability tor stimulation also contributes to proprioception due to
because repetitive activation of specific sensory-motor superficial tissue deformation during joint movement.4,9
 32  Management of the Sensorimotor System 323

coordinated activity of the dynamic restraints to optimize

joint stability.8,11 Different training methods elicit differ-
ent sensorimotor control training adaptations, and thor-
ough exercise therapy for lower limb joint injuries must
include several different types of exercise selected within
a clinically reasoned and goal-directed process.122–124
The muscle spindle is the most potent mechanorecep-
tor which is always stimulated with active movements as
a result of alpha-gamma co-activation.4,10 The Golgi
tendon organ is also a potent mechanoreceptor, being
very sensitive to forces generated by active movements.4,10
Any active exercise can, therefore, be considered pro-
prioceptive training since it will generate a barrage of
impulses from muscle mechanoreceptors.122 Open kinetic
chain and closed kinetic chain exercise generate proprio-
ceptive feedback to the CNS,125–127 although closed
kinetic chain exercise results in better proprioception
defined by less error in active joint repositioning
tasks,125,127 and full weight-bearing exercise enhances pro-
prioceptive feedback more than partial weight-bearing
exercise.128 Long-term lower limb strength training,129,130
balance training131,132 and plyometric training133 have all
been reported to significantly improve active measures
of proprioception.
Repeated use of the CNS is necessary to facilitate the
neurological changes necessary for long-term learning of
enhanced sensorimotor control programmes.95,96 Activa-
tion of all components of the sensorimotor system is
FIGURE 32-6  ■  Example of a knee taping technique. (From Cal-
laghan et al. 2002.111)
evident with the short-term active performance of repeti-
tive goal-directed tasks.134,135 Long-term strength and
skill training stimulates spinal and cortical plastic adapta-
The application of athletic tape, elastic bandages or neo- tions that enhance both muscle performance characteris-
prene sleeves can immediately reduce the intensity of tics and the execution of coordinated tasks.136–138
knee pain.103–107 The application of athletic tape can also The sensorimotor system coordinates activation of
immediately enhance proprioception of the ankle108–110 skeletal muscle to optimize joint stability, posture and
and knee,111,112 as can wearing of elastic bandages and movement.1,5 Goal-directed repeated movements result
neoprene sleeves.26,113,114 Furthermore, knee athletic tape in learning new sensorimotor motor control programmes
and neoprene sleeves are able to modulate activity of the and enhanced functional properties of extrafusal muscle
sensorimotor cortex,115,116 and application of athletic tape fibres,95,96,139 which then manifest with changes in pos-
has been reported to enhance lower limb muscle activa- tural stability and the kinematics and kinetics of human
tion characteristics.117–120 Stimulation of the skin, there- movement. Strength training can enhance muscle perfor-
fore, can be an important part of lower limb sensorimotor mance characteristics, postural stability and the kinemat-
system rehabilitation.121 Stimulation of the skin via ath- ics of walking.140–142 Balance and perturbation training
letic tape, elastic bandages and neoprene sleeves is capable can enhance muscle activation patterns, muscle perfor-
of immediately reducing pain and beneficially affecting mance characteristics, postural stability, the kinematics of
all components of the sensorimotor system. Lower limb walking, and the kinematics and kinetics of landing
taping (Fig. 32-6) and bracing is, therefore, a further tasks.52,143–148 Plyometric training can alter muscle activa-
potential intervention that clinicians can employ to help tion patterns, muscle performance characteristics, and
patients prepare for exercise therapy sessions and the the kinematics and kinetics of running and landing
performance of functional movement patterns. tasks.147–151
Exercise therapy integrates all components of the sen-
sorimotor system to generate coordinated activity of skel-
EXERCISE THERAPY AND THE etal muscle. Active exercises (Fig. 32-7) are the most
SENSORIMOTOR SYSTEM effective intervention for stimulating all components of
the sensorimotor system. A variety of exercise therapy
Exercise therapy refers to repeated movements per- training methods can positively affect proprioception,
formed within structured and goal-directed exercise pro- CNS processing, and the coordination of skeletal muscle
grammes. Repeated movements must be active versus activation. A selection of training methods is required to
passive in order to optimally and simultaneously stimu- induce beneficial changes in lower limb muscle perfor-
late all components of the sensorimotor system. mance, joint stability, postural stability, kinematics and
The objective of exercise therapy is to integrate all com- kinetics due to plastic adaptation in different parts of the
ponents of the sensorimotor system and generate sensorimotor system.
324 PART III  Advances in Clinical Science and Practice

4. Rothwell J. Control of Human Voluntary Movement. 2nd ed.

London: Chapman Hall; 1994.
5. Lephart S, Riemann B, Fu F. Introduction to the sensorimotor
system. In: Lephart S, Fu F, editors. Proprioception and Neuro-
muscular Control in Joint Stability. Illinois: Human Kinetics;
2000. p. xvii–xxiv.
6. Borsa P, Sauers E, Lephart S. Functional training for the restora-
tion of dynamic stability in the PCL-injured knee. J Sport Rehabil
1999;8:362–78.
7. Lephart S, Pincivero D, Rozzi S. Proprioception of the ankle and
knee. Sports Med 1998;25(3):149–55.
8. Swanik C, Lephart S, Giannantonio F, et al. Reestablishing pro-
prioception and neuromuscular control in the ACL-injured
athlete. J Sport Rehabil 1997;6:182–206.
9. Martin J, Jessell T. Modality coding in the somatic sensory
system. In: Kandel E, Schwartz J, Jessell T, editors. Principles
of Neural Science. 3rd ed. London: Prentice-Hall; 1991.
p. 341–52.
10. Gordon J, Ghez C. Muscle receptors and spinal reflexes: the
stretch reflex. In: Kandel E, Schwartz J, Jessell T, editors. Prin-
ciples of Neural Science. 3rd ed. London: Prentice-Hall Interna-
tional; 1991. p. 564–80.
11. Lephart S, Pincivero D, Giraldo J, et al. The role of propriocep-
tion in the management and rehabilitation of athletic injuries. Am
J Sports Med 1997;25(1):130–7.
12. Barrack R, Lund P, Skinner H. Knee joint proprioception revis-
FIGURE 32-7  ■  Example of closed kinetic chain exercise tech- ited. J Sport Rehabil 1994;3(1):18–42.
nique on an unstable base-of-support. 13. Day B, Mackenzie W, Shim S, et al. The vascular and nerve supply
of the human meniscus. Arthroscopy 1985;1(1):58–62.
14. Kennedy J, Alexander I, Hayes K. Nerve supply of the human knee
and its functional importance. Am J Sports Med 1982;10(6):
329–35.
SUMMARY 15. Michelson J, Hutchins C. Mechanoreceptors in human ankle liga-
ments. J Bone Joint Surg Am 1995;77B(2):219.
Normal human movement depends on effective senso- 16. Moraes M, Cavalcante M, Leite J, et al. Histomorphometric
evaluation of mechanoreceptors and free nerve endings in human
rimotor control. Sensorimotor control is achieved by lateral ankle ligaments. Foot Ankle Int 2008;29(1):87–90.
the sensorimotor system which includes sensory, process- 17. Schutte M, Dabezies E, Zimny M, et al. Neural anatomy of the
ing and motor components. All components of the sen- human anterior cruciate ligament. J Bone Joint Surg Am
sorimotor system are affected by lower limb joint injury. 1987;69A(2):243–7.
18. Moraes M, Cavalcante M, Leite J, et al. The characteristics of the
The effects of lower limb joint injury on the sensorimo- mechanoreceptors of the hip with arthrosis. J Orthop Surg Res
tor system can be widespread and extend far beyond the 2011;6:58.
site and side of injury. Joint manual therapy, taping and 19. Freeman M, Wyke B. The innervation of the knee joint. An ana-
bracing can all immediately reduce pain, stimulate the tomical and histological study in the cat. J Anat 1967;101(Pt
sensory (proprioception) and processing (CNS) compo- 3):505–32.
20. Assimakopoulos A, Katonis P, Agapitos M, et  al. The innervation
nents of the sensorimotor system, and enhance lower of the human meniscus. Clin Orthop Relat Res 1992;275:
limb postural stability and kinematics during functional 232–6.
tasks. Joint manual therapy has also been reported to 21. Kararizou E, Manta P, Kalfakis N, et al. Morphometric study of
immediately stimulate motor function defined by the human muscle spindle. Anal Quant Cytol Histol 2005;27(1):
1–4.
increases in muscle strength. An integrated model for 22. Spiro A, Beilin R. Human muscle spindle histochemistry. Arch
clinical management of the lower limb sensorimotor Neurol 1969;20(3):271–5.
system, therefore, includes joint manual therapy, taping 23. Johansson R, Vallbo Å. Tactile sensory coding in the glabrous skin
and bracing as effective interventions employed to help of the human hand. Trends Neurosci 1983;6:27–32.
patients prepare for more active rehabilitation in the 24. Dhillon M, Bali K, Vasistha R. Immunohistological evaluation of
proprioceptive potential of the residual stump of injured anterior
form of exercise therapy and the performance of func- cruciate ligaments (ACL). Int Orthop 2010;34(5):737–41.
tional movement patterns. Exercise therapy can then 25. Bali K, Dhillon M, Vasistha R, et al. Efficacy of immunohistologi-
elicit long-term beneficial adaptations in all components cal methods in detecting functionally viable mechanoreceptors in
of the sensorimotor system that manifest with measurable the remnant stumps of injured anterior cruciate ligaments and its
clinical importance. Knee Surg Sports Traumatol Arthrosc
improvements in lower limb joint stability, postural sta- 2012;20(1):75–80.
bility, kinematics and kinetics. 26. Borsa P, Lephart S, Irrgang J, et al. The effects of joint position
and direction of joint motion on proprioceptive sensibility in ante-
rior cruciate ligament-deficient athletes. Am J Sports Med
REFERENCES 1997;25(3):336–40.
1. Riemann B, Lephart S. The sensorimotor system, part I: the 27. Lephart S, Kocher M, Fu F, et al. Proprioception following ante-
physiologic basis of functional joint stability. J Athl Train rior cruciate ligament reconstruction. J Sport Rehabil 1992;1(3):
2002;37(1):71–9. 188–98.
2. Shumway-Cook A, Woollacott M. Motor Control. Theory and 28. Safran M, Allen A, Lephart S, et al. Proprioception in the poste-
Practical Applications. 2nd ed. Philadelphia: Lippincott; 2001. rior cruciate ligament deficient knee. Knee Surg Sports Traumatol
3. Ghez C. The control of movement. In: Kandel E, Schwartz J, Arthrosc 1999;7(5):310–17.
Jessell T, editors. Principles of Neural Science. 3rd ed. London: 29. Swanik C, Lephart S, Rubash H. Proprioception, kinesthesia, and
Prentice-Hall; 1991. p. 533–47. balance after total knee arthroplasty with cruciate-retaining and
 32  Management of the Sensorimotor System 325

posterior stabilized prostheses. J Bone Joint Surg Am 2004; affects knee joint mechanics during a single-legged drop landing.
86A(2):328–34. Am J Sports Med 2007;35(8):1269–75.
30. Valeriani M, Restuccia D, Di Lazzaro V, et al. Central 52. Stokes M, Young A. The contribution of reflex inhibition to
nervous system modifications in patients with lesion of the arthrogenous muscle weakness. Clin Sci 1984;67(1):7–14.
anterior cruciate ligament of the knee. Brain 1996;119: 53. Rozzi S, Lephart S, Sterner R, et al. Balance training for persons
1751–62. with functionally unstable ankles. J Orthop Sports Phys Ther
31. Valeriani M, Restuccia D, Di Lazzaro V, et al. Clinical and neu- 1999;29(8):478–86.
rophysiological abnormalities before and after reconstruction of 54. Lysholm M, Ledin T, Odkvist L, et al. Postural control – a com-
the anterior cruciate ligament of the knee. Acta Neurol Scand parison between patients with chronic anterior cruciate ligament
1999;99(5):303–7. insufficiency and healthy individuals. Scand J Med Sci Sports
32. Kapreli E, Athanasopoulos S, Gliatis J, et al. Anterior cruciate 1998;8(6):432–8.
ligament deficiency causes brain plasticity: a functional MRI study. 55. Mohammadi F, Salavati M, Akhbari B, et al. Static and dynamic
Am J Sports Med 2009;37(12):2419–26. postural control in competitive athletes after anterior cruciate
33. Konishi Y, Fukubayashi T, Takeshita D. Possible mechanism ligament reconstruction and controls. Knee Surg Sports Trauma-
of quadriceps femoris weakness in patients with ruptured tol Arthrosc 2012;20(8):1603–10.
anterior cruciate ligament. Med Sci Sports Exerc 2002;349: 56. Fontboté C, Sell T, Laudner K, et  al. Neuromuscular and bio-
1414–18. mechanical adaptations of patients with isolated deficiency of the
34. Snyder-Mackler L, De Luca P, Williams P, et al. Reflex inhibition posterior cruciate ligament. Am J Sports Med 2005;33(7):
of the quadriceps femoris muscle after injury or reconstruction of 982–9.
the anterior cruciate ligament. J Bone Joint Surg Am 1994; 57. Seeley M, Park J, King D, et al. A novel experimental knee-pain
76A(4):555–60. model affects perceived pain and movement biomechanics. J Athl
35. Chmielewski T, Stackhouse S, Axe M, et al. A prospective analysis Train 2013;48(3):337–45.
of incidence and severity of quadriceps inhibition in a consecutive 58. Vairo G, Myers J, Sell T, et al. Neuromuscular and biomechanical
sample of 100 patients with complete acute anterior cruciate liga- landing performance subsequent to ipsilateral semitendinosus and
ment rupture. J Orthop Res 2004;22(5):925–30. gracilis autograft anterior cruciate ligament reconstruction. Knee
36. De Mont R, Lephart S, Giraldo J, et  al. Muscle preac- Surg Sports Traumatol Arthrosc 2008;16(1):2–14.
tivity of anterior cruciate ligament-deficient and -reconstructed 59. Hengeveld E, Banks K, Maitland G, et al. Maitland’s Peripheral
females during functional activities. J Athl Train 1999;34(2): Manipulation. Edinburgh: Butterworth-Heinemann; 2005.
115–20. 60. Kaltenborn F. Manual Mobilizations of the Joints: The Kalten-
37. Swanik C, Lephart S, Giraldo J, et al. Reactive muscle firing of born Method of Joint Examination and Treatment. Oslo: Olaf
anterior cruciate ligament-injured females during functional activ- Norlis Bokhandel; 1999.
ities. J Athl Train 1999;34(2):121–9. 61. Mulligan B. Manual Therapy: NAGs, SNAGs, MWMs. Minne-
38. Bullock-Saxton J. Local sensation changes and altered hip muscle apolis: Orthopaedic Physical Therapy Products; 2010.
function following severe ankle sprain. Phys Ther 1994;74(1): 62. Greenman P. Principles of Manual Medicine. Philadelphia: Lip-
17–28. pincott; 2003.
39. Roberts D, Fridén T, Stomberg A, et al. Bilateral proprioceptive 63. Jessell T, Kelly D. Pain and analgesia. In: Kandel E, Schwartz J,
defects in patients with a unilateral anterior cruciate ligament Jessell T, editors. Principles of Neural Science. London: Prentice-
reconstruction: a comparison between patients and healthy indi- Hall; 1991. p. 385–99.
viduals. J Orthop Res 2000;18(4):565–71. 64. Melzack R, Wall P. Pain mechanisms: a new theory. Science
40. Arockiaraj J, Korula R, Oommen A, et al. Proprioceptive changes 1965;150(3699):971–9.
in the contralateral knee joint following anterior cruciate injury. 65. Yeo H, Wright A. Hypoalgesic effect of a passive accessory mobili-
Bone Joint J 2013;95B(2):188–91. sation technique in patients with lateral ankle pain. Man Ther
41. Konishi Y, Konishi H, Fukubayashi T. Gamma loop dysfunction 2011;16(4):373–7.
in quadriceps on the contralateral side in patients with ruptured 66. Moss P, Sluka K, Wright A. The initial effects of knee joint mobi-
ACL. Med Sci Sports Exerc 2003;35(6):897–900. lization on osteoarthritic hyperalgesia. Man Ther 2007;12(2):
42. Urbach D, Nebelung W, Weiler H, et al. Bilateral deficit of vol- 109–18.
untary quadriceps muscle activation after unilateral ACL tear. 67. Pedowitz R, Gershuni D, Crenshaw A, et al. Intraarticular pres-
Med Sci Sports Exerc 1999;31(12):1691–6. sure during continuous passive motion of the human knee.
43. Matre D, Arendt-Neilsen L, Knardahl S. Effects of localization J Orthop Res 1989;7(4):530–7.
and intensity of experimental muscle pain on ankle joint proprio- 68. Ikomi F, Schmid-Schönbein G. Lymph pump mechanics in the
ception. Eur J Pain 2002;6(4):245–60. rabbit hind leg. Am J Physiol 1996;271(1 Pt 2):H173–83.
44. Rossi S, della Volpe R, Ginanneschi F, et al. Early somatosensory 69. McGeown J, McHale N, Thornbury K. The role of external
processing during tonic muscle pain in humans: relation to loss of compression and movement in lymph propulsion in the sheep
proprioception and motor defensive strategies. Clin Neurophysiol hind limb. J Physiol 1987;387:83–93.
2003;114:1351–8. 70. Sojka P, Johansson H, Sjölander P, et al. Fusimotor neurones can
45. Graven-Nielsen T, Lund H, Arendt-Nielsen L, et al. Inhibition be reflexly influenced by activity in receptor afferents from the
of maximal voluntary contraction force by experimental muscle posterior cruciate ligament. Brain Res 1989;483(1):177–83.
pain: a centrally mediated mechanism. Muscle Nerve 2002;26(5): 71. Johansson H, Lorentzon R, Sjölander P, et  al. The anterior cruci-
708–12. ate ligament: a sensor acting on the γ-muscle-spindle systems of
46. Farina D, Arendt-Nielsen L, Merletti R, et al. Effect of experi- muscles around the knee joint. Neuro Orthop 1990;9(1):1–23.
mental muscle pain on motor unit firing rate and conduction 72. Johansson H, Sjölander P, Sojka P. Activity in receptor afferents
velocity. J Neurophysiol 2004;91(3):1250–9. from the anterior cruciate ligament evokes reflex effects on fusi-
47. Graven-Nielsen T, Svensson P, Arendt-Nielsen L. Effects of motor neurones. Neurosci Res 1990;8(1):54–9.
experimental muscle pain on muscle activity and co-ordination 73. Sjölander P, Djupsjöbacka M, Johansson H, et al. Can receptors
during static and dynamic motor function. Electroencephalogr in the collateral ligaments contribute to knee joint stability and
Clin Neurophysiol 1997;105(2):156–64. proprioception via effects on the fusimotor-muscle-spindle
48. Salomoni S, Ejaz A, Laursen A, et al. Variability of three- system? Neuro Orthop 1994;15(2):65–80.
dimensional forces increase during experimental knee pain. Eur J 74. Needle A, Charles BBS, Farquhar W, et al. Muscle spindle traffic
Appl Physiol 2013;113(3):567–75. in functionally unstable ankles during ligamentous stress. J Athl
49. Henriksen M, Rosager S, Aaboe J, et al. Experimental knee pain Train 2013;48(2):192–202.
reduces muscle strength. J Pain 2011;12(4):460–7. 75. Petty N, Maher C, Latimer J, et al. Manual examination of acces-
50. Baxendale R, Ferrell W. Disturbances of proprioception at the sory movements – seeking R1. Man Ther 2002;7(1):39–43.
human knee resulting from acute joint distension. J Physiol 76. Venturini C, Penedo M, Peixoto G, et al. Study of the force
1987;392:60. applied during anteroposterior articular mobilization of the talus
51. Palmieri-Smith R, Kreinbrink J, Ashton-Miller J, et al. Quadri- and its effect on the dorsiflexion range of motion. J Manipulative
ceps inhibition induced by an experimental knee joint effusion Physiol Ther 2007;30(8):593–7.
326 PART III  Advances in Clinical Science and Practice

77. Silvernail J, Gill N, Teyhen D, et  al. Biomechanical measures 100. Wassinger C, Rockett A, Pitman L, et al. Acute effects of rearfoot
of knee joint mobilization. J Man Manip Ther 2011;19(3): manipulation on dynamic standing balance in healthy individuals.
162–71. Man Ther 2013;(Accepted manuscript).
78. Ju Y, Wang C, Cheng H. Effects of active fatiguing movement 101. Delahunt E, Cusack K, Wilson L, et al. Joint mobilization acutely
versus passive repetitive movement on knee proprioception. Clin improves landing kinematics in chronic ankle instability. Med Sci
Biomech (Bristol, Avon) 2010;25(7):708–12. Sports Exerc 2012;45(3):514–19.
79. Vicenzino B, Jordan K, Brandjerporn M, et al. Mobilization with 102. Hunt M, Di Ciacca S, Jones I, et al. Effect of anterior tibiofemoral
movement treatment of the ankle changes joint position sense in glides on knee extension during gait in patients with decreased
subjects with recurrent sprains: a preliminary report. J Orthop range of motion after anterior cruciate ligament reconstruction.
Sports Phys Ther 2005;35(5):A–21. Physiother Can 2010;62(3):235–41.
80. Learman K, Myers J, Lephart S, et al. Effects of spinal manipula- 103. Hinman R, Bennell K, Crossley K, et al. Immediate effects of
tion on trunk proprioception in subjects with chronic low back adhesive tape on pain and disability in individuals with knee osteo-
pain during symptom remission. J Manipulative Physiol Ther arthritis. Rheumatology 2003;42(7):865–9.
2009;32(2):118–26. 104. Wilson T, Carter N, Thomas G. A multicenter, single-masked
81. Martin J, Jessell T. Anatomy of the somatic sensory system. In: study of medial, neutral, and lateral patellar taping in individuals
Kandel E, Schwartz J, Jessell T, editors. Principles of Neural with patellofemoral pain syndrome. J Orthop Sports Phys Ther
Science. 3rd ed. London: Prentice-Hall; 1991. p. 353–66. 2003;33(8):437–43.
82. Pitman M, Nainzadeh N, Menche D, et al. The intraoperative 105. Aminaka N, Gribble P. Patellar taping, patellofemoral pain syn-
evaluation of the neurosensory function of the anterior cruciate drome, lower extremity kinematics, and dynamic postural control.
ligament in humans using somatosensory evoked potentials. J Athl Train 2008;43(1):21–8.
Arthroscopy 1992;8(4):442–7. 106. Bryk F, Jesus J, Fukuda T, et al. Immediate effect of the elastic
83. Saygi B, Yildirim Y, Berker N, et al. Evaluation of the neurosen- knee sleeve use on individuals with osteoarthritis. Rev Bras Reu-
sory function of the medial meniscus in humans. Arthroscopy matol 2011;51(5):440–6.
2005;21(12):1468–72. 107. Hassan B, Mockett S, Doherty M. Influence of elastic bandage on
84. Saper C, Iversen S, Frackowiak R. Integration of sensory and knee pain, proprioception, and postural sway in subjects with knee
motor function: the association areas of the cerebral cortex and osteoarthritis. Ann Rheum Dis 2002;61(1):24–8.
the cognitive capabilities of the brain. In: Kandel E, Schwartz J, 108. Heit E, Lephart S, Rozzi S. The effect of ankle bracing and taping
Jessell T, editors. Principles of Neural Science. 4th ed. New York: on joint position sense in the stable ankle. J Sport Rehabil
McGraw-Hill; 2000. p. 349–80. 1996;5(3):206–13.
85. Riemann B, Lephart S. The sensorimotor system, part II: the role 109. Simoneau G, Degner R, Kramper C, et al. Changes in ankle joint
of proprioception in motor control and functional joint stability. proprioception resulting from strips of athletic tape applied over
J Athl Train 2002;37(1):80–4. the skin. J Athl Train 1997;32(2):141–7.
86. Friemert B, Faist M, Spengler C, et al. Intraoperative direct 110. Jerosch J, Hoffstetter I, Bork H, et al. The influence of orthoses
mechanical stimulation of the anterior cruciate ligament elicits on the proprioception of the ankle joint. Knee Surg Sports Trau-
short-and medium-latency hamstring reflexes. J Neurophysiol matol Arthrosc 1995;3(1):39–46.
2005;94(6):3996–4001. 111. Callaghan M, Selfe J, Bagley P, et al. The effects of patellar taping
87. Huston L, Wojtys E. Neuromuscular performance characteristics on knee joint proprioception. J Athl Train 2002;37(1):19–24.
in elite female athletes. Am J Sports Med 1996;24(4):427–36. 112. Callaghan M, Selfe J, McHenry A, et al. Effects of patellar taping
88. Beard D, Kyberd P, Fergusson C, et al. Proprioception after rupture on knee joint proprioception in patients with patellofemoral pain
of the anterior cruciate ligament. An objective indication of the syndrome. Man Ther 2008;13(3):192–9.
need for surgery? J Bone Joint Surg Am 1993;75B(2):311–15. 113. Barrett D, Cobb A, Bentley G. Joint proprioception in normal,
89. Buchanan T, Kim A, Lloyd D. Selective muscle activation follow- osteoarthritic and replaced knees. J Bone Joint Surg Am 1991;
ing rapid varus/valgus perturbations at the knee. Med Sci Sports 73B(1):53–6.
Exerc 1996;28(7):870–6. 114. Jerosch J, Prymka M. Knee joint proprioception in normal volun-
90. Dhaher Y, Tsoumanis A, Houle T, et al. Neuromuscular reflexes teers and patients with anterior cruciate ligament tears, taking
contribute to knee stiffness during valgus loading. J Neurophysiol special account of the effect of a knee bandage. Arch Orthop
2005;93(5):2698–709. Trauma Surg 1996;115(3–4):162–6.
91. Yerys S, Makofsky H, Byrd C, et al. Effect of mobilization of the 115. Callaghan MJ, McKie S, Richardson P, et al. Effects of patellar
anterior hip capsule on gluteus maximus strength. J Man Manip taping on brain activity during knee joint proprioception tests
Ther 2002;10(4):218–24. using functional magnetic resonance imaging. Phys Ther
92. Makofsky H, Panicker S, Abbruzzese J, et al. Immediate effect of 2012;92(6):821–30.
Grade IV inferior hip joint mobilization on hip abductor torque: 116. Thijs Y, Vingerhoets G, Pattyn E, et al. Does bracing influence
a pilot study. J Man Manip Ther 2007;15(2):103–10. brain activity during knee movement: an fMRI study. Knee Surg
93. Suter E, McMorland G, Herzog W, et al. Conservative lower back Sports Traumatol Arthrosc 2010;18(8):1145–9.
treatment reduces inhibition in knee-extensor muscles: a random- 117. Karlsson J, Andreasson G. The effect of external ankle support in
ized controlled trial. J Manipulative Physiol Ther 2000;23(2): chronic lateral ankle joint instability. An electromyographic study.
76–80. Am J Sports Med 1992;20(3):257–61.
94. Suter E, McMorland G, Herzog W, et  al. Decrease in quadriceps 118. Briem K, Eythörsdöttir H, Magnúsdóttir R, et al. Effects of
inhibition after sacroiliac joint manipulation in patients with ante- kinesio tape compared with nonelastic sports tape and the untaped
rior knee pain. J Manipulative Physiol Ther 1999;22(3):149–53. ankle during a sudden inversion perturbation in male athletes.
95. Dishman J, Ball K, Burke J. Central motor excitability changes J Orthop Sports Phys Ther 2011;41(5):328–85.
after spinal manipulation: a transcranial magnetic stimulation 119. Chou E, Kim K, Baker A, et al. Lower leg neuromuscular changes
study. J Manipulative Physiol Ther 2002;25(1):1–9. following fibular reposition taping in individuals with chronic
96. Ghez C. The cerebellum. In: Kandel E, Schwartz J, Jessell T, ankle instability. Man Ther 2013;18(4):316–20.
editors. Principles of Neural Science. 3rd ed. London: Prentice- 120. Csapo R, Herceg M, Alegre L, et al. Do kinaesthetic tapes affect
Hall; 1991. p. 626–46. plantarflexor muscle performance? J Sports Sci 2012;30(14):
97. Kandel E. Cellular mechanisms of learning and the biological 1513–19.
basis of individuality. In: Kandel E, Schwartz J, Jessell T, editors. 121. Lewit K. Manipulative Therapy in Rehabilitation of the Locomo-
Principles of Neural Science. London: Prentice-Hall; 1991. p. tor System. Oxford: Butterworth Heinemann; 1999.
1009–31. 122. Clark N, Herrington L. The knee. In: Comfort P, Abrahamson
98. Vaillant J, Rouland A, Martigné P, et al. Massage and mobilization E, editors. Sports Rehabilitation and Injury Prevention. Chiches-
of the feet and ankles in elderly adults: effect on clinical balance ter: John Wiley; 2010. p. 407–63.
performance. Man Ther 2009;14(6):661–4. 123. Clark N. Principles of injury rehabilitation. SportEx Medicine
99. Ferreira G, Viero C, Silveira M, et al. Immediate effects of hip 2004;19:6–10.
mobilization on pain and baropodometric variables – A case 124. Clark N. Functional rehabilitation of the lower limb. SportEx
report. Man Ther 2013;18(6):628–31. Medicine 2003;18:16–21.
 32  Management of the Sensorimotor System 327

125. Andersen S, Terwilliger D, Denegar C. Comparison of open 140. Bruhn S, Kullmann N, Gollhofer A. The effects of a sensorimotor
versus closed kinetic chain test positions for measuring joint posi- training and a strength training on postural stabilisation, maximum
tion sense. J Sport Rehabil 1995;4:165–71. isometric contraction and jump performance. Int J Sports Med
126. Benjaminse A, Sell T, Abt J, et al. Reliability and precision of hip 2004;25(1):56–60.
proprioception methods in healthy individuals. Clin J Sport Med 141. Aagaard P, Simonsen E, Andersen J, et al. Increased rate of force
2009;19(6):457–63. development and neural drive of human skeletal muscle following
127. Drouin J, Houglum P, Perrin D, et al. Weight-bearing and non- resistance training. J Appl Physiol 2002;93(4):1318–26.
weight-bearing knee-joint reposition sense and functional perfor- 142. Snyder-Mackler L, Delitto A, Bailey S, et al. Strength of the
mance. J Sport Rehabil 2003;12:54–66. quadriceps femoris muscle and functional recovery after recon-
128. Bullock-Saxton J, Wong W, Hogan N. The influence of age on struction of the anterior cruciate ligament. A prospective, random-
weight-bearing joint reposition sense of the knee. Exp Brain Res ized clinical trial of electrical stimulation. J Bone Joint Surg Am
2001;136(3):400–6. 1995;77A(8):1166–73.
129. Docherty C, Moore J, Arnold B. Effects of strength training on 143. Chmielewski T, Hurd W, Rudolph K, et al. Perturbation training
strength development and joint position sense in functionally improves knee kinematics and reduces muscle co-contraction after
unstable ankles. J Athl Train 1998;33(4):310–14. complete unilateral anterior cruciate ligament rupture. Phys Ther
130. Friemert B, Bach C, Schwarz W, et al. Benefits of active motion 2005;85(8):740–9.
for joint position sense. Knee Surg Sports Traumatol Arthrosc 144. Gruber M, Gollhofer A. Impact of sensorimotor training on the
2006;14:564–70. rate of force development and neural activation. Eur J Appl
131. Eils E, Rosenbaum D. A multi-station proprioceptive exercise Physiol 2004;92(1–2):98–105.
program in patients with ankle instability. Med Sci Sports Exerc 145. Hurd W, Chmielewski T, Snyder-Mackler L. Perturbation-
2001;33(12):1991–8. enhanced neuromuscular training alters muscle activity in female
132. Waddington G, Adams R, Jones A. Wobble board (ankle disc) athletes. Knee Surg Sports Traumatol Arthrosc 2006;14(1):60–9.
training effects on the discrimination of inversion movements. 146. Heitkamp H, Horstmann T, Mayer F, et al. Gain in strength and
Aust J Physiother 1999;45:95–101. muscular balance after balance training. Int J Sports Med
133. Waddington G, Seward H, Wrigley T, et al. Comparing wobble 2001;22(4):285–90.
board and jump-landing training effects on knee and ankle move- 147. Myer G, Ford K, McLean S, et al. The effects of plyometric versus
ment discrimination. J Sci Med Sport 2000;3:449–59. dynamic stabilization and balance training on lower extremity
134. Lagerquist O, Mang C, Collins D. Changes in spinal but not biomechanics. Am J Sports Med 2006;34(3):445–55.
cortical excitability following combined electrical stimulation of 148. Myer G, Ford K, Brent J, et al. The effects of plyometric vs.
the tibial nerve and voluntary plantar-flexion. Exp Brain Res dynamic stabilization and balance training on power, balance, and
2012;222(1–2):41–53. landing force in female athletes. J Strength Cond Res 2006;20(2):
135. Perez M, Lungholt B, Nyborg K, et al. Motor skill training 345–53.
induces changes in the excitability of the leg cortical area in 149. Lephart S, Abt J, Ferris C, et al. Neuromuscular and biomechani-
healthy humans. Exp Brain Res 2004;159(2):197–205. cal characteristic changes in high school athletes: a plyometric
136. Jensen J, Marstrand P, Nielsen J. Motor skill training and strength versus basic resistance program. Br J Sports Med 2005;39(12):
training are associated with different plastic changes in the central 932–8.
nervous system. J Appl Physiol 2005;99(4):1558–68. 150. Chimera N, Swanik K, Swanik C, et al. Effects of plyometric
137. Adkins D, Boychuk J, Remple M, et al. Motor training induces training on muscle-activation strategies and performance in
experience-specific patterns of plasticity across motor cortex and female athletes. J Athl Train 2004;39(1):24–31.
spinal cord. J Appl Physiol 2006;101(6):1776–82. 151. Irmischer B, Harris C, Pfeiffer R, et al. Effects of a knee ligament
138. Rosenkranz K, Kacar A, Rothwell J. Differential modulation of injury prevention exercise program on impact forces in women.
motor cortical plasticity and excitability in early and late phases of J Strength Cond Res 2004;18(4):703–7.
human motor learning. J Neurosci 2007;27(44):12058–66.
139. Flück M. Functional, structural and molecular plasticity of mam-
malian skeletal muscle in response to exercise stimuli. J Exp Biol
2006;209(12):2239–48.
 CHAPTER 33 

Consideration of Cognitive and

Behavioural Influences on
Physiotherapy Practice
Justin Kenardy Kim Bennell
●

Cognitive and behavioural factors may need to be con- depression and anxiety. Activity levels will be reduced,
sidered in dealing with people with persistent/chronic sometimes on the basis of health care or other advice, and
musculoskeletal disorders. This chapter will provide a thoughts emerge that physical activity and pain associ-
background to consideration of cognitive and behav- ated with physical activity is harmful to recovery. The
ioural influences in dealing with patients with persistent patient may avoid actions or situations out of fear that
musculoskeletal disorders and how they may be managed these might trigger or exacerbate pain. As activity is
in physiotherapy practice. It will also provide a practical reduced depression can often develop, compounded by a
guide to applying some important aspects of psychologi- reduction in physical fitness and increased fatigue and
cal care and behaviour change using cognitive and behav- lethargy. In summary, these factors can occur individually
ioural interventions. Rather than being separate and and together, and they can interact with each other to
ancillary, cognitive and behaviour change will be described create vicious cycles of physical factors, thinking and
as an integral part of usual treatment. However, informa- behaviour. This can be understood as the biopsychosocial
tion will also be provided on management of significant model of chronic pain.1
psychological co-morbidity in this population when the The physiotherapist may choose to evaluate the per-
problem falls outside the scope of physiotherapy practice. son’s presentation using this model through interview
Understanding the context and function of cognitive and and careful assessment. The physiotherapist can also
behavioural factors will provide the groundwork for the choose to use self-report tools as part of that assessment
subsequent section on practical skills of relaxation, to assist in the formulation. Some examples of these are
problem solving, coping skills training and graded the Tampa Kinesiophobia Scale,2 the Pain Self Efficacy
activity. Questionnaire,3 the Pain Catastrophizing Scale,4 and the
Fear Avoidance Beliefs Questionnaire.5
UNDERSTANDING THE PROBLEM
PRESENTATION PSYCHOLOGICAL CO-MORBIDITY AND
WHAT TO DO ABOUT IT?
Chronic pain can have a complex presentation. A better
understanding of the psychological factors that are part Patients who experience chronic illness may also experi-
of chronic pain will assist the treating therapist in provid- ence a history of co-occurring psychological distress that
ing a better service for their patient. As pain transitions may include mental illness. There is an increasing aware-
from acute to persistent, the patient will engage in think- ness among the general public and healthcare practitio-
ing and behaviours that will be counterproductive and ners about mental illness. However in the context of a
will contribute to ongoing distress and disability. These physical injury, it may well be overlooked as the focus
behaviours and thoughts will be influenced by people and is on physical rehabilitation and recovery. Mental illness
environmental factors in their lives. The patient may is a relatively common occurrence in the population at
change their work, either reducing their work capacity, large, with one in six people experiencing clinical depres-
requiring workplace and work role changes and conces- sion and one in four experiencing clinical anxiety during
sions, or even ceasing work. These changes can often be their lives.6 Adversity, including chronic illness and pain,
a consequence of advice from healthcare providers, but can lead to the development of a mental illness, or exac-
can also come from the workplace directly or from family. erbate an existing one. Unfortunately there is a widely
Clearly these changes can have a stressful impact on the held and counterproductive view that the chronic pain
lives of patients, including financial stress. Successive itself is the psychological disorder.7 This view should
interventions that are not effective in reducing the pain be avoided as much as possible unless the objective evi-
can often be demoralizing and lead to depression. Cata- dence is available to the contrary. Furthermore pain
strophic thoughts may emerge that the pain will go on behaviours (e.g. fear of movement) and pain cognitions
endlessly and that problems cannot be resolved. In addi- (e.g. pain catastrophizing) can occur with and without
tion, extended use of analgesic medications can have sig- clinically significant distress, although distress is usually
nificant physical consequences that can also contribute to concomitant.
328
 33  Consideration of Cognitive and Behavioural Influences on Physiotherapy Practice 329

Both depression and anxiety have the potential to for the technique is that stress can change our breath-
influence the patient’s ongoing experience of pain and ing patterns, and that can lead to changes in our body’s
disability and their capacity to recover physically.8,9 It capacity to deal with stress and can create symptoms
should be stated that the presence of mental illness in the that can be stress-provoking in themselves such as short-
patient with chronic musculoskeletal pain should not ness of breath and dizziness. Breathing retraining is
necessarily prevent the progress of physical rehabilita- designed to be used both on a regular basis to help
tion. Recognizing the psychological co-morbidity and reduce overall stress levels and at times where the patient
understanding the impact on the chronic pain condition might feel particularly stressed and overwhelmed. The
are essential to good patient management. Unfortunately physiotherapist can use the following script to help to
recognition is not always easy. Patients may be reluctant teach the technique and should demonstrate the steps
to discuss their mental health with a physiotherapist before observing the patient doing them.
whose focus is on the physical rehabilitation. In the
patient’s mind there may be a stigma associated with the ‘Find a quiet place and sit comfortably with your back
mental illness. They may believe that the acknowledge- straight. Put one hand on your diaphragm, between your
ment of a mental illness will ‘discount’ the validity of the belly button and the bottom of your ribcage, and the other
physical disorder in the mind of the physiotherapist. The hand on your upper chest. Close your eyes and breathe
patient themselves may not even recognize their experi- through your nose. Try to make the hand on your
ence as a mental illness. Also, many of the symptoms of abdomen rise, while keeping the hand on your chest still.
a mental illness will overlap with the presentation of a Exhale through your mouth, allowing your breath out
chronic musculoskeletal disorder (e.g. reduced activity) and your abdominal muscles to contract. Count to three
and increased weight, thereby complicating possible slowly as you inhale through your nose, pause and then
identification by the physiotherpist. Finally, the physio- count to three slowly as you exhale through your mouth.
therapist might be reluctant to address mental health Continue breathing in. And out.’
issues within their treatment sessions through concerns
about practicing outside their competance, or disenfran- The physiotherapist should provide encouragement and
chising their patient. However, there are a number of constructive feedback as it is sometimes difficult for the
simple and brief tools that can be given to patients that patient to perform the technique. While the technique
will help to identify mental illness if there is some concern should be able to be done in any position, it is sometimes
that it might be present and impeding the effectiveness easier for the patient to lie down to begin with, as this
of physical rehabilitation. The Kessler Psychological provides better feedback to the patient. Also some
Distress Scale (K10)10 is a commonly used measure in patients will attempt to breathe very deeply during the
general practice medicine to assess significant psycho- technique, this can be associated with light headedness
logical distress. Its ten items can be completed quickly by and therefore can also be distressing. The depth of the
the patient and has cut-points that provide an indication breath should be guided by the simple rule that the tech-
of clinically elevated anxiety and depression.11 Alterna- nique is about the type of breathing rather than depth
tively the PHQ-4, derived from the PHQ-9 and GHQ- of breathing. Patients should be encouraged to breathe
712 is a four-item screener that can detect possible clinical to a normal depth and use the diaphragm instead of the
anxiety or depression (see www.phqscreeners.com). upper body.
Either of these brief questionnaires could be adminis- A second technique can also be taught that focuses on
tered if there was some concern by the physiotherapist breathing and body tension. The body scan is so called
about failure to progress in treatment. Referral for further because the idea is to review the body for stress and
assessment and care can then be negotiated with the tension and then undertake a brief muscular relaxation in
patient. combination with diaphragmatic breathing. The tech-
nique can be done at any time including before, during
and after a treatment session. The steps are simple and
SKILLS AND PROCEDURES OF COGNITIVE the patient is taught to:
1. Undertake a self-evaluation of stress and tension
BEHAVIOURAL THERAPY RELEVANT TO using a ten-point scale.
PHYSIOTHERAPY PRACTICE 2. Take a slow breath in, and then breathe out saying
to ‘relax’ to yourself.
Stress, or distress, is common in injury and certainly 3. Begin to focus on sensations of relaxation within
present to some degree in most patients with chronic the body as you breathe out and allow sensations
pain. There are a few simple skills that can be taught to of heaviness and warmth to flow downwards
patients that will help them to manage their stress. through shoulders, arms and hands, stomach, legs
and feet.
Breathing Retraining and 4. Remain as long as they wish in this state, relaxing
more with each breath out.
Body Scan Relaxation The technique should be conducted once only or
Physiologically stress can manifest in increased body repeatedly, and can be performed in any position
tension and arousal. A simple skill to manage that including standing. However, as with diaphragmatic
manifestation of stress is breathing retraining, using breathing it may be easier if the patient starts in a
abdominal or diaphragmatic breathing. The rationale lying position.
330 PART III  Advances in Clinical Science and Practice

Problem Solving continuing with the feared activity, and in reinforcing

their new behaviour.
Problem solving is a skill used to develop a plan to Hence the concept for the patient is that some thoughts
manage difficulties identified by the patient including work for them and others work against them. A first step
overcoming barriers to self-management. It is a useful is identifying unhelpful thoughts. This if followed by
life skill that promotes self-efficacy through helping replacing these with more helpful coping statements.
to improve a patient’s capacity to overcome adversities. Unhelpful thoughts increase stress and avoidance and
It should be said that the goal of problem solving is decrease use of helpful coping skills such as problem
not to resolve the ‘problem’ of pain, which would be solving and relaxation. Examples of unhelpful thoughts
counterproductive and stressful,13 but rather to develop are: ‘This is too hard’, ‘I can’t handle this’ or ‘I give up’.
solutions to specific life events and obstacles to recov- In contrast, helpful thoughts decrease stress and avoid-
ery. The problem-solving approach should be modelled ance and increase use of helpful coping skills such as
by the physiotherapist when a patient presents a dif- problem solving and relaxation. Examples of helpful
ficulty as part of the therapy, for example finding thoughts are: ‘I can handle this’, ‘This feeling will pass’
time to complete an exercise. Problem solving is an or ‘This is not dangerous’.
iterative process with up to seven steps. The seven The physiotherapist can assist the patient identify
steps are: unhelpful thoughts that increase stress and promote
1. Identify the problem: A problem that is solvable avoidance by using examples but then encouraging the
must be defined and it needs be broken down into patient to generate their own, especially by remembering
separate and smaller components. Each component what these might be from previous experience. The phys-
then becomes the focus of a problem-solving iotherapist then assists the patient to generate their own
process. cognitive coping statements. The use of examples helps
2. Explore the problem: The aim is to better under- to prompt the patient, but such thoughts always have
stand the scope of the problem, why it is relevant greater valence when generated by the patient. A ques-
at this point in time, and in what ways it affects the tion that the therapist could ask is ‘What could you say
patient. to yourself to increase your confidence and help yourself
3. Set goals: Problem solving implies that there is an manage the situation?’ The physiotherapist could prac-
end point to be achieved if the problem is resolved, tice a scenario with the patient where they might use
this needs to be defined in order to understand pos- these statements and then suggest that the patient record
sible solutions. these statements on a card for use in situations outside of
4. Think of all possible solutions: There are no bad the treatment setting.
ideas at this stage, creativity is encouraged. Consul-
tation with others may be helpful.
5. Select a possible solution: Evaluate the generated BEHAVIOURAL GRADED ACTIVITY
solutions by asking how helpful, realistic, relevant, APPROACHES
and manageable they are. Evaluate the pros and
cons for each solution and ask whether the solution Graded exercise or activity encourages continued activity
achieves the goals that are desired. despite the presence of pain through the use of specific
6. Implement a possible solution: Plan how and behavioural goals and systematic reinforcement for effort
when the solution will be applied, and provide or achievement.14 In a graded exercise approach, pain is
encouragement for attempting. not used to determine exercise or activity level. Instead,
7. Evaluate: Was the solution effective? Did the solu- dosage is increased by preset quota in a time-contingent
tion achieve the personally relevant goals? Does manner. A baseline exercise or activity level is first deter-
another solution need to be sought? mined by having the patient perform a task until pain
If there is a need for further problem solving then the limits the patient’s ability to perform the task. This level
process should be repeated until a satisfactory endpoint of exercise or activity provides the initial therapeutic
is achieved. quota. Subsequent sessions are based on this quota and if
the patient reaches the quota, reinforcement is provided
(e.g. verbal praise or some other reward). The quota is
Cognitive Coping Skills gradually increased across sessions. If the patient does not
Patients with chronic pain can experience a range of meet the quota, the therapist does not offer reinforce-
negative thoughts that will interfere with recovery. These ment and instead discusses the importance of continuing
thoughts can focus on the perceived negative conse- the activity and provides assistance for the patient to
quences of pain, in particular where physical activity is achieve the set goals.
avoided because of its believed deleterious effect on pain. Another graded activity approach is graded exposure.
To overcome these thoughts the patient may need to This approach can be useful for patients who have
engage in a process of actively engaging in the avoided chronic pain and report high levels of fear of pain or
activities in a graded fashion. In order to assist in injury and avoidance behaviours. It first involves patients
approaching these previously avoided activities it can be identifying activities that they are highly fearful of per-
helpful for patients to substitute the negative and some- forming because of their pain. Following this, a highly
times catastrophic thinking for thinking that will assist feared activity is incorporated into the rehabilitation pro-
them in engaging in the approach behaviour, in gramme first at a low level that elicits minimal fear and
 33  Consideration of Cognitive and Behavioural Influences on Physiotherapy Practice 331

sequentially increased until the fear declines. A key aspect motivation to form an intention to change; (b) help the
of graded exposures it that the exposure must also occur person to convert that intention into action and mainte-
outside of the clinical setting.14 nance; and (c) effective communication of information
between the patient and the health professional. In
essence, this can be simplified to several questions that
PROMOTING BEHAVIOUR CHANGE the patient asks themselves: ‘Do I know what to do?’, ‘Do
I want to do it?’ and ‘Am I able to do it?’. From the clini-
A key part of many healthcare practices involve engaging cian’s perspective the question becomes: ‘Are there tech-
with the patient to change their behaviours. A medical niques that can be applied to influence the patient’s
practitioner may prescribe a drug to control cholesterol answers to these questions?’.
with an implicit direction to the patient to adhere to The first question, ‘Does the patient know what to
the prescription. The patient must change their daily do?’ relates to the effective communication of knowledge
routine to incorporate the consistent and regular taking between the health practitioner and the patient. This
of the drug. Whether that occurs will depend on a mul- relies on the ‘therapeutic approach’ taken by the clini-
titude of factors, but an often overlooked yet key influ- cian. A patient-centred approach where the patient’s
ence is the actions of the prescriber which will help or autonomy is respected and they are involved in collabora-
hinder the behaviour change. For a physiotherapist, a tive decision making, is generally considered to be more
central part of patient recovery is providing advice on effective than a ‘traditional approach’, where the patient
undertaking new behaviours such as strengthening exer- is simply told what to do.16,17 Once the patient knows
cises. It might be assumed that all patients are motivated what to do, the challenge for the clinician is to ensure
by their desire to recover and that this is sufficient to that the patient is willing and able to act on their advice.
ensure that they commence and maintain their changed Motivation (the desire to take action) and self-efficacy
behaviours. However this is a false assumption. As with (the belief you can take action) are considered to be the
the example of the medical practitioner prescribing a two most important cognitive drivers of behaviour
drug treatment, the beliefs, behaviours and communica- change.18 The widely used model of stages of change19
tions of the physiotherapist will have a profound impact encapsulates these concepts. Readiness can be conceptu-
on the behaviours that are to be changed. In the case alized as the resultant combined effect of thinking that it
of a patient with a persistent musculoskeletal disorder, is important to take action, being somewhat confident of
if the physiotherapist believes that the patient cannot or success and it being the right time to take action. Readi-
will not change their behaviours, these beliefs will implic- ness can be influenced using interventions such as moti-
itly impact on the physiotherapist’s behaviours and com- vational interviewing (a collaborative conversation that
munications, and therefore on their capacity to influence seeks to identify, examine and resolve ambivalence about
the patient to change their behaviour. If the physiothera- changing behaviour) and decisional balance (exploring
pist provides complex instructions for the patient to the pros and cons of different choices). Once a patient
undertake their new behaviours without checking for has formed a goal intention, the clinician may need to
patient understanding of those instructions, it should assist them to engage in action and self-regulation leading
come as no surprise that the patient is unable to complete to maintenance of behaviour change. It is recommended
the new behaviours. If, at the end of a treatment session, that the goal-setting and action-planning process should
the physiotherapist gives the patient instruction on com- identify and address barriers to change and take into
pleting a series of regular exercises by the following account strategies to identify when and how to act in a
session, and then fails to follow-up with a review of variety of situations.
progress in the following session, there is less likelihood
that the patient will continue with the exercise. Behaviour
change is not about prescribing a set of new behaviours INTEGRATING PSYCHOLOGICAL
and expecting the prescription to be followed, it is an FACTORS IN TO CLINICAL PRACTICE
interactive and iterative process between the patient and
the physiotherapist. The physiotherapist must see the There are many challenges to integrating psychological
patient as a collaborator in the process of change and perspectives within traditional physiotherapy clinical
the patient must be willing to hold the same view. The practice. Foster and Delitto20 suggest a pyramid approach
physiotherapist must understand and define what behav- to this (Fig. 33-1). At the base of the pyramid are the
iour change is needed and the extent and circumstances common key psychological obstacles to recovery that are
of the change. The patient must share that understand- relatively easy to incorporate into physiotherapy practice,
ing and be willing to accept, at least tentatively, that the such as enhancing personal control and self-efficacy and
behaviour change is what they will attempt. But there reducing fear of movement in patients with pain. Identi-
must also be an open process of collaborative negotiation fying and addressing these factors is unlikely to require
about the behaviour to be changed in which the phys- intensive additional education and skill development for
iotherapist’s expert knowledge and patient’s needs and physiotherapists. Moving up the pyramid are the psycho-
circumstances have equal value. logical factors and intervention techniques that are likely
There are three main processes required to facilitate to require more specialist training to identify and address,
health behaviour change:15 (a) assist the person to form a but that can and should be part of at least some physio-
behavioural goal intention – this relates to whether a therapists’ practice and skill set. At the top of the pyramid
person has the required knowledge and sufficient are the patients with psychological obstacles to recovery
332 PART III  Advances in Clinical Science and Practice

Onward referral to a mental health professional or

multidisciplinary team

Examples: Psychopathology or ‘orange flags’ Onward

referral
Requires additional training for physical therapists

Examples: Eliciting and addressing unhelpful Some

cognitions and low-mood, motivational interviewing physical therapist
practice
Relatively easy to incorporate into
physical therapist practice
All physical therapist practice
Examples: Identifying and enhancing
patients’ perceptions and expectations,
effective reassurance, positive
reinforcement, enhancing personal
control and self-efficacy, reducing fear
of movement

FIGURE 33-1  ■  A suggested model for integration: the psychosocial factors pyramid. (Reproduced from Foster and Delitto.20)

that are most likely to require onward referral to mental BOX 33-1 
health professionals.
Many physiotherapists feel ill-equipped to deal with ‘[the workshop] was the tip of the iceberg … it set the
psychological factors possibly because most training is groundwork or sort of gave us a taste of it, but then it was
biomedical in orientation with less attention paid to prac- the weekly meetings we had with the psychologist that really
tical implementation of a biopsychosocial approach.21 concreted everything for us’
Certainly, incorporating higher-level psychological ap-
From Neilsen et al.23
proaches into physiotherapy management of chronic
conditions (Fig. 33-1, middle tier of the pyramid) re-
quires additional training that can be extensive. For ex- BOX 33-2 
ample, in a recent study investigating the effects of a
physiotherapy-delivered integrated exercise and cogni- ‘… because it’s not a straightforward competency of just a
tive behavioural pain-coping skill training programme, performer’s skill. It’s a skill that has to adapt under the
physiotherapists underwent lengthy training in order to pressure of doing the interview. And that’s a far more
achieve a high degree of competence. This involved an advanced skill than simply learning to be able to – I don’t
initial 4-day group workshop followed by formal group know – take a foot through a movement. If I learn that
mentoring and instruction, role-playing and performance skill, then I’ve got that and I can go on. Whereas this sort of
skill, I walk in and the client throws me a curve ball and
feedback from a psychologist over the course of 3–6
I’ve got to adapt and make it all work.’
months and continued throughout the study.22 Interviews
with the physiotherapists at the conclusion of the study From Neilsen et al.23
found that they believed the extensive training to be criti-
cal to their ability to effectively deliver the intervention
and to problem solve issues that arose (Boxes 33-1 patients and negotiate with them to gain appropriate
and 33-2).23 The fact that such extensive training is not psychological management. Such patients stand to gain
feasible to implement widely in the real world, supports better outcomes from multiprofessional management of
physiotherapy practice models whereby some practitio- the painful musculoskeletal condition.
ners gain the additional skills necessary to competently
deliver higher-level psychological interventions.
REFERENCES
1. Gatchel RJ, Peng YB, Peters ML, et al. The biopsychosocial
approach to chronic pain: scientific advances and future directions.
CONCLUSION Psychol Bull 2007;133:581–624.
2. Lundberg M, Styf J, Carlsson S. A psychometric evaluation of the
Cognitive and behavioural factors often require consid- tampa scale for kinesiophobia – from a physiotherapeutic perspec-
eration in people with persistent/chronic musculoskeletal tive. Physiother Theory Pract 2004;20:121–33.
disorders. Physiotherapists need to recognize and posi- 3. Nicholas MK. The pain self-efficacy questionnaire: taking pain into
account. Eur J Pain 2007;11:153–63.
tively manage these factors as part of usual physiotherapy 4. Sullivan MJL, Bishop SR, Pivik J. The pain catastrophizing scale:
practice. They can use techniques such as relaxation, development and validation. Psychol Assess 1995;7(4):524–32.
problem solving, coping skills training and graded activ- 5. Waddell G, Newton M, Henderson I, et al. A Fear-Avoidance
ity, which are well within their scope of practice. However Beliefs Questionnaire (FABQ) and the role of fear-avoidance beliefs
in chronic low back pain and disability. Pain 1993;52:157–68.
some patients may present with significant psychological 6. Australian Bureau of Statistics. 2007 National Survey of Mental
co-morbidity which falls outside the scope of physio- Health and Wellbeing: Summary of Results. Canberra: Australian
therapy practice. It is important to recognize these Bureau of Statistics; 2008 Contract No.: 4326.0.
 33  Consideration of Cognitive and Behavioural Influences on Physiotherapy Practice 333

7. Crombez G, Beirens K, Van Damme S, et al. The unbearable light- 17. Wagner EH, Bennett SM, Austin BT, et al. Finding common
ness of somatisation: a systematic review of the concept of somatisa- ground: patient-centeredness and evidence-based chronic illness
tion in empirical studies of pain. Pain 2009;145:31–5. care. J Altern Complement Med 2005;11(Suppl.):S7–15.
8. Surah A, Baranidharan G, Morley S. Chronic pain and depression. 18. Bandura A. Social cognitive theory: an agentic perspective. Annu
Cont Edu Anaesth Crit Care Pain 2014;14(2):85–9. Rev Psychol 2001;52:1–26.
9. Liedl A, O’Donnell M, Creamer M, et al. Support for the mutual 19. Prochaska JO, DiClemente CC. The Transtheoretical Approach:
maintenance of pain and post-traumatic stress disorder symptoms. Crossing Traditional Boundaries of Therapy. Homewood, Ill.: Dow
Psychol Med 2010;40:1215–23. Jones-Irwin; 1984.
10. Kessler RC, Walters EE, Zaslavsky AM, et al. Screening for serious 20. Foster NE, Delitto A. Embedding psychosocial perspectives within
mental illness in the general population. Arch Gen Psychiatry clinical management of low back pain: integration of psychosocially
2003;60:184–9. informed management principles into physical therapist practice –
11. Andrews G, Slade T. Interpreting scores on the Kessler Psychologi- challenges and opportunities. Phys Ther 2011;91:790–803.
cal Distress Scale (K10). Aust N Z J Public Health 2001; 21. Main CJ, George SZ. Psychologically informed practice for man-
25:494–7. agement of low back pain: future directions in practice and research.
12. Kroenke K, Spitzer RL, Williams JBW, et al. An ultra-brief screen- Phys Ther 2011;91(5):820–4. PubMed PMID: 21451091. [Epub
ing scale for anxiety and depression: the PHQ-4. Psychosomatics 2011/04/01].
2009;50:613–21. 22. Bennell KL, Metcalf B, Egerton T, et al. A physiotherapist-
13. Eccleston C, Crombez G. Worry and chronic pain: a misdirected delivered integrated exercise and pain coping skills training inter-
problem solving model. Pain 2007;132:233–6. vention for individuals with knee osteoarthritis: a randomised
14. Michael KN, Steven ZG. Psychologically informed interventions controlled trial protocol. BMC Musculoskelet Disord 2012;
for low back pain: an update for physical therapists. Phys Ther 13(1):129.
2011;91:765–76. 23. Nielsen M, Keefe FJ, Bennell K, et al. Physical therapist-delivered
15. Gale J, Skouteris H. Health coaching: facilitating health behaviour cognitive-behavioral therapy: a qualitative study of physical thera-
change for chronic condition prevention and self-management. In: pists’ perceptions and experiences. Phys Ther 2014;94(2):
Caltabiano M, Ricciardelli L, editors. Applied Topics in Health 197–209.
Psychology. Brisbane: John Wiley & Sons; 2012. p. 15–28.
16. Moller AC, Ryan RM, Deci EL. Self-determination theory and
public policy: improving the quality of consumer decisions without
using coercion. J Public Policy Mark 2006;25:104–16.
 CHAPTER 34 

Adjunct Modalities for Pain

CHAPTER OUTLINE

Editor’s Introduction Ch 34.3  The Use of Tape in Managing Spinal

Pain  339
Ch 34.1  Electrophysical Agents  334
Jenny McConnell
Tim Watson
Ch 34.2  Acupuncture/Dry Needling  336
Panos Barlas

EDITOR’S INTRODUCTION

The case for the integration of multimodalities summary of how electrophysical agents,
in the management of complex musculoskeletal acupuncture/dry needling and taping can
presentations is strong, as there is no panacea facilitate the treatment of musculoskeletal pain.
for musculoskeletal pain. It can be difficult to The potential is discussed for electrophysical
know what modality is the most ‘effective/ agents to both address the underlying pathology
active’ component within a programme of of musculoskeletal pain presentations and
management, and thus what is the adjunct relieve musculoskeletal pain as a distinct
modality increasing effectiveness is equally objective. Dry needling has become a popular
difficult to establish. These treatment modality and the theory underpinning needling
approaches, termed adjunct modalities, will is discussed in some detail, as are some of the
undoubtedly continue to be crucial issues regarding the evidence base for
considerations in musculoskeletal management acupuncture. To complete a picture of the
and will continue to attract similar levels of rationale for the use of taping within a
clinical and research interest as manual therapy programme of management for spinal pain has
and exercise. been described and some treatment examples
In this chapter three internationally renowned are included.
experts in their respective fields have provided a

CHAPTER 34.1  ■  ELECTROPHYSICAL AGENTS

Tim Watson

Electrophysical agents (EPAs, a term with greater accu- an EPA is most effectively employed in isolation. Trans-
racy and currency than the older term ‘electrotherapy’) cutaneous electrical nerve stimulation (TENS) for
have an established place as a component of therapy example, may provide an effective and clinically useful
clinical practice, though their utilization appears to method by which symptomatic pain relief can be
vary between professional groups, between countries achieved. Used in conjunction with a holistic treatment
and indeed within both of these. There is a substantial package, it can make a valuable contribution. Used alone,
evidence to support their use but, for some clinical pre- it will have an effect, evidenced and measurable, but it
sentations, there appears to be a fundamental mismatch is unlikely to be optimal. It is the integration of manual
between the supportive evidence and current practice. therapy, exercise therapy, advice, education and, where
Historically, it is almost certainly the case that these appropriate, EPAs that is most likely to achieve optimal
‘modalities’ were over-employed, with many, if not all, outcome.
patients with a whole range of musculoskeletal presenta- In general, there has been a shift away from EPAs
tions receiving some kind of electrotherapy. Given the being delivered purely in the clinical environment. TENS
current evidence base, the continued use of these inter- was probably one of the first modalities provided as a
ventions can be justified in some, but certainly not all, ‘home-based’ treatment – the therapist teaching the
clinical circumstances. It is rarely, if ever, the case that patient how best to employ the machine, and the patient
334
 34  Adjunct Modalities for Pain 335

(or carer) being responsible for the day-to-day delivery. this phenomenon in considerable detail. If TENS, ultra-
The machines were inexpensive and relatively easy to sound or laser is applied at what is known to be a clini-
manage, making this a real-world possibility. Over time cally effective dose, its use is supported by the evidence
this approach has been adopted with other devices. There across the musculoskeletal physiotherapy range. If applied
are now interferential therapy, neuromuscular electrical at an ineffective (or at least sub-optimal) dose, then it
stimulation devices, therapy ultrasound, microcurrent would be difficult to rationalize how a beneficial effect
and several others which can be delivered in this way.1–6 could be achieved, as would be the case with manual
Some clinics encourage patients to purchase their own therapy, exercise, drug therapy or any other relevant
machines while others lease, loan or rent to patients. intervention method.
That notwithstanding, the concept of home-based EPA In conclusion, various EPAs are evidenced as being
treatment delivery is evidenced as being effective, and effective when applied optimally and in line with best
serves to ‘free up’ clinic time for those aspects of treat- evidence. They can be used as a means to influence the
ment which cannot be easily or effectively delivered by underlying tissue problem (tissue damage, inflammation)
the patient at home. or can be used as a means to change perception of pain
In terms of potential uses in the musculoskeletal arena, or other disabling symptoms. One approach is not ‘more
there are two fundamental approaches that are employed valid’ than another. They both have a potential value as
for the use of EPAs. Firstly one can use the modality as a component of a therapeutic package of care, but none
a means to deal with the underlying pathology (e.g. to are evidenced as being optimal if used in isolation.
enhance repair of a damaged tissue). There are several
modalities that are supported by the evidence base
that can be used in this context such as ultrasound,7–9 REFERENCES
laser,10,11 pulsed-shortwave therapy,12,13 shockwave14–16 1. Yik YI, Ismail KA, Hutson JM, et al. Home transcutaneous electri-
cal stimulation to treat children with slow-transit constipation.
and microcurrent.5,17,18 Other modalities are sometimes J Pediatr Surg 2012;47(6):1285–90.
also included in this group, for example radiofrequency 2. Bruce-Brand RA, Walls RJ, Ong JC, et al. Effects of home-based
applications that are similar to shortwave modalities but resistance training and neuromuscular electrical stimulation in knee
actually utilize electromagnetic energy delivered at osteoarthritis: a randomized controlled trial. BMC Musculoskelet
slightly different frequencies19,20 and magnetic-based Disord 2012;13:118.
3. Brown AS. At-home laser and light-based devices. Curr Probl Der-
therapies.21–23 However, there is a need for more compre- matol 2011;42:160–5.
hensive clinical trial data before these can be confirmed 4. Watanabe Y, Matsushita T, Bhandari M, et al. Ultrasound for frac-
as being supported by the evidence for this purpose, ture healing: current evidence. J Orthop Trauma 2010;24(Suppl.
though such trials are currently underway, and the foun- 1):S56–61.
5. Poltawski L, Johnson M, Watson T. Microcurrent therapy in the
dation studies (e.g. cell, animal) strongly suggest that they management of chronic tennis elbow: pilot studies to optimize
have this tissue repair capability. parameters. Physiother Res Int 2012;17(3):157–66.
The second, and equally valid approach would be to 6. Persson AL, Lloyd-Pugh M, Sahlström J. Trained long-term
employ an EPA modality as a means to change the TENS users with chronic non-malignant pain. A retrospective
patient’s perception of their pain without necessarily questionnaire study of TENS usage and patients’ experiences. Phys
Ther Rev 2010;15(4):294–301.
changing the underlying problem. EPA modalities in this 7. Watson T. Ultrasound in contemporary physiotherapy practice.
group would most obviously include TENS;24–26 interfer- Ultrasonics 2008;48:321–9.
ential therapy;27–29 various other forms of electrical stimu- 8. Yildirim MA, Ones K, Celik EC. Comparision of ultrasound
lation30,31 together with heat- and cold-based therapies,32–37 therapy of various durations in the treatment of subacromial
impingement syndrome. J Phys Ther Sci 2013;25(9):1151–4.
and laser-based intervention.38–41 9. Kinami Y, Noda T, Ozaki T. Efficacy of low-intensity pulsed ultra-
A detailed review of each of these modalities is clearly sound treatment for surgically managed fresh diaphyseal fractures
beyond the remit of this short overview. The essential/ of the lower extremity: multi-center retrospective cohort study.
indicative references provided will provide a preliminary J Orthop Sci 2013;18(3):410–18.
source of information for further evaluation. 10. Alayat MS, Elsodany AM, El Fiky AA. Efficacy of high and low level
laser therapy in the treatment of Bell’s palsy: a randomized double
Several reviews (Cochrane, systematic reviews and blind placebo-controlled trial. Lasers Med Sci 2014;29(1):335–42.
meta analyses) and clinical guidelines (e.g. NICE) have 11. Sussmilch-Leitch SP, Collins NJ, Bialocerkowski AE, et al. Physical
commonly drawn equivocal conclusions when these therapies for Achilles tendinopathy: systematic review and meta-
interventions have been considered. While not trying to analysis. J foot Ankle Res 2012;5(1):15.
12. Al Mandeel M, Watson T. Pulsed and continuous shortwave
defend the indefensible, one of the key issues is that these therapy. In: Watson T, editor. Electrotherapy: Evidence Based
reviews tend not to consider treatment dose. Essentially, Practice. Edinburgh: Churchill Livingstone/Elsevier; 2008.
if five randomized controlled trial papers were shortlisted p. 137–60.
to the review, three demonstrating benefit whereas two 13. Jan MH, Chai HM, Wang CL, et al. Effects of repetitive shortwave
do not, the common conclusion would be that there was diathermy for reducing synovitis in patients with knee osteoarthri-
tis: an ultrasonographic study. Phys Ther 2006;86(2):236–44.
insufficient supportive evidence. Taking into account the 14. Schmitz C, Csaszar NB, Rompe JD, et al. Treatment of chronic
totality of the evidence base, there is strong support for plantar fasciopathy with extracorporeal shock waves (review).
a ‘dose’ dependency when using EPAs.42 Strangely, dose- J Orthop Surg 2013;8(1):31.
related issues do not often feature in the reviews. A 15. Reznik JE, Milanese S, Golledge J, et al. Extracorporeal shock wave
therapy as a treatment for heterotopic ossification. Phys Ther Rev
detailed analysis of the effective and ineffective random- 2013;18(4):300–7.
ized controlled trials commonly reveals that the settings 16. Dizon JN, Gonzalez-Suarez C, Zamora MT, et al. Effectiveness of
(dose) at which the EPA is delivered is key to a positive extracorporeal shock wave therapy in chronic plantar fasciitis: a
outcome. Several eminent authors24,43–45 have explained meta-analysis. Am J Phys Med Rehabil 2013;92(7):606–20.
336 PART III  Advances in Clinical Science and Practice

17. Poltawski L, Watson T. Bioelectricity and microcurrent therapy 32. Thym DBM, Olmedija dAR, Dall’-Aqua JMG, et al. Evaluation of
for tissue healing – a narrative review. Phys Ther Rev 2009;14(2): pain relief using a combination of TENS and cryotherapy. Kranken-
104–14. Gymnastik 2005;57(5):894–901.
18. Rockstroh G, Schleicher W, Krummenauer F. Effectiveness of 33. Ansari NN, Naghdi S, Naseri N, et al. Effect of therapeutic infra-
microcurrent therapy as a constituent of post-hospital rehabilitative red in patients with non-specific low back pain: a pilot study.
treatment in patients after total knee alloarthroplasty – a random- J Bodyw Mov Ther 2014;18(1):75–81.
ized clinical trial. Rehabilitation (Stuttg) 2010;49(3):173–9. 34. Lewis SE, Holmes PS, Woby SR, et al. Short-term effect of super-
19. Guo L, Kubat NJ, Nelson TR, et al. Meta-analysis of clinical effi- ficial heat treatment on paraspinal muscle activity, stature recovery,
cacy of pulsed radio frequency energy treatment. Ann Surg and psychological factors in patients with chronic low back pain.
2012;255(3):457–67. Arch Phys Med Rehabil 2012;93(2):367–72.
20. Guo L, Kubat NJ, Isenberg RA. Pulsed radio frequency energy 35. Kettenmann B, Wille C, Lurie-Luke E, et  al. Impact of continu-
(PRFE) use in human medical applications. Electromagn Biol Med ous low level heatwrap therapy in acute low back pain patients:
2011;30(1):21–45. subjective and objective measurements. Clin J Pain 2007;23(8):
21. Ueno S, Okano H. Static, Low-frequency and pulsed magnetic 663–8.
fields in biological systems. In: Lin JC, editor. Electromagnetic 36. Chou R, Huffman LH. Nonpharmacologic therapies for acute and
Fields in Biological Systems. CRC Press; 2012. chronic low back pain: a review of the evidence for an American
22. Assiotis A, Sachinis NP, Chalidis BE. Pulsed electromagnetic fields Pain Society/American College of Physicians clinical practice
for the treatment of tibial delayed unions and nonunions a prospec- guideline. Ann Intern Med 2007;147(7):492–504.
tive clinical study and review of the literature. J Orthop Surg 37. Bleakley CM, Costello JT. Do thermal agents affect range of move-
2012;7(1):24. ment and mechanical properties in soft tissues? A systematic review.
23. Rosen AD. Studies on the effect of static magnetic fields on biologi- Arch Phys Med Rehabil 2013;94(1):149–63.
cal systems. PIERS Online 2010;6(2):133–6. 38. Al Rashoud AS, Abboud RJ, Wang W, et al. Efficacy of low-level
24. Sluka KA, Bjordal JM, Marchand S, et al. What makes transcutane- laser therapy applied at acupuncture points in knee osteoarthritis:
ous electrical nerve stimulation work? making sense of the mixed a randomised double-blind comparative trial. Physiotherapy 2014;
results in the clinical literature. Phys Ther 2013;93(10):1397–402. 100(3):242–8.
25. Johnson MI, Bjordal JM. Transcutaneous electrical nerve stimula- 39. Maia ML, Bonjardim LR, Quintans Jde S, et  al. Effect of low-
tion for the management of painful conditions: focus on neuro- level laser therapy on pain levels in patients with temporoman-
pathic pain. Expert Rev Neurother 2011;11(5):735–53. dibular disorders: a systematic review. J Appl Oral Sci 2012;20(6):
26. Johnson MI. Transcutaneous elecetrical nerve stimulation (TENS). 594–602.
In: Watson T, editor. Electrotherapy: Evidence Based Practice. 40. Jovicic M, Konstantinovic L, Lazovic M, et al. Clinical and func-
Edinburgh: Elsevier/Churchill Livingstone; 2008. p. 253–96. tional evaluation of patients with acute low back pain and radicu-
27. Rocha CS, Lanferdini FJ, Kolberg C, et al. Interferential therapy lopathy treated with different energy doses of low level laser
effect on mechanical pain threshold and isometric torque after therapy. Vojnosanit Pregl 2012;69(8):656–62.
delayed onset muscle soreness induction in human hamstrings. J 41. Jang H, Lee H. Meta-analysis of pain relief effects by laser irradia-
Sports Sci 2012;30(8):733–42. tion on joint areas. Photomed Laser Surg 2012;30(8):405–17.
28. Gundog M, Atamaz F, Kanyilmaz S, et al. Interferential current 42. Watson T. Narrative review: key concepts with electrophysical
therapy in patients with knee osteoarthritis: comparison of the agents. Phys Ther Rev 2010;15(4):351–9.
effectiveness of different amplitude-modulated frequencies. Am J 43. Bjordal JM, Lopes Martins RAB, Klovning A. Is quality control of
Phys Med Rehabil 2012;91(2):107–13. Cochrane reviews in controversial areas sufficient? J Altern Com-
29. Hurley DA, McDonough SM, Dempster M, et al. A randomized plement Med 2006;12(2):181–3.
clinical trial of manipulative therapy and interferential therapy for 44. Bjordal JM, Lopes-Martins R, Johnson MI, et al. Inaccuracies in
acute low back pain. Spine 2004;29(20):2207–16. laser therapy meta-analysis for neck pain? J Physiother 2010;56(4):
30. Ediz L, Ceylan MF, Turktas U, et al. A randomized controlled trial 282.
of electrostimulation effects on effussion, swelling and pain recov- 45. Bjordal JM, Johnson MI, Lopes-Martins RA, et al. Short-term effi-
ery after anterior cruciate ligament reconstruction: a pilot study. cacy of physical interventions in osteoarthritic knee pain. A system-
Clin Rehabil 2012;26(5):413–22. atic review and meta-analysis of randomised placebo-controlled
31. Lowry AM, Simopoulos TT. Spinal cord stimulation for the treat- trials. BMC Musculoskelet Disord 2007;8(1):51.
ment of chronic knee pain following total knee replacement. Pain
Physician 2010;13(3):251–6.

CHAPTER 34.2  ■  ACUPUNCTURE/DRY NEEDLING

Panos Barlas

Acupuncture is a modality popular among physiothera- modern, evidence-based, medical thinking. It is these
pists as a safe and effective technique for the relief of pain. developments that have shaped contemporary acupunc-
It was introduced to the physiotherapy profession in the ture to an amalgam of Traditional Chinese practices
early 1980s, and has steadily grown in popularity. It is and modern needling techniques.
estimated that over 10 000 physiotherapists in the UK This short review will provide an overview of the main
alone have been trained in acupuncture and regularly use physiological effects of acupuncture and review its clinical
it for the treatment of musculoskeletal pain. efficacy on common musculoskeletal disorders, including
While acupuncture is an integral part of Traditional a discussion on optimal stimulation parameters.
Chinese Medicine, recent scientific advances have deep-
ened our understanding of the physiological mechanisms
involved in sensory stimulation for the relief of pain PHYSIOLOGICAL EFFECTS OF
and a number of other processes (e.g. healing). Fur- ACUPUNCTURE
thermore, the traditional practice of acupuncture has
evolved through the dissemination of acupuncture Since the publication of Melzack and Wall’s ‘gate control
throughout the Western world and the influence of theory’ in 1965, and the subsequent development of
 34  Adjunct Modalities for Pain 337

transcutaneous electrical nerve stimulation (TENS), a milestone for acupuncture since, for the first time, it was
considerable amount of research effort has been dedi- accepted by the medical establishment (in the United
cated to the physiological mechanisms of analgesia Kingdom) as a credible form of treatment for such a
through sensory stimulation. The historical coincidence common condition. This recommendation was based on
of the publication of the ‘gate control theory’ (1965), the a range of clinical studies that showed acupuncture to be
development of TENS (1967), the discovery of opiate- superior to the control intervention and placebo/sham
like substances in the cow’s brain (1972) and the discovery interventions. Following this, a further review has dem-
of the opiate receptors (1975)1 provided the necessary onstrated that the effect of acupuncture on chronic mus-
environment for the scientific establishment to accept culoskeletal pain is specific and significantly different to
that somatic stimulation is capable of stimulating endog- a sham procedure.7 Earlier studies have also shown that
enous pain-relieving mechanisms, which would explain acupuncture is an effective treatment for chronic knee
the reported efficacy of traditional practices such as acu- pain,8 and that this effect is dependent on a number of
puncture and soft tissue techniques. parameters, namely the number of treatments, the inten-
The following decades showed an explosion in acu- sity and duration of stimulation as well as the repetition
puncture research that examined the physiological effects (treatment frequency) and the total number of treat-
of such modalities (i.e. TENS, acupuncture and elec- ments.9 A similar recommendation was included in the
troacupuncture) and their clinical efficacy. NICE guidelines for the management of headache.10
The realization that Aδ and C fibres contribute to not These recommendations were further validated in a later
only the generation and maintenance of pain, but also the study that showed a positive correlation to the number
stimulation of endogenous analgesic reflexes was perhaps of needles per session and the total number of treatments
the key to unlock the puzzle of the therapeutic effects of to successful treatment outcomes.11
sensory stimulation modalities since they are designed to Other popular applications of acupuncture include
evoke stimuli capable of exciting such fibres.2 Further treatment of the hip, shoulder, elbow and neck pain. The
research3 showed the effects of somatosensory stimula- evidence for the conditions needs further exploration and
tion on the autonomic system, paving the way for further support from large clinical trials; nevertheless, they do
work in this area and explaining the effects of acupunc- point towards effectiveness of acupuncture as an adjunct
ture on conditions such as migraine, infertility, etc. to conventional treatment.12,13 An interesting observation
The key points that emerge from this wealth of inves- from the available trials is that acupuncture and sham
tigation are that acupuncture has peripheral, spinal acupuncture frequently outperform ‘standard care’ which
(segmental) and supraspinal effects, and that these physi- may include a range of physiotherapy and manual medi-
ological responses to sensory stimulation (acupuncture) cine techniques.14,15
account for the analgesic, healing and mood effects Acupuncture is also useful for the relief of myofascial
observed after acupuncture treatment.4 Full accounts of pain and myofascial trigger points. It has been demon-
the complex events that take place after acupuncture strated that, when compared with other modalities, nee-
stimulation are beyond the scope of this short review. An dling seems to be the most effective method for the
up-to-date account can be found in Zhang et al.5 deactivation of myofascial trigger points.16 Frequently
Despite the abundance of scientific evidence on the mentioned as ‘dry needling’ it is safe to say that there is
physiological effects of acupuncture, the issue of its clini- no difference between the two modalities, other than the
cal efficacy remains perhaps one of the most hotly etymological one.
disputed subjects in the field of physical medicine. Pro- Despite the positive reports regarding the clinical effi-
ponents of acupuncture argue that traditional research cacy of acupuncture on a range of conditions, closer
methods employing double-blind, placebo-controlled examination of the literature reveals wide variation in
designs fail to detect the full effect of complex therapies practice and a lack of standardization of treatment param-
(such as acupuncture and exercise). Sceptics argue that eters, namely number of needles, intensity and duration
acupuncture should provide a very robust set of evidence of stimulation and total number of treatments. As early
if it is to be included in the arsenal of the practitioner as 2001, it was proposed that these parameters are crucial
and should withstand the scrutiny of modern scientific for the success to treatment,17 and as a result of such
investigation methods. Thankfully, the last decade has observations, a consensus opinion for the reporting and
seen a significant amount of high-quality randomized designing clinical trials was proposed.18 Perhaps more
clinical trials of acupuncture on a range of musculoskel- significantly the dose of acupuncture treatment has been
etal conditions, which seem to overcome the method- discussed in relation to data from neurophysiological
ological faults of earlier attempts. As such, the clinician studies,19 paving the way for a robust and science-based
can now make a reasoned, evidence-based decision as to approach to designing effective clinical protocols.
whether acupuncture should feature in the rehabilitation Evident from these discussions is the fact that param-
programme of patients with musculoskeletal disorders eters such as intensity of stimulation, duration of treat-
and pain. ment and frequency of treatment seem to be the
determinants of treatment adequacy, moving away from
the Traditional Chinese Medical model which places
ACUPUNCTURE IN THE TREATMENT equal emphasis on point selection to the aforementioned
OF MUSCULOSKELETAL PAIN variables.
Since the scientific validation of the mechanisms
The inclusion of acupuncture in the NICE guidelines for implicated in the analgesic effect of acupuncture, research
the management of low back pain6 was perhaps the has started to explore the effects of acupuncture in a
338 PART III  Advances in Clinical Science and Practice

number of other clinically relevant applications, namely 9. National Institute of Health and Clinical Excellence (NICE).
its anti-inflammatory effects20 and effects on mood21,22 Headaches: diagnosis and management of headaches in young
people and adults. NICE Clin Guide 2012;150. <http://
and the clinical efficacy of acupuncture on such condi- www.nice.org.uk/guidance/CG150>.
tions.23,24 Such investigations further elaborate on the 10. White A, Cummings M, Barlas P, et al. Defining an adequate dose
applications of sensory stimulation for the care of the of acupuncture using aneurophysiological approach–a narrative
patients with musculoskeletal pain, since depression and review of the literature. Acupunct Med 2008;26(2):111–20.
11. MacPherson H, Maschino AC, Lewith G, et al. Acupuncture Trial-
insomnia are common co-morbidities.25,26 ists’ Collaboration. Characteristics of acupuncture treatment asso-
Acupuncture has evolved in recent years to become ciated with outcome: an individual patient meta-analysis of 17,922
a useful and effective tool in the arsenal of the musculo- patients with chronic pain in randomised controlled trials. PLoS
skeletal pain therapist. Frequently, its origins from Tra- ONE 2013;8(10):e77438.
ditional Chinese Medicine create friction with an 12. Green S, Buchbinder R, Hetrick S. Acupuncture for shoulder pain.
Cochrane Database Syst Rev 2005;18(2):CD005319.
establishment whose point of reference is the Western 13. Trinh KV, Phillips SD, Ho E, et al. Acupuncture for the alleviation
medical model; however, as evidence for its physiological of lateral epicondyle pain: a systematic review. Rheumatology
and clinical effects become available its acceptance as 2004;43(9):1085–90.
a valid, biologically plausible method of treatment is 14. Stener-Victorin E, Kruse-Smidje C, Jung K. Comparison between
electro-acupuncture and hydrotherapy, both in combination with
increasing. The biomedical model of clinical reasoning patient education and patient education alone, on the symptomatic
as evidenced from Western medical acupuncture seems treatment of osteoarthritis of the hip. Clin J Pain 2004;20(3):
to be the most promising development in the field of 179–85.
acupuncture or needling-based therapies in general.27 15. Witt CM, Jena S, Brinkhaus B, et al. Acupuncture for patients with
The reports which show that the inclusion of acupunc- chronic neck pain. Pain 2006;125(1-2):98–106. [Epub 2006 Jun 14].
16. Cummings TM, White AR. Needling therapies in the management
ture in a package of care for conditions prevalent in of myofascial trigger point pain: a systematic review. Arch Phys
primary care such as back pain,28 knee pain,29 neck pain30 Med Rehabil 2001;82(7):986–92.
and headache,31 is a cost-effective measure, adds to the 17. Ezzo J, Hadhazy V, Birch S, et al. Acupuncture for osteoarthritis
confidence of the therapist when choosing to include of the knee: a systematic review. Arhtritis Rheum 2001;44(4):
819–25.
acupuncture in their treatment options. 18. MacPherson H, Altman DG, Hammershlag R, et al. Revised stan-
The time has perhaps come to consider acupuncture darts for teporting interventions in clinical trials of acupuncture
(or dry needling) as a core skill in physiotherapy and (STRICTA): extending the CONSORT statement. J Evid Based
advocate its inclusion to the core curriculum of physio- Med 2010;3(3):140–55.
therapy education. Experience throughout the Western 19. White A, Cummings M, Barlas P, et al. Acupunct Med 2008;26(2):
111–20.
world has shown that physiotherapists are perhaps the 20. Kavoussi B, Ross BE. The neuroimmune basis of anti-inflammatory
best-suited practitioners to apply acupuncture since they acupuncture. Integr Cancer Ther 2007;6(3):251–7.
have the scientific background, technical and clinical 21. da Silva MA, Dorsher PT. Neuroanatomic and clinical correspon-
skills to effectively incorporate acupuncture in the care dences: acupuncture and vagus nerve stimulation. J Altern Comple-
ment Med 2014;20(4):233–40.
of their patients. 22. Hui KK, Marina O, Liu J, et al. Acupuncture, the limbic system,and
the anticorrelated networks of the brain. Auton Neurosci
2010;157(1-2):81–90.
REFERENCES 23. Hopton A, Macpherson H, Keding A, et al. Acupuncture, counsel-
1. Hughes J, Kosterlitz HW, Smith TW. The distribution of ling or usual care for depression and comorbid pain: secondary
methionine-enkephalin and leucine-enkephalin in the brain and analysis of a randomised controlled trial. BMJ Open 2014;4(5):
peripheral tissues. Br J Pharmacol 1997;120(4 Suppl.):428–36. e004964. doi:10.1136/bmjopen-2014-004964.
2. Sprenger C, Bingel U, Büchel C. Treating pain with pain: supra- 24. Spence DW, Kayumov L, Chen A, et al. Acupuncture increases
spinal mechanisms of endogenous analgesia elicited by heterotopic nocturnal melatonin secretion and reduces insomnia and anxiety: a
noxious conditioning stimulation. Pain 2011;152(2):428–39. preliminary report. J Neuropsychiatry Clin Neurosci 2004;16(1):
3. Sato A, Sato Y, Schmidt RF. The impact of somatosensory input 19–28.
on autonomic functions. Rev Physiol Biochem Pharmacol 25. Lavigne GJ, Nashed A, Manzini C, et al. Does sleep differ among
1997;130(130):1–328. patients with common musculoskeletal pain disorders? Curr Rheu-
4. Kawakita K, Gotoh K. Role of polymodal receptors in the matol Rep 2011;13(6):535–42.
acupuncture-mediated endogenous pain inhibitory systems. Prog 26. Gorevic PD. Osteoarthritis. A review of musculoskeletal aging and
Brain Res 1996;113:507–23. treatment issues in geriatric patients. Geriatrics 2004;59(8):28–32.
5. Zhang ZJ, Wang XM, McAlonan GM. Neural acupuncture unit: a 27. Kavoussi B. The untold story of acupuncture. FACT 2009;14(4):
new concept for interpreting effects and mechanisms of acupunc- 276–85.
ture. Evid Based Complement Alternat Med 2012;2012:429412. 28. Ratcliffe J, Thomas KJ, MacPherson H, et al. A randomised con-
doi:10.1155/2012/429412; [Epub 2012 Mar 8]. trolled trial of acupuncture care for persistent low back pain: cost
6. National Institute of Health and Clinical Excellence (NICE). Low effectiveness analysis. BMJ 2006;333(7569):626.
back pain: early management of persistent low back pain. NICE 29. Whitehurst DG, Bryan S, Hay EM, et al. Cost-effectiveness of
Clin Guide 2009;88. <http://www.nice.org.uk/guidance/CG88>. acupuncture care as an adjunct to exercise-based physical therapy
7. Vickers AJ, Cronin AM, Maschino AC, et  al. Acupuncture for osteoarthritis of the knee. Phys Ther 2011;91(5):630–41.
Trialists’ Collaboration. Acupuncture for chronic pain: individual 30. Willich SN, Reinhold T, Selim D, et al. Cost-effectiveness of acu-
patient data meta-analysis. Arch Intern Med 2012;172(19): puncture treatment in patients with chronic neck pain. Pain
1444–53. 2006;125(1-2):107–13.
8. White A, Foster NE, Cummings M, et al. Acupuncture treatment 31. Wonderling D, Vickers AJ, Grieve R, et al. Cost effectiveness
for chronic knee pain: a systematic review. Rheumatology (Oxford) analysis of a randomised trial of acupuncture for chronic headache
2007;46(3):384–90. in primary care. BMJ 2004;328(7442):747.
 34  Adjunct Modalities for Pain 339

CHAPTER 34.3  ■  THE USE OF TAPE IN

MANAGING SPINAL PAIN
Jenny McConnell

Patients with musculoskeletal problems usually present homoeostasis.10 Dye contends that symptoms will not be
to physiotherapists for the treatment of pain. Treatment present if an individual is operating inside his/her enve-
for chronic conditions frequently has to be modified lope of function, but as soon as a threshold is reached a
because the patient experiences increased pain during complex biological cascade of trauma and repair will
treatment. Modifying the treatment can impede the occur, which will be manifested clinically by pain and
recovery of the patient. The practitioner therefore needs swelling. In this model there are four factors determining
to employ strategies that will minimize the aggravation the size of an individual’s envelope of function: (a) ana-
of symptoms and facilitate the rehabilitation of the tomical (e.g. involving the morphology, structural integ-
patient. Appropriate taping of a painful area has been rity and biomechanical characteristics of the tissue); (b)
found to decrease pain, alter muscle activity, change joint kinematic (e.g. the dynamic control of the joint involving
range of motion, improve joint loading and provide proprioceptive sensory output, cerebral and cerebellar
support for the injured area.1–5 sequencing of motor units, spinal reflex mechanisms,
muscle strength and motor control); (c) physiological
(e.g. the genetically determined mechanisms responsible
WHAT IS PAIN? for the quality and rate of repair of damaged tissues; and
(d) treatment (e.g. the type of rehabilitation or surgery
Pain has been defined as an unpleasant sensory or emo- received).
tional experience associated with actual or potential tissue
damage (nociception). Pain involves the patient’s reaction
to the nociception, so it is very much an individual expe- WHERE IS THE PAIN COMING FROM?
rience with a learned component.6 Pain can become
memorized because pain mechanisms are not fixed or In the first instance, pain will come from increased sen-
hard-wired, but are plastic or soft-wired.7 Through neu- sitivity of structures in the vicinity of the problem which
roplasticity, hyperalgesia can be learned and unlearned, will be mostly soft-tissue-related. Many soft tissues such
from both tissue-based and environmental afferent as ligaments and tendons have tensile properties but these
inputs.7 properties are affected when the ligament or tendon is
Musculoskeletal pain syndromes are seldom caused by disrupted so the tissues respond adversely to stretch,
isolated precipitating events, but are the consequences of whereas other soft tissues such as menisci and discs are
habitual imbalances in the movement system. The one-off designed to minimize compressive stress but when they
injury such as the torn anterior cruciate ligament, can and are damaged compression increases the sensitivity of the
does occur, but more often than not, physiotherapists are structures. Adams11 has introduced the concept of ‘func-
dealing with more complex pain syndromes such as low tional pathology’, whereby back pain can arise because
back pain and patellofemoral pain, so the problem is postural habits generate painful stress concentrations
often multifactorial and the cause of the pain may be within innervated tissues, even though the stresses are
remote from the site of the symptoms. not high enough to cause physical disruption.
A study by Solomonow and colleagues12 examining the
effect of creep after loaded spinal flexion in the in vivo
WHY ARE SOME INDIVIDUALS MORE feline found that creep developed in the tissues during
SUSCEPTIBLE TO PAIN? the 20 minutes of static or cyclic flexion and did not fully
recover over the 7 hours of following rest. Histological
An individual’s mechanics has a marked effect on their data from the supraspinous ligament showed a tenfold
inherent stability and passive control and hence their increase in neutrophil density in the ligament 2 hours
propensity for experiencing pain. Panjabi described a into the recovery and a hundredfold increase 6 hours into
stability model for the spine which involves passive the recovery from the 20 minutes of sustained and cyclic
structures (osseus, ligamentous, tendinous and capsular flexion, indicating an acute soft tissue inflammation. A
structures of the joint), active structures (muscles) and neuromuscular disorder of a decreasing magnitude of
neural control (centrally and peripherally. This means reflexive EMG from the multifidus upon flexion and
that a joint can be passively unstable, but dynamically superimposed spasms developed during and after the
stable, as the muscles via the neural control subsystem static and cyclic flexion. The recovery period was char-
can compensate for the lack of stability in the passive acterized by an initial muscle hyperexcitability, a slowly
structures.9 increasing reflexive EMG and a delayed hyperexcitability.
The amount of load through the soft tissues or the The authors concluded that sustained static or cyclic
frequency of the loading will also affect joint structures loading of the lumbar viscoelastic tissues caused micro-
and may result in tissue failure, as an individual may damage in the collagen structure resulting in spasms in
breach his/her threshold and stray out of the zone of the multifidus and hyperexcitability early in recovery
340 PART III  Advances in Clinical Science and Practice

when the majority of the creep occurs. The micro-

damage caused the time-dependent development of
inflammation and the resultant spasms (i.e. initial and
delayed hyperexcitabilities) represented the increased
muscular forces applied across the intervertebral joints in
an attempt to limit the range of motion and unload the
viscoelastic tissues in order to prevent further damage
and to promote healing. The authors felt that this may
give insight into development of idiopathic low back
pain.12 Thus, in the acute low back situation, it may be
possible for clinicians to minimize the protective spasm
of the erector spinae by improving the stability of vulner-
able lumbar segments using firm tape (Fig. 34-1).
Unloading painful structures by using a firm, non-
elastic, rayon-based tape with a hypoallergenic tape
underneath allows the patient to exercise and train in a
pain-free manner, which enhances treatment outcomes
and further improves compliance. The principle of
unloading is based on the premise that inflamed soft
tissue does not respond well to stretch.
Hypomobility, which is a lack of flexibility of joint
structures, neural, fascial and muscle tissues, can increase
the stress on other relatively more mobile structures. An
example would be tight hamstrings affecting forward
flexion, so the lumbar spine demonstrates relatively more FIGURE 34-2  ■  Firmly tape across musculotendinous junction of
flexibility; firm tape across the muscle, perpendicular to hamstrings to help improve hamstring flexibility.
the fibres at the musculotendinous junction is effective in
decreasing hamstring tightness, allowing the patient to
stretch the area more effectively (Fig. 34-2).
Hypermobility/instability, which is a lack of passive
and dynamic control, can compromise joint function.
Tape can be used to improve stability by being applied
parallel to the muscle fibres to facilitate muscle activity.
For control post whiplash, tape can be used to provide
stability and minimize excessive protective spasm, par-
ticularly from the upper trapezius and scalenes.
(Fig. 34-3).
If the pain persists central sensitization occurs, where
extrinsic factors can amplify the pain experience. Fear-
avoidance has long been recognized as an important
factor in the development of pain-related disability.
Exposure to stress initiates the secretion of several

FIGURE 34-1  ■  Taping for acute low back pain. Tape towards the
direction of pain with the horizontal strips, starting at the waist FIGURE 34-3  ■  Tape to facilitate stability post whiplash – unload
crease level. The diagonal strips start on the superior horizontal the upper trapezius by lifting soft tissue towards neck and tape
tape to the opposite buttock. to support the scapular stabilizers.
 34  Adjunct Modalities for Pain 341

hormones as part of the survival mechanism, including minimal or no equipment, with a maximum of four exer-
corticosterone/cortisol, catecholamines, prolactin, oxyto- cises, taking no more than 5 minutes when on mainte-
cin and renin. Such conditions are often referred to nance, otherwise they will not be compliant.
as ‘stressors’ and can be divided into three categories:
(a) external conditions resulting in pain or discomfort; REFERENCES
(b) internal homoeostatic disturbances; and (c) learned or 1. Crossley K, Bennell K, Green S, et al. Physical therapy for patel-
associative responses to the perception of impending lofemoral pain: a randomized, double-blinded, placebo-controlled
endangerment, pain or discomfort.13 To test whether fear trial. Am J Sports Med 2002;30(6):857–65.
2. Derasari A, Brindle T, Alter K, et  al. McConnell taping shifts the
changes the motor control of the segment or whether the patella inferiorly in patients with patellofemoral pain: a dynamic
diminished motor control amplifies the fear of pain, pain magnetic resonance imaging study. Phys Ther 2010;90(3):
has been induced in asymptomatic individuals in the 411–19.
lumbar spine. During anticipation of experimentally 3. Gilleard W, McConnell J, Parsons D. The effect of patellar taping
induced back pain, with repetitive arm movements there on the onset of vastus medialis obliquus and vastus lateralis muscle
activity in persons with patellofemoral pain. Phys Ther
was decreased activity of the deep trunk muscles as well 1998;78(1):25–32.
as a shift from biphasic to monophasic activation. 4. Kilbreath SL, Perkins S, Crosbie J, et al. Gluteal taping improves
Increased activity occurred in the superficial trunk hip extension during stance phase of walking following stroke. Aust
muscles. These changes were similar to those observed J Physiother 2006;52(1):53–6.
5. McConnell J, Donnelly CJ, Hamner S, et al. Effect of shoulder
in patients with recurrent back pain.14 The implication is taping on maximum shoulder external and internal rotation range
that if the patient is fearful about a movement causing in uninjured and previously injured overhead athletes during a
pain, that alone will have a dramatic effect on muscle seated throw. J Orthop Res 2011;29(9):1406–11.
performance. It is important for clinicians to do whatever 6. McConnell J, Donnelly CJ, Hamner S, et al. Is passive rotation
they have in their kitbag of treatment modalities to shoulder range of motion indicative of active range of motion
during throwing? PMR 2012;4(2):111–16.
decrease pain so that the detrimental effects of pain and 7. Bogduk N. The anatomy and physiology of nociception. In:
fear of pain can be reduced as soon as possible and muscle Crosbie J, McConnell J, editors. Key issues in Musculoskeletal
function can return to normal. Tape can be extremely Physiotherapy. Oxford: Butterworth-Heinemann; 1993.
successful in achieving this goal, particularly for control- 8. Shacklock M. Central Pain Mechanisms: a new horizon in manual
therapy. Aust J Physiother 1999;45(2):83–92.
ling chronic low back and leg symptoms.15 Using tape to 9. Panjabi M. The stabilising system of the spine. Part I. J Spinal
unload inflamed tissues will decrease the pain and fear of Disord 1992;5(4):383–9.
pain, enabling the clinician to implement muscle-training 10. Dye S. The knee as a biologic transmission with an envelope of
strategies to provide a long-term control of symptoms for function: a theory. Clin Orthop 1996;325:10–18.
the patient.15,16 11. Adams MA. Biomechanics of back pain. Acupunct Med
2004;22(4):178–88.
Chronic musculoskeletal conditions are managed, not 12. Solomonow M, Baratta RV, Zhou BH, et al. Muscular dysfunction
cured. Taping should be used as an adjunct to treatment elicited by creep of lumbar viscoelastic tissue. J Electromyogr Kine-
to decrease pain and improve control while normal siol 2003;13(4):381–96.
mechanics are restored. The patient therefore needs to 13. Van de Kar LD, Blair ML. Forebrain pathways mediating stress-
induced hormone secretion. Front Neuroendocrinol 1999;20(1):
do something daily to ensure that the muscles stay 1–48.
working well and their symptoms do not recur. It is 14. Moseley GL, Nicholas MK, Hodges PW. Does anticipation of back
essential to improve the patient’s awareness of the effects pain predispose to back trouble? Brain 2004;127(Pt 10):2339–47.
of uncontrolled sustained posture and to give them simple 15. McConnell J. Recalcitrant chronic low back and leg pain – a new
strategies so that they can cope with everyday life – how theory and different approach to management. In: Karen B, editor.
Manual Therapy in Masterclasses – The Vertebral Column.
to stand, how to sit and how to get from sitting to stand- London: Churchill Livingstone; 2003.
ing, what type of mattress and pillow they need, what 16. McConnell J. Management of a difficult knee problem. Man Ther
type of chair, position of arms on chairs, workstation 2013;18(3):258–63.
advice, etc. They also need a home programme that uses
 CHAPTER 35 

Cautions in Musculoskeletal
Practice

CHAPTER OUTLINE

Editor’s Introduction Ch 35.3  Pre-Manipulative Screening for

Craniocervical Ligament Integrity  352
Ch 35.1  Masqueraders  343
Peter Osmotherly
Susan Greenhalgh  •  James Selfe
Ch 35.2  Haemodynamics and Clinical Practice  347
Alan Taylor  •  Roger Kerry

EDITOR’S INTRODUCTION

Physiotherapists assessing, treating and exclude instability in the upper cervical spine
providing guidance to people presenting with region as the source of symptoms. This
musculoskeletal conditions are, in many highlights the importance of including a chapter
countries, primary contact practitioners who discussing cautions in musculoskeletal practice.
make autonomous decisions and provide the Chapter 35 brings together international experts
highest levels of care possible. Referrals for in these fields of musculoskeletal practice to
management may also come from other health provide the reader with an essential overview of
professionals. Irrespective of the method of areas of concern that impact on clinical practice.
referral, physiotherapists must be accountable Each subchapter provides invaluable information
for their clinical practice. They must ensure that that will be indispensable to clinicians.
they remain vigilant to sinister conditions that Information includes methods of identifying
may masquerade as musculoskeletal symptoms sinister pathology and guidance on critical time
or that may be derived from non- frames required to respond to certain presenting
musculoskeletal sources, such as the vascular symptoms. Guidance is provided
system. They must also be aware of the possible to help identify clinical signs that may be
side effects of medicines that may masquerade associated with vascular impairment and
as musculoskeletal symptoms. It is highly methods of management. Finally a review
relevant that one of the most common of craniocervical ligament integrity assessment
presenting symptoms of vascular pathology is will provide important guidance for those using
pain, and that neoplasms may mimic the these tests to assess the stability of
symptoms of musculoskeletal conditions. In the upper cervical spine as well as part of
addition, physiotherapists assessing pre-cervical spine manipulation screening.
musculoskeletal conditions, such as symptoms Chapter 35 is essential reading for all
emanating from structures associated with musculoskeletal physiotherapists, those
cervical spine, must be aware of the value as newly qualified and those with considerable
well as the limitations of tests to implicate or clinical experience.

342
 35  Cautions in Musculoskeletal Practice 343

CHAPTER 35.1  ■  MASQUERADERS

Susan Greenhalgh  •  James Selfe

INTRODUCTION sometimes deceptive nature of symptoms referred from

the viscera and from changes within metabolic systems
Musculoskeletal physiotherapists may be ‘first contact’ (Fig. 35-1). In this short section it is impossible to discuss
clinicians or receive referrals from other health speciali- all the possible musculoskeletal masqueraders, or even to
ties. It remains our duty of care to refer patients to an produce a comprehensive list. We have therefore chosen
appropriate speciality in a timely manner if the present- to focus on a small number of areas that are slightly more
ing condition proves not to be musculoskeletal in origin. common and have important implications for musculo-
Although masqueraders of musculoskeletal conditions skeletal practitioners.
are rare in the general population, timely recognition of It is essential not to underestimate the power of sound
these presentations is essential. A key challenge for prac- anatomical knowledge in clinical reasoning. For example,
titioners managing patients presenting to musculoskele- anatomical knowledge clearly illustrates why a Pancoast
tal services is that the source of symptoms is frequently tumour could produce symptoms in a C8/T1 distribu-
extensive and may not originate from musculoskeletal tion. Clinicians must also consider the wider holistic
tissues. The pathological mechanisms responsible for picture and actively listen to the patient’s experiences (i.e.
generating nociceptive signals may, particularly in the what makes symptoms worse, what improves the symp-
early stages of a non-musculoskeletal condition, present toms, when did it start, has anything else changed). The
a confusing and indistinct clinical picture. For example thoracic spine has a complex neural anatomy leading to
serious pathology of the spine can initially masquerade as difficulty in differentiating between visceral and somatic
simple back pain (Box 35-1). The difficulties associated pain.7 The close proximity of the intercostal nerves and
with early identification of serious causes of back pain are the sympathetic plexus to the zygoapophyseal, costo-
compounded by the sheer number of people suffering transverse and costovertebral joints, disc and vertebral
from low back pain and the variety and vagueness of body account for referred band-like pain with any lesion
symptoms articulated by the patients. It is also important compressing neural structures within this spinal complex.
to recognize that patients suffering with complex chronic As with dermatomal distribution, there are discrepancies
pain states are not immune to other forms of pathology, relating to the exact locations for some of these referred
and that musculoskeletal disorders may often coexist with pains from viscera, which are often vague and ill-defined
other pathologies. in nature. Figure 35-1 illustrates some of the less conten-
Masqueraders are usually related to a lesion of a tious areas. For more detailed information on this inter-
system unrelated to the perceived site and nature of esting subject see; Topical Issues in Pain 3e edited by Louis
symptoms. The clinical severity of masqueraders covers Gifford.8
a broad spectrum ranging from emergency life-
threatening conditions (e.g. aortic aneurysm) through to
minor disorders (e.g. carpal tunnel syndrome). Grieve CAUDA EQUINA SYNDROME
first approached the subject of masqueraders in 1986
(p. 848),4 he observed that: ‘Neoplasms are sly surrepti- The estimated yearly incidence of cauda equina syn-
tious things, often masquerading as quite ordinary mus- drome (CES) in England is 2 per 100 000.9 It is a rare
culoskeletal syndromes’. condition accounting for 2% of all herniated discs.
Those involved in musculoskeletal medicine work in
an arena with some element of risk, with aspects of confu-
sion and doubt occurring on a daily basis. Our clinical
What is It?
skills should guide us to reach a conclusion of greatest CES occurs as a consequence of the loss of function of
belief by considering the inherent likelihood of the cause two or more of the 18 nerve roots that comprise the
(or causes) of a patient’s pain and dysfunction. In order cauda equina.10 CES is a potential emergency.11,12 Conse-
to do this accurately we must possess knowledge of the quently, it is mandatory that physiotherapists should rou-
tinely ask about bladder and bowel functions during the
subjective examination.3,13,14 Early diagnosis and surgical
BOX 35-1  Definitions of Terms decompression are essential. Jalloh and Minhas15 and
Gleave and Macfarlane16 suggest that spinal surgery
Masquerader: A condition that ‘appears in disguise or within 48 hours of an individual developing sphincter
assumes a false appearance’ dysfunction will optimize post-operative recovery. If left
Red Herring:1 Misleading biomedical or psychosocial factor untreated, CES may lead to permanent loss of bowel and
that could deflect the course of accurate clinical
reasoning
bladder control, sexual dysfunction or even paralysis.17
Red Flag:2 Possible indicator of serious pathology Current evidence regarding the clinical presentation of
Serious pathology:3 Fracture, cancer, infection, cauda CES demonstrates marked discrepancies related to its
equina syndrome, inflammatory disorder definition, with 17 different definitions of CES recorded.11
Fraser et al.11 have suggested that one or more of the
344 PART III  Advances in Clinical Science and Practice

Diaphragm
(C3–5)

Heart
(C8–T4)

Pancreas Stomach
(T6–10) (T6–10)
Gall bladder Liver
(T7–8) (T7–8)

Bladder Kidney
(T11–L1) (T10–L1)

FIGURE 35-1  ■  Common sites of visceral pain referral.5,6 For colour version see Plate 22.

following must be present in order to make a provisional BOX 35-2  Sexual Dysfunction Associated
diagnosis of CES: bladder and/or bowel dysfunction; with CES18
reduced sensation in the saddle area; sexual dysfunction
(Box 35-2). SEXUAL DYSFUNCTION
Clinicians commonly consider CES as either incom- Vaginal anaesthesia and numbness
plete (CES-I) or complete (CES-R).19 Incontinence during intercourse
Decreased intensity and/or inability to achieve orgasm
Inability to achieve erection
CES-I (48-Hour Emergency Window Open Inability to achieve ejaculation
Where Surgery is Likely to be Helpful)
• Unilateral or bilateral sciatica may be present and
increasing.
• Neurological deficit progressing.
• Unilateral or patchy perineal/perianal numbness. • No bladder sensation or control.
• Anal sphincter tone may be reduced. • Faecal incontinence.
• Loss of desire to void, poor stream, strain to mictur-
ate but with sensation of full bladder. Important Issues
• Early diagnosis provides the best chance of optimal
CES-R (Emergency Window Passed Where
recovery.
Surgery is Less Likely to be Beneficial)
• Diagnosis in early stages is not easy, yet is an
• May have no leg pain or may have unilateral/ orthopaedic/neurological emergency.
bilateral sciatica. • To confound early diagnosis, the patient’s experi-
• May have unilateral or bilateral neurological deficit. ence of CES symptoms can be difficult for them to
• Widespread perineal sensory deficit. recognize or articulate.20
• No anal sphincter tone. • It can be a highly litigious condition; damages on
• Painless urinary retention with full bladder and average can be £300 00017 because many cases are
overflow incontinence. preventable.20
 35  Cautions in Musculoskeletal Practice 345

• Approximately 20% will have poor outcome (e.g. A CES guideline has recently been published by
sexual dysfunction, self-catheterization, colostomy, Gloucestershire Hospitals NHS (UK) that is designed to
psychosocial support). advance critical thinking skills and evidence-based man-
• Potentially improved outcome if retention rather agement of CES.24
than incontinence present.
• Erectile dysfunction uncommon but a strong indi-
cator of a poor prognosis. METASTATIC SPINAL CORD
• Early recognition is essential as decompression is COMPRESSION
preferably within 24–48 hours.
Gleave and Macfarlane16 reported that the emergency The guidelines for the physiotherapy management of low
surgical window is very small (48 hours) and they state back pain14 reported that there were 163 individual items
that ‘the die is cast at the time of the prolapse’ depending that could be considered as Red Flags. Clearly this pres-
on the speed of development and the severity of compres- ents a major problem in terms of the practical and clinical
sion. This paper has been used subsequently to inform utility of the current system of spinal Red Flags; none of
court decisions in the UK.21 There is still debate sur- the 163 items had been identified as being specific to
rounding the optimum point of surgical intervention metastatic spinal cord compression (MSCC).
with many authors suggesting that surgery should take The true incidence of MSCC is unknown; post-
place at the early stages of CES. This has been defined mortem evidence indicates that it is present in 5–10% of
as unilateral or bilateral sensory/motor deficit in the patients with advanced cancer. In total, there are approxi-
lower extremities, prior to sphincter involvement.22,23 mately 4000 new cases of MSCC reported in England
and Wales per year.25
What Causes Confusion?
Variations in presentation may range from rapid onset of
What is It?
CES without previous history of back pain to acute MSCC is a well-recognized complication of cancer. The
bladder dysfunction with a history of back pain and sci- condition occurs when there is pathological vertebral
atica, or even chronic backache and sciatica with gradual body collapse or direct tumour growth causing compres-
progression to CES.9 In addition, a number of confound- sion of the spinal cord leading to irreversible neurological
ing factors may influence excretory organ dysfunction; damage. In addition to the agonizing pain and spinal
these include medication (opioid salts; anticonvulsants; instability that the condition can cause; compression on
antidepressants), co-morbidity (prostate conditions; the spinal cord can also lead to paraplegia or quadriplegia
stress incontinence) or pain (acute or chronic). and double incontinence.26

Emerging Issues Important Issues

The pattern of symptom progression in CES has not • Frequently missed oncological emergency.26
been defined.22 Knowing that there appears to be no • At diagnosis 82% of patients with MSCC are unable
chronological pattern to symptoms developing may actu- to walk or only able to do so with help.26
ally be clinically valuable. In 2013, in the UK a lengthy • Life expectancy significantly reduced once paraple-
debate took place on the Chartered Society of Physio- gia has developed.27
therapy website (iCSP) relating to the definition of saddle • Those with established paraparesis and loss of
anaesthesia. Part of the discussion involved the exact bladder control by the time of treatment are unlikely
location of the saddle (bicycle versus horse). Personal to regain useful function.28
communication with the CES UK Charity confirms that • The best outcome for MSCC in terms of function
amongst their members, the anatomical area that would and prognosis depends on a high index of suspicion,
be in contact with a horse’s saddle (including buttocks) is early diagnosis, onward referral for urgent investi-
affected. gation ideally within 24 hours25 and prompt treat-
ment in order to prevent or limit neurological
damage.
New Advances • Whole spinal scan required within 24 hours.25
A review of CES patient records has confirmed that these
cases were regularly being missed in the early stages of
symptom development.20 A subsequent service improve-
What Causes Confusion?
ment using an experience-based design model suggested MSCC may appear as simple mechanical back pain ini-
that when suffering severe pain, bladder function was tially. Early detection and diagnosis of MSCC, before the
often not the main cause of a patient’s concern. development of neurological symptoms relies solely on
For example the following quote was reported in sheer the subjective history taking. This is extremely challeng-
disbelief by the patient as she perceived the question was ing when considering that on average patients present to
‘stupid’. ‘I was crawling on the floor in agony when the a variety of non-specialist practitioners in a broad range
ambulance man asked if me if I had any bladder prob- of locations within three weeks of the onset of back
lems?’ This illustrates the importance of patients under- pain.26 Physical neurological examination is unremark-
standing the significance of Red Flag questions within the able until later stages in the disease process. Subjective
context of their suffering. leg symptoms may be vague: ‘my legs feel odd and weak’.29
346 PART III  Advances in Clinical Science and Practice

Emerging Issues New Advances

Studies have reported that around 25% of patients A new eight-item tool aimed at helping clinicians to iden-
present with spinal cord compression as the first sign of tify the early signs and symptoms of MSCC has been
malignancy with no previous diagnosis of primary developed and produced in the form of a credit card.30
cancer.25 A combination of Red Flags increases suspicion, The Greater Manchester and Cheshire Cancer Network
the more Red Flags the higher the risk and the greater (UK) brought together oncology expertise from the
the urgency. Regional Cancer Centre (Christie) and primary care
musculoskeletal physiotherapy, to produce a user-friendly
list of MSCC Red Flags for non-specialist front-line cli-
nicians working in primary care settings.
TABLE 35-1  Musculoskeletal Side Effects of Referred back pain that is multisegmental or band-like
Medication32–35 Escalating pain which is poorly responsive to treat-
ment (including medication)
Musculoskeletal Different character or site to previous symptoms
Side Effects: Signs
and Symptoms Medication
Funny feelings, odd sensations or heavy legs
(multisegmental)
Mild aches, pains Oral contraceptives (e.g. Lying flat increases back pain
Microgynon)
Statins (e.g. atorvastatin)
Agonizing pain causing anguish and despair
Muscle cramps Diuretics (e.g.
Gait disturbance, unsteadiness, especially on stairs
bendroflumethiazide) (not just a limp)
Calcium channel blockers (e.g. Sleep grossly disturbed due to pain being worse at
verapamil) night.
Beta-agonists (e.g. salbutamol) It is important to emphasize that established motor,
Proximal muscle Oral corticosteroids sensory, bladder and bowel disturbances are considered
weakness, (e.g. prednisolone)
atrophy >10 mg daily dose, for at least 30 to be late signs.
days
Severe pain, Statins
myopathy, 0.1–0.2% of patients in clinical MEDICATION
malaise, fever, trials have side effects
dark urine
In the UK, Chartered Physiotherapists have been
Osteoporosis, Oral corticosteroids
fracture Doses >5 mg daily lead to
performing injections since 1995; they were given
significant and rapid bone loss. supplementary prescribing rights in 2005 and indepen-
A cumulative dose of >30 g dent prescribing rights in 2013.31 Even if physiotherapy
associated with a high incidence practice does not encompass these extended roles,
of fracture 53%. Excessive risk knowledge of side effects of common medications
of fracture disappears within 1
year of stopping therapy which masquerade as musculoskeletal problems is useful
Avascular necrosis Corticosteroids in the clinical reasoning processes (Table 35-1). Medi-
5–40% of patients on long-term cations can produce side effects, and it is essential for
therapy physiotherapists to be aware of these as they may
Tendinopathy, Injected corticosteroids include muscle pain, bladder and bowel dysfunction,
tendon rupture Oral corticosteroids osteoporosis, fractures and tendon ruptures. A large
myopathy Glucocorticoids have a direct
catabolic effect on skeletal
proportion of the structures within the musculoskeletal
muscle tissue system have a high metabolic rate and blood flow. As
Myalgia, arthralgia, Quinalones (synthetic broad- a consequence the musculoskeletal system has a high
arthritis, spectrum antibiotics) (e.g. exposure to circulating medications.32 Within the clini-
tendinitis ciprofloxacin) cal reasoning process the chronological sequence of
World-wide incidence of side symptoms is important. One of the main clues sug-
effects estimated as 15–20 per
100,000 patients treated gesting that the symptoms are caused by the medication
Bladder and bowel Opioid salts; constipation (e.g. is that the symptoms began after the medication was
dysfunction tramadol, codeine) started and resolved once the medication had ceased.
Anticonvulsants; urinary
incontinence (e.g. gabapentin, REFERENCES
pregabalin) 1. Sykes JB, editor. Concise Oxford Dictionary. 6th ed. Oxford: Clar-
Antidepressants; retention, sexual endon Press.; 1978.
dysfunction (e.g. amitriptyline, 2. Greenhalgh S, Selfe J. Red Flags: A Guide to Identifying Serious
nortriptyline) Pathology of the Spine. Churchill Livingstone, Elsevier; 2006.
Muscle cramp, Thyroid hormones (e.g. 3. Clinical Standards Advisory Group. Report of a Clinical Standards
muscle weakness levothyroxine sodium) at Advisory Group on Back Pain. London: HMSO; 1994.
excessive dosage 4. Grieve G. Modern Manual Therapy of the Vertebral Column.
Joint aches and Antithyroid drugs used to treat Edinburgh and New York: Churchill Livingstone; 1986.
pains (arthralgia) hyperthyroidism (e.g. 5. Standring S, editor. Gray’s Anatomy: the Anatomical Basis of Clini-
carbimazole) cal Practice. 39th ed. Edinburgh: Elsevier Churchill Livingstone;
2005.
 35  Cautions in Musculoskeletal Practice 347

6. Ombregt L, Bisschop O, J ter Veer H. A System of Orthopaedic 22. Sun JC, Xu T, Chen KF, et al. Assessment of cauda equina syn-
Medicine. 2nd ed. Elsevier Science Limited; 2003. drome progression pattern to improve diagnosis. Spine 2013; Spine
7. Boyling J, Jull G. Grieve’s Modern Manual Therapy: The Vertebral publish ahead of print, doi:10.1097/BRS.0000000000000079.
Column. 3rd ed. Churchill Livingstone; 2005. 23. Todd NV. Causes and outcomes of Cauda Equina Syndrome in
8. Gifford L, Thacker M. Complex regional pain syndrome: part 1. medico-legal practice: a single neurosurgical experience of 40 con-
In: Gifford L, editor. Topical Issues in Pain 3. Sympathetic Nervous secutive cases. Br J Neurosurg 2011;25(4):503–8. [Epub 2011 Apr
System and Pain. Pain Management. Clinical Effectiveness. Fal- 22].
mouth: CNS Press; 2002. p. 53–74. 24. © GHNHSFT. Physiotherapy Guideline Cauda Equina Syndrome
9. Gitelman A, Hishmeh S, Morelli B, et al. Cauda equina syndrome: (CES) – Early Recognition v2 ISSUE DATE: v1 July 2012, v2 Apr
a comprehensive review. Am J Orthop 2008;37(11):556–62. 2013. [On line]. Available from: <www.esp-physio.co.uk>; 2013
10. Woolsley R, Martin D. Spinal cord and cauda equina syndromes. [Accessed 14th November 2013].
In: Lin V, Cardenas D, Cutter N, et al., editors. Spinal Cord Medi- 25. National Institute for Health and Clinical Excellence (NICE).
cine: Principles and Practice. New York Demos Medical Publish- Metastatic Spinal Cord Compression: Diagnosis and Management
ing; 2003. of Patients at Risk of or with Metastatic Spinal Cord Compression.
11. Fraser S, Roberts L, Murphy E. Cauda equina syndrome: a litera- Clinical Guideline 75. 2008. [On line]. Available from: <www.nice
ture review of its definition and clinical presentation. Arch Phys .org.uk/Guidance/CG75>; [Accessed 14th November 2013].
Med Rehabil 2009;90:1964–8. 26. Levack P, Graham J, Collie D, et al. Don’t wait for a sensory
12. Mestrum R, De Vooght P, Vanelderen P, et al. Cauda equina syn- level – listen to the symptoms: a prospective audit of the delays in
drome secondary to lumbar disc herniation: pitfalls in clinical pain diagnosis of malignant cord compression. Clin Oncol 2002;14:
management. Eur J Pain 2009;13:S138–9. 472–80.
13. Royal College of General Practitioners. Clinical guidelines for 27. Patchell RA, Tibbs PA, Regine WF. Direct decompressive surgical
the management of acute low back pain. [On line]. Available from: resection in the treatment of spinal cord compression caused by
<http://www.rcgp.org.uk/clinspec/guidelines/backpain/index.asp>; metastatic cancer: a randomised trial. Lancet 2005;266:643–8.
2001 [Accessed 14th November 2013]. 28. Christie Hospital NHS Foundation Trust. Spinal Cord Compres-
14. The Chartered Society of Physiotherapy. Clinical guidelines for the sion Guidelines. Manchester; 2008.
effective physiotherapy management of persistent low back pain. 29. Greenhalgh S, Selfe J. A qualitative investigation of red flags for
[On line]. Available from: <http://corporate.csp.midev.rroom.net/ serious spinal pathology. Physiotherapy 2009;95:224–7.
director/libraryandpublications/publications.cfm?item_id=562CC 30. Turnpenney J, Greenhalgh S, Richards L, et al. Developing an
348D28AC0F97B2AA357019A7C7C>; [Accessed 6 September early alert system for metastatic spinal cord compression. Prim
2010]. Health Care Res Dev 2013;1–7. [Epub ahead of print] [On line].
15. Jalloh I, Minhas P. Delays in the treatment of cauda equina syn- Available from: DOI: <http://dx.doi.org/10.1017/S1463423613000
drome due to its variable clinical features in patients presenting to 376>; [Accessed 14th November 2013].
the emergency department. Emerg Med J 2007;24(1):33–4. 31. Chartered Society of Physiotherapy. CSP History. [On line]. Avail-
16. Gleave JRW, Macfarlane R. Cauda equina syndrome: what is the able from: <http://www.csp.org.uk/about-csp/history/csp-history>;
relationship between timing of surgery and outcome? Br J Neuro- [Accessed 14th November 2013].
surg 2002;16(3):325–8. 32. Randall C. Chapter 11. Musculoskeletal disorders; 293–325. In:
17. Markham DE. Cauda equina syndrome: diagnosis, delay and litiga- Lee A, editor. Adverse Drug Reactions. 2nd ed. London: Pharma-
tion risk. Curr Orthop 2004;18(1):58–62. ceutical Press.; 2006.
18. Shapiro S. Medical realities of cauda equina syndrome secondary 33. BNF 65. March-September. BMA. Royal Pharmaceutical Society;
to lumbar disc herniation. Spine 2000;25:348–52. 2013.
19. Gardner A, Gardner E, Morley T. Cauda equina syndrome: a 34. UPTODATE. Glucocorticoids. [On line]. Available from: <http://
review of the current clinical and medico-legal position. Eur Spine www.uptodate.com/contents/glucocorticoid-induced-myopathy
J 2011;20:690–7. ?source=search_result&search=corticosteroids&selectedTitle=11
20. Anthony S. Cauda equina syndrome. UK Casebook 2003;20: %7E150>; [Accessed 14th November 2013].
9–13. 35. Powell C, Chang C, Naguwa S, et al. Steroid induced osteonecro-
21. Oaks v Neininger, et al. [Online]. Available from: <http:// sis: an analysis of steroid dosing risk. Autoimmun Rev 2010;9:
www.bailii.org/ew/cases/EWHC/QB/2008/548.html>; [Accessed 721–43.
15th July 2013].

CHAPTER 35.2  ■  HAEMODYNAMICS AND CLINICAL

PRACTICE
Alan Taylor  •  Roger Kerry

This chapter highlights key advances in haemodynamic

INTRODUCTION science that are relevant to the everyday practice of mus-
culoskeletal physiotherapy.
Altered haemodynamics is the forgotten Red Flag of The International Federation of Orthopaedic Manip-
manual therapy. While it is well understood in medicine ulative Therapists (IFOMPT) produced a consensus
that a failure to assess the vascular system could lead to document for cervical spine risk assessment,1 which
dire consequences (limb loss, death) for patients, it seems details a shift in thinking pertaining to manual therapy
manual therapists are less well versed in the art of vascular and vascular risk. This chapter provides an overview of
assessment. It is a sobering thought that most vascular this document for clinicians from a practical perspective,
pathologies, from deep vein thrombosis to stroke, have and goes on to consider how this change of practice may
pain as their initial presenting feature – precisely the have implications when considering other anatomical
symptom for which patients may seek manual therapies. regions.
348 PART III  Advances in Clinical Science and Practice

The IFOMPT document recommends a number of of ‘is manipulation dangerous for the vertebral artery and
evidence-informed changes to practice relating to cervi- should I do the vertebral artery test?’. The model gives
cal arterial dysfunction (CAD). Of note, the use of ver- consideration of all movements known to influence vessel
tebral artery testing receives short thrift, in favour of a mechanics (e.g. active and passive exercise and manual
‘systems approach’ based on existing reviews of the best therapy techniques) in the context of the patient’s hae-
of scientific evidence in the area.2 This new model con- modynamic status and with a background knowledge of
siders the whole vascular system, including knowledge a range of pathologies.
of flow dysfunction, vessel mechanics and pertinent sys- Subjective history taking requires clinicians to pay spe-
temic pathologies. Clinicians are guided towards holistic cific attention to known cardiovascular risk factors. This
assessment, incorporating general cardiovascular health serves as a reminder for clinicians of the importance of
and a consideration of pain as a symptom of arterial detail, which should consider family history, as well as
pathology, or impending events such as transient isch- individual predilection towards cardiovascular disease.
aemic attack or stroke. Haemodynamic principles are summarized in Box 35-3.
The idea that cardiovascular status can inform judge- Of interest to clinicians is that more is now known
ment on the likelihood of a haemodynamic event, or about the subtle descriptors patients use which may alert
predict such, is controversial in manual therapy.3,4 therapists to the presence of underlying or impending
However, these studies have over-focused on isolated vascular pathology. Table 35-2 presents typical subtle
pathologies, such as dissection events, and do not repre- clinical presentation for CAD. Table 35-3 details the
sent the range of presentations relevant to musculoskel- range of descriptors used for peripheral vascular pain.
etal therapists. Decades of data from medical literature Utilizing the evidence and knowledge of CAD and
leave little doubt that such a relationship exists.2,5,6 The haemodynamic science, attempts may be made to develop
idea that pain is an early presenting feature of vascular
dysfunction is clear.7–9 The CAD model is well-aligned
to the best of contemporary evidence regarding local BOX 35-3  Principles of Clinical Reasoning
vessel disease.10–13 It utilizes the best of the medical data, as Illustrated by the IFOMPT
demonstrating the relationship between mechanical Framework, Related to
vessel stress, fluid flow changes and disease formation.14,15 Haemodynamics
It is suggested that an awareness of CAD is ‘an important • Haemodynamic science allows us to understand clinical
consideration as part of an orthopaedic manual therapy aspects of vascular pathologies
assessment’. Secondly, attention is drawn to the fact that, • Vascular pathologies present in pre-ischaemic and is­
‘there are serious conditions which may mimic musculo- chaemic stages
skeletal dysfunction in the early stages of their pathologi- • Pain is often an early (pre-ischaemic) symptom of
cal progression’.1 vascular pathology; neurology is a late (ischaemic)
Clinicians should be aware that patients with poten- presentation
tially serious pathology (e.g. impending stroke) may • Vascular pathologies vary in nature and are not confined
attend for manual therapy treatment in the belief that to dissection events
• Cardiovascular and hereditary risk factors predispose to a
they have a benign headache or migraine. Patterns of range of vascular pathologies
vascular pathologies are well known and should be central • Clinical tests currently used have poor diagnostic utility
to clinical reasoning.5 • Reliance on any single clinical test is misleading, and
An important subtle change in risk assessment has physical findings should be considered in context with the
taken place. Attention is shifted away from specific struc- subjective history
tures, dysfunctions and tests, for example it is not a matter

TABLE 35-2  Clinical Presentations Related to CAD in Different Stages of the Pathologies

Pre-Ischaemic Ischaemic
Internal Carotid Artery Internal Carotid
Vertebral Artery Pathology Pathology Vertebral Artery Pathology Artery Pathology

Ipsilateral posterior neck Parietal, temporal headache; Hind-brain transient ischaemic attacks Transient ischaemic
pain/occipital headache unilateral neck pain; jaw (dizziness, diplopia, dysarthria, attack
pain dysphagia, drop attacks, nausea, Ischaemic stroke
Horner’s syndrome, pulsatile nystagmus, facial numbness, (usually middle
tinnitus ataxia, vomiting, hoarseness, loss cerebral artery
Cranial nerve (CN) palsies of short-term memory, vagueness, territory)
(most commonly CN IX to hypotonia/limb weakness (arm or Retinal infarction
XII) leg), anhidrosis (lack of facial Amaurosis fugax
Less common local signs and sweating), hearing disturbances,
symptoms include: malaise, perioral dysthesia,
ipsilateral carotid bruit, scalp photophobia, papillary changes,
tenderness, neck swelling, clumsiness and agitation)
CN VI palsy, orbital pain and Hind-brain stroke (e.g. Wallenberg’s
anhidrosis (facial dryness) syndrome, locked-in syndrome)
 35  Cautions in Musculoskeletal Practice 349

Table 35-3  Descriptors Associated with Vascular Dysfunction in the Peripheral Regions

Upper Limb Lower Limb

Sign/Symptom Arterial Dysfunction Venous Dysfunction Arterial Dysfunction Venous Dysfunction
Exercise-induced pain   
Numbness/tingling   
Cold   
Hot  
Blue (back pressure of vein)   
Fatigue/weak  
Non-dermatomal pain    
Cramp    
Whitened skin/blanching  
Swelling  
Subjective swelling (none seen)   
Redness  
Band of pain  
Throbbing/pulsatile  

(From detailed reviews of multiple case studies; case series; epidemiological studies; experimental studies; and clinical observations.)
Acknowledgments to Simon Meadows, Physiotherapist, for producing this table.

FIGURE 35-2  ■  The Nottingham Cervical Arterial Dysfunction (nCAD) sub-classification system for profiling the haemodynamic status
of a patient presenting with neck and/or head pain. Classes 3 to 5 represent patients presenting with haemodynamic pathology and
medical referral should be considered. Disease progression is represented by the classification order (class 5 is advanced pathol-
ogy). NMS, neuromusculoskeletal.

sub-classification systems to categorize patients. Figure BOX 35-4  Haemodynamic Considerations for
35-2 demonstrates a proposed system known as the Not- Manual Therapists
tingham Cervical Arterial Dysfunction sub-classification
(nCAD). The system categorizes patients first of all into 1. What is the haemodynamic status of the patient?
whether they present with the potential of CAD (classes 2. Should manual therapy assessment proceed in the ‘usual’
1 and 2) or whether they present with signs and symp- way or be modified?
toms of actual CAD pathology (classes 3–5). This enables 3. Are there haemodynamic considerations for treatment/
the clinician to make a decision on whether to continue management of the patient?
with assessment or not, with a view to manual therapy
treatment (classes 1 and 2), or to refer for medical assess-
ment (classes 3–5). CASE STUDIES
The generic principles detailed in Box 35-3 may be
distilled into a small number of clinical questions that the In all musculoskeletal physiotherapy cases, regardless of
manual therapist can use to shape their evidence-informed proposed management strategies, a targeted subjective
reasoning. Box 35-4 summarizes these consideration. history should elucidate clues to potential underlying
350 PART III  Advances in Clinical Science and Practice

vascular pathology, or the need to explore this further attacks’. Importantly, her neck pain cleared completely
using appropriate objective testing. Two short case sce- following the surgery.
narios, one involving a person with a cervical condition
(Case Study 35-1) and one involving a person with a Case Analysis
peripheral condition (Case Study 35-2), will follow which
will illustrate key considerations. What Was the Haemodynamic Status of the
Patient?  The vascular status of the patient was known
to the treating physiotherapist. The case notes detailed
the vascular history and the drugs used to manage it.
CASE STUDY 35-1  MANUAL THERAPY- However, this knowledge did not appear to factor into
INDUCED TRANSIENT the clinical reasoning. This patient would have reason-
ISCHAEMIC ATTACK ably been classified into class 3 or 4 on the nCAD system,
A 75-year-old female with cervical spondylosis is referred indicating medical referral.
for a ‘flare up of neck pain’ by her GP. She had a history
of angina, heart disease and peripheral vascular disease Should Manual Therapy Assessment Have Pro-
(PVD) for which she was taking appropriate medications ceeded in the ‘Usual’ Way or Been Modified?  There
under the care of cardiac and vascular specialists.
are strong indicators that further vascular assessment
should have been undertaken. With the presenting vas-
cular history there should have been a high index of
suspicion for vascular pathology as it is well known that
CASE STUDY 35-2  DYNAMIC UPPER LIMB cardiac disease is associated with carotid disease.16 Pulse
ARTERIAL OCCLUSION palpation or auscultation may have revealed the abnor-
An 18-year-old male competitive swimmer reported poor
mality.17 Blood pressure examination may have been a
competitive performance associated with upper limb pertinent aid to risk assessment prior to treatment.18
‘fatigue’ and weakness when swimming (freestyle). The Cranial nerve testing may have been performed at any
reported symptoms had been getting worse over the last stage, but particularly after the patient’s report of an
3 months and he and his mother were concerned that he adverse response to treatment.
may lose his place on the county team due to his deterio-
rating times/performance.
Were There Haemodynamic Considerations for
Treatment/Management of the Patient?  Where a
patient details a range of vascular risk factors/events there
Case Study 1 is always a consideration for manual therapists to modify
treatment. The belief that only manipulation is ‘risky’ is
The patient was examined by a domiciliary physiothera- a dangerous fallacy; simple movement or exercise may
pist who took a subjective history (including the above have a haemodynamic effect that requires careful consid-
detail). A routine objective examination revealed minor eration, particularly in the presence of an adverse response
loss of cervical range globally. The therapist proceeded to treatment. Empirically, it is known that normal physi-
to treat the patient with longitudinal distraction mobili- ological movements affected vessel mechanics.18
zations in sitting. Re-examination revealed mild gains
(5°) in cervical rotation. At the follow-up visit the patient Clinical Reasoning Note
reported ‘feeling funny’ after the treatment, which was
detailed further as ‘feeling uncomfortable, light headed The therapist detailed all the vascular risk factors in the
and woozy for a few hours’. This was ascribed to treat- notes, but failed to raise an index of suspicion for con-
ment soreness and manual therapy treatment continued. comitant carotid artery disease in a patient already under
Variations of the same treatment continued for four ses- the care of the vascular team for heart disease, angina and
sions in total, with the ‘treatment soreness’ being reported peripheral vascular disease. When the patient reported
after each session. Management was discontinued when an adverse response to the intervention, no further sig-
the patient reported that her reaction to treatment was nificant clinical reasoning took place and the patient was
getting worse, ‘post treatment arm and facial numbness/ offered variations of a similar intervention until
discomfort’ and a report sent to the GP detailing the treatment was eventually halted. Furthermore, from a
outcome. medico-legal perspective the surgeon’s note relating to
At her routine visit to see her specialist she reported ‘physiotherapy-induced transient ischaemic attacks’ may
that her angina was stable, that her walking distance was have had deleterious effects, had a medico-legal case
the same, but that she had had some ‘funny turns’ follow- ensued. The patient’s pain may have been associated with
ing the visits of the domiciliary therapist. The vascular the carotid disease or ‘carotidynia’.19 Repeated movement
surgeon listened carefully to her description of events, of the head on neck might have been sufficient for micro-
palpated her carotid pulses and sent her for immediate embolic events. Beyond the transient ischaemic attacks,
ultrasound scans of her carotid arteries. She was found to no apparent neurology readily manifested itself during
have significant atherosclerotic stenosis bilaterally. She assessment. Clinicians should raise an index of suspicion
was listed for urgent carotid endarterectomy and made a for carotid disease in the presence of co-existing vascular
full recovery. The surgeon’s notes included the entry disease and other cardiovascular risk factors1 and modify
‘possible physiotherapy-induced transient ischaemic examination accordingly.
 35  Cautions in Musculoskeletal Practice 351

Case Study 2 in the light of findings. In this case, glenohumeral

joint instability resulted in functional positional stenosis
The patient was fit and healthy, taking no medications of of the axillary artery, and the therapist’s role was to
any sort and had no history of trauma. The reported identify the problem and then rehabilitate the underly-
family history was unremarkable. Subjective history ing musculoskeletal cause, while monitoring key vascular
revealed an emphasis on upper limb fatigue/weakness and markers.
mild discomfort rather than pain. The symptoms were
associated with swimming only (high-intensity training
or competition) and did not manifest in normal activity. CONCLUSION
Physical examination revealed glenohumeral joint
instability and significant weakness of glenohumeral joint Haemodynamic science has advanced substantially over
lateral rotation. The examination findings were reported the last decade. However, clinical practice has been
to the patient and the mother by the therapist. The slow to adapt. The IFOMPT risk assessment docu-
mother asked ‘could this be circulatory? …because it only ment for the cervical spine is an excellent example
happens during exercise’. She was reassured by the thera- of how the evidence base should be used to inform
pist that this was unlikely, considering the patient’s age clinical practice and reasoning. This chapter illustrates
and lack of vascular risk factors. However, the therapist how clinicians can integrate that knowledge and apply
suggested this would be checked at the next visit. it to real clinical situations. Above all it demonstrates
how sound clinical reasoning allows for modification
Case Analysis of physical examination and management for the benefit
of the patient and the therapist. The fundamentals of
What Was the Haemodynamic Status of the simple vascular assessment together with a sound
Patient?  Because of the patient’s age and activity levels, knowledge of haemodynamic principles and pathologies
there appears to be no apparent traditional vascular risk are an essential tool for the modern musculoskeletal
factors. However, in certain populations the repetitive therapist.
limb movement associated with that sport, together with
mild anomalous body forms, may predispose vascular
compromise.20 REFERENCES
1. Rushton A, Rivett D, Carlesso L, et al. International framework for
Should Manual Therapy Assessment Have Pro- examination of the cervical region for potential of cervical arterial
ceeded in the ‘Usual’ Way or Been Modified?  Although dysfunction prior to orthopaedic manual therapy intervention. Man
subtle, there are sufficient historical indicators that would Ther 2013;pii:S1356-689X(13)00192-6. doi:10.1016/j.math.2013.
11.005.
justify haemodynamic examination. At the follow-up 2. Taylor AJ, Kerry R. A ‘system based’ approach to risk assessment
visit, pulses and blood pressure were taken at rest and of the cervical spine prior to manual therapy. Int J Osteopath Med
found to be entirely normal. Radial pulses were dimin- 2010;13:85–93.
ished in full glenohumeral joint flexion (compared to 3. Mitchell J. Vertebral artery atherosclerosis: a risk factor in the use
of manipulative therapy? Physiother Res Int 2002;7:122–35.
normal). Blood pressure readings were then performed 4. Thomas LC, Rivett DA, Attia JR, et al. Risk factors and clinical
in a temperate setting, with the person quiet and seated, presentation of craniocervical arterial dissection: a prospective
with their arm outstretched and supported. This revealed study. BMC Musculoskelet Disord 2012;3;13:164. doi:10.1186/1471
the following results: left arm resting 124/82, elevated -2474-13-164.
80/62; right arm resting 118/78, elevated 76/60. 5. Kerry R, Taylor AJ. Haemodynamics. In: McCarthy C, editor.
Chapter 6 in: Combined Movement Theory. London: Elsevier;
2010. p. p79–99.
Were There Haemodynamic Considerations for 6. Romero JR, Wolf PA. Epidemiology of stroke: legacy of the fram-
Treatment/Management of the Patient?  The patient ingham heart study. Glob Heart 2013;8(1):67–75.
was referred for further vascular testing and found to 7. Taylor AJ, George KP. Exercise induced leg pain in young athletes
misdiagnosed as pain of musculoskeletal origin. Man Ther
have restricted arterial flow in both upper limbs related 2001;6(1):48–52.
to flexion/elevation. This was due to compression of 8. Kerry R, Taylor AJ. Arterial pathology and cervicocranial pain –
the vessels by the humeral head. He was referred for differential diagnosis for manual therapists and medical practitio-
intensive shoulder rehabilitation, with the goal of improv- ners. Int Musculoskelet Med 2008;30(2):70–7.
ing glenohumeral stability, to address the mechanical 9. Gottesman RF, Sharma P, Robinson KA. Clinical characteristics of
symptomatic vertebral artery dissection: a systematic review. Neu-
impingement of the artery. Importantly, positional blood rologist 2012;18(5):245–54.
pressure readings were used as a primary objective 10. Engelter ST, Grond-Ginsbach C, Metso TM, et al. Cervical artery
measure throughout the process. The patient returned to dissection: trauma and other potential mechanical trigger events.
full competition 4 months later and achieved personal Neurology 2013;80(21):1950–7.
11. Lichy C, Metso A, Pezzini A, et al. Predictors of delayed stroke in
best times in all events after a period of re-conditioning. patients with cervical artery dissection. Int J Stroke 2012;doi:10.11
11/j.1747-4949.2012.00954.
12. Metso AJ, Metso TM, Debette S, et al. Gender and cervical artery
Clinical Reasoning Note dissection. Eur J Neurol 2012;19(4):594–602.
Not all vascular problems are ‘sinister’ or require medical 13. Debette S, Leys D. Cervical-artery dissections: predisposing
factors, diagnosis, and outcome. Lancet Neurol 2009;8(7):
or surgical intervention. Some may respond to phys- 668–78.
iotherapy. It is the role of the clinician to modify 14. Cecchi E, Giglioli C, Valente S, et al. Role of hemodynamic shear
examination and implement appropriate further testing stress in CV disease. Atherosclerosis 2011;214(2):249–56.
352 PART III  Advances in Clinical Science and Practice

15. Anssari-Benam A, Korakianitis T. Atherosclerotic plaques: is 18. Taylor AJ, Kerry R. Vascular profiling: Should manual therapists
endothelial shear stress the only factor? Med Hypotheses take blood pressure? Man Ther 2013;18(4):351–3.
2013;81(2):235–9. 19. Al-Obaidi SM, Asbeutah A, Al-Sayegh N, et al. To establish
16. Aboyans V, Lacroix P. Indications for carotid screening in patients whether McKenzie lumbar flexion and extension mobility exercises
with coronary artery disease. Presse Med 2009;38(6):977–86. performed in lying affect central as well as systemic hemodynamics:
17. Cournot M, Boccalon H, Cambou JP, et al. Accuracy of the screen- a crossover experimental study. Physiotherapy 2013;99(3):258–65.
ing physical examination to identify subclinical atherosclerosis and 20. Stanbro M, Gray BH, Kellicut DC. Carotidynia: revisiting an unfa-
peripheral arterial disease in asymptomatic subjects. J Vasc Surg miliar entity. Ann Vasc Surg 2011;25(8):1144–53.
2007;46(6):1215–21.

CHAPTER 35.3  ■  PRE-MANIPULATIVE SCREENING FOR

CRANIOCERVICAL LIGAMENT
INTEGRITY
Peter Osmotherly

highlighting the considerable disagreement regarding

INTRODUCTION the actual symptoms and signs exhibited by an individual
with craniocervical ligament lesions.16 A summary of the
Pre-manipulative screening to assess the integrity of the more commonly described signs and symptoms is given
craniocervical junction is used to guide and alert clini- in Table 35-4. Many patients exhibit no symptoms at all,
cians who are considering manual treatments including even in the presence of demonstrable instability.4,19 In
end-range or high-velocity techniques to the upper isolation, many of the described symptoms could be
cervical spine which, in the presence of hypermobility associated with other disorders of the cervical spine
or instability, could result in adverse outcomes. The and cannot be considered indicative of craniocervical
application of mechanical force in the presence of insta-
bility can result in catastrophic medical consequences1
that may include motor incoordination,2–4 disturbance TABLE 35-4  Described Signs and Symptoms
of bladder or bowel control,5–7 bilateral, hemilateral of Craniocervical Instability
or quadrilateral paraesthesia or hypoaesthesia,2,4,7–9 or
even death from spinal cord compression or vascular Symptoms Signs
injury secondary to excessive craniocervical range of Bilateral or quadrilateral Altered proprioception2,7–9
rotation.3,5,10 limb paraesthesia Altered sensation for
Stability within the craniocervical complex is achieved reproduced by active or vibration and deep
by a complex interaction between the osseoligamentous passive movement2,17,18 pressure2,7–9
Buzzing in the ears/ Altered sphincter control
and neuromuscular systems of this region.11 Central to tinnitus18,19 (bladder/bowel)5–7,14,22
this interaction is the role of the ligaments that span the Dizziness2,19,20 Pain within range of
occipito-atlantoaxial complex,12,13 particularly the trans- Facial pain or cervical motion26–29
verse ligament of the atlas, the alar ligaments and the paraesthesia18,19 Ataxia2–4,14,22
Feeling of a lump in the Cardiac distress2,30
tectorial membrane.14,15 Trauma, inflammatory disease or throat Hyper-reflexia7,8,14,17,31
infection involving the craniocervical ligaments may Headache3,14,20,21 Increased mobility on
result in injury or laxity to these structures. In conjunc- Hypoaesthesia of both passive movement
tion with pertinent aspects of the patient history and hands or both feet2 testing of the upper
physical examination, the performance of clinical screen- Metallic taste in the cervical spine32
mouth18 Loss of cervical lordosis26
ing tests developed to assess hypermobility or instability Nausea or vomiting22 Nystagmus on head/ neck
of the craniocervical ligaments is designed to inform the Occipital numbness or movement8,14,19
clinician to seek alternative management if appropriate, paraesthesia23 Lingual deviation2
or to select treatment techniques with a lower risk of Paraesthesia of the lips Persistent, pain-free
reproduced by active or torticollis (‘cock robin’
potential consequences in patients where ligamentous passive movement24 position)19,33
compromise may be suspected.16 Popping in the ears18 Respiratory distress2,30
Retro-ocular pain25 Syncope14,17
Reflex swallowing or
gagging2
SCREENING FOR CRANIOCERVICAL Upper cervical or
suboccipital pain3,19,26
INSTABILITIES Pain on sudden movement
of the head and neck22
The type and nature of symptoms associated with cranio- Vagal nerve symptoms
e.g. chest and
cervical instability are extremely diverse. One narrative abdominal pain,
literature review compiled 42 signs and symptoms tachycardia10
associated with instability of the craniocervical region
 35  Cautions in Musculoskeletal Practice 353

instability on their own.15,16,34 Currently, there is a lack of sliding motion of the head when pressure was applied in
consensus as to any distinctive cluster of symptoms indi- a posterior direction indicated atlanto-axial instabil-
cating the presence of clinical instability in this region.4,16,35 ity.2,14,22,39 Other descriptions of the interpretation of this
The severity of symptoms has been reported to vary from test relate to symptom modification. As the test is
vague discomfort to severe distress indicative of long proposed to relocate the odontoid process against the
tract compromise of the spinal cord.17,36 Published anterior arch of the atlas, it is considered that
clinical reports suggest that severe presentations are symptoms associated with this position may be relieved
rare.25,27,37–39 Many patients will tolerate marked instabil- or ablated.15,24,44–47 A ‘clunk’ on relocation of the atlas has
ity without exhibiting neurological symptoms or signs, also been interpreted as a positive finding.15,22,24
instead presenting with a wide variety of less severe Exploration of the validity of this test has yielded sen-
symptoms. Furthermore, symptom severity often appears sitivity ranging from 43%48 to 69%39 and specificity from
unrelated to the degree of pathological change present,40,41 77%48 to 98%.4 The higher estimate of specificity would
necessitating that assessment of instability occurs within suggest that the test, when positive, is potentially clini-
a strong clinical reasoning framework. cally useful in a rheumatoid arthritis population because
A number of linear stress tests have been proposed to of its low false-positive rate. However, estimates of both
assess craniocervical ligament integrity. While descrip- intra- and inter-observer reliability for the test are
tions of many of these tests may be found else- poor.42,48 Assessments of the validity and reliability of this
where,9,14,15,42,43 the more commonly described linear test have all been performed in non-traumatic popula-
stress tests used to assess this region are presented in tions, notably adults with rheumatoid arthritis and chil-
Table 35-5 and discussed below. dren with Down syndrome. While we may infer that the
mechanism by which the test is proposed to be effective
is the same, the applicability of the test to a traumatic
Tests for Transverse Ligament Integrity population under conditions of acute pain and muscle
spasm is not truly known.
Sharp-Purser Test
Originally proposed as a clinical method of assessing Anterior Shear Test
spontaneous atlanto-axial dislocation in individuals with
ankylosing spondylitis and rheumatoid arthritis, the Unlike the Sharp-Purser test, the anterior shear test is
Sharp-Purser test is commonly recommended to assess potentially a provocation test. For this reason, some
for integrity of the transverse ligament of the atlas. Inter- authors have urged caution in its use, suggesting it should
pretation of this test in its original form was that any only be used in the presence of a negative Sharp-Purser

Table 35-5  Descriptions of Commonly Used Stress Tests to Assess Craniocervical Ligament Integrity
Test Patient Position Therapist Position Action
Sharp-Purser Seated with neck Palm of one hand is placed on the Using pressure of the palm on the
test relaxed in a patient’s forehead patient’s forehead, the occiput
semi-flexed Spinous process of the axis is gently and atlas are translated
position fixed by a ‘pinch grip’ of thumb posteriorly15,26
and fingertip of other hand
Anterior shear Supine lying with Standing or seated at head of couch Gentle pressure is applied to the
test cervical spine Both index fingers are placed posterior arch of the atlas. The
neutrally posteriorly against the atlas and head and atlas move anteriorly as
positioned fingers III and IV resting against a unit while gravity fixes the
the occiput lower portion of the cervical spine
Axis is fixed by stabilization on the
anterior aspect of the transverse
processes by the clinician’s thumbs
Side-bending Sitting or supine Spinous process and lamina of axis Slight compression is applied
stress test are stabilized by placing the thumb through the crown of the head to
along one side of the neural arch facilitate atlanto-occipital side-
and the index finger along the bending. Passive side-bending
other, preventing both side- then applied using pressure
bending and rotation of the through the patient’s head14,15,22,44
segment14 Test in upper cervical spine neutral,
flexion and extension
Rotation stress Sitting or supine Axis is stabilized around its lamina Head rotated, the occiput taking the
test and spinous process using a atlas segment with it, to the end
lumbrical grip. The cranium is of available range
grasped with a wide hand span Test in upper cervical spine neutral,
flexion and extension
Distraction test Supine with head Therapist at the head of the plinth Manual traction is then applied to
resting on a pillow Fixate the axis around its neural arch the head
with the lower hand Test in upper cervical spine neutral,
Cup the occiput with the upper hand flexion and extension
354 PART III  Advances in Clinical Science and Practice

test.14,22 No movement should be detected or symptoms published estimates. Cadaveric research has demon-
produced on testing if the transverse ligament is strated a 30% increase in the range of contralateral
normal.14,15,17,22,45,47 An abnormal response occurs when rotation following unilateral alar ligament transection.53
the atlas glides forward on the axis, potentially allowing Therefore, it is possible that a person without alar liga-
the dens to move into the space available for the spinal ment integrity may also have movement within these
cord. In addition to movement, symptoms may be pro- suggested ranges. This possibility presents difficulties
voked or reproduced, including cardinal signs or a sensa- in the interpretation of a test finding based upon range
tion of a ‘lump in the throat’. A ‘clunk’ may indicate the of rotation alone.
atlas translating anteriorly on the axis.14,15,22 While the construct validity of both the side-bending
Although no data on the reliability or validity of this and rotation stress tests have been demonstrated in a
test have been published, the mechanism of the test has normal population using magnetic resonance imaging,54
been demonstrated using magnetic resonance imaging to no examinations in any population of either the validity
measure anterior displacement of the atlas against the axis or reliability of these clinical tests in regard to detection
in a normal population.49 of alar ligament lesions have been published. Investiga-
tions of this type remain unlikely in the absence of an
accurate and reliable radiological gold standard for
Tests for Alar Ligament Integrity detecting and interpreting alar ligament injury.
Stress tests for integrity of the alar ligaments are based
upon preventing the inherent coupling of rotation and Distraction Test for the
lateral flexion in the occipito-atlantoaxial complex. Side-
bending of the occiput on the atlas is accompanied by
Tectorial Membrane
immediate ipsilateral rotation of the axis beneath the Distraction testing is used to assess the integrity of the
atlas. This rotation is proposed to result from tension tectorial membrane because of its described role as a
generated in the alar ligaments.50 limiting factor in vertical translation.55,56 The patient is
positioned in supine lying with their head resting on a
pillow. This is proposed to relax the upper cervical mus-
Side-Bending Stress Test
culature22 and to eliminate the stabilizing effect of liga-
The side-bending stress test may be performed in mentum nuchae.15 The test is performed in three positions
sitting44,47 or supine lying.24 To account for variations in with the upper cervical spine positioned in neutral, flexion
alar ligament orientation, testing is performed in three where the tectorial membrane is tensioned as it passes
positions: (a) neutral posture of the upper cervical spine; over the tip of the dens and extension.14,22,24
(b) upper cervical flexion; and (c) upper cervical exten- Some movement on application of a distraction force
sion.14,22 For a side-bending stress test to be considered is normal. A positive test response is considered to be
positive for an alar ligament lesion, excessive movement excessive vertical translation when distraction is applied.
in all three planes of testing should be evident.15,22 Separation should not be greater than 1–2 mm.22,24,47
It has been proposed that testing in both directions is There have been no examinations of the validity and reli-
required to stress the alar ligament on one side.22 It has ability of this test published to date.
been assumed that the occipital portion of the alar liga-
ment contralaterally and the atlantal portion ipsilaterally
will both be tensioned during side-bending. However, CONTROVERSIES IN CRANIOCERVICAL
the importance of the atlantal portion of the alar ligament LIGAMENT TESTING
has recently been questioned,51 suggesting that directing
testing towards this component may be unnecessary. Testing for instability of the craniocervical region remains
a controversial aspect of physiotherapy practice. While
many authors have considered these tests to be a routine
Rotation Stress Test
component of pre-manipulative screening for the upper
The rotation stress test is regarded as primarily stressing cervical spine,24,42,47 others have considered them to be
the contralateral alar ligament. The test is described in provocative, potentially harmful and lacking validation.2,7
both sitting15,22 and supine lying24 and no lateral flexion The predominant area of controversy regarding
is permitted during the test. Similar to the side-bending screening tests for this region pertains to their ability to
stress test, the rotation test is repeated in positions of discriminate individuals with lesions of the craniocervical
upper cervical spine neutral, flexion and extension, with ligaments from others in a neck pain population. While
laxity in all three positions necessary to establish a posi- construct validity has been demonstrated for some of the
tive test finding.15,22,24 Reports in standard textbooks of clinical tests, little assessment of individuals with con-
the amount of rotation that should be possible in the firmed pathology of these ligaments has been under-
presence of intact alar ligaments has been inconsistent. taken. The impediment to completing this work at this
While some rotation will occur during performance of time is technological. The consideration of magnetic
the test, suggestions of the normal range of movement resonance imaging being a ‘gold standard’ for the detec-
vary between 20° to 40°.15,22,24,44,47 In the only study tion of lesions of the craniocervical ligaments has been
to quantify rotation occurring during this test, the seriously questioned due to the lack of reproducibility of
maximum range measured using magnetic resonance interpretation of high-intensity signal changes within the
imaging was 22°,52 a finding consistent with the lower cross-section of the ligaments and the consequent
 35  Cautions in Musculoskeletal Practice 355

inability to determine pathological from normal 16. Osmotherly PG, Rivett DA. Knowledge and use of craniovertebral
ligaments.57–59 Further investigation of highly reproduc- instability testing by Australian physiotherapists. Man Ther 2011;
16:357–63.
ible methods to assess and measure ligament integrity is 17. Meadows JTS. Orthopedic Differential Diagnosis in Physical
required before comparison of clinical tests against an Therapy. New York: McGraw-Hill; 1999.
acceptable reference standard may be undertaken. 18. Pettman E, editor. Subcranial Anatomy and Stress Testing the
The second major area of contention involves the use Anatomy. International Federation of Orthopaedic Manipulative
Therapists 5th International Conference. Vail, Colorado; 1992.
of tests where provocation of symptoms is required. This 19. Swinkels RAHM, Oostendorp RAB. Upper cervical instability: fact
is particularly in regard to instability at the atlanto-axial or fiction. J Manipulative Physiol Ther 1996;19(3):185–94.
joint. Given how rarely cardinal signs present in physio- 20. Dvorak J, Hayek J, Zehnder R. CT-Functional diagnostics of the
therapy practice, rapid relocation of the atlanto-axial rotatory instability of the upper cervical spine. Part 2 An evaluation
joint may be difficult when the clinician is working under on healthy adults and patients with suspected instability. Spine
1987;12:726–31.
the unfamiliar stress of a patient who may suddenly be 21. Coutts MB. Atlanto-epistropheal subluxations. Arch Surg
demonstrating cardinal signs or gagging severely.2 It is 1934;29(2):297–311.
proposed that this may subject the transverse ligament to 22. Beeton K. Instability in the upper cervical region; clinical presenta-
sustained stress and potentially further injury. Further, it tion, radiological and clinical testing. Manipulative Physiother
1995;27(1):19–32.
is suggested that these tests have little practical applica- 23. Dugan M, Locke S, Gallagher J. Occipital neuralgia in adolescents
tion since patients with central nervous system signs and young adults. NEJM 1962;267:1166–72.
should be appropriately referred for management else- 24. Hing W, Reid D. Cervical Spine Management. Pre-screening
where.2 Certainly, the administration of tests to provoke Requirement for New Zealand. New Zealand Manipulative Phys-
cardinal signs is undesirable when there is any reasonable iotherapists Association; 2004.
25. Derrick LJ, Chesworth BM. Post-motor vehicle accident alar liga-
expectation that these symptoms may be present. ment laxity. J Orthop Sports Phys Ther 1992;16(1):6–11.
However, it should be kept in mind that the tests described 26. Sharp J, Purser DW. Spontaneous atlanto-axial dislocation in anky-
are screening tests designed to identify previously uniden- losing spondylitis and rheumatoid arthritis. Ann Rheum Dis
tified risk factors to manipulation in a largely unaffected 1961;20:47–77.
27. Niibayashi H. Atlantoaxial rotatory dislocation. Spine 1998;23(13):
population. As such, the tests are not intended to be 1494–6.
diagnostic of craniocervical instability but rather high- 28. Hunter G. Non-traumatic displacement of the atlanto-axial joint.
light those individuals at greater risk of adverse outcome J Bone Joint Surg 1968;50-B(1):44–51.
for whom other investigation and management may be 29. Stauffer E. Subaxial injuries. Clin Orthop Relat Res 1989;239:
instigated. 30–9.
30. Akpinar G, Tekkok IH, Sumer M. Grisel’s syndrome: a case of
potentially lethal spinal cord injury in the adult. Br J Neurosurg
REFERENCES 2002;16(6):592–6.
1. Mathers KS, Schneider M, Timko M. Occult hypermobility of the 31. Floyd AS, Learmonth ID, Mody G, et al. Atlantoaxial instability
craniocervical junction: a case report and review. J Orthop Sports and neurologic indicators in rheumatoid arthritis. Clin Orthop
Phys Ther 2011;41(6):444–57. Relat Res 1989;241:177–82.
2. Meadows J. The Sharp-Purser test: a useful clinical tool or an 32. Kaale BR, Krakenes J, Albrektsen G, et al. Clinical assessment
exercise in futility and risk. J Man Manip Ther 1998;6(2):97–100. techniques for detecting ligament and membrane injuries in the
3. Nguyen HV, Ludwig SC, Silber J, et al. Rheumatoid arthritis of upper cervical spine region – a comparison with MRI results. Man
the cervical spine. Spine J 2004;4:329–34. Ther 2008;13(5):397–403.
4. Stevens JC, Cartlidge NEF, Saunders M, et al. Atlanto-axial sub- 33. Parker DA, Selwyn P, Bradley PJ. Subluxation of the atlanto-axial
luxation and cervical myelopathy in rheumatoid arthritis. Q J Med joint. Br J Oral Maxillofac Surg 1985;23:275–8.
1971;40:391–408. 34. Rosa C, Alves M, Querios MV, et al. Neurologic involvement in
5. Meijers KAE, van Beusekom GT, Luyendijk W, et al. Dislocation patients with rheumatoid arthritis with atlatoaxial subluxation – a
of the cervical spine with cord compression in rheumatoid arthritis. clinical and neuriphysiological study. J Rheumatol 1993;20:
J Bone Joint Surg 1974;56(B)(4):668–80. 248–52.
6. Rahman N, Jamjoom ZA, Jamjoom A. Ruptured transvesre liga- 35. Osmotherly PG, Rivett DA. Screening for craniovertebral instabil-
ment: an injury that is often forgotten. Br J Neurosurg ity; a new look at the evidence. Aust J Physiother 2005;51(4):S17.
2000;14(4):373–7. 36. Fielding JW, Griffin PP. Os odontoideum: an acquired lesion.
7. Rana NA, Hancock DO, Taylor AR, et al. Atlanto-axial subluxation J Bone Joint Surg 1974;56-A(1):187–90.
in rheumatoid arthritis. J Bone Joint Surg 1973;55-B(3):458–70. 37. BenEliyahu DJ. Conservative management of posttraumatic
8. Hensinger RN. Osseous anomalies of the craniovertebral junction. cervical intersegmental hypermobility and anterior subluxation.
Spine 1986;11(4):323–33. J Manipulative Physiol Ther 1995;18(5):315–21.
9. Mathews JA. Atlano-axial subluxation in rheumatoid arthritis. Ann 38. Swinkels R, Beeton K, Alltree J. Pathogenesis of upper cervical
Rheum Dis 1969;28:260–5. instability. Man Ther 1996;1:127–32.
10. Braaf M, Rosner S. Trauma of the cervical spine as a cause of 39. Uitvlugt G, Indenbaum S. Clinical assessment of atlantoaxial insta-
chronic headache. J Trauma 1975;15(5):441–6. bility using the sharp-purser test. Arthritis Rheum 1988;
11. Crisco JJI, Oda T, Panjabi MM, et al. Transections of the C1-C2 31(7):918–22.
joint capsular ligaments in the cadaveric spine. Spine 1991;16(10S): 40. Castor WR, Miller JDR, Russell AS, et al. Computed tomography
S474–9. of the craniocervical junction in rheumatoid arthritis. J Comput
12. Levine AM, Edwards CC. Traumatic lesions of the occipitoatlan- Assist Tomogr 1983;7(1):31–6.
toaxial complex. Clin Orthop Relat Res 1989;239:53–68. 41. Grieve G. Common Vertebral Joint Problems. Edinburgh:
13. Harris MB, Duval MJ, Davis JAJ, et al. Anatomical and roentgeno- Churchill Livingstone; 1981.
graphic features of atlantooccipital instability. J Spinal Disord 42. Cattrysse E, Swinkels RAHM, Oostendorp RAB, et al. Upper cer-
1993;6(1):5–10. vical instability: are clinical tests reliable? Man Ther
14. Aspinall W. Clinical testing for the craniovertebral hypermobility 1997;2(2):91–7.
syndrome. J Orthop Sports Phys Ther 1990;12(2):47–54. 43. van der El A. Manuelle Diagnostiek. Rotterdam: Wervelkolom
15. Pettman E. Stress tests of the craniovertebral joints. In: Boyling Manthel; 1992.
JD, Palastanga N, editors. Grieve’s Modern Manual Therapy The 44. Gibbons P, Tehan P. Manipulation of the Spine, Thorax and Pelvis;
Vertebral Column. 2nd ed. Edinburgh: Churchill Livingstone; An Osteopathic Perspective. Edinburgh: Churchill Livingstone;
1994. p. 529–37. 2004.
356 PART III  Advances in Clinical Science and Practice

45. Mintken PE, Metrick L, Flynn T. Upper cervical ligament testing 53. Dvorak J, Panjabi MM, Gerber M, et al. CT – functional diagnos-
in a patient with os odontoideum presenting with headaches. tics of the rotatory instability of upper cervical spine. 1. An experi-
J Orthop Sports Phys Ther 2008;38(8):465–75. mental study on cadavers. Spine 1987;12(3):197–205.
46. Lincoln J. Clinical instability of the upper cervical spine. Man Ther 54. Osmotherly PG, Rivett DA, Rowe LJ. Construct validity of clinical
2000;5(1):41–6. tests for alar ligament integrity: an evaluation using magnetic reso-
47. Westerhuis P. Cervical instability. In: von Piekartz HJM, editor. nance imaging. Phys Ther 2012;92(5):718–25.
Craniofacial Pain Neuromusculoskeletal Assessment, Treatment 55. Werne S. Factors limiting the range of movement of the craniover-
and Management. Edinburgh: Butterworth Heinemann Elsevier; tebral joints. Acta Orthop Scand Suppl 1957;23(Pt 1):38–62.
2007. p. 119–47. 56. White AAI, Panjabi MM. Clinical Biomechanics of the Spine. 2nd
48. Forrester GA, Barlas P. Relaibility and validity of the sharp-purser ed. Philadelphia: J.B. Lippincott Company; 1990.
test in the assessment of atlanto-axial instability in patients with 57. Dullerud R, Gjertsen O, Server A. Magnetic resonance imaging of
rheumatoid arthritis. Physiotherapy 1999;85(7):376. ligaments and membranes in the craniocervical junction in
49. Osmotherly PG, Rivett DA, Rowe LJ. The anterior shear and whiplash-associated injury and in healthy control subjects. Acta
distraction tests for craniocervical instability. An evaluation using Radiol 2010;51:207–12.
magnetic resonance imaging. Man Ther 2012;17:416–21. 58. Myran R, Kvistad KA, Nygaard OP, et al. Magnetic resonance
50. Dvorak J, Schneider E, Saldinger P, et al. Biomechanics of the imaging assessment of the alar ligaments in whiplash injuries. Spine
craniocervical region: the alar and transverse ligaments. J Orthop 2008;33(18):2012–16.
Res 1988;6(3):452–61. 59. Vetti N, Krakenes J, Damsgaard E, et al. Magnetic resonance
51. Osmotherly PG, Rivett DA, Mercer SR. Revisiting the clinical imaging of the alar and transverse ligaments in acute whiplash-
anatomy of the alar ligaments. Eur Spine J 2013;22(1):60–4. associated disorders 1 and 2. Spine 2011;36:E434–40.
52. Osmotherly PG, Rivett DA, Rowe LJ. Toward understanding
normal craniocervical rotation occurring during the rotation stress
test for the alar ligaments. Phys Ther 2013;93(7):986–92.
 SECTION 3 . 2

THE BROADER SCOPE

OF MANAGEMENT

The personal and financial burden of musculoskeletal considers the important area of musculoskeletal health in
disorders is increasing worldwide, reflecting numerous the workplace. Here it is necessary to develop effective
factors (e.g. the ageing population, the recurrent and strategies for primary, secondary and tertiary prevention
progressive nature of many musculoskeletal disorders and of work-related musculoskeletal disorders both to
more sedentary lifestyles). Therefore, as well as conven- improve the workers’ and management’s outcomes. In
tional practitioner–patient encounters in the clinical the ideal world, prevention of musculoskeletal disorders
setting, there is an increasingly broader scope to muscu- would be the optimal management. No method or prac-
loskeletal physiotherapy in both the prevention and man- tice has yet achieved the ideal of prevention. Towards this
agement of musculoskeletal pain to manage this global ambition, the issue of musculoskeletal screening is dis-
problem. cussed and an example of a musculoskeletal screening,
This section presents four key areas in this broader testing and assessment model is presented.
scope of patient management. The first is the concept Finally, over the last decade there has been a broader
and context of self-management that could arguably be a scope of management for physiotherapists. Advanced
mandatory component of management for all patients, practice roles have developed internationally in response
whether part of one-to-one patient/clinician encounters to increased demand and the need to provide high-
or when delivered more specifically to patient groups. quality cost-effective services. Musculoskeletal physio-
The second explores the role of physiotherapy in lifestyle therapists with appropriate knowledge and skills are
and health promotion in musculoskeletal conditions. ideally placed to take up these new opportunities. These
This is another area where increased engagement is nec- roles include triage, referral for imaging and blood tests,
essary. For people suffering musculoskeletal conditions, listing for surgery, performing injections and indepen-
clinical outcomes may be improved if lifestyle and health dent prescribing. This chapter explores service models
promotion interventions for behaviours such as smoking, and evaluates their impact for patients as well as the
sub-optimal nutrition, unhealthy body mass, physical health economy. It highlights professional issues associ-
inactivity, low physical activity, sub-optimal sleep quality ated with innovative practice and calls for further high-
and quantity, and anxiety, depression and stress are quality research to quantify the impact of these roles
included in patient management. The third chapter accurately as they continue to evolve.

357
 CHAPTER 36 

Supported Self-Management and an

Overview of Self-Help
Ann Moore

and Shea5 took the concept to a wider stance and contex-

INTRODUCTION tualized self-management as ‘the ability of the individual in
conjunction with family, community and health care profes-
This chapter provides an overview of the context and sionals to manage symptoms, treatments, lifestyles changes and
definitions of self-management and self-help, and dis- psycho-social, cultural and spiritual consequences of health con-
cusses the principles and theories underpinning success- ditions’ (p. 261). This is in contrast to Richard and Shea’s
ful self-management approaches. The perceptions of feelings about self-care which they contend ‘broadly delin-
patients and clinicians of self-management and the impli- eates the health lifestyle behaviours undertaken by individuals
cations of these perceptions for practice are also discussed for optimal growth and development or the preventative strate-
with the main focus being on what patients’ perspectives gies performed or maintain health’ (p. 261).5
and expectations of self-management are. Chronic disease across the world contributes to 60%
of the global disease burden.6 In terms of musculoskeletal
physiotherapy, chronic low back pain, for example, has a
CONTEXT AND DEFINITION high prevalence rate and is very costly in relation to
health-care expenditure, the personal impact it has on
The concept of self-management has been around for patients, as well as the social and economic burden it
many years in the field of health education. The term places on society due to work absence and work loss.7,8
‘self-management’ was first used in a text by Creer et al.1 Consequently, there is a strategic move by governments
which focused on the rehabilitation of chronically ill chil- and health departments nationally and internationally to
dren. Overall, however, there is a lack of clarity about the increase the focus on self-management in health services
meaning of self-management from a range of stakeholder in order to reduce the impact of chronic diseases/disorders
perspectives. Lorig and Holman2 stressed that ‘the issue of on society.9,10 While health-service strategies are commit-
self-management is especially important for those with chronic ted to reducing the burden of chronic disease on indi-
disease, where only the patient can be responsible for his or her viduals and society in general, for some patients this may
day to day care over the length of the illness, and for most of only be seen as a money-saving venture. In contrast,
these people, self-management is a lifetime task’ (p. 1).2 Lorig others may celebrate the move as the concept of self-
has much experience in the development of self- management appears to support their own needs and
management programmes for patients with chronic desired personal direction.
disease, for example chronic arthritis. These programmes
are often delivered for groups of patients and not neces-
sarily on a one-to-one basis as is a common patient–
clinician encounter in the musculoskeletal physiotherapy PATIENT EDUCATION AND
setting.2 SELF-MANAGEMENT
The term self-management is often used in a similar
context to ‘self-help’ and ‘self-treatment’. The following For many decades, patient education has been one of the
definition of self-management by Gruman and Von key elements of a multimodal approach to musculoskel-
Korff3 is a helpful basis for this chapter: etal patient care provided by musculoskeletal physiother-
apists. Patient education is inextricably linked with
‘Self-management involves (the person with chronic self-management facilitation. Some authors, however,
disease) engaging in activities that protect and promote make the distinction between patient education and self-
health, monitoring and managing symptoms and signs of management education. Patient education has core com-
illness, managing the impacts of illness on function, ponents that are identifying, caring about and respecting
emotions and interpersonal relationships and adhering to patients’ preferences, values, differences and expressed
treatment regimes’.3 needs.11 Self-management education, however, has been
described as follows:
Barlow et al.4 defined self-management as ‘the indi- It should teach patients to:
vidual’s ability to manage the symptoms, treatment, physical • access the information they seek
and psychological consequences and lifestyle changes inherent in • ensure they are proficient in carrying out medically
living with a chronic condition’ (p. 178).4 Further, Richard related behaviours (e.g. insulin injections or using
358
 36  Supported Self-Management and an Overview of Self-Help 359

an inhaler) and non-medically related behaviours modified and extended by their professional education
(e.g. interacting with their doctor, exercising, etc.) and experience.
• enhance their levels of confidence (i.e. perceived It is imperative to understand one’s own (the physio-
self-efficacy) in their ability to engage with these therapist’s) knowledge, beliefs, values and standards,
behaviours while also understanding the patient’s beliefs, values and
• ensure they are proficient in problem-solving.12 standards from their point of view and to recognize that
The interesting component of self-management is the you, the clinician, the patients and others you work with,
understanding of the perceptions and expectations of may differ in knowledge, beliefs, values and standards.
self-management from both the patient’s and the clini- This will ensure that adequate communication occurs in
cian’s perspectives and how enmeshed or un-enmeshed the therapeutic workplace. It should be recognized that
they are at the first consultation. It is also important to any differences do not imply that your views as a clinician
note how these perceptions and expectations may change are of greater worth than your patient’s.15 This is particu-
over time. larly relevant when considering the perceptions of
Self-care is distinguished from self-management as self-management from both patients’ and clinicians’ per-
more broadly delineating healthy lifestyle behaviours spectives. Some would agree, and some would not, with
undertaken by individuals for optimal growth and devel- certain perspectives as illustrated by the work of Stenner
opment, or the preventative strategies performed to et al.16 The acknowledgement of differences in perspec-
promote or maintain health.5 This is an important tives is vital in order to help the patient in their self-
concept that should be considered by all musculoskeletal management journey.
physiotherapists during each consultation. The concept
relates to significant public health issues, for example,
obesity, alcohol and drug abuse and lack of exercise. EVIDENCE AND SELF-MANAGEMENT
Another two terms are linked to patient education and
subsequently to patient self-management, namely self- In this section, some of the more recent evidence for
efficacy and patient empowerment. Empowerment is an self-management programmes will be presented. Butow
outcome of patient education as a result of which patients and Sharpe17 reviewed the research investigating the
gain power, access to relevant resources to enable them impact of communication on adherence to pain manage-
to gain or take control over their lives.13 Self-management ment strategies. Their conclusion was that although the
education is an empowerment strategy in itself and treatment of chronic pain is challenging, good commu-
enables patients to problem solve and make decisions nication between health providers and patients can
about their condition and their approach to it. Self- promote adherence and improve outcomes, and an inter-
efficacy, on the other hand, is related to patient education vention needs to be tailored to individuals’ reasons for
and is related to a person’s belief or confidence in their non-adherence. Du et  al.18 conducted a systematic review
ability to do something.14 The two concepts are of course of 19 trials of self-management programmes for chronic
very much linked, as lack of self-confidence can signifi- musculoskeletal pain conditions. They concluded that
cantly impact on self-management. self-management programmes have small to moderate
effects on improving pain and disability in the long term
but more research into self-management was needed,
SELF-MANAGEMENT STRATEGIES for example, on self-management for chronic low back
pain. Since self-management as an approach is very
Lorig and Holman2 identified five core self-management complex and dependent on a range of factors, it is dif-
skills which need to be facilitated within a treatment self- ficult to know from the review how tailored the self-
management session. The five core self-management management programmes included in the studies were
skills are: to patient needs.
• problem solving Schulman-Green et al.19 studied processes of self-
• decision making management in chronic illness. They highlighted the
• resource utilization importance of health-care providers’ ongoing communi-
• the forming of a patient/health-care provider cation with patients to explore their self-management
partnership preferences and how these may change over time. Their
• taking action. study was focused generally on chronic illness and disease
Ewles and Simnett15 made some useful suggestions as to and was not specific to chronic musculoskeletal condi-
how clinicians can help patients take more control of tions; however, the findings were broadly relevant to
their health by: musculoskeletal patients and practitioners. They identi-
• encouraging patients to make decisions fied three categories of self-management processes and
• encouraging patients to think things out for delineated the tasks and skills required for each:
themselves • focusing on illness needs
• respecting any unusual ideas that individuals may • activating resources
have about their health • living with a chronic disease.
• acceptance of individuals rather than judging them. In a qualitative meta-synthesis of living with low back
This means recognizing that the individual’s knowledge pain20 it was found that professional and family support,
and beliefs have emerged from their own life experiences, self-efficacy, motivation, work conditions and exercise
whereas the clinician’s knowledge and beliefs have been opportunities influenced the patient’s pain experience.
360 PART III  Advances in Clinical Science and Practice

This suggests that all need to be incorporated into self- Considering other delivery mediums, Zufferey and
management strategies in some way. Furthermore, a Schulz.24 noted that patient-centred websites were useful
small qualitative study by Morris,21 which explored in enhancing self-management of chronic low back pain.
patients’ perspectives on self-management following a However, patient engagement appeared to depend on
spinal rehabilitation programme, found a range of obsta- their stage of advancement in the self-management
cles to continuing with exercise that included pain, time process. It seems that website information needs to be
and family constraints. Some participants indicated that tailored to peoples’ stage of self-management advance-
there were limitations to the extent to which their chronic ment. The authors identified and defined four types of
low back pain would allow them to undertake certain self-management website users:
activities and those activity limitations were perhaps • The selective user: Experienced self-managers, who
inadvertently reinforced by physiotherapists in the reha- have a high level of awareness and experience of
bilitation sessions. Overall the study highlighted the need self-management of low back pain to good effect.
for very clear communication between the patient and Their expectation was to find tailored information
their physiotherapist, and also the need for clinicians to on the website to further support their ongoing
have an understanding of patients’ expectations and self-management.
beliefs prior to engagement in a rehabilitation/self-man- • The enthusiastic user: Novices in self-management.
agement programme.21 They were aware that a medical cure for chronic
In a qualitative study, Cooper et al.22 explored patients’ low back pain did not exist and accepted that they
expectations of self-management of chronic low back had to be involved in their own care, but admitted
pain. It appeared that self-management strategies that that they did not know how to do it. They wanted
were largely focused on exercise were not always adopted the best way to deal with chronic low back pain from
by the patients/participants. There was a need for ongoing the website.
self-management support for patients following discharge • The magic user: Passive self-managers who adhere to
to ensure that they more readily conformed to the exer- a traditional biomedical model of chronic low back
cises prescribed. Participants felt that physiotherapy had pain, and were expecting that clinicians would find
little influence on the management of chronic low back a cure/solution to their problem. They were mainly
pain following discharge from treatment. Cooper et al.22 new to the problem of low back pain. This group
concluded that self-management could be better facili- expected the website to contain definitive solutions
tated and should include education on self-management, to the problem and, when not found, they became
patient information and other aspects of patient educa- confused and felt discouraged.
tion, as well as putting in place support for self- • The ‘wait and see’ user: Latent self-managers where
management via the telephone or by review appointments chronic low back pain was quite marginal and inter-
with the physiotherapist. mittent. They felt that they did not need to engage
Sokunbi et al.23 conducted a randomized controlled in long-term self-management.
trial investigating the effects of stabilization exercises for Zufferey and Schulz.24 concluded that information and
patients with chronic low back pain. An extensive educa- support should be tailored to pave the way for people’s
tion programme was included in the study which was stages of advancement. This indicates again the need
designed to facilitate self-management. It included video for good communication between the clinician and the
footage of the spine and its movements, the effects of patient.
certain positions on the spine and detailed descriptions A systematic review and meta-analysis of the effec-
of stabilization exercises. There were clear educational tiveness of self-management of low back pain by Oliveira
discussions with each participant on a one-to-one basis et  al.25 indicated that there is moderate quality evi-
and many opportunities throughout the sessions for par- dence that self-management has a small effect on pain
ticipants to ask questions and seek advice. The outcome and disability in people with low back pain. They
of the patients’ experiences of the programme was gath- challenged the endorsement of self-management in
ered using focus group interviews. Participants indicated treatment guidelines.25 However, unless the approaches
that overall, they had found the whole process was to self-management are clearly expressed and fully
enlightening and very positive, and that their confidence understood, it is difficult to make this challenge in a
in relation to their problem had increased. The relation- robust way.
ship that they had had with the lead researcher/clinician Johnston et  al.26 provided a detailed approach to the
they felt was very open and their low back pain problems use of self-management in facilitating workers with
had reduced significantly. However, during the interviews chronic musculoskeletal conditions to return to or
it became very clear that the patients were not committed remain in work. In particular, they highlighted the use-
to carrying on with the management programme that fulness of the readiness to return to work scale.27 They
they had received. They felt so much better that they emphasized the need for detailed communication
wanted simply to get back to normal life and did not have between the clinician and patient and the need for clini-
the time to spend on the programme! This may indicate cians to ensure that they have the right skills to facilitate
that the patient management programme may have positive self-management behaviour in order to enable
lacked a key communication strategy which could help patients to return to work or stay in work. They pre-
patients realize the need for ongoing self-management sented a useful table of practical tips for the incorporation
activities even when their pain has reduced or by clinicians of self-management into musculoskeletal
disappeared.23 practice.26
 36  Supported Self-Management and an Overview of Self-Help 361

SELF-MANAGEMENT – PATIENTS’ AND DISCUSSION

CLINICIANS’ VIEWPOINTS
Clearly the philosophies, structures and processes associ-
A recent study by our research team looked in detail ated with self-management are well grounded, but all
at the perceptions of both patients (with chronic low those involved in facilitating self-management must be
back pain) and clinicians (from a variety of professions) fully aware of these models and approaches, and develop
of self-management. The work consisted of a detailed strategies to incorporate them into routine day-to-day
literature review (Defever et  al., manuscript in prepara- practice. In this context, the definitions of and approaches
tion) and a series of focus groups involving patients to empowerment and self-efficacy are very important.
and clinicians. Based on the findings, a further piece Self-management should not be seen as a separate
of research took place utilizing statements on self- entity from an overall assessment and treatment strategy.
management gleaned from the literature and from the There are a series of stages in a successful treatment
focus group data. The study involved the use of pathway and self-management has to be part of these.
Q-methodology28 to explore patients’ and health pro- Many stages of a successful treatment pathway depend on
viders’ viewpoints on the concept of self-management clear two-way communication between the clinician and
in the context of chronic low back pain16 (Stenner the patient which was clearly articulated some years ago
et  al. 2014, unpublished data). A set of 60 statements in a UK Department of Health document; ‘the importance
of opinion on self-management of chronic low back of patients may not always be appreciated by patients who feel
pain was developed (a ‘Q set’). Subsequently, a wider talked at rather than listened to’.29 This led to the priority
group of stakeholders, which included 60 patients with for more patient information, greater patient choice and
chronic low back pain and 60 health-care practitioners, more patient-centredness.29
ranked the statements on a continuum from ‘strongly The patient care continuum of Barr and Threlkeld30
agree’ to ‘strongly disagree’ (‘Q-sort’). The data were is a useful model in terms of the balance of patient/
analysed by the research team which included clini- clinician partnership. The continuum has high control
cians, researchers and service users. What emerged which is clinician-centred at one end of the spectrum
from the data were four distinct viewpoints on self- and high control which is patient-centred at the other
management in chronic low back pain. The four view- end of the continuum. Patient/clinician partnership is
points were: developed and comes to the fore throughout the treat-
• ‘Changing myself’: This viewpoint took a strong psy- ment continuum. Early in treatment, there often needs
chological approach, needing a lifestyle/mind-set to be a strong clinician-centred approach followed
change. This viewpoint was the largest perspective quickly by the development of a patient/clinician part-
expressed mainly by health-care providers but also nership. This then leads to patients’ high control related
shared by some patients. to empowerment of self-efficacy and successful self-
• ‘Changing what I do’: This was a strongly pragmatic management strategies.
approach to self-management guided by accurate The importance of good-quality, effective and timely
information and practical strategies. This viewpoint communication has been highlighted over the years.
was shared mostly by patients and some health-care Richardson and Moran31 suggest that good-quality com-
practitioners. munication can lead to patients’ empowerment, advance-
• ‘Not sure what to change’: This viewpoint focused on ment, enhancement of quality of care, improved patient
managing medical uncertainty with a need for access satisfaction, improved health outcomes and modification
to health-care resources and assistance. This was of practice in response to patients’ needs.31 Some of the
expressed mostly by patients and a few health-care complexities of communication and its use in clinical
providers. practice are addressed in Chapter 27a.
• ‘The others must change’: This viewpoint was based Clinicians need to demonstrate good knowledge of the
on a concern with the stigmatic perception of being area, high-quality therapeutic skills, communication skills
in chronic pain, with reliance on health-care provid- and also listening skills. Clinicians should offer high-
ers to acknowledge and validate their problem. This quality tailored explanations, education and advice to
viewpoint was only voiced by patients. patients, as well as clear guidance on the therapist’s role.
Overall, the study provided valuable insights into the A consultative process within treatment sessions should
diversity, complexity and tensions in and between view- be adopted. The facility of a flexible appointment system
points in relation to self-management in chronic low back with ‘SOS’ appointment availability is important, par-
pain. It shows that it is essential to address these issues ticularly for patients who are at one end of the spectrum
and the resulting differences in expectations of care and in their preparedness for self-management processes.
self-management in order to establish more successful Patients need to be facilitated to empower themselves.
engagement in and accomplishment of effective self- Self-efficacy needs to be facilitated in relation to behav-
management. Further research in education is needed ioural change. It is important that clinicians give time to
both for those experiencing problems and those provid- ensuring that these foci are addressed. This can present
ing services to support the process of achieving effective quite a challenge in some health services where, to
and inclusive self-management in chronic low back become cost-effective, the numbers of treatments and
pain, and most likely in a range of musculoskeletal treatment time available to patients is being reduced!
conditions. Another challenge to self-management relates to the lack
362 PART III  Advances in Clinical Science and Practice

of, or low level of, pre-qualification training/education in self-management process. Unless detailed and clear com-
patient education theories and practices. Post-registration, munication can be held acknowledging that there may be
Masters level modules/courses are quite widely available differences in the perceptions of self-management, then
but these are taken up only by a small percentage of clini- self-management is unlikely to increase its effectiveness.
cians. This is an important area for future development. Finally, it is important that all clinicians recognize that
Fundamentally, successful self-management by pa­ their perceptions, expectations and perspectives on self-
tients is the result of patient-focused care in which the management can vary considerably from those of their
balance of the therapeutic partnership, consisting of patients. It is extremely important that practitioners can
trust, respect and understanding of patients’ ideas, beliefs, spend time, at the initial meeting with their patients, to
knowledge and values, is in place, when patients are in- understand where they are coming from in terms of their
volved in decision making and also when patients’ needs perspectives on self-management and, indeed, on patient
and expectations are shared and discussed and their ex- education.
pression of these is encouraged and facilitated. The issue
for some clinicians working in some health service envi- REFERENCES
ronments may be the time availability to engage with the 1. Creer T, Renne C, Christian W. Behavioral contributions to reha-
patient at a personal level in order to explore their view- bilitation and childhood asthma. Rehabil Lit 1976;37:226–32.
points on self-management and their learning needs in 2. Lorig KR, Holman HR. Self-management education: history, defi-
relation to resources, to help them decide on what ap- nition, outcomes, and mechanisms. Anns Behav Med
2003;26:1–7.
proach to self-management would be best suited to their 3. Gruman J, Von Korff M. Indexed Bibliography on Self-Management
needs. This needs time which, well spent, could poten- for People with Chronic Disease. Washington, DC: Center for
tially be personally beneficial to the patient and cost ef- Advancement in Health; 1996.
fective for governments and health services if patients 4. Barlow JH, Wright CC, Sheasby J, et al. Self-management
self-manage effectively and do not then need to receive approaches for people with chronic conditions: a review. Patient
Educ Couns 2002;48:177–87.
or request further referrals for treatment. Having the 5. Richard A, Shea K. Delineation of self-care and associated con-
opportunity for a review contact (i.e. SOS appointments) cepts. J Nurs Scholarsh 2011;43:255–64.
would lead to improved patient confidence in the support 6. Murray CJL, Lopez AD, editors. The Global Burden of Disease:
available to them and would also give clinicians insight A Comprehensive Assessment of Mortality and Disability from
Diseases, Injuries and Risk Factors in 1990 and Projected to 2020.
to whether their approaches to self-management are Cambridge, MA: Harvard University Press on behalf of the World
being effective. The most important message from this Health Organization and the World Bank; 1996.
chapter is the need for both the clinician and the patient 7. Katz JN. Lumbar disc disorders and low-back pain: socioeconomic
to understand the range of perceptions of self-management factors and consequences. J Bone Joint Surg Am 2006;88(Suppl.
that exist, and for clinicians to understand that the patient 2):21–4.
8. Johannes CB, Le TK, Zhou X, et al. The prevalence of chronic
may be in a very different place along their perception pain in United States adults: results of an internet-based survey.
of self-management according to their stage of advance- J Pain 2010;11:1230–9.
ment24 which will alter their perception of self- 9. Department of Health. The Expert Patient: A New Approach to
management. If clinicians can understand this spectrum Chronic Disease Management for the 21st Century. London:
Department of Health; 2001.
of perceptions of self-management and make time to 10. Department of Health. Self-Care – A Real Choice Self-Care
explore the patients’ position then this is likely to lead to Support: A Practical Option. London: Department of Health;
an improved take up of a well-tailored self-management 2005.
strategy. 11. Barlow JH. How to use education as an intervention in osteoarthri-
Patient education skills play an important role in self- tis. In: Docherty M, Dougados M, editors. Osteoarthritis: Balliere’s
Best Practice and Research. London: Harcourt; Clinical Rheuma-
management, empowerment and self-efficacy. However, tology, 15(4), 545–558; 2001.
the term patient education is often used loosely in clinical 12. World Health Organization. Preparing a Health Care Workforce
practice so that clinicians very often take a didactic for the 21st Century: The Challenge of Chronic Conditions.
approach to education with little recognition of the Geneva: WHO; 2005.
13. Lorig K. Self-management of chronic illness: a model for the
patient’s needs and learning styles. It is likely that more future. Generations 1993;XVII(3):11–14.
educational philosophies, principles and methods should 14. Bandura A. Self-Efficacy: The Exercise of Control. New York:
be incorporated into health professionals’ undergraduate Freeman; 1977.
and postgraduate curricula. The issue of patient educa- 15. Ewles L, Simnett I. Promoting Health: A Practical Guide. 5th ed.
tion is discussed in Chapter 27b. Edinburgh: Ballière Tindall; 2003.
16. Stenner P, Cross V, McCrum CA, et al. Patient and healthcare
provider viewpoints on the concepts of self-management in the
context of chronic low back pain. Submitted for review in Social
SUMMARY Science and Medicine (in review).
17. Butow P, Sharpe L. The impact of communication on adherence
in pain management. Pain 2013;154:S101–7.
This chapter has highlighted a number of issues relating 18. Du S, Yuan C, Xiao X, et al. Self-management programs for
to self-management. Firstly, there are a number of defini- chronic musculoskeletal pain conditions: a systematic review and
tions associated with self-management and self-care meta-analysis. Patient Educ Couns 2011;85:299–e310.
which need to be clarified for the users. Secondly, there 19. Schulman-Green D, Jaser S, Martin F, et  al. Processes of
is a range of different interpretations and usages of self-management in chronic illness. J Nurs Scholarsh 2012;44:
136–44.
the term self-management and self-care. Thirdly, there 20. Snelgrove S, Liossi C. Living with chronic low back pain: a
may not be a full understanding of the variety of view- metasynthesis of qualitative research. Chronic Illn 2013;9(4):
points that might be held by all those involved in the 283–301.
 36  Supported Self-Management and an Overview of Self-Help 363

21. Morris AL. Patients’ perspectives on self-management following work with a chronic musculoskeletal condition. Masterclass. Man
a back rehabilitation programme. Musculoskeletal Care Ther 2013;18(4):274–80.
2004;2(3):165–79. 27. Franche RL, Corbiere M, Lee H, et al. Readiness for Return-To-
22. Cooper K, Smith BH, Hancock E. Patients’ perceptions of self- Work (RRTW) scale: development and validation of a self-report
management of chronic low back pain: evidence for enhancing staging scale in lost-time claimants with musculoskeletal disorders.
patient education and support. Physiotherapy 2009;95(1):43–50. J Occup Rehabil 2007;17(3):450–72.
23. Sokunbi O, Cross V, Watt P, et al. A randomised controlled trial 28. Stenner P, Stainton Rogers R. Q methodology and qualiquantol-
(RCT) on the effects of frequency of application of spinal stabilisa- ogy: the example of discriminating between emotions. In: Todd Z,
tion exercises on multifidus cross sectional area (MFCSA) in par- Nerlich B, McKeown S, et al., editors. Mixing Methods in Psychol-
ticipants with chronic low back pain. Physiotherapy Singapore ogy: The Integration of Qualitative and Quantitative Methods
2008;11(2):9–17. in Theory and Practice. Hove, UK: Psychology Press; 2004.
24. Zufferey MC, Schulz PJ. Self-management of chronic low back p. 101–20.
pain: an exploration of the impact of a patient-centered website. 29. Department of Health. The NHS Plan. London: Stationery Office;
Patient Educ Couns 2009;77(1):27–32. 2000.
25. Oliveira VC, Ferreira PH, Maher CG, et al. Effectiveness of self- 30. Barr J, Threlkeld JA. Patient-practitioner collaboration in clinical
management of low back pain: systematic review with meta-analysis. decision-making. Physiother Res Int 2002;5:254–60.
Arthritis Care & Research 2012;64(11):1739–48. 31. Richardson KE, Moran S. Developing standards for patient infor-
26. Johnston V, Jull G, Sheppard DM, et al. Applying principles of mation. Int J Health Care Qual Assur 1995;8(7):27–31.
self-management to facilitate workers to return to or remain at
 CHAPTER 37 

Role of Physiotherapy in Lifestyle

and Health Promotion in
Musculoskeletal Conditions
Elizabeth Dean  •  Anne Söderlund

INTRODUCTION PHYSIOTHERAPISTS AS
HEALTH ADVOCATES
There are two principal reasons why physiotherapists
who specialize in musculoskeletal conditions, including Motivating a patient to change health behaviour can
treatment of spinal conditions, need to address risk appear daunting both to the physiotherapist and the
factors for non-communicable diseases (NCDs) in their patient. They both should be encouraged by the fact that
patients, which include ischaemic heart disease, smoking- healthy lifestyle practices and health benefits are dose-
related conditions, hypertension, stroke and cancer. dependent.8 Although strict dietary and activity changes
Firstly, risk factors for back problems are comparable to do need to be instituted to reverse atherosclerosis,8,9 high
those for NCDs (i.e. smoking, prolonged sitting, inactiv- blood pressure,10 type 2 diabetes mellitus11 and reduce the
ity, being overweight, and depression and stress).1,2 Sec- growth of some tumors,12 partial changes have substantial
ondly, contemporary physiotherapists focus on the benefits.
comprehensive care of their patients consistent with the
International Classification of Functioning, Disability
and Health (ICF).3 In this chapter, the authors translate HEALTH AND RISK ASSESSMENTS
evidence-based knowledge about the association between AND INTERVENTIONS
healthy living and musculoskeletal health that was syn-
thesized in Chapter 11, to the musculoskeletal physio- To comprehensively manage the needs of a person expe-
therapy context. They first outline assessment and riencing symptoms arising from the musculoskeletal
evaluation tools for lifestyle-related health practices and system, the physiotherapist first needs to assess that per-
risk factors, and then strategies and interventions for son’s health and lifestyle health practices. Based on these
health behaviour change that can be readily integrated assessments, appropriate health education interventions
into physiotherapists’ practices. Attention to alcohol and may be negotiated between the physiotherapist and
drug abuse is beyond the scope of this chapter. Many of patient. Consistent with the ICF adopted by the World
the behaviour change principles presented in this chapter Confederation for Physical Therapy, a holistic approach
may, however, be used to support change in these behav- is indicated with health as the base (see Chapter 11).
iours as well. Although other professionals may be pri- Based on this perspective, physiotherapy assessment
marily involved, the physiotherapist has a role in should include assessments of health, lifestyle-related
supporting and following their initiatives. health behaviours, lifestyle-related health risk, as well as
any manifestations of lifestyle-related conditions (i.e. the
signs and symptoms that constitute part of conventional
physiotherapy management) (Box 37-1). The elements of
CLUSTERING OF UNHEALTHY LIFESTYLE- these assessments are described below with the exception
RELATED BEHAVIOURS AND RISKS of the manifestations of lifestyle-related conditions,
which is considered to be a fundamental physiotherapy
The clustering of commonalities among lifestyle- practice whose resources can be found elsewhere.
related NCDs, including chronic systemic low-grade
inflammation4 and contributing factors, have become a
focus in the literature.5–7 Understanding the role of the
Health Assessment
commonalities of these conditions provides valuable Health is a multifactorial construct, thus there is no
insight into best practices for their prevention, reversal single metric to quantify it. The ICF has provided guid-
and management. ance to clinicians to consider its multiple determinants
364
 37  Role of Physiotherapy in Lifestyle and Health Promotion in Musculoskeletal Conditions 365

BOX 37-1  Tools for Assessing Health Status of lifestyle behaviours itself may be a superior focus than
risk factor assessment.
GLOBAL HEALTH STATUS
Short Form 12 and Short Form 36 Lifestyle-Related Health Risk Assessment
Health-related quality of life tools
Life satisfaction tools There are multiple health risk assessment tools. These
typically focus on risk for a particular NCD (e.g. isch-
HEALTH-RELATED BEHAVIOUR aemic heart disease, hypertension, stroke, type 2 diabetes
ASSESSMENT/EVALUATION
mellitus and cancer). It is not feasible for the physio-
Health behaviours including smoking questionnaires therapist to administer all disease-specific risk assessment
(e.g. WISDOM and The WHY Test; and smoking tools to every patient. Given there are common risks for
abstinence self-efficacy questionnaire)
these lifestyle-related conditions, assessment of risk
Nutrition logs (in accordance with national food guide-
lines, e.g. Canada’s Food Guide13) factors for common lifestyle-related conditions however
Physical activity and exercise logs (in accordance with can yield important information. For example, the Cana-
physical activity pyramid) dian Diabetes Risk Questionnaire or CANRISK17 has 12
Exercise self-efficacy assessment items (Fig. 37-2). The questionnaire can be readily com-
Sleep questionnaires pleted by the patient without the need for invasive pro-
Stress questionnaires cedures and blood tests, which some risk assessment
tools require. CANRISK may be used to assess general
RISK FACTOR ASSESSMENT/EVALUATION FOR THE
LIFESTYLE-RELATED CONDITIONS lifestyle-related disease risk including type 2 diabetes
mellitus. This tool has been expanded for use by Cana-
Ischaemic heart disease risk factor assessments (e.g.
dian pharmacists and this version also has utility for
Grundy et al. 199914 and Harvard School of Public
Health Disease Risk website15) physiotherapists;18 recommendations for specific inter-
ventions based on the individual’s response are described.
ASSESSMENT/EVALUATION OF THE MANIFESTATIONS OF Other tools that are clinically applicable include cardio-
LIFESTYLE-RELATED CONDITIONS vascular disease risk14 and stroke risk.19 Also, a range of
Established medical and surgical history taking lifestyle-related risk factor tools can be accessed from
Assessment and evaluation methods the Harvard University School of Public Health website
(e.g. heart disease, stroke, diabetes, cancer and osteopo-
rosis).15 Routine use of one of these tools, such as
and assess these and evaluate changes in them at its CANRISK, can provide a general assessment of lifestyle-
various levels (i.e. function and structure, activity and related health and disease risk, and be used to evaluate
participation; see Chapter 11, Fig. 11-1). change over time with health behaviour change interven-
Despite its limitations, self-report is typically how an tion education and other physiotherapy or medical/
individual’s overall health and wellness are assessed. surgical interventions. They also serve as effective patient
Functional status and independence are central to peo- education tools.
ple’s overall health and well-being, and these indices are
reported to be singularly important within a social context Multisystem Review
(e.g. social participation, life satisfaction and health-
related quality of life). The multisystem review (Fig. 37-3) can be an effective
way of identifying risk factors and the presence of chronic
Assessment of Lifestyle-Related co-morbid conditions expediently, with the opportunity
for more detailed questioning of the patient. Three
Health Behaviours levels of information can be gleaned that elucidate con-
Lifestyle-related health behaviours are strongly associ- tributors to presenting musculoskeletal complaints, and
ated with health status (see Chapter 11). Assessment of insight into how these can be best managed. Firstly, the
health behaviours (Fig. 37-1) enables the physiotherapist physiotherapist can identify lifestyle-related, non-
to identify the adequacy of the quality and quantity of musculoskeletal causes and conditions that contribute to
these behaviours in terms of maximizing health (i.e. a patient’s musculoskeletal complaints; secondly, lifestyle-
achieving the highest status possible at each level of the related non-musculoskeletal conditions that can be
ICF and self-reported quality of life). They include the adversely affected by back complaints (e.g. a person with
individual’s status related to smoking, nutrition, body NCDs or their risk factors reducing activity level); and
composition, activity and exercise, sleep, and anxiety, thirdly, insights into the ‘best’ strategies for managing
depression and stress. Assessment of lifestyle behaviours patient’s back pain including lifestyle behaviour change
has some benefit over risk factor assessment for specific with traditional management, or alone.
NCDs. The field of risk factor assessment is advancing Vital sign measurement has become an essential
rapidly with established tools being revised and new ones component of contemporary physiotherapy assessment.
emerging. Thus tracking patients’ risks over time or Heart rate and blood pressure are key indicators of
using these tools as outcome measures may be challeng- physical health status and health risk.20,21 These need to
ing. Basic lifestyle recommendations for maximal health be recorded at the patient’s initial visit and then as
(Box 37-2) are changing less quickly and dramatically indicated.
than for risk factor assessment tools, therefore assessment Text continued on p. 371
366 PART III  Advances in Clinical Science and Practice

Smoking
q Non-smoker q Life-long non-smoker

q Past smoker Amount: q <½ pk/day q between ½ to 1 pk/day q between 1–2 pk/day q >2 pk/day

q I smoke. Amount: q >20 cigarettes/day q between 10 and 20 cigarettes/day q <10 cigarettes/day

Duration: q <5yr q 6–9 yr q 10–19 yr q >19 yr

If you smoke, what would help you to quit smoking?

q Counselling q Medication to help q Knowledge of quitting methods q Will power q Support from a professional
q Fewer worries and stress q Other______________________________________

If you don’t smoke, are you exposed to the smoke of someone in your household or work place that smokes?
q No q Yes If yes, how much for how long__________________________________

Plan: Smoking cessation

Diet and Nutrition

Body Composition

Weight (kg)_____________ Height (m)________________ Body mass index (BMI (kg/m2)______________ Waist girth (cm)________
Hip girth___________ Waist–hip ratio (WHR)_____________
Goal: WHR <85 cm for women and <90 cm for men

Plan: Achieve Recommended Food Guide Servings

Nutrition (example based on the Canada Food Guide [Health Canada13])

Recommended Number of Food Guide Servings per Day*

Children Teens Adults
2–3 4–8 9–13 14–18 Years 19–50 Years 51+ Years
Girls and Boys Female Male Female Male Female Male
Vegetables and Fruit 4 5 6 7 8 7–8 8–10 7 7
Grain Products 3 4 6 6 7 6–7 8 6 7
Milk and Alternatives 2 2 3–4 3–4 3–4 2 2 3 3
Meat and Alternatives 1 1 1–2 2 3 2 3 2 3

*Serving Sizes for Each Food Group:

Vegetables and Fruit

125 mL (½ cup) fresh, frozen or canned vegetable or fruit or 100% juice
250 mL (1 cup) leafy raw vegetables or salad
1 piece of fruit

Grain Products
1 slice (35 g) bread or ½ bagel (45 g)
½ pita (35 g) or ½ tortilla (35 g)
125 mL (½ cup) cooked rice, pasta, or couscous
30 g cold cereal or 175 mL (¾ cup) hot cereal

Milk and Alternatives

250 mL (1 cup) milk or fortified soy beverage
175 g (¾ cup) yogurt
50 g (1½ oz.) cheese

Meat and Alternatives

75 g (2 ½ oz.)/125 mL (½ cup) cooked fish, shellfish, poultry or lean meat
175 mL (¾ cup) cooked beans
2 eggs
30 mL (2 Tbsp) peanut butter
FIGURE 37-1  ■  Assessment of lifestyle-related health behaviours.
Physical Activity

Hours sitting with minimal activity in typical work day________________

Steps/day (measured by valid pedometer reading)___________
Weekly hours of structured exercise_____________

During a week, how often do you accumulate at least 30 minutes of moderately intense physical activity a day. Circle the number of days that
you achieve this?

0 1 2 3 4 5 6 7

0–2 days: design a walking plan

3–4 days: if not adding up to 150 minutes, introduce additional brisk walks and regular activity on another couple of days
5+ days: Goal met

Plan: Goal of at least 150 minutes of moderately intense activity a week (2008 Physical Activity Guidelines14)

*Recommendation may need to be modified based on patient’s disability and progressed accordingly under the physiotherapist’s supervision
Strengthening exercise____________

Sleep

Hours sleep/typical night____________

Times up during a typical night___________
Feels restored in the morning (0 is not at all to 10 maximally restored)__________
Sleep Inventory (Coren 200915) to assess sleep quality and sleep debt: Score: _________

Plan: Achieve optimal sleep between 7 and 10 hours depending on the individual

Stress

Self-rated daily stress 0 (none) to 10 (maximal, unbearable)___________________

Stress triggers________________________ Stress relievers___________________________
Psychological Stress Measure-9 (Lemyre et al 200916) score:________
Holmes-Rahe Stress Test17 score:_______

Plan: Achieve manageable stress levels

FIGURE 37-1, cont’d

BOX 37-2  Guidelines on Nutrition and Physical Activity for Prevention of All-Cause Premature
Mortality and Related Morbidity
ACHIEVE AND MAINTAIN A HEALTHY WEIGHT Limit sedentary behaviour such as sitting, lying down,
THROUGHOUT LIFE watching TV and other forms of screen-based
Be as lean as possible throughout life without being entertainment
underweight Doing some physical activity above usual activities, no
Avoid excess weight gain at all ages. For those who are matter what one’s level of activity, can have many health
overweight or obese, losing even a small amount of benefits
weight has health benefits and is a good place to start EAT A HEALTHY DIET, WITH AN
Get regular physical activity and limit intake of high- EMPHASIS ON PLANT FOODS
calorie foods and drinks as keys to help maintain a
healthy weight Choose foods and drinks in amounts that help you get to
and maintain a healthy weight
BE PHYSICALLY ACTIVE Limit how much processed meat and red meat you eat
Adults Eat at least 2 1 2 cups of vegetables and fruits each day
Choose whole grains instead of refined grain products
Get at least 150 minutes of moderate intensity or 75
minutes of vigorous intensity activity each week (or a IF YOU DRINK ALCOHOL, LIMIT YOUR INTAKE
combination of these), preferably spread throughout the Drink no more than one drink per day for women or two
week per day for men
Children and Teens
Get at least 1 hour of moderate or vigorous intensity activ-
ity each day, with vigorous activity on at least 3 days each
week

SOURCE: McCullough et al, 2011; American Cancer Society. American Cancer Society guidelines on nutrition and physical activity for cancer prevention,
<http://www.cancer.org/cancer/news/news/cancer-prevention-guidelines-also-helpful-against-other-diseases>.16
368 PART III  Advances in Clinical Science and Practice

FIGURE 37-2  ■  Prototype of a lifestyle-related health risk assessment tool: CANRISK. (Source: The Canadian Diabetes Risk Assessment
Questionnaire. Public Health Agency of Canada; 2009. <http://www.diabetes.ca/documents/for-professionals/NBI-CANRISK.pdf>.17) (Source:
© All rights reserved. Public Health Agency of Canada. Reproduced with permission from the Minister of Health, 2014.)
 37  Role of Physiotherapy in Lifestyle and Health Promotion in Musculoskeletal Conditions 369

FIGURE 37-2, cont’d

370 PART III  Advances in Clinical Science and Practice

FIGURE 37-3  ■  Multisystem Review.

 37  Role of Physiotherapy in Lifestyle and Health Promotion in Musculoskeletal Conditions 371

Health Improvement Card investigators identified an operant treatment approach as

a promising behavioural strategy to prevent chronic back
The World Health Professions Alliance published the pain, and one that can be readily integrated into ambulant
Health Improvement Card22 to provide a common tool physiotherapy practice.
for health professionals that could be readily used and Comparable to behavioural theories and models
implemented to address patients’ lifestyle behaviours in underlying lifestyle behaviour change in relation to
terms of both basic lifestyle assessment and recommenda- patients with back problems, their applications have not
tions for health behaviour change. The World Health been sufficiently studied. Their applications in relation
Professions Alliance also supports a practitioner NCD to pain, its experience and remediation, may help inform
toolkit to further foster health promotion practice within best practice management of back pain. Although back
the daily clinical context.23 pain was not a focus of a Cochrane review of weight loss
The Health Improvement Card consists of two pages strategies in people who were overweight or obese,
(Fig. 37-4). Page one outlines the patient’s biometric weight loss was greatest when diet and exercise were
information and includes lifestyle behaviours and some combined with behaviour therapy.26 Another review of
laboratory test results (cholesterol and blood sugar). the literature supported a behavioural approach to the
Colour coding is used to indicate whether these are management of acute whiplash-associated disorders.27
acceptable, caution is needed, or the patient is at high Such behavioural approaches may be applicable to
risk. Page two consists of colour-coded action items. patients with whiplash and concurrent lifestyle-related
Green signifies the lifestyle behaviour is within healthy conditions and by extension, those with thoracic and
limits and the person should continue accordingly. lumbar involvement. Study of the combined outcomes of
Yellow signifies warning and need for remediation, and physical and behavioural approaches in the management
red signifies risky health behaviour warranting priority of spinal conditions is needed.
attention by the patient and health practitioner. The
Health Improvement Card provides a foundation for Cognitive Behaviour Therapy
initiating a conversation with the patient about health
behaviour change and realistic tangible targets. These Cognitive behaviour therapy (CBT) is an approach to
targets are measurable and can be readily followed by behaviour change that focuses on the patient’s emotional
the physiotherapist. and behavioural responses as a vehicle for such change.28
It is based on the assumption that emotional and behav-
ioural responses are largely learned. The goal of therapy
HEALTH BEHAVIOUR CHANGE is for the patient to learn adaptive ways of responding
INTERVENTIONS emotionally and behaviourally to health problems, and to
unlearn maladaptive responses. CBT is well suited for
A contemporary physiotherapy priority is to maximize application to health behaviour change in the clinical
health overall even in people living with chronic condi- setting. Intervention is focused, directed and brief, and
tions. In addition, across health behaviour change initia- often associated with rapid results. The therapeutic rela-
tives, a primary goal is to avoid or reduce reliance on tionship needs to be empathetic and based on rapport.
pharmacologic interventions as much as possible. The CBT enables the patient to accept a health or personal
health psychology literature describes a range of strate- concern so that personal resources such as intelligence,
gies and interventions that can be incorporated into phys- knowledge and energy can be effectively harnessed to
iotherapy practice, to effect health behaviour change. address it. CBT also uses elements of a Socratic method
Some established evidence-based interventions and to enable patients to gain insight into their problems by
related approaches are described below. posing questions to themselves and to the clinician.
Overall, CBT has been promoted as a clinically useful
evidence-based intervention to enable patients to better
Interventions manage chronic back pain.29
Behaviour Modification
Motivational Interviewing
Physiotherapy-provided operant conditioning or behav-
iour modification has been a focus in multiple studies of Motivational interviewing (MI) has become a leading
chronic low back pain disability. In one recent systematic evidence-based interviewing strategy to enable patients
review, such intervention (described as a time-contingent, to identify their health behaviour change needs and moti-
graduated increase in activity including goal setting and vation. MI is a collaborative person-centred form of vali-
the education and reinforcement of positive pain behav- dating the patient’s behaviours and guiding him or her
iours with the ultimate aim of decreasing disability and to elicit and strengthen motivation for change.30 A unique
increasing function) was considered efficacious in the feature of MI is that it is ‘evocative’ in that it is designed
treatment of low back pain.24 Thus, physiotherapists may to elicit the person’s own motivation and commitment
also consider operant conditioning for its additional to change in a supportive, non-coercive manner. A
effect on reducing long-term disability associated with patient’s ambivalence about change is anticipated and MI
chronic back pain. Another systematic review examined strategies are designed to enable the patient to identify,
the use of behavioural strategies used by physiotherapists examine and resolve any ambivalence. Examples of MI
for the prevention of chronic low back pain.25 The questions to identify the patient’s ‘positive motivation’ to
372 PART III  Advances in Clinical Science and Practice

FIGURE 37-4  ■  Health Improvement Card. For colour version see Plates 23–24. (Source: Health Improvement Card. World Health
Professions Alliance. Reprinted with permission. <http://www.ifpma.org/fileadmin/content/Publication/2011/ncd_Health-Improvement-Card
_web-1.pdf>.22)
 37  Role of Physiotherapy in Lifestyle and Health Promotion in Musculoskeletal Conditions 373

FIGURE 37-4, cont’d

374 PART III  Advances in Clinical Science and Practice

participate in health behaviour change and ‘perceived what has been tried, how many times and level of success.
barriers’ to change, appear in Box 37-3. One barrier can be lack of systematic support and
accountability to help sustain patient’s efforts. With some
modicum of interest by the patient in being supported
Decision Balance Analysis
for an attempt at behaviour change, the physiotherapist
Decision balance analysis is based on principles associ- has an inroad. If the patient demonstrates readiness to
ated with MI and CBT.31,32 It is a strategy that enables change (Table 37-1) (i.e. is at the contemplative, prepara-
the patient to identify and reflect on the pros and tion or action stages), the physiotherapist can initiative
cons of changing a specific health behaviour and, as and/or support the patient with appropriate interventions
importantly, the pros and cons of not changing that or referral to other professionals with use of the 5 As
behaviour. Completion of such a grid by the patient endorsed by the World Health Organization.33,34 The 5
aims to increase his or her self-awareness of the facili- As include Assess, Advise, Agree, Assist and Arrange.
tators to health behaviour change and to reduce the Their descriptions appear in Box 37-4. The 5 As consti-
perceived barriers to such change. In addition, this tutes a systematic sequential approach to effecting health
information is useful to the physiotherapist in targeting behaviour change.
health behaviour and health behaviour change strategies The physiotherapist needs to accept that a patient may
to the patient’s needs. be pre-contemplative and disinterested in considering
change at this time. Given changing health behaviour is
challenging and can appear formidable to a patient (e.g.
The 5 As and the 5 Rs
one who smokes a pack of cigarettes a day or more to
At various points in their lives, patients are keen to consider abstinence, or having to lose 25 kg), the 5 Rs
address negative health behaviours such as quitting can provide a systematic approach for the physiothera-
smoking, improving nutrition, losing weight, being less pist, to enable the patient to consider changing a health
sedentary and more physically active, sleeping better and behaviour despite apparent lack of interest or motivation.
reducing stress. Their histories of health behaviour The 5 Rs stand for Relevance, Resistance, Rewards,
change attempts are important to identify in terms of Roadblocks and Repetition.36 These are also described in
Box 37-4.
Finally, even if the patient is referred to one or more
other health professionals, the physiotherapist has a role
in continuing to follow the patient’s progress in a manner
BOX 37-3  Motivational Interviewing: that is as systematic as if that physiotherapist had initiated
Examples of Questions and Their the behaviour change programme.
Interpretation; Implications for an
Action Plan and Follow-Up
Other Behaviour Change Strategies
QUESTION: Designed to elicit positive motivational state- A physiotherapy clinic or department can take advantage
ments from the patient about changing a given behaviour of many resources available to health professionals to
‘Pick a number from 1 to 10 (ten highest) that describes how
motivated or interested you are in changing behaviour X?’
support health promotion. Ministries of Health in most
Follow-up probing question that would identify the countries, for example, circulate regular updated health
degree to which the patient has no-to-low motivation bulletins, reports and information. User-friendly credible
‘Why did you not pick a lower number?’ information is available on the Internet, available for
QUESTION: Designed to identify the patient’s barriers to clinic or department use, or to have the patient use at
making a given health behaviour change home as part of a take home assessment or health
‘Pick a number from 1 to 10 (ten highest) that describes how education strategy. The World Health Organization
confident you are in changing behaviour X?’ has identified key days of the year to promote specific
Follow-up probing question to identify factors that would health initiatives (e.g. May 31st is World No Tobacco
indicate patient’s increased confidence Day). Resources are available for practitioners to
‘Why did you not pick a higher number?’
promote such days in their settings. Disease/condition
ACTION PLAN agencies and associations (e.g. heart, stroke, hyperten-
• Summarize the patient’s/client’s responses for wanting sion, diabetes and cancer) exist in most countries, and
and not wanting to change they too are eager to have their evidence-based resources
• Prompt patient/client to come up with solutions fully used by patients, health professionals as well as
• Add other solutions that have worked for others (with the general public.
patient’s/client’s permission) Engaging and informative clips are available in the
• Systematic and agreed upon follow-up form of ‘edu-tainment’ through Internet sites such as
FOLLOW-UP STRATEGY TED talks® and YouTube®. Although local professional
associations need to preview these for quality and accu-
• Set a follow-up date
• Clarify what the patient will do in terms of realistic
racy, some are well suited to being screened in waiting
expectations for changing behaviours areas of clinics. A couple of evidence-based recommenda-
• What the practitioner will do tions are Dean Ornish’s healing through diet37 and Dr.
• Deliverables at follow-up Mike’s 23 and 1 2 hours, on the effects of physical activity
on health and disease prevention.38
 37  Role of Physiotherapy in Lifestyle and Health Promotion in Musculoskeletal Conditions 375

TABLE 37-1  Assessment of Readiness to Change Health Behaviour

Circle a response to each question using the ‘Y’ or the ‘N.’
Y = Yes, I meet my health objective on this question.
N = For each ‘N’ you circle, circle the readiness to change number that applies:
1 = Not thinking about change at this time (pre-contemplative)
2 = Thinking about change (contemplative)
3 = Preparing to change (preparation)

Readiness to Change Checklist* Response Readiness to Change

†
Do you exercise moderately intensely at least three times a week for 20 to 40 minutes? Y N 1 2 3
Are you physically active during your average day (walk, walk briskly, take stairs)? Y N 1 2 3
Is your weight within normal range? Y N 1 2 3
Do you eat at least five servings of fruit and vegetables daily? Y N 1 2 3
Do you minimize the trans and saturated fats in your diet? Y N 1 2 3
Do you minimize highly refined carbohydrates in your diet (sugar and white flour)? Y N 1 2 3
Do you drink alcohol less often than five times a week? Y N 1 2 3
Are you a non-smoker? Y N 1 2 3
Are you generally relaxed during your day and do you feel in control? Y N 1 2 3

Modified from: The Stages of Readiness to Change defined within the Transtheoretical Model of behaviour change (DiClemente and
Prochaska, 1998)35 is designed to help people adopt new health behaviours. Knowing where you are in the stages of readiness to
change helps you to understand the steps you should take to move to subsequent stages to achieve lifelong sustainable health
behaviours.
*Behaviours that are consistent with healthy living. If patients give a No response to a question, then their readiness to change that
behaviour is evaluated.
†
Given patients vary with their capacity for exercise, the requirement for health should be adjusted.

BOX 37-4  The 5 As and the 5 Rs

Assess or re-evaluate with Initiate and
Indication for the 5 As: The patient is ready to change health pre-set follow-ups and/or Support/Reinforce
behaviour (i.e. either contemplating or preparing to change). scheduled reports from lifestyle behavior change
• Ask about the target health behaviour other practitioners education strategies
• Advise to change the behaviour
• Assess willingness to attempt to change the • Health
behaviour • Health knowledge
• Lifestyle behaviors Initiate and Refer
• Assist in changing the behaviour Smoking cessation to other practitioner (e.g.
• Arrange follow-up Optimal nutritional choices counsellor, nurse
Indication for the 5 Rs: The patient is not interested in ↓ Prolonged periods of practitioner, physical
changing a health behaviour at this time (i.e. at the pre- inactivity therapist, physician,
contemplative stage); the purpose is to maintain an open ↑ General physical activity psychologist)
door for conversation should the patient become interested. ↑ Cumulative aerobic
• Determine the Relevance of changing behaviour to exercise of moderate and
patient exertion for 20–30
• Discuss the Risks of patient’s continued deleterious minutes 3–5 days a week Support/Reinforce
• Lifestyle-related health risk the initiatives of these
behaviour factors practitioners
• Explore Rewards of changing behaviour
• Examine possible Roadblocks to changing behaviour
• Continue Repetition of the discussion
FIGURE 37-5  ■  Process of health behaviour change in the phys-
iotherapy context. (Source: Adapted from Dean et al. 2012.53)

complaints, baselines of lifestyle-related health behav-

Examples of Physiotherapy-Directed iours as well as risk factors need to be assessed and
Health Behaviour Change Initiatives addressed as indicated, in the interest of comprehensive
patient care that is consistent with the ICF philosophy
The steps in the process for effecting lifestyle behaviour and goals.
change with a patient are shown in Figure 37-5. This Comparable to conventional assessments, self-reported
figure details the decision-making points for initiating assessments of smoking, basic nutrition, physical activity
health behaviour change or not; and whether to refer to and structured exercise, sleep habits and stress are funda-
another professional. mental, despite the limitation of self-reported informa-
The key elements for assessing/evaluating and target- tion. To maximize validity, patients are encouraged to
ing strategies and interventions for modifying health record these behaviours as specifically and accurately
behaviours are presented in Table 37-2. Comparable to as possible over a representative number of days.
physiotherapy assessment of a patient’s musculoskeletal Quality baseline data are essential if the goals for health
376 PART III  Advances in Clinical Science and Practice

TABLE 37-2  Examples of Evidence-Based Lifestyle-Related Assessment/Evaluation Tools and

Strategies/Interventions for Health Behaviour Change Within an Orthopaedic
Physiotherapy Context
SMOKING CESSATION

Assessment and Evaluation Tools

Smoking history and current practices (see Fig. 37-1 Smoking section)
The WHY test39 (unvalidated) (helps to identify why the person smokes, i.e. stimulation, handling, pleasure, relaxation, habit,
weight, image and social)

Strategies and Interventions

Brief advice (Bodner and Dean 2009;40 Frerichs et al., 201241)
Referral to physician for potential pharmaceutical support and/or health psychologist/counsellor

OPTIMIZING NUTRITION AND HEALTHY WEIGHT

Assessment and Evaluation Tools

Detailed multi-day nutrition logs can be laborious and de-motivating, and may lack validity
Weight, height and body mass index
Waist–hip ratio (Zhu et al. 2002;42 Janssen et al. 2004;43 Yusuf et al. 2004;44 Yusuf et al. 200545)
Use established and accepted food guides to establish a patient’s typical consumption patterns related to servings of the basic
food groups daily to identify gross excesses and deficits: servings of vegetables, fruit, whole grain, refined foods, dairy,
animal protein (meat, poultry vs. fish sources), sweets
Added sweetener, salt, butter and oil
Food preparation: steam, bake and broil over frying and deep frying
Fast food meals per week
DETERMINE Your Nutritional Health Questionnaire (Morris et al. 200946)
Mini-Nutritional Assessment-SF (Morris et al. 200946)
Establish need for nutritionist intervention (beyond basic recommendations)

Strategies and Interventions

Implement basic nutrition education based on established guidelines (e.g. plant-based diets such as the Mediterranean diet)
Irrespective of body mass and waist–hip ratio, most patients can benefit from nutritional assessment and reinforcement of
healthy food choices
Patients who are overweight and obese do require special consideration, however a healthy diet will help to modify body
composition
Referral to dietician or nutritionist

MOTIVATING PATIENTS TO BE PHYSICALLY ACTIVE

Assessment and Evaluation Tools

International Physical Activity Questionnaire (IPAQ website47) (long and short versions in multiple languages that classify a
person’s general physical activity as low, medium, or high)
Pedometer to establish physical activity level, and whether is sedentary (<5000 step criterion) (Tudor-Locke et al. 200448)

Strategies and Interventions

Action planning worksheet (Rhodes et al. 200949)
Exercise barrier sheet (Rhodes et al. 200949)
Exercise enjoyment sheet (identifies suitable activities based on proximity, aesthetics and interest) (Rhodes et al. 200949)

OPTIMIZING SLEEP

Assessment and Evaluation Tools

Sleep inventory questionnaire (17 questions) (Coren 200950) (helps to establish evidence for patient’s sleep debt/deprivation
and risk of related health problems)
Need to distinguish pathologically disturbed sleep versus functionally/behaviourally disturbed sleep (if the former, may need
to refer to sleep specialist and potential for sleep laboratory investigation)

Strategies and Interventions

Sleep is a physiological necessity but its quality and effectiveness to restore is highly behaviourally dependent
Sleep hygiene recommendations:
Regular hours
Quiet, no light (including electronic clock/TV lights), comfortable ventilated room
Avoid heavy meals, caffeine, alcohol within hours of bed

STRESS MANAGEMENT

Assessment and Evaluation Tools

Distinguish acute (daily hassle) type stress and chronic stress
Psychological Stress Measure-9 (nine questions) (Lemyre et al. 200951) (evaluates short-term stress, past 4–5 days)
Holmes-Rahe Social Readjustment Stress Scale (Holmes-Rahe Stress Test52) (evaluates major life stressors over the past year
and predicts health risks for the subsequent year)

Strategies and Interventions

Establish need for referral to other professionals
Methods based on principles of cognitive behavioural therapy and motivational interviewing
 37  Role of Physiotherapy in Lifestyle and Health Promotion in Musculoskeletal Conditions 377

behaviour change are to be S.M.A.R.T. (i.e. Specific, 12. Ornish D, Weidner G, Fair WR, et al. Intensive lifestyle changes
Measurable, Attainable, Realistic and Timely). Such goal may affect the progression of prostate cancer. J Urol 2005;174(3):
1065–9, discussion 1069–70.
characteristics are necessary if effective change is to be 13. Eating Well with Canada’s Food Guide [Internet]. Ottawa, ON:
demonstrated. Health Canada; 2007. Available from: <http://www.has.uwo.ca/
hospitality/nutrition/pdf/foodguide.pdf>; [cited 2014 Feb 22].
14. Grundy SM, Pasternak R, Greenland P, et al. Assessment of car-
CONCLUSION diovascular risk by use of multiple-risk-factor assessment equations:
a statement for healthcare professionals from the American Heart
Association and the American College of Cardiology. Circulation
This chapter builds on the evidence and epidemiological 1999;100(13):1481–92.
base described in Chapter 11. It introduced physiothera- 15. Disease Risk Index [Internet]. Harvard School of Public Health;
pists involved in the management of people with muscu- 2008. Available from: <http://www.diseaseriskindex.harvard.edu/
update/>; [cited 2014 Feb 21].
loskeletal conditions to established assessment and 16. 2008 Physical Activity Guidelines for Americans: Be Active,
evaluation tools, and theory- and evidence-based strate- Healthy, and Happy [Internet]. U.S. Department of Health and
gies and interventions to change their patients’ lifestyle Human Services; 2008. Available from: <http://www.health.gov/
behaviours. Behaviours warranting assessment and poten- paguidelines/pdf/paguide.pdf>; [cited 2014 Feb 22].
17. The Canadian Diabetes Risk Assessment Questionnaire [Internet].
tial intervention include smoking, sub-optimal nutrition, Public Health Agency of Canada; 2009. Available from: <http://
unhealthy body mass, regular prolonged periods of physi- www.diabetes.ca/documents/for-professionals/NBI-CANRISK
cal inactivity, low physical activity and exercise, sub- .pdf>; [cited 2014 Feb 21].
optimal sleep quality and quantity, and anxiety, depression 18. Canrisk: The Canadian Diabetes Risk Questionnaire: User
and stress. Assessment tools and behavioural interven- Guide for Pharmacists [Internet]. Public Health Agency of Canada.
Available from: <http://www.pharmacists.ca/cpha-ca/assets/File/
tions are described that can be integrated into busy, education-practice-resources/Canriskuserguideforpharmacists
resource-constrained physiotherapists’ practices. With EN.pdf>; [cited 2014 Feb 21].
systematic attention to health behaviour change, physio- 19. Pearson TA, Blair SN, Daniels SR, et al. AHA guidelines for
therapy outcomes related to musculoskeletal complaints primary prevention of cardiovascular disease and stroke: 2002
update: Consensus Panel guide to comprehensive risk reduction for
including pain can be augmented as well as patients’ adult patients without coronary or other atherosclerotic vascular
general health and well-being improved. Both are priori- diseases. American Heart Association Science Advisory and Coor-
ties in contemporary physiotherapy practice. dinating Committee. Circulation 2002;106(3):388–91.
20. Inoue T, Iseki K, Ohya Y. Heart rate as a possible therapeutic guide
for the prevention of cardiovascular disease. Hypertens Res
REFERENCES 2013;36(10):838–44.
1. Huan HC, Chang HJ, Lin KC, et al. A closer examination of the 21. Handler J. The importance of accurate blood pressure measure-
interaction among risk factors for low back pain. Am J Health ment. Perm J 2009;13(3):51–4.
Promot 2014;28:372–9. 22. Health Improvement Card [Internet]. World Health Professions
2. Melloh M, Elfering A, Stanton TR, et al. Low back pain risk factors Alliance; 2014. Available from: <http://www.ifpma.org/fileadmin/
associated with persistence, recurrence and delayed presentation. content/Publication/2011/ncd_Health-Improvement-Card_
J Back Musculoskelet Rehabil 2014;27(3):281–9. web-1.pdf>; [cited 2014 Feb 21].
3. Sykes C, Myers B. Annual WHO Family of International Classifi- 23. Non Communicable Diseases: An Action Toolkit for Health
cations Network Meeting: ICF Activities by the World Confedera- Professionals, Patients and Public [Internet]. World Health Profes-
tion for Physical Therapy and Its Member Organisations [Internet]. sions Alliance. Available from: <http://www.whpa.org/ncd_Action
Seoul, Republic of Korea: World Confederation for Physical Toolkit_cover.pdf>; [cited 2014 Feb 21].
Therapy; 2009. Available from: <http://www.who.int/classifications/ 24. Bunzli S, Gillham D, Esterman A. Physiotherapy-provided operant
network/WHOFIC2009_D041p_Sykes.pdf>; [cited 2014 Feb 22]. conditioning in the management of low back pain disability: a
4. Dean E, Gormsen Hansen R. Prescribing optimal nutrition and systematic review. Physiother Res Int 2011;16(1):4–19.
physical activity as ‘first–line’ interventions for best practice man- 25. Brunner E, De Herdt A, Minguet P, et al. Can cognitive behav-
agement of chronic low-grade inflammation associated with osteo- ioural therapy based strategies be integrated into physiotherapy for
arthritis: evidence synthesis. Arthritis 2012;2012:560634. the prevention of chronic low back pain? A systematic review.
5. Buck D, Frosini F. Clustering of Unhealthy Behaviours Disabil Rehabil 2013;35(1):1–10.
Over Time: Implications for Policy and Practice [Internet]. 26. Shaw K, O’Rourke P, Del Mar C, et al. Psychological interventions
London, UK: The King’s Fund; 2012. Available from: <http:// for overweight or obesity. Cochrane Database Syst Rev 2005;(2):
www.kingsfund.org.uk/sites/files/kf/field/field_publication_file/ CD003818.
clustering-of-unhealthy-behaviours-over-time-aug-2012.pdf>; 27. Soderlund A, Sweden V. The role of educational and learning
[cited 2014 Feb 21]. approaches in rehabilitation of whiplash associated disorders in
6. Schuit AJ, van Loon AJ, Tijhuis M, et al. Clustering of lifestyle risk lessening the transition to chronicity. Spine 2011;36(Suppl. 25):
factors in a general adult population. Prev Med 2002;35(3): S280–5.
219–24. 28. NACBT Online Headquarters [Internet]. National Association of
7. Spring B, Moller AC, Coons MJ. Multiple health behaviours: over- Cognitive-Behavioral Therapists. 2010. Available from: <http://
view and implications. J Public Health 2012;34(Suppl. 1):i3–10. www.nacbt.org/whatiscbt.htm>; [cited 2014 Feb 21].
8. Ornish D. Avoiding revascularization with lifestyle changes: the 29. Gatchel RJ, Rollings KH. Evidence-informed management of
multicenter lifestyle demonstration project. Am J Cardiol 1998; chronic low back pain with cognitive behavioral therapy. Spine J
82(10B):72T–76T. 2008;8(1):40–4.
9. Ornish D, Scherwitz LW, Billings JH, et al. Intensive lifestyle 30. Rollnick S, Miller WL, Butler C. Motivational Interviewing in
changes for reversal of coronary heart disease. JAMA 1998;280(23): Health Care: Helping Patients Change Behavior (Applications of
2001. Motivational Interviewing). New York, NY: The Guilford Press;
10. Your Guide to Lowering Your Blood Pressure with DASH [Inter- 2008.
net]. U.S Department of Health and Human Services; 2006. Avail- 31. Decisional balance worksheet [Internet]. Available from:
able from: <http://www.nhlbi.nih.gov/health/public/heart/hbp/ <http://motivationalinterview.net/clinical/decisionalbalance.pdf>;
dash/new_dash.pdf>; [cited 2014 Feb 21]. [cited 2014 Feb 21].
11. Norris SL, Engelgau MM, Venkat Narayan KM. Effectiveness of 32. Lipschitz JM, Fernandez AC, Larson HE, et al. Validation of deci-
self-management training in type 2 diabetes: a systematic review of sional balance and self-efficacy measures for HPV vaccination in
randomized controlled trials. Diabetes Care 2001;24(3):561–87. college women. Am J Health Promot 2013;27(5):299–307.
378 PART III  Advances in Clinical Science and Practice

33. 5 A’s behavior change model adapted for self-management 44. Yusuf S, Hawken S, Ounpuu S, et al. Effect of potentially modifi-
support improvement [Internet]. 2002. Available from: <http:// able risk factors associated with myocardial infarction in 52 coun-
www.improvingchroniccare.org/downloads/3.5_5_as_behaviior_ tries (the INTERHEART study): case-control study. Lancet
change_model.pdf>; [cited 2014 Feb 21]. 2004;364(9438):937–52.
34. Fiore MC, Jaen CR, Baker TB. A clinical practice guideline for 45. Yusuff S, Hawken S, Ôunpuu S, et al. Obesity and the risk of
treating tobacco use and dependence: 2008 Update. A U.S. Public myocardial infarction in 27 000 participants from 52 countries: a
Health Service report. Am J Prev Med 2008;35(2):158–76. case-control study. Lancet 2005;366(9497):1640–9.
35. DiClemente CC, Prochaska JO. Toward a comprehensive, trans- 46. Morris DM, Kitchin EM, Clark DE. Strategies for optimizing
theoretical model of change: stages of change and addictive behav- nutrition and weight reduction in physical therapy practice: the
iors. In: Miller WR, Heather N, editors. Treating Addictive evidence. Physiother Theory Pract 2009;25(5–6):408–23.
Behaviors. 2nd ed. New York, NY: Plenum Press; 1998. p. 3–24. 47. International Physical Activity Questionnaire: IPAQ: short last 7
36. Newson RS, Lion R, Crawford RJ, et al. Behaviour change for days self administered format. [Internet]. IPAQ website; 2001.
better health: nutrition, hygiene and sustainability. BMC Public Available from: <http://www.ipaq.ki.se/questionnaires/IPAQ_S7S_
Health 2013;13(Suppl. 1):S1. FINAL_MAY_01.pdf>; [cited 2014 Feb 22].
37. Dean Ornish: Healing through diet | Video on TED.com [Inter- 48. Tudor-Locke C, Bassett DR Jr. How many steps/day are enough?
net]. Ted Conferences; 2004. Available from: <http://www.ted.com/ Preliminary pedometer indices for public health. Sports Med
talks/dean_ornish_on_healing.html>; [cited 2014 Feb 21]. 2004;34(1):1–8.
38. 23 and 1/2 hours: What is the single best thing we can do for our 49. Rhodes RE, Fiala B. Building motivation and sustainability into the
health? [Internet]. You Tube; 2011. Available from: <http:// prescription and recommendations for physical activity and exercise
www.youtube.com/watch?v=aUaInS6HIGo>; [cited 2014 Feb 21]. therapy: the evidence. Physiother Theory Pract 2009;25(5–6):
39. The ‘Why I Smoke’ Test [Internet]. University of Virginia Health 424–41.
System. Available from: <http://uvahealth.com/patients-visitors- 50. Coren S. Sleep health and its assessment and management in physi-
guide/smoke-free/smoke-free-pdfs/test.pdf>; [cited 2014 Feb 22]. cal therapy practice: the evidence. Physiother Theory Pract 2009;
40. Bodner ME, Dean E. Advice as a smoking cessation strategy: a 25(5–6):442–51.
systematic review and implications for physical therapy. Physiother 51. Lemyre L, Lalonde-Markon MP. Psychological stress measure
Theory Pract 2009;25(5):369–407. (PM-9): integration of an evidence-based approach to assessment,
41. Frerichs W, Kaltenbacher E, van de Leur JP, et al. Can physical monitoring, and evaluation of stress in physical therapy practice.
therapists counsel patients with lifestyle-related health conditions Physiother Theory Pract 2009;25(5–6):453–62.
effectively? A systematic review and implications. Physiother 52. Holmes-Rahe Stress Test [Internet]. Fort Worth, TX: The Ameri-
Theory Pract 2012;28(8):571–87. can Institute of Stress. Available from: <http://www.stress.org/
42. Zhu S, Wang Z, Heshka S, et al. Waist circumference and obesity- holmes-rahe-stress-inventory/>; [cited 2014 Feb 22].
associated risk factors among whites in the third National Health 53. Dean E, Li Z, Wong WP, et al. Cardiology best practice – effective
and Nutrition Examination Survey: clinical action thresholds. Am health education meets biomedical advances: Reducing the ultimate
J Clin Nutr 2002;76(4):743–9. knowledge translation gap. In: Lakshmanadoss U, editor. Novel
43. Jannsen I, Katzharzyk PT, Ross R. Waist circumference and not Strategies in Ischemic Heart Disease. InTech Publishing; 2012. p.
body mass index explains obesity-related health risk. Am J Clin 301–18 [Online access].
Nutr 2004;79(3):379–84.
 CHAPTER 38 

Musculoskeletal Health in the

Workplace
Venerina Johnston  •  Leon Straker  •  Martin Mackey

to the greater severity of injuries requiring longer recov-

INTRODUCTION ery time.8,9 In order to ensure the health and safety of
older workers within the workplace, organizational prac-
There is international consensus that work is generally tices will need to be adjusted, new technologies adopted
good for health.1 Maintenance of musculoskeletal health and assistance given to help mature workers cope with
of the individual worker is a shared responsibility between work demands to ensure work ability is optimized in the
the work organization and the worker. The organization face of increasing challenges to working life.10–13 The
has a responsibility to ensure the workplace and the way physical changes with ageing need to be considered to
work is performed are safe and not detrimental to health enable workers to age productively.
and well-being. The worker has a responsibility to main- The prevalence of some lifestyle risk factors for
tain their own health and ensure that work is practiced chronic disease is increasing, particularly physical inac-
in the prescribed safe way. This symbiotic relationship tivity and obesity across workers of all ages.14 Asthma,
between work organization and worker is confirmed in cancer, cardiovascular disease, diabetes, arthritis, osteo-
legislation in most developed countries. However, several porosis and other musculoskeletal conditions, including
features of modern society pose new challenges to this those associated with exposure to hazards in the work-
relationship – changes in workers themselves reflected in place, are of particular concern.14 These chronic diseases
the ageing population and the increase in chronic dis- represent a major challenge for industry as they result
eases, and changes in the nature of work such as increases in substantial absenteeism as well as presenteeism
in precarious work and sedentary work. This chapter (reduced performance while at work).14 In response to
discusses contemporary approaches to assist the worker the growing impact of chronic disease on the health
retain and regain musculoskeletal health within a con- of workers and health-care systems, governments are
stantly changing work environment. currently implementing preventive strategies such as
anti-smoking campaigns and lifestyle programmes to
promote healthy eating choices and exercise participa-
Factors Threatening Worker Health tion including within the workplace.15 With the majority
Population ageing is occurring globally due to a sustained of working-age people having one or more risk factors,16
reduction in fertility rates and a decline in mortality asso- it is incumbent on health practitioners to assist workers
ciated with improvements in health care and technology.2 to understand how these risk factors may impact on
Ageing of the working population has significant social, working life.
economic and political implications for government, The nature of work is diversifying in many societies.
industry and the health professions.3 For instance, in the Lifelong employment with a single organization in a
future more mature-aged workers will need to remain single industry is becoming rarer, with more workers in
active in the workforce beyond the current retirement precarious employment such as contract, temporary or
age to meet workforce demands, and this is being encour- part-time work. These work arrangements have been
aged by a range of legislative and social policy initiatives. linked with negative health outcomes due to their asso-
There are several implications of an ageing workforce for ciations with lower material well-being, adverse physical
workplace health and safety. Physical work capacity and psychosocial working conditions, less positive social
(impacted by changes in cardiovascular and musculoskel- contacts, and weaker support from supervisors and
etal capacity) declines with increasing age, and after 50 co-workers.17,18 Concurrently, there is an increasing
years the deterioration is more marked.4 If a worker’s demand for greater flexibility in the location and timing
physical capacity cannot match the task demands, it could of work. This is driven in part by portable technology,
result in excessive fatigue, leading to a poor quality of economic globalization and the desire of workers to
work along with an increased risk of industrial accidents.5 combine family commitments and lifestyle interests while
Older workers also tend to experience a higher rate of remaining in employment. Knowledge workers and those
some work-related injuries (e.g. falls) than their younger in information technology often have the option of
counterparts.6,7 Work injuries in mature-aged workers working from home, whereas workers in the resource
are more costly in terms of lost productivity partly due industry may utilize organization-sponsored ‘fly-in
379
380 PART III  Advances in Clinical Science and Practice

fly-out’ work arrangements. The changing nature of injury or illness.24 As a result, there is increased recogni-
work requires clinicians to consider the current physical tion that the workplace is an ideal venue for health inter-
and psychosocial work environment and implement ventions and that work should be used not only for
(often creative) strategies to increase the workers’ knowl- rehabilitation from injury but also to enhance and
edge and skills to ensure maintenance and/or improve- promote health.32
ment of musculoskeletal health. Health professionals such as physiotherapists who spe-
There has also been an increase in sedentary work, cialize in the preservation and improvement of move-
with a shift in the proportion of workers employed in ment for positive health and functional outcomes33 have
‘blue collar’ industries to ‘white collar’ industries.19 This a key role to play in the prevention of work-related
increase in sedentary work is thought to be a significant injuries34–36 and in the prevention of work disability fol-
contributor to the obesity epidemic facing many societ- lowing a work-related injury or other pre-existing mus-
ies.20 Even within traditionally physically demanding culoskeletal health problem. While health professionals
industries such as mining, forestry and agriculture, many have traditionally focused mainly on management of
tasks are now mechanized, creating sedentary jobs.21 symptoms related to MSDs, there is increasing awareness
Some job tasks still remain that are physically demanding, of their role in preventing subsequent disability (tertiary
such as hotel bed making, and there are other jobs that prevention) and also help prevent development of MSDs
require only light physical exertion but are highly repeti- (primary and secondary prevention). The following pres-
tive, such as electronics manufacturing. Thus there needs ents a discussion of recent advances for the prevention
to be an awareness of the different types of work and and management of work-related MSDs.
current strategies to reverse the negative impact of sed-
entary work while maintaining employee musculoskeletal
health. Such strategies include the use of adjustable sit– PREVENTION
stand workstations in office environments22 and initia-
tives to encourage increased physical activity in the Prevention is often conceptualized in three stages:
workplace.23 primary, secondary and tertiary. Primary prevention aims
to avoid a health problem before it occurs; secondary
What is a Work-Related prevention to minimize disability and recurrence in the
early stages of a health problem; and tertiary prevention
Musculoskeletal Disorder? to reduce morbidity arising from a chronic health
Work-related musculoskeletal disorders (MSDs) are problem.37 The definitions infer discreet phases, but
musculoskeletal conditions that may be caused, aggra- taking the example of back or neck pain, the first episodes
vated, accelerated or exacerbated by (non-accidental) of spinal pain often occur during adolescence, prior to
work activities. They include disorders of inflammation, adult working life.38,39 Similarly, the first experiences of
degeneration and physiological disruption of muscles, disability associated with spinal pain often occur during
tendons, ligaments, nerves, synovia and cartilage of the adolescence.40 For many MSDs there is a gradual onset
limbs and/or trunk. MSDs are considered work-related and symptoms follow an episodic pattern.38,41 Given these
when the work environment and performance of work common life-course and episodic characteristics of many
contribute significantly to the condition but may be only MSDs, the precise phase of prevention may not be clear
one of a number of factors contributing to the causation for many MSDs’ preventive activities. This chapter will
of a multifactorial disease.24,25 These entities are included discuss advances related to interventions aimed at primary
in categories 353–355, 722–724 and 726–729 of the Inter- prevention in the general workforce (‘primary’) and at
national Classification of Diseases (commonly referred to as those who have developed an MSD (‘secondary’ and
ICD-9).26 MSDs may include clinical syndromes such as ‘tertiary’).
tendon inflammations and related conditions (tenosyno-
vitis, epicondylitis, bursitis), nerve compression disorders
(carpal tunnel syndrome, sciatica) and osteoarthrosis, as
Primary Prevention
well as conditions without clear diagnostic criteria such The traditional intervention for primary prevention of
as myalgia, low back pain and other regional pain syn- spinal work-related MSDs was training in lifting tech-
dromes not attributable to known pathology. Body nique. Several decades of research has provided evidence
regions most commonly involved in prevalence order are which questions the physical validity of recommended
the low back; hand, fingers and thumb; shoulder; and lifting techniques.42–45 Further, high-quality intervention
knee.27,28 MSDs are associated with high costs to organi- studies have been unable to demonstrate an improvement
zations in terms of absenteeism, lost productivity, and in MSD outcomes.46 Systematic reviews have concluded
increased health-care, disability and worker’s compensa- that there is moderate evidence that training in manual
tion costs. For example, workers’ compensation claims handling techniques is not effective in preventing back
for MSDs account for over 40% of the $57.5 billion pain.47 This has prompted a change in approach to injury
annual expenditure of work-related injuries and diseases prevention – from changing the individual to meet the
in Australia29 and upto 1.6% of the gross domestic demands of the job (e.g. manual handling training) to a
product of some European states.30 MSDs are the most risk-management approach, creating a safe system of
common cause of chronic severe pain and long-term work. This approach is based on two models – an ergo-
physical disability, work limitations and unemployment.31 nomics human–technology systems model and a risk-
They are often more severe than the average non-fatal management model.
 38  Musculoskeletal Health in the Workplace 381

Ergonomics Human–technology is a product of the likelihood and consequences of harm

Systems Model being caused by the hazard. Likelihood is usually charac-
terized as a probability, say a 1 in 5 chance each year of
The ergonomics human–technology systems model is experiencing an MSD. Consequence is the outcome,
illustrated in Figure 38-1. Briefly, the model’s focus is on which for MSDs would range from mild discomfort
the interaction between the human and the technology through to severe disability (more severe non-MSD con-
they are using to perform a task within a work environ- sequences would include fatality).
ment, positioned within a broader organizational and
societal context. It is becoming increasingly accepted in Work-Related MSD Hazards.  The main hazards iden-
MSD management. Physical, psychological and social tified as risks for MSDs are related to the different types
aspects of the interaction are important in the prevention of physical demands in work and psychosocial issues.
of MSDs.48 The aim of ergonomics is for the non-human Additional hazards are created by work organization
aspects of the system to match the capabilities and limita- factors (e.g. excessive work hours and shift systems) and
tions of the human. It is hypothesized that this will result work environment factors (e.g. high heat, inadequate
in better health, satisfaction and productivity outcomes. lighting and arm or whole body vibration).
Physical hazards include individual technology and
task aspects. Key physical hazards include:49
Risk-management Model
• Repetitive force – for example, repetitive gripping
Figure 38-2 illustrates the risk-management model. of bricks or using a nail gun to fix palings to a fence;
Briefly, hazards within the work environment are identi- • Sustained force – for example, holding a plaster
fied and the risk for injury assessed. Measures to control sheet while fixing it to a ceiling or supporting a
the risks are identified and implemented and the impact patient limb during surgery;
of these changes is evaluated. Hazards are entities with • High force – for example, lifting a large container
the potential to cause harm (examples provided below). or cutting wire with pliers;
With respect to work-related MSDs these are commonly • Sudden force – for example, restraining an animal
classified into hazards of physical aspects of work and or catching a falling patient;
hazards of psychosocial aspects of work. Risk, in contrast, • Repetitive movement – for example cutting grape
vines or typing;
• Awkward posture – for example, neck flexed and
rotated to read document or arms reaching around
Society an engine to adjust a bolt;
• Sustained posture – for example, continually stand-
ing on one leg or using a computer mouse.
Work organization
Psychosocial hazards include individual task aspects in
addition to broader job and organization aspects.48 Key
Work environment
psychosocial hazards include:
Task
• High mental workload – for example, excessive cog-
nitive task demands where tasks have high percep-
tual demands with short time deadlines;
Human Technology • Low control over work – for example, assembly line
tasks where task pace is set by the conveyor belt;
• Low social support – for example, from work peers
and supervisors.
There has been considerable debate about the level of
FIGURE 38-1  ■  The ergonomics human–technology systems evidence for work factors contributing to MSDs,27,50,51
model. and therefore what the hazards are and what should be
addressed in risk control measures. The continued debate
about hazards is not surprising given the wide variety of
Hazard work-related MSDs, the range of potential aetiological
identified pathways, the cumulative nature and life-course of many
MSDs and the difficulty in accurately assessing exposure
to hazards and accurately defining MSD outcomes.
However, a substantial body of evidence has now amassed
Risk that is convincing to most.27,48,52
assessed
Tools Available for Risk Management.  A number of
Evaluate tools have been developed to assist practitioners assess
the degree of risk associated with work. Often the rele-
Risk
vant occupational safety and health authority will have
controlled produced guidelines, codes of practice or advice material
which commonly include simple checklists (e.g. Safe
FIGURE 38-2  ■  The risk-management model. Work Australia49). For more detailed assessments, there
382 PART III  Advances in Clinical Science and Practice

are a variety of tools to choose from. Macdonald and or health condition to find or keep a job when they are
Evans48 provide an accessible summary of tools available unable to return to their pre-injury occupation. These
for assessment of posture (OWAS53 and RULA54), loads interventions include job capacity and functional capacity
(Health and Safety Executive55, NIOSH lifting equation56 assessments to identify transferable skills and physical
and Liberty Mutual psychophysical tables57), repetition capacity for realistic vocational options.
(Job Strain Index58), multiple physical hazards There is consistent evidence that the longer a person
(ManTRA59), psychosocial hazards (Job Content Ques- is away from work, the longer it will take them to return
tionnaire60) and both physical and psychosocial hazards to work and the likelihood of prolonged disability is
(Quick Exposure Check61). increased.65–67 Health professionals such as general prac-
titioners and physiotherapists are intimately involved in
Risk Control.  Potential control options to reduce the the treatment of injured workers. The primary focus is
risk of MSDs are often informed by the risks assessed. often on relief of symptoms and restoration of function.
There is a recommended hierarchy of controls62 where Return to pre-injury work activities is the expected but
the strategy with the highest confidence for sustained often the secondary outcome of treatment. Increasingly,
success is to remove the hazard. An example would be a health-care practitioners are being encouraged and
change in work processes to replace manual handling of expected to take a more active role in the return to work
bags of potatoes with forklift handling of pallets of pota- (RTW) of the injured worker.68–70 This is driven not
toes. The second group of strategies recommended are only by the insurance authorities,68 but also by the
based around engineering controls to control the hazard mounting evidence for the negative impact of workless-
at its source. These do not rely on individual workers’ ness.71 For some practitioners, this may require a para-
behaviour. An example is the use of roller conveyors to digm shift or, at least, clarification of the patient’s
eliminate the need to lift objects from the floor. The last treatment goals. RTW was once considered the end of
group of strategies to deploy are administrative controls the rehabilitation phase but complete recovery cannot
which rely on worker behaviour with protocols, training always be assumed. There is evidence that for many
and the use of personal protective equipment. These workers the RTW was not sustained, with as many as
administrative controls are the least reliable, and as stated two-thirds of workers experiencing a subsequent injury-
earlier there is evidence that training in manual handling related work absence.72 Possible reasons are the recurrent
alone is not effective. nature of many MSDs, pressure from the organization
to return sooner than ready or an organization’s inability
to modify the work environment. RTW is now recog-
Evidence of the Efficacy of the Ergonomics/
nized as a dynamic process, the success of which is
Risk-Management Approach
dependent on the coordination of the various players in
In developed countries it is now very difficult to conduct the process each with their own (sometimes competing)
controlled trials of the efficacy of ergonomics/risk-man- needs and demands.73–76 This section will discuss three
agement approach as most work situations have already features of the advances made in the sphere of work
had some risk control measures implemented and ethics disability prevention: adopting a systems approach to
would not allow workers to be put at undue risk by rein- work disability prevention; looking beyond the physical
troducing prior risks. Despite this challenge, a number symptoms; and the need to promote ability not disability
of studies have demonstrated the efficacy of this approach. in workers.
A randomized controlled trial tested this risk-management
approach across 48 workplaces from three high-risk A Systems Approach to Work
industry sectors in Queensland, Australia (food process- Disability Prevention
ing, aged care and construction related). The approach
resulted in reduced risk based on occupational health and It is well-accepted that musculoskeletal conditions are
safety inspector audits.63 Similarly, an intervention in 66 best understood and managed according to a biopsycho-
computer workers in Israel was able to show improve- social model that includes biological, psychological and
ments in physical risk indicators and MSDs.64 social dimensions.77–81 Yet this model does not reflect the
complexity of issues surrounding RTW after injury,
Prevention of Work Disability – which is influenced by a complex interaction of the indi-
vidual and their health condition and the various stake-
Secondary and Tertiary Prevention holders and systems (political, legislative, social, work
The desired outcome of all primary prevention interven- environment, health care).82 One model that reinforces
tions in the workplace is an absence of injuries. However, the biopsychosocial perspective but also considers the
the reality is that inevitably, some workers will sustain an various actors in the work disability prevention arena is
MSD and that a small proportion will experience a that developed by Loisel et al.82 This is an operational
chronic MSD. This section discusses the advances made rather than an explanatory model to guide the manage-
for the secondary prevention of work disability immedi- ment and understanding of the various systems on the
ately following an MSD and tertiary prevention of work disability process. The worker is at the centre of the
disability for people with a chronic MSD. Inclusive of recovery process and is exposed to the influence of four
tertiary prevention, but not discussed further in this main systems (Fig. 38-3):
chapter, are vocational rehabilitation interventions that • their own personal resources to manage their condi-
assist and support people who have an injury, disability tion and the impact on their life and family
 38  Musculoskeletal Health in the Workplace 383

Overall societal context

Culture and politics

Workplace system
Work relatedness, employees’ assistance plans,
workplace accommodation

External environment

Interdisciplinary and interorganizational team

Organization

Legislative and insurance system

Department
Variety of care management

Provincial and Federal laws

Regulations of jurisdictions
Multidisciplinary team
Health-care system

Society’s safety net

Other health-care
Job position

professionals

case worker
sation agent
physicians
Attending

Compen-

Insurer’s
Worker
with disability from
musculoskeletal pain

Physical

Cognitive

Affective

Social relationships

Personal system/Personal coping

FIGURE 38-3  ■  The work disability prevention arena. (Reprinted from Loisel et al 2005. Copyright with permission from Springer.)

• the health-care system and various providers and rehabilitation and occupational intervention with the aim
their unique and overlapping roles of returning workers with subacute back pain to their
• the workplace system with its various policies and regular job. The clinical rehabilitation aspect involved a
procedures to follow and multidisciplinary approach whereas the occupational
• the legislative and insurance system with the various intervention included visits to the workplace by an occu-
actors and steps to follow. pational medicine physician, ergonomist, the injured
By conceptualizing RTW as the result of an intricate worker, the supervisor, and management and union rep-
interplay between various systems, it is necessary to resentatives. A participatory ergonomicsa intervention
accept that a transdisciplinary approach is required. This was included to ensure that any work modifications or
means that work optimization requires the involvement changes recommended would be feasible and acceptable
of professionals from various health disciplines such as to the organization that was at liberty to implement them
medicine, occupational therapy, physiotherapy, nursing, or not. A 1-year follow-up revealed that the model was
psychology and ergonomics, as well as members of the effective. Workers returned to pre-injury work 2.4 times
organization such as human resource management, line faster than workers in usual care88 and the model was cost
manager, insurance and compensation systems. Thus, effective in the long term for the insurer.89 This Canadian
successful reintegration for work is a shared responsibil- intervention was replicated to suit the Dutch socioeco-
ity between the worker, health providers, the workplace nomic context by Anema et al.90 and used for workers
and the insurance provider. The involvement of each absent from work for 2–6 weeks due to non-specific low
stakeholder group from onset of injury is an important back pain. In comparison to usual care, workers returned
change in the way RTW is managed. Examples of system to work sooner (77 versus 104 days) when participating
approaches include the ‘Sherbrooke’ model,83 ‘integrated in this active workplace intervention. The cost–benefit
care’,84 ‘multifaceted’ intervention,85 coordinated and tai- analyses showed that every £1 invested in integrated care
lored work rehabilitation,86 and the Return2Health pro-
gramme.87 Common to all these interventions is the a
active involvement of the worker and organization in Participatory ergonomics is defined as ergonomics with participation
of the necessary actors in problem solving. A characteristic feature is
addition to the health-care team. the formation of an ergonomics team typically made up of employees
The Sherbrooke model was developed and piloted or their representatives, managers, ergonomists, health and safety
by Loisel et al.83 It consisted of a combined clinical personnel, and research experts.
384 PART III  Advances in Clinical Science and Practice

would return an estimated £26 with a net societal benefit (e.g. high physical demands), interactions with the insur-
of integrated care compared with usual care of £5744.84 ance system (e.g. access to treatment; questions of legiti-
Evidence of the success of multi-stakeholder interven- macy) or the organization (e.g. availability of alternative
tions in countries without a workers’ compensation duties) in which the injury is managed. The term ‘proce-
insurance scheme is available from the UK and Denmark. dural justice’ refers to the worker’s experience of the
In the UK, the Return2Health intervention was imple- justice of the compensation process which has been
mented to minimize the costs of long-term sickness linked with work absenteeism, high levels of stress and
absence and its adverse impact on health.87 This inter- poorer long-term recovery.92 Blue Flags may potentially
vention included representatives from the main stake- be modifiable by therapeutic interventions whereas Black
holders – human resource professionals, managers, Flags require greater negotiation and often changes to
employees and clinicians (occupational health physician, the legislation or organizational policy and outside clini-
psychologist and physiotherapist). The focus of the inter- cians’ influence.
vention was restoration of function using a biopsycho- In general, clinicians believe in the importance
social approach, coordinated by a case manager. As a of assessing the psychosocial obstacles but may find
result of this intervention, the proportion of staff off management of these issues challenging.93 There is
work longer than 8 weeks decreased from 51.7% to preliminary evidence that few clinicians consider the
45.9% while increasing from 51.2% to 56.1% in the work-relevant Blue Flags in their assessment.94 Reasons
control group. Similarly, in Denmark workers receiving offered include a lack of confidence in this area, not
coordinated care by an interdisciplinary team had sig- part of their professional role and the uncertainty in
nificantly fewer sickness absence hours than controls with the assessment of these factors and interpretation of
savings of US$1366 per worker at 6-month review.86 results. There are several tools available for use to assist
In Australia, a multifaceted intervention was trialled in the assessment of psychosocial barriers to work. Yellow
that included early reporting, employee-centred case Flags are addressed in the Örebro Musculoskeletal Pain
management by an experienced injury manager and Questionnaire,95 STarT Back Screening Tool96 or the
removal of barriers to RTW through active involvement Fear Avoidance beliefs questionnaire.97 For a compre-
of the workplace. It resulted in a 40% reduction in the hensive assessment of Blue Flags, the Obstacles to Return
number of days on compensation and reduction in the to Work Questionnaire98 has been recommended,
average cost of claims by AUD$2329.85 although its length may prohibit routine use in clinical
These studies demonstrate that a systems approach to practice.99 Another option is to adopt the six-stage
RTW after injury can result in benefits to the individual, strategy recommended by Shaw et  al.69 as a means of
the organization and the disability insurance scheme. incorporating workplace issues into usual clinical prac-
This win–win approach is only possible when each stake- tice. Assessment of recovery expectations, one of the
holder recognizes the differing perspective of each while most consistent predictors of work disability and pain
sharing the ultimate goal of sustained RTW for the indi- outcomes, can be assessed by the Return to Work Self-
vidual. The health-care provider can enhance this process Efficacy Scale.100 No one scale currently exists to measure
by providing regular feedback regarding progress of the all aspects of Black Flags; however, the physical demands
worker to the individual, insurer and organization to of work may be assessed by a visit to the workplace
maintain or increase the stakeholders’ levels of commit- or the Job Requirements and Physical Demands Scale.101
ment and involvement and assist in the development of Procedural justice may be assessed by the Perceived
the RTW plan. Justice of the Compensation Process Scale.102
With so many psychosocial factors implicated as
important for the recovery from injury, the clinician may
Beyond Physical Symptoms
be at a loss to decide which to focus on as it is impossible
The concept of Red Flags as signs of serious pathology to include all. A recent review by Laisné et al.81 found
is well engrained in a clinician’s assessment of patients strong evidence for two psychosocial constructs as pre-
with musculoskeletal conditions. Less well known and dictors of work participation – recovery expectation and
assessed are the Yellow, Blue and Black Flags introduced disability management systems such as availability of
to increase the focus on the psychological and workplace modified work or workplace accommodations. While
factors contributing to back disability after injury onset.79 psychosocial factors were once considered more relevant
The flag concept has been extended for use in the second- in the transition from acute to chronic state, this system-
ary and tertiary prevention of disability after any muscu- atic review suggests that an integrated biopsychosocial
loskeletal injuries, not only the back. Yellow Flags refer approach early in the acute phase is important as many
to those psychological features that may be considered factors predate the injury or may have even contributed
normal but unhelpful reactions to pain such as the belief to the onset.
that pain implies damage; the Orange, less modifiable Much research has focused on low back pain as it is a
Flags are considered to be those conditions meeting the common work-related MSD. Eight workplace factors are
criteria for psychopathology (e.g. post-traumatic stress, considered strong predictors of poor recovery from this
major depression).91 Blue Flags refer to the worker’s (neg- injury: heavy physical demands at work, the inability to
ative) perceptions about the workplace such as poor modify work, job stress, low social support from
expectations for RTW, that work is stressful or harmful, co-workers or supervisors, short job tenure, job dissatis-
and the workplace is unsupportive. Black Flags refer to faction, poor expectation for return to work, and fear of
the existing work conditions external to the individual re-injury.69,103 Thus clinicians are advised to include
 38  Musculoskeletal Health in the Workplace 385

assessment of these factors with either targeted question- must consider all the stakeholders and RTW barriers.
ing or the scales mentioned above in both the manage- Clinicians are thus well placed to move ‘beyond the
ment of acute/subacute MSD and chronic MSD. clinic’ to maximize the worker’s opportunity to recover
musculoskeletal health for a sustained return to work
following an acute MSD or to remain at work with a
Promoting Ability Not Disability
chronic MSD.
There is evidence that workers who have sustained a
work-related injury feel disempowered by the compensa- REFERENCES
tion process, experience difficulty navigating the social
1. Dodu N. Is employment good for well-being? A literature review.
and procedural environment of RTW and are frustrated J Occup Psychol Employ Disabil 2005;7:17–33.
with the information imbalance between themselves, 2. World Health Organisation. Global Health and Aging. National
insurers and health-care providers. They are concerned Institute on Aging; National Institutes of Health; 2011 Contract
about repercussions from disclosing their condition in No.: Contract No.: NIH Publication no. 11-7737.
the workplace, the perceived legitimacy of their injury 3. NOHSC. Surveillance alert – OHS and the ageing workforce
[Internet]. National Occupational Health and Safety Commission,
and associated stigma with being injured.104–108 Adopting Commonwealth of Australia; 2005.
a client-centred orientation and communication style 4. Ilmarinen J. The ageing worker. J Occup Environ Med 2001;58:
may create an environment in which the worker feels 546–52.
comfortable discussing these concerns.109 This opens dis- 5. Shephard R. Age and physical work capacity. Exp Aging Res 1999;
25:331–43.
cussions in which the clinician can help the worker iden- 6. Kemmlert K, Lundholm L. Slips, trips and falls in different work
tify and problem-solve their concerns about re-injury groups – with reference to age and from a preventive perspective.
and their capacity to work, stigma and pressure from Appl Ergon 2001;32:149–53.
co-workers or supervisors to undertake more than they 7. Walton M. Graying, not falling. Occupa Health Saf 1999;
feel able. Techniques such as motivational interviewing,87 68:85–7.
8. Safe Work Australia. Australian work-related injury experience by
problem solving110 and goal setting with structured activ- sex and age 2009–10 [Internet]. Commonwealth of Australia.
ity plans111 have been successfully delivered by physio- Available from: <http://www.safeworkaustralia.gov.au/>; 2012.
therapists to benefit workers returning to work. These 9. US Bureau of Labor Statistics. Non-fatal injuries and illnesses
techniques motivate and empower the worker to self- among older workers [Internet]. Available from: <http://
www.bls.gov/>; 2009.
manage obstacles to return to and remain at work and are 10. Gould R, Ilmarinen J, Järvisalo J, et  al. Dimensions of work
particularly important for ongoing chronic MSD man- ability: results of the health 2000 survey. In: Helsinki: Finnish
agement. For practical tips on incorporating self- Centre for Pensions TSII, National Public Health Institute,
management strategies into practice when managing editor. Finland: Finnish Institute of Occupational Health;
patients with a chronic musculoskeletal condition see 2008.
11. Ilmarinen J. The ageing workforce – challenges for occupational
Johnston et al.112 health. Occup Med 2006;56:362–4.
12. Ilmarinen J. Work ability – a comprehensive concept for occupa-
tional health research and prevention. Scand J Work Environ
SUMMARY Health 2009;35:1–5.
13. Ilmarinen J, Rantanen J. Promotion of work ability during ageing.
Am J Ind Med 1999;36:21–3.
Musculoskeletal health in the workplace is important for 14. Australian Institute of Health and Welfare. Chronic dsease and
individuals, the work organizations and for society more participation in work. In: Australian Institute of Health and
broadly. Being able to work in a suitable job provides a Welfare, editor. Canberra: Australian Government; 2009.
very positive influence on a person’s health and well- 15. Department of Health. Healthy workers initiative. Common-
wealth of Australia. Available from: <www.healthyworkers.gov.au>;
being. Clinicians have traditionally had a strong role in 2013 [updated 12.11.13; cited 2013 13.12.13.].
the management of MSDs and this role can be enhanced 16. Australian Institute of Health and Welfare. Risk factors and par-
and extended to acknowledge and utilize the important ticipation in work. In: Australian Institute of Health and Welfare,
influence of work in helping to prevent the development editor. Canberra: Australian Government; 2010.
17. Quinlan M, Mayhew C, Bohle P. The global expansion of precari-
of MSDs and the disability related to them. Clinicians ous employment, work disorganization, and consequences for
are ideally placed to be the conduit between the clinic occupational health: placing the debate in a comparative historical
and the workplace due to their proximity to the worker, context. Int J Health Serv 2001;31:507–36.
their understanding of physical and psychosocial barriers 18. Benach J, Muntaner C, Santana V. Employment Conditions and
to recovery and sustaining available ability, and their Health Inequalities Labor Markets and Welfare States: A Country
Perspective. Barcelona: Final report to the WHO Commission on
highly developed communication skills. However, to Social Determinants of Health: Employment Conditions Knowl-
maximize their contribution to the musculoskeletal edge Network (EMCONET); 2007.
health of the working population, it is important for 19. Straker L, Mathiassen SE. Increased physical work loads in
clinicians to stay abreast of the changes within society, modern work – a necessity for better health and performance?
Ergonomics 2009;52:1215–25.
such as the ageing population, and the work environ- 20. Mummery WK, Schofield GM, Steele R, et al. Occupational
ment, such as the increase in precarious work. Evidence sitting time and overweight and obesity in australian workers. Am
for the ergonomic/risk-management approach to injury J Prev Med 2005;29:91.
prevention suggests that identifying and assessing the 21. Church TS, Thomas DM, Tudor-Locke C, et al. Trends over 5
risks for injury is worthwhile with ample resources avail- decades in U.S. occupation-related physical activity and their asso-
ciations with obesity. PLoS ONE 2011;6(5):e19657.
able to assist the clinician gain appropriate skills in this 22. Alkhajah TA, Reeves MM, Eakin EG, et al. Sit–stand worksta-
area. There is also evidence to support the systems tions: a pilot intervention to reduce office sitting time. Am J Prev
approach for the prevention of work disability which Med 2012;43:298–303.
386 PART III  Advances in Clinical Science and Practice

23. Conn VS, Hafdahl AR, Cooper PS, et al. Meta-analysis of work- 47. Verbeek JH, Martimo KP, Karppinen J, et al. Manual material
place physical activity interventions. Am J Prev Med 2009;37: handling advice and assistive devices for preventing and treating
330–9. back pain in workers. Cochrane Database Syst Rev 2011.
24. Centers for Disease Control and Prevention C. Work-Related 48. Macdonald W, Evans O. Research on the prevention of work-
Musculoskeletal Disorders (Wmsd) Prevention. Atlanta, US: related musculoskeletal disorders. Stage 1 – literature review. In:
Centers for Disease Control and Prevention; 2013. Available Australian Safety and Compensation Council, editor. Canberra:
from: <http://www.cdc.gov/workplacehealthpromotion/implemen Australian Government; 2006.
tation/topics/disorders.html>; [cited 2013 23rd October.]. 49. Safe Work Australia. Hazardous manual tasks code of practice. In:
25. World Health Organization. Identification and Control of Work- Australian Government, editor. Canberra: Australian Govern-
Related Diseases: Report of a WHO Expert Committee. Geneva: ment; 2011.
World Health Organisation; 1985 Technical Report Series 714. 50. da Costa BR, Vieira ER. Risk factors for work related musculosk-
26. World Health Organisation W. World Health Classification: eletal disorders: a systematic review of recent longitudinal studies.
Manual of the International Statistical Classification of Diseases, Am J Ind Med 2010;53:285–323.
Injuries, and Causes of Death. Geneva, Switzerland: World Health 51. Bernard B, Putz-Anderson V, Burt SE. Musculoskeletal Disorders
Organization; 1977. and Workplace Factors: a Critical Review of Epidemiologic Evi-
27. Punnett L, Wegman DH. Work-related musculoskeletal disor- dence for Work-Related Musculoskeletal Disorders of the Neck,
ders: the epidemiologic evidence and the debate. J Electromyogr Upper Extremity and Low Back. Cincinatti: U.S. Department of
Kinesiol 2004;14:13–23. Health and Human Services; 1997 Publication No. 97–141 Con-
28. Safe Work Australia. Compendium of Workers’ Compensation tract No.: July, 1997.
Statistics Australia 2010–11. Canberra: Commonwealth of Austra- 52. Xu Y-Y, Cheng ASK, Li-Tsang CWP. Prevalence and risk factors
lia; 2013. p. 112; ISBN 978-1-74361-036-7 (Online PDF) ed. of work-related musculoskeletal disorders in the catering industry:
29. Zheltoukhova K, Bevan S, Reich A. Fit for Work? Musculoskeletal a systematic review. Work 2013;44:107–16.
Disorders and the Australian Labour Market. The Work Founda- 53. Kilbom A. Assessment of physical exposure in relation to work-
tion, Part of Lancaster University; 2012. related musculoskeletal disorders – what information can be
30. European Agency for Safety and Health at Work. A European obtained from systematic observations? Scand J Work Environ
campaign on musculoskeletal disorders (en4): work-related mus- Health 1994;20:30–45.
culoskeletal disorder-prevention report. In: Office for Official 54. McAtamney L, Corlett NE. Rula: a survey method for the inves­
Publications of the European Communities, editor. Luxembourg: tigation of work-related upper limb disorders. Appl Ergon 1993;
2008. 24:91–9.
31. Woolf AD, Vos T, March LM. How to measure the impact of 55. HSE HaSE. Manual handling assessment charts. In: Executive
musculoskeletal conditions. Best Pract Res Clin Rheumatol HaS, editor. UK: 2003.
2010;24:723–32. 56. Waters TR, Putz-Anderson V, Garg A, et al. Revised niosh equa-
32. Kuoppala J, Lamminpa L, Husman P. Work health promotion, tion for design and evaluation of manual lifting tasks. Ergonomics
job well-being, and sickness absences – a systematic review and 1993;36:749–76.
meta-analysis. J Occup Environ Med 2008;50:1216–27. 57. Snook SH, Ciriello VM. The design of manual handling tasks:
33. World Confederation for Physical Therapy. Position Statement: revised tables of maximum acceptable weights and forces. Ergo-
Description of Physical Therapy. London: 2007. nomics 1991;34:1197–213.
34. Proper K, Koning M, van der Beek A, et al. The effectiveness of 58. Moore JS, Garg A. The strain index: a proposed method to
worksite physical activity programs on physical activity, physical analyze jobs for risk of distal upper extremity disorders. Am Ind
fitness, and health. Clin J Sport Med 2003;13:106–17. Hyg Assoc J 1995;56:443–58.
35. Verhagen AP, Karels C, Bierma-Zeinstra SMA, et al. Ergonomic 59. Burgess-Limerick R, Egeskov R, Straker L, et al. Manual tasks
and physiotherapeutic interventions for treating work-related risk assessment tool (mantra) v2. 2004.
complaints of the arm, neck or shoulder in adults. Cochrane Data- 60. Karasek RA, Berisson C, Kawakami N, et al. The Job Content
base Syst Rev 2006;(3):CD003471. Questionnaire (JCQ): an instrument for internationally compara-
36. Verhagen AP, Karels C, Bierma-Zeinstra SMA, et al. Exercise tive assessments of psychosocial job characteristics. J Occup
proves effective in a systematic review of work-related complaints Health Psychol 1998;3:322–56.
of the arm, neck, or shoulder. J Clin Epidemiol 2007;60:110–17. 61. Li G, Buckle P. Evaluating Change in Exposure to Risk for Mus-
37. Institute for Work & Health. At work, Issue 43. Toronto: Institute culoskeletal Disorders – A Practical Tool. London: Health and
for Work & Health; 2006. Available from: <http://www.iwh.on.ca/ Safety Executive; 1999.
system/files/at-work/at_work_43.pdf>; [cited January 2014.]. 62. ILO-OSH. Guidelines on Occupational Safety and Health Man-
38. Dunn KM, Jordan KP, Mancl L, et al. Trajectories of pain in agement Systems. Geneva: International Labour Office; 2001.
adolescents: a prospective cohort study. Pain 2011;152:66–73. 63. Straker LM, Burgess-Limerick R, Pollock C, et al. A randomized
39. Rees C, Smith A, O’Sullivan P, et al. Back and neck pain are and controlled trial of a participative ergonomics intervention to
related to mental health problems in adolescence. BMC Public reduce injuries associated with manual tasks: physical risk and
Health 2011;11:382. legislative compliance. Ergonomics 2004;47:166–88.
40. O’Sullivan PB, Beales DJ, Smith AJ, et al. Low back pain in 17 64. Levanon Y, Gefen A, Lerman Y, et al. Reducing musculoskeletal
year olds has substantial impact and represents an important disorders among computer operators: comparison between ergo-
public health disorder: a cross-sectional study. BMC Public Health nomics interventions at the workplace. Ergonomics 2012;55:
2012;12:100. 1571–85.
41. Axen I, Leboeuf-Yde C. Trajectories of low back pain. Best Pract 65. Krause N, Dasinger L, Neuhauser F. Modified work and return
Res Clin Rheumatol 2013;27:601–12. to work: a review of the literature. J Occup Rehabil 1998;8:
42. Straker L. Evidence to support using squat, semi-squat and stoop 113–39.
techniques to lift low-lying objects. Int J Ind Ergon 2003; 66. Australian Institute for Social Research. The Role of the Work-
31:149–60. place in Return to Work: Discussion Paper. WorkCover SA;
43. Straker LM. A review of research on techniques for lifting low- 2008.
lying objects: 1. Criteria for evaluation. Work 2002;19:9–18. 67. Watson PJ, Booker CK, Moores L, et al. Returning the chroni-
44. Straker LM. A review of research on techniques for lifting low- cally unemployed with low back pain to employment. Eur J Pain
lying objects: 2. Evidence for a correct technique. Work 2003; 2004;8:359–69.
20:83–96. 68. Johnston V, Nielsen M, Corbiere M, et al. Experiences and per-
45. Van Dieen JH, Hoozemanns MJM, Toussaint HM. Stoop or spectives of physical therapists managing patients covered by
squat: a review of biomechanical studies on lifting technique. Clin workers’ compensation in Queensland, Australia. Phys Ther
Biomech 1999;14:685–96. 2012;92:1306–15.
46. Daltroy LH, Iversen MD, Larson MG, et al. A controlled trial of 69. Shaw WS, Main CJ, Johnston V. Addressing occupational factors
an educational program to prevent low back injuries. NEJM in the management of low back pain: implications for physical
1997;337:322–8. therapist practice. Phys Ther 2011;91:1–13.
 38  Musculoskeletal Health in the Workplace 387

70. Pincus T, Greenwood L, McHarg E. Advising people with back 92. Grant GM, O’Donnell ML, Spittal MJ, et al. Relationship
pain to take time off work: a survey examining the role of private between stressfulness of claiming for injury compensation and
musculoskeletal practitioners in the uk. Pain 2011;152:2813–18. long-term recovery: a prospective cohort study. JAMA Psychiatry
71. Australasian Faculty of Occupational & Environmental Medicine. In press.
Realising the Health Benefits of Work: A Position Statement. 93. Sanders T, Foster NE, Bishop A, et al. Biopsychosocial care and
Sydney: The Royal Australasian College of Physicians; 2010. the physiotherapy encounter: physiotherapists’ accounts of back
72. Baldwin ML, Butler RJ. Upper extremity disorders in the work- pain consultations. BMC Musculoskelet Disord 2013;14:65.
place: costs and outcomes beyond the first return to work. J Occup 94. Gray H, Howe T. Physiotherapists’ assessment and management
Rehabil 2006;16:303–23. of psychosocial factors (yellow and blue flags) in individuals with
73. Franche RL, Baril R, Shaw W, et al. Workplace-based return-to- back pain. Phys Ther Rev 2013;18:379–94.
work interventions: optimizing the role of stakeholders in imple- 95. Linton SJ, Hallden K. Can we screen for problematic back pain?
mentation and research. J Occup Rehabil 2005;15:525–42. A screening questionnaire for predicting outcome in acute and
74. Young AE, Roessler RT, wasiak R, et al. A developmental concep- subacute back pain. Clin J Pain 1998;14:209–15.
tualization of return towork. J Occup Rehabil 2005;15:557–68. 96. Hill JC, Dunn KM, Lewis M, et al. A primary care back pain
75. Kosny A, MacEachen E, Ferrier S, et al. The role of health care screening tool: identifying patient subgroups for initial treatment.
providers in long term and complicated workers’ compensation Arthritis Rheum 2008;59:632–41.
claims. J Occup Rehabil 2011;21(4):582–90. 97. Waddell G, Newton M, Henderson I, et al. A fear-avoidance
76. Wynne-Jones G, Buck R, Porteous C, et al. What happens to beliefs questionnaire (fabq) and the role of fear-avoidance beliefs
work if you’re unwell? Beliefs and attitudes of managers and in chronic low back pain and disability. Pain 1993;52:157–68.
employees with musculoskeletal pain in a public sector setting. 98. Marhold C, Linton S, Melin L. Identification of obstacles for
J Occup Rehabil 2011;21:31–42. chronic pain patients to return to work: evaluation of a question-
77. Engel GL. The need for a new medical model: a challenge for naire. J Occup Rehabil 2002;12:65–75.
biomedicine. Science 1977;196:129–36. 99. Gray H, Adefolarin AT, Howe TE. A systematic review of instru-
78. Linton SJ. A review of psychological risk factors in back and neck ments for the assessment of work-related psychosocial factors
pain. Spine 2000;25:1148–56. (blue flags) in individuals with non-specific low back pain. Man
79. Kendall NAS. Psychosocial approaches to the prevention of Ther 2011;16:531–43.
chronic pain: the low back paradigm. Baillieres Best Practice Res 100. Brouwer S, Franche RL, Hogg-Johnson S, et al. Return-to-work
Clin Rheumatol 1999;13:545–54. self-efficacy: development and validation of a scale in claimants
80. Pincus T, Burton AK, Vogel S, et al. A systematic review of psy- with musculoskeletal disorders. J Occup Rehabil 2010;21:
chological factors as predictors of chronicity/disability in prospec- 244–58.
tive cohorts of low back pain. Spine 2002;27:E109–20. 101. Daniels C, Huang GD, Feuerstein M, et al. Self-report measure
81. Laisné F, Lecomte C, Corbière M. Biopsychosocial predictors of of low back-related biomechanical exposures: clinical validation.
prognosis in musculoskeletal disorders: a systematic review of the J Occup Rehabil 2005;15:113–28.
literature. Disabil Rehabil 2012;34:355–82. 102. Franche R-L, Severin C, Lee H, et al. Perceived justice of com-
82. Loisel P, Buchbinder R, Hazard R, et al. Prevention of work dis- pensation process for return-to-work: development and validation
ability due to musculoskeletal disorders: the challenge of imple- of a scale. Psychol Inj Law 2009;2:225–37.
menting evidence. J Occup Rehabil 2005;15:507–24. 103. Costa-Black KM, Loisel P, Anema JR, et al. Back pain and work.
83. Loisel P, Durand P, Abenhaim L, et al. Management of occupa- Best Pract Res Clin Rheumatol 2010;24:227–40.
tional back pain: the Sherbrooke model. Results of a pilot and 104. Eggert S. Psychosocial factors affecting employees’ abilities to
feasibility study. Occup Environ Med 1994;51:597–602. return to work. AAOHN J 2010;58:51–5.
84. Lambeek LC, Bosmans JE, Van Royen BJ, et al. Effect of inte- 105. MacEachen E, Clarke J, Franche RL, et al. Systematic review of
grated care for sick listed patients with chronic low back pain: the qualitative literature on return to work after injury. Scand J
economic evaluation alongside a randomised controlled trial. Br Work Environ Health 2006;32:257–69.
Med J 2010;341:c6414. 106. Baril R, Clarke J, Friesen M, et al. Management of return-to-work
85. Iles RA, Wyatt M, Pranksy G. Multi-faceted case management: programs for workers with musculoskeletal disorders: a qualitative
reducing compensation costs of musculoskeletal work injuries in study in three canadian provinces. Soc Sci Med 2003;57:
Australia. J Occup Rehabil 2012;22:478–88. 2101–14.
86. Bultmann U, Sherson D, Olsen J, et al. Coordinated and tailored 107. Roberts-Yates C. The concerns and issues of injured workers in
work rehabilitation: a randomized controlled trial with economic relation to claims/injury management and rehabilitation: the need
evaluation undertaken with workers on sick leave due to muscu- for new operational frameworks. Disabil Rehabil 2003;25:
loskeletal disorders. J Occup Rehabil 2009;19:81–93. 898–907.
87. Smedley J, Harris EC, Cox V, et al. Evaluation of a case manage- 108. Young AE, Wasiak R, Phillips L, et al. Workers’ perspectives on
ment service to reduce sickness absence. Occup Med 2013;63: low back pain recurrence: ‘it comes and goes and comes and goes,
89–95. but it’s always there’. Pain 2011;152:204–11.
88. Loisel P, Abenhaim L, Durand P, et al. A population-based, ran- 109. Shaw WS, Chin EH, Nelson CC, et al. What circumstances
domized clinical trial on back pain management. Spine 1997;22: prompt a workplace discussion in medical evaluations for back
2911–18. pain? J Occup Rehabil 2012;23(1):125–34.
89. Loisel P, Lemaire J, Poitras S, et al. Cost-benefit and cost- 110. van den Hout JH, Vlaeyen JWS, Heuts PH, et al. Secondary
effectiveness analysis of a disability prevention model for back pain prevention of work-related disability in non-specific low back
management: a six year follow up study. Occup Environ Med pain: does problem-solving therapy help? A randomized clinical
2002;59:807–15. trial. Clin J Pain 2003;19:87–96.
90. Anema JR, Steenstra IA, Bongers PM, et al. Multidisciplinary 111. Sullivan MJL, Ward CL, Tripp D, et al. Secondary prevention of
rehabilitation for subacute low back pain: graded activity or work- work disability: community-based psychosocial intervention for
place intervention or both? A randomized controlled trial. Spine musculoskeletal disorders. J Occup Rehabil 2005;15:377–92.
2007;32:291–8. 112. Johnston V, Jull G, Sheppard DM, et al. Applying principles of
91. Nicholas M, Linton SJ, Watson PJ, et al. Early identification and self-management to facilitate workers to return to or remain at
management of psychological risk factors (‘yellow flags’) in work with a chronic musculoskeletal condition. Man Ther
patients with low back pain: a reappraisal. Phys Ther 2011; 2013;18:274–80.
91:1–7.
 CHAPTER 39 

Screening
CHAPTER OUTLINE

Editor’s Introduction Ch 39.2  What is Our Baseline for Movement? The

Clinical Need for Movement Screening, Testing
Ch 39.1  Screening for Musculoskeletal and Assessment  394
Disorders  388
Gray Cook  •  Kyle Kiesel
Tania Pizzari  •  Carolyn Taylor

EDITOR’S INTRODUCTION

Screening in health care is used to identify injury is previous injury. As such, attempts to
potential risk factors for people without reduce recurrence are warranted and welcome.
symptoms that, if left untreated, may lead to The first subchapter deals mainly with athletic
serious illness. Examples include assessment of populations and identifies the independent
blood pressure, monitoring blood glucose levels predictors, risk factors and associated factors
and bowel cancer screening programmes. The measured using field-expedient screening tests
management of musculoskeletal conditions has that have consistently been linked to future
not taken this approach and traditionally has injury. The second subchapter presents a
involved assessment and management of method and structure for undertaking
symptoms as and when they present. The musculoskeletal screening. Screening functional
authors invited to contribute the two movement patterns, rather than single
musculoskeletal screening chapters are musculoskeletal variables, as predictors for
international leaders in the field of injury is becoming increasingly popular and this
musculoskeletal screening. These chapters is discussed in the two subchapters. The
explore the potential role of screening as a synthesis of these two subchapters will provide
method to prevent musculoskeletal symptoms, the reader with an understanding of the
as well as providing guidance when treating potential value for screening in musculoskeletal
individuals with symptoms with a view of conditions. It will also highlight uncertainties
preventing or reducing recurrence. This is and areas where our knowledge base with
relevant as recurrence rates associated with respect to screening for musculoskeletal
musculoskeletal conditions are high, and the conditions requires further research.
number one risk factor for musculoskeletal

CHAPTER 39.1  ■  SCREENING FOR MUSCULOSKELETAL

DISORDERS
Tania Pizzari  •  Carolyn Taylor

attempt to reduce this injury burden. This screening is

INTRODUCTION often called ‘pre-participation examination’ and is con-
ducted by sports medicine personnel with the aim of
Injury can detrimentally affect an athlete’s performance, identifying risk of illness, injury or sudden death in
their team’s success and, in extreme cases, curtail their athletes.4,5 Assessment prior to commencing organized
career. Injuries may linger after the athlete has finished sport is compulsory in some areas of the world (such
competing and result in long-term disability,1,2 with an as Italy and some parts of the United States of America)6
associated high cost for both the individual and society.3 and is also mandated by some sporting organizations.2
Screening of athletes for current injury and risk of future However, in other places, this screening is voluntary
injury is common practice throughout the world in an (United Kingdom and Australia).4,5 A pre-participation
388
 39  Screening 389

examination may have multiple components and include The time, cost, equipment and expertise required to
screening for cardiovascular, neurological, pulmonary, conduct screening are an important consideration.11,13
urogenital and musculoskeletal injury.2,4,7,8 This chapter Interpretation of screening outcomes is also compli-
is concerned with musculoskeletal screening. cated. No screening test is 100% accurate and therefore
athletes may be falsely identified as having a positive or
negative risk based on a test result. An athlete estimated
THE IMPORTANCE OF to be at risk might then undertake unnecessary, costly and
MUSCULOSKELETAL SCREENING onerous steps in an attempt to minimize this risk.

Although there are many reasons to conduct musculo­

skeletal screening, the most common are to identify RISK FACTORS AND INJURY
current injuries or physical deficits due to previous inju-
ries and to identify potentially modifiable intrinsic risk The identification of risk factors for injury using
factors that may predispose the athlete to future injury.4 tests with predictive validity is an essential aspect of the
Intrinsic risk factors may be present as a result of an musculoskeletal screening process. There are three dif-
inadequately rehabilitated previous injury2 or be an ferent levels of ‘risk factor’: associated factors, risk factors
inherent physical characteristic of that athlete, such as and independent predictors. An associated factor is iden-
limited joint range of motion. The identification of mod- tified when a positive musculoskeletal test is associated
ifiable risk factors may then allow counselling of athletes with an injury in a cross-sectional cohort study.14 A risk
with sports-specific deficits and rehabilitation or preven- factor is where a musculoskeletal test is related to an
tion programmes to be implemented with the aim of injury in a prospective study using univariate or bivariate
reducing the risk of future injury.7,9,10 analysis.15 An independent predictor is where the outcome
Other potential benefits of screening include building of a musculoskeletal test has a significant contribution to
a professional rapport with the athlete, having first-hand an injury in a prospective study using a multivariate anal-
knowledge of current and previous musculoskeletal inju- ysis, where all identified risk factors are included and
ries and physical deficits, educating athletes4 and provid- where all other risk factors are controlled for.16 A mus-
ing research data. culoskeletal test used to identify an independent predic-
tor is said to have ‘predictive validity’, that is, the ability
to predict future injury; however, a very limited number
THE DIFFICULTIES OF SCREENING of independent predictors for injury in sport have been
identified.4
The identification of potential risk factors for injury is an While there are a small number of risk factors with
underdeveloped area of sports medicine research and predictive validity for injury risk, there are some with
there are few proven risk factors for injury.2,6,8 In part this established links to injury risk. Table 39-1 outlines
is because large, well-designed, cohort studies employing commonly used field-expedient screening tests with
appropriate and generalizable outcome measures that known reliability properties and some level of predictive
screen uninjured athletes for potential risk factors and validity.
then follow them up for 1 to 2 years, without preventative There is a need for normative data for many of the
intervention, are difficult to conduct.9 Scientifically tests used for musculoskeletal screening and a need to
robust screening protocols based on evidence for the identify the threshold for abnormality.63 It is important
incidence of injury, the mechanism of injury and the to establish what is normal and does not pose an increased
established risk factors that utilize tests with predictive injury risk, and what is an abnormal test result that could
validity and reliability to identify those risk factors are mean an increased risk of injury and allow for preventa-
required to conduct longitudinal cohort studies of value. tive strategies to be adopted. It should be noted that
Research into musculoskeletal injury has predomi- normative values and threshold might vary depending on
nantly yielded single variables as predictors of injury and the type and level of activity and the personal character-
these may vary depending on the requirements of the istics of the athlete.
sport and the athlete characteristics. It is unrealistic to Many non-modifiable risk factors such as age, gender,
identify individual tests to predict every musculoskeletal height, race, previous history, sport and climate, have
injury in all athlete types and to conduct screening for been implicated in altering the risk of musculoskeletal
each potential risk factor.10,11 The multifactorial aetiology injury.64–67 The majority of such factors can be collated
of most injuries means that a focus on single predictors using a questionnaire and may be used together with
neglects the inter-relationship between the intrinsic risk screening tests to build a risk profile for an individual
factors and extrinsic risks present at the moment of an athlete.11
inciting injury event.12
Musculoskeletal screening protocols are highly vari-
able4,6 and are often developed on an ad hoc basis based SCREENING AND PREVENTION
on practitioner preferences with no regard for the reli-
ability or the predictive validity of the tests. Problems also The assumption of screening is that the identification
arise when the musculoskeletal tests are conducted differ- of risk factors and protective factors may then inform
ently by different sports medicine personnel.4 The field- the development of preventative strategies. To date,
expedience of screening protocols may also limit their use. however, there has been limited evidence that risk
390 PART III  Advances in Clinical Science and Practice

TABLE 39-1  Commonly Used Field-Expedient Screening Tests: Independent Predictors, Risk Factors
and Associated Factors with Injury
Independent Predictors

Test Intra-Rater Reliability Inter-Rater Reliability Predictive Validity

Prone passive hip ICC >0.94 (95%CI range ICC >0.30 (95%CI range Reduced hip IR on ipsilateral leg
internal rotation 0.68–0.97)17–21 0.00–0.87)19–21 independent predictor for lower limb/back
injury in amateur cricket players.22 Hip
IR ≤ 30°: OR = 0.20 (0.06–0.073), p = 0.045,
Hip IR = 31–40°: OR = 0.36 (0.12–1.11),
p = 0.045
Modified Thomas ICC >0.9917 ICC = 0.90 (95% CI Reduced quadriceps flexibility (<50° of knee
test (quadriceps ICC = 0.69 (95%CI 0.72–0.96)18 flexion) independent predictor of time to
flexibility) 0.29–0.88)18 sustaining a hamstring injury. More
flexible amateur Australian football
players had a lower risk of sustaining a
hamstring injury.23 RR >51° knee flexion:
RR = 0.3 (0.1–0.8), p = 0.022
Reduced hip flexibility (hip neutral/flexion)
was an associated factor for sustaining a
hamstring injury in professional Australian
football players. RR = 1.47 (0.77–2.82)15
Hip muscle strength ICC >0.77 (95% CI range ICC >0.62 (95% CI Strength of adductor muscles independent
with HHD – hip 0.24–0.99)24–28 range 0.19– predictor for groin injury in amateur
adduction and 0.97)24,26,28–41 soccer players.32 Adjusted OR = 4.28
abduction (1.38–14.0), p = 0.02
Hip adduction to hip abduction strength
ratio a risk factor for groin injury
(adductor strain) (p = 0.01) and
independent predictor (p = 0.03) RR = 17:1
based on hip adduction strength less than
80% of abduction strength in professional
ice hockey players33
Ankle dorsiflexion ICC >0.97 (95% CI range ICC >0.96 (95% CI Reduced ankle dorsiflexion on contralateral
lunge 0.92–0.99)19,34,35 range 0.89–0.99)19,34 leg an independent predictor for lower
limb/back injury in amateur cricket
players22
Reduced ankle dorsiflexion (<10 cm) an
independent predictor for hamstring injury
in professional Australian football
players15
Reduced ankle dorsiflexion (≤12 cm) a risk
factor for lower limb injury in amateur
Australian football players36
Single leg balance ICC = 0.88 (95%CI ICC = 0.83 (95%CI A positive SLB test independent predictor
0.76–0.94)37 0.71–0.91)37 for ankle sprains in varsity and
Kappa = 0.9038 intercollegiate athletes, OR = 2.54
(1.02–6.03) p < 0.0538
Beighton score/ % agreement = 69% % agreement = 51% Female amateur soccer players who had
general Spearman rho = 0.8639 Spearman rho = 0.8739 general joint laxity (Beighton score <4)
hypermobility were at great risk of any injury OR = 5.3
(2.0–13.5), p < 0.001. Joint laxity was an
independent predictor of knee injury,
OR = 5.0 (1.3–18.9), p < 0.0540
Beighton score ≤5 a risk factor for traumatic
leg injuries in female soccer players41
Beighton score <4 a risk factor for any injury
in male rugby players42
General laxity (≥5 regions) a risk factor for
non-contact ACL injury in both male and
female military cadets43
Knee ICC >0.88 (SEM = 1.8 ICC >0.48 (SEM = 2.9 Knee hyperextension an independent
hyperextension degrees)44 degrees)44 predictor for traumatic leg injuries
(genu recurvatum) Kappa >0.85 (95% CI in female soccer players, OR = 3.84
0.64–1.06)45 (1.51–9.79), p = 0.00541
Knee hyperextension a risk factor for ACL
injury in male American football players
OR = 15.56 (3.61–138.32)46
 39  Screening 391

TABLE 39-1  Commonly Used Field-Expedient Independent

ScreeningPredictors
Tests: Independent Predictors, Risk Factors
Test and Associated
Intra-RaterFactors with Injury
Reliability (Continued)
Inter-Rater Reliability Predictive Validity

Risk Factors

Test Intra-Rater Reliability Inter-Rater Reliability Predictive Validity

Prone passive hip ICC >0.88 (95% CI ICC = 0.66 (95% CI Restricted hip external rotation range of
external rotation 0.54–0.96)17,19 0.25–0.90)19 motion a risk factor for groin injury in
amateur soccer players. OR = 1.53
(1.13–2.07) p < 0.0132
Supine passive hip ICC >0.88 (95% CI ICC >0.75 (95% CI Restricted total hip rotation was a risk factor
internal rotation 0.84–0.91)21,47 0.60–0.84)21,48 for groin injury. For each degree increase
with hip at 90° in hip rotation there was a 10% reduction
in injury rate in professional Australian
football players49
Supine passive hip ICC >0.91 (95%CI ICC = 0.63 (95%CI Restricted total hip rotation was a risk factor
external rotation 0.93–0.96)21,47 0.44–0.76)21 for groin injury. For each degree increase
with hip at 90° in hip rotation there was a 10% reduction
in injury rate in professional Australian
football players49
Adductor squeeze ICC >0.76 (95%CI range ICC >0.77 (95%CI range Hip adductor strength decreased 2 weeks
test 0.61–0.97)20,50–52 0.62–0.96)20,51,52 preceding and during the onset of groin
injury during in-season monitoring of
junior elite Australian football players53
Single leg ICC = 0.56 (95%CI Amateur and semi-elite Australian football
hamstring bridge 0.00–0.83)19 players who sustained right-sided
test hamstring strains had significantly lower
preseason single leg bridge scores than
uninjured players54
Biering-Sorenson ICC = 0.69 (95%CI ICC >0.59 (95%CI Extensor muscle endurance was a risk factor
test 0.59–0.85)55 0.44–0.97)55–60 for serious low back pain at 36 months
follow-up (p = 0.01), but not at 12 months
follow-up (p = 0.133)61
Risk factor for predicting first-time low back
pain in 12-month follow-up period in men
(p = 0.029), but not in women (p = 0.34)62
Associated Factors

Test Intra-Rater Reliability Inter-Rater Reliability Predictive Validity

Supine active hip ICC = 0.83 (95%CI ICC = 0.94 (95%CI Reduced active hip internal rotation was
internal rotation 0.57–0.94)18 0.82–0.98)18 associated with hamstring injury in
professional Australian football players15

ACL, Anterior cruciate ligament; CI, Confidence interval; HHD, Hand-held dynamometer; ICC, Interclass correlation coefficient; IR, Internal
rotation; OR, Odds ratio; RR, Relative risk; SEM, Standard error of measurement.

profiles can be altered with intervention11 or that pre- relatively short amount of time to conduct and not involve
vention programmes implemented to address risk factors complicated tests or expensive equipment. The informa-
reduce the risk of injury.5 The cost benefit of screening tion should also follow the athlete as they progress
must be questioned if it does not reduce the frequency through their career and move between teams.
and severity of musculoskeletal injury. Labelling an Musculoskeletal screening has two components: a
athlete ‘at risk’ without the ability to reduce injury questionnaire and a physical examination.7,68 Since one
may have a detrimental impact on an individual. Improv- of the most consistent predictors of injury is previous
ing the quality of screening protocols may enhance injury,15,65,67 the questionnaire should identify current
the relationship between risk identification and injury and previous injuries. Caution needs to be adopted
prevention. when relying on the information provided in the ques-
tionnaire as athletes’ recall of injuries beyond the
previous 12 months is poor.69 Athletes may also be less
DEVELOPING A SCREENING TOOL inclined to disclose a complete injury history if they
believe the outcome of a potential contract may depend
Ideally, a screening protocol should be highly relevant to on the extent of their previous injuries. The physical
a specific sport, and if a team sport, relevant to the indi- examination component of the musculoskeletal screen
viduals and their specific roles. The protocol should should include tests to identify physical deficits that
include reliable tests that are able to predict injuries and may require further comprehensive assessment, and not
identify risk factors for those injuries. The tool should be to comprehensively assess every area of the athlete at
simple, financially viable, easy to administer, take a that time.13,68
392 PART III  Advances in Clinical Science and Practice

WHEN TO SCREEN CLINICAL SCREENING

Musculoskeletal screening is conducted at various points While this chapter has concentrated on screening for
in the season or the athlete’s career. Screening may be sport and exercise, future research may identify the value
prior to signing a contract, during the preseason, of screening people presenting to physiotherapists with a
in-season or at the end of the season.2,7 Preseason screen- range of musculoskeletal conditions. Screening for
ing should be conducted at least 6 to 8 weeks prior to the general strength, endurance, range of motion and func-
commencement of the competition season to allow for tion might identify deficits in addition to the presenting
further investigation and rehabilitation if problems are musculoskeletal problem. Identifying and addressing
identified.4 In-season screening monitors athletes during these deficits may improve the rehabilitation outcomes
the season with the aim to identify risk factors that arise and reduce future injury incidence.
as a result of training and competition.53 The end of For example, an elderly individual presenting with
season screening identifies issues that the athlete needs a fractured neck of humerus or massive inoperable
to work on during the off-season. rotator cuff tear who may normally have relied on
both upper and lower limbs to stand up from a chair,
or ascend stairs, would now have reduced function due
to the inability to effectively use the upper limb. If
SCREENING FUNCTIONAL rehabilitation concentrates on re-establishing upper limb
MOVEMENT PATTERNS function without using reliable, age- and function-
specific screening to identify if the lower limbs have
In response to the difficulties of screening to date, appropriate capacity to address the loss of upper limb
musculoskeletal evaluations have more recently shifted contribution to these activities, it is arguable that clini-
towards the identification of deficits in fundamental cal practice should be deemed as sub-standard. The
movement patterns.10,11 The assumption that individuals value of screening across all musculoskeletal presenta-
who display poor movement patterns have an elevated tions, ages, co-morbidities and functional needs should
risk of injury has been shown to be accurate in a number be considered.
of studies.70,71 Movement deficits are believed to limit
performance and render the athlete susceptible to injury.
The Lower Quarter Y Balance Test™ and the Func- REFERENCES
tional Movement Screen™ are two examples of reliable, 1. Oiestad BE, Engebretsen L, Storheim K, et al. Knee osteoarthritis
field-expedient screening protocols that use grading of after anterior cruciate ligament injury. Am J Sports Med
movement to develop an injury risk profile for an 2009;37(7):1434–43.
2. Tscholl PE, Dvorark J. Pre-competition orthopaedic assessment in
athlete.11 Assessment of movement patterns attempts to elite athletes: experiences and general considerations from interna-
combine multiple potential risk factors of muscle tional football. Eur Musculoskel Rev 2011;6(4):260–4.
strength, flexibility, range of motion, coordination, 3. Dallinga JA, Benjaminse A, Lemmink KAPM. Which screening
balance and proprioception into one test, and might tools can predict injury to the lower extremities in team sports: a
systematic review. Sports Med 2012;42(9):791–815.
better account for the multifactorial nature of injury. 4. Brukner P, White S, Shawdon A, et al. Screening of athletes: Aus-
Screening is not sport-specific and allows the imple- tralian experience. Clin J Sport Med 2004;14(3):169–77.
mentation of training programmes based around move- 5. Carek PJ. Evidence-based preparticipation physical examination.
ment patterns rather than individual joints and muscles. In: MacAuley D, Best TM, editors. Evidence-Based Sports Medi-
This new generation of screening assessments shows cine. 2nd ed. Carlton, Vic: Blackwell Publishing Asia; 2007.
p. 18–35.
promise; however, further research is required to estab- 6. Wingfield K, Matheson GO, Meeuwisse WH. Preparticipation
lish the predictive validity of the tools across a range evaluation. Clin J Sport Med 2004;14(3):109–22.
of populations, reliability across varying examiner levels 7. Batt ME, Jaques R, Stone M. Preparticipation examination (screen-
and their ability to assist in the prevention of injury. ing): practical issues as determined by sport: a United Kingdom
The impracticalities of assessor training and equipment Perspective. Clin J Sport Med 2004;14(3):178–82.
8. Garrick JG. Preparticipation orthopedic screening evaluation. Clin
are also a consideration with the tools currently avail- J Sport Med 2004;14(3):123–6.
able. Care should also be taken to interpret the outcome 9. Finch CF. A new framework for research leading to sports injury
of movement screening appropriately. The protocols prevention. J Sci Med Sport 2006;9(1–2):3–9.
are not diagnostic tools and simply highlight an increase 10. Schneiders AG, Davidsson A, Horman E, et al. Functional move-
ment screen normative values in a young, active population. Int J
in the risk of injury. Sports Phys Ther 2011;6(2):75–82. [Epub 2011/06/30].
The move towards quantifying movement patterns 11. Lehr ME, Plisky PJ, Butler RJ, et al. Field-expedient screening and
as an indicator of injury risk signifies an important injury risk algorithm categories as predictors of noncontact lower
advancement in the sports medicine and injury preven- extremity injury. Scand J Med Sci Sports 2013;23(4):e225–32.
[Epub 2013/03/23].
tion fields. The clinical evaluation of functional move- 12. Bartlett RBM. Sports biomechanics: reducing injury risk and
ment has been a part of clinical practice for many years improving sports performance. London; New York: Routledge;
but failed as a screening tool due to subjectivity and 2012.
reduced reliability. The current movement screening 13. Gomez JE, Landry GLB. Critical evaluation of the 2-minute ortho-
tools attempt to objectively grade movement using pedic screening examination. Am J Dis Child 1993;147(10):
1109–13.
explicit criteria. No doubt there will be continual evolu- 14. Cowan SM, Schache AG, Brukner P, et al. Delayed onset of trans-
tion of fundamental movement pattern screening in years versus abdonimus in long-standing groin pain. Med Sci Sports
to come. Exerc 2004;36(12):2040–5.
 39  Screening 393

15. Gabbe BJ, Bennell KL, Finch CF, et al. Predictors of hamstring 38. Trojian TH, McKeag DB. Single leg balance test to identify risk
injury at the elite level of Australian football. Scand J Med Sci of ankle sprains. Br J Sports Med 2006;40(7):610–13. [Epub
Sports 2006;16(1):7–13. 2006/05/12].
16. Brotman DJ, Walker E, Lauer MS, et al. In search of fewer inde- 39. Boyle KL, Witt P, Riegger-Krugh C. Intrarater and interrater reli-
pendent risk factors. Arch Intern Med 2005;165(2):138–45. ability of the Beighton and Horan joint mobility index. J Athl Train
17. Bullock-Saxton J, Bullock M. Repeatability of muscle length mea- 2003;38(4):281–5. [Epub 2004/01/23].
sures around the hip. Physiother Can 1994;46(2):105. 40. Ostenberg A, Roos H. Injury risk factors in female European foot-
18. Gabbe B, Bennell K, Wajswelner H, et al. Reliability of common ball. A prospective study of 123 players during one season. Scand
lower extremity musculoskeletal screening tests. Phys Ther Sport J Med Sci Sports 2000;10(5):279–85. [Epub 2000/09/23].
2004;5(2):90–7. 41. Soderman K, Alfredson H, Pietila T, et al. Risk factors for leg
19. Dennis RJ, Finch CF, Elliott BC, et al. The reliability of musculo- injuries in female soccer players: a prospective investigation during
skeletal screening tests used in cricket. Phys Ther Sport 2008;9(1): one out-door season. Knee Surg Sports Traumatol Arthrosc
25–33. [Epub 2008/12/17]. 2001;9(5):313–21. [Epub 2001/10/31].
20. Malliaras P, Hogan A, Nawrocki A, et al. Hip flexibility and 42. Stewart DR, Burden SB. Does generalised ligamentous laxity
strength measures: reliability and association with athletic groin increase seasonal incidence of injuries in male first division club
pain. Br J Sports Med 2009;43(10):739–44. [Epub 2009/03/14]. rugby players? Br J Sports Med 2004;38(4):457–60. [Epub
21. Prather H, Harris-Hayes M, Hunt DM, et al. Reliability and agree- 2004/07/27].
ment of hip range of motion and provocative physical examination 43. Uhorchak JM, Scoville CR, Williams GN, et al. Risk factors associ-
tests in asymptomatic volunteers. PM R 2010;2(10):888–95. [Epub ated with noncontact injury of the anterior cruciate ligament: a
2010/10/26]. prospective four-year evaluation of 859 West Point cadets. Am J
22. Dennis RJ, Finch CF, McIntosh AS, et al. Use of field-based tests Sports Med 2003;31(6):831–42. [Epub 2003/11/19].
to identify risk factors for injury to fast bowlers in cricket. Br J 44. Shultz SJ, Nguyen AD, Windley TC, et al. Intratester and intert-
Sports Med 2008;42(6):477–82. [Epub 2008/04/09]. ester reliability of clinical measures of lower extremity anatomic
23. Gabbe BJ, Finch CF, Bennell KL, et al. Risk factors for hamstring characteristics: implications for multicenter studies. Clin J Sport
injuries in community level Australian football. Br J Sports Med Med 2006;16(2):155–61. [Epub 2006/04/11].
2005;39(2):106–10. 45. Juul-Kristensen B, Rogind H, Jensen DV, et al. Inter-examiner
24. Kelln BM, McKeon PO, Gontkof LM, et al. Hand-held dynamom- reproducibility of tests and criteria for generalized joint hypermo-
etry: reliability of lower extremity muscle testing in healthy, physi- bility and benign joint hypermobility syndrome. Rheumatology
cally active, young adults. J Sport Rehabil 2008;17(2):160–70. 2007;46(12):1835–41. [Epub 2007/11/17].
[Epub 2008/06/03]. 46. Nicholas JA. Injuries to knee ligaments: relationship to loose-
25. Thorborg K, Petersen J, Magnusson SP, et al. Clinical assessment ness and tightness in football players. JAMA 1970;212(13):
of hip strength using a hand-held dynamometer is reliable. Scand 2236–9.
J Med Sci Sports 2010;20(3):493–501. [Epub 2009/06/30]. 47. Nussbaumer S, Leunig M, Glatthorn JF, et al. Validity and test-
26. Krause DA, Schlagel SJ, Stember BM, et al. Influence of lever arm retest reliability of manual goniometers for measuring passive hip
and stabilization on measures of hip abduction and adduction range of motion in femoroacetabular impingement patients. BMC
torque obtained by hand-held dynamometry. Arch Phys Med Musculoskelet Disord 2010;11:194. [Epub 2010/09/03].
Rehabil 2007;88(1):37–42. [Epub 2007/01/09]. 48. Wyss TF, Clark JM, Weishaupt D, et al. Correlation between inter-
27. Phillips BA, Lo SK, Mastaglia FL. Muscle force measured using nal rotation and bony anatomy in the hip. Clin Orthop Relat Res
‘break’ testing with a hand-held myometer in normal subjects aged 2007;460:152–8. [Epub 2007/02/10].
20 to 69 years. Arch Phys Med Rehabil 2000;81(5):653–61. [Epub 49. Verrall G, Slavotinek J, Barnes P, et al. Hip joint range of motion
2000/05/12]. restriction precedes athletic chronic groin injury. J Sci Med Sport
28. Scott DA, Bond EQ, Sisto SA, et al. The intra- and interrater reli- 2007;10(6):463–6.
ability of hip muscle strength assessments using a handheld versus 50. Delahunt E, McEntee BL, Kennelly C, et al. Intrarater reliability
a portable dynamometer anchoring station. Arch Phys Med Rehabil of the adductor squeeze test in gaelic games athletes. J Athl Train
2004;85(4):598–603. [Epub 2004/04/15]. 2011;46(3):241–5. [Epub 2011/06/15].
29. Katoh MYH. Comparison of reliability of isometric leg muscle 51. Fulcher ML, Hanna CM, Raina Elley C. Reliability of handheld
strength measurements made using a hand-held dynamometer with dynamometry in assessment of hip strength in adult male football
and without a restraining belt. J Phys Ther Sci 2009;21(1): players. J Sci Med Sport 2010;13(1):80–4. [Epub 2009/04/21].
37–42. 52. Mens JM, Vleeming A, Snijders CJ, et al. Reliability and validity of
30. Thorborg K, Serner A, Petersen J, et al. Hip adduction and abduc- hip adduction strength to measure disease severity in posterior
tion strength profiles in elite soccer players: implications for clinical pelvic pain since pregnancy. Spine 2002;27(15):1674–9. [Epub
evaluation of hip adductor muscle recovery after injury. Am J Sports 2002/08/07].
Med 2011;39(1):121–6. [Epub 2010/10/12]. 53. Crow JF, Pearce AJ, Veale JP, et al. Hip adductor muscle strength
31. Lu YM, Lin JH, Hsiao SF, et al. The relative and absolute reli- is reduced preceding and during the onset of groin pain in elite
ability of leg muscle strength testing by a handheld dynamometer. junior Australian football players. J Sci Med Sport 2010;13(2):
J Strength Cond Res 2011;25(4):1065–71. [Epub 2010/09/15]. 202–4.
32. Engebretsen AH, Mykelurst G, Holme I, et al. Intrinsic risk factors 54. Freckleton G, Cook J, Pizzari T. The predictive validity of a single
for groin injuries among male soccer players: a prospective cohort leg bridge test for hamstring injuries in Australian Rules Football
study. Am J Sports Med 2010;38(10):2051–7. Players. Br J Sports Med 2013;[Epub 2013/08/07].
33. Tyler T, Nicholas S, Campbell R, et al. The association of hip 55. Lindell O, Eriksson L, Strender LE. The reliability of a 10-test
strength and flexibility with the incidence of adductor muscle package for patients with prolonged back and neck pain: could an
strains in professional ice hockey players. Am J Sports Med 2001; examiner without formal medical education be used without loss
29(2):124–8. of quality? A methodological study. BMC Musculoskelet Disord
34. Bennell KL, Talbot RC, Wajswelner H, et al. Intra-rater and inter- 2007;8:31. [Epub 2007/04/05].
rater reliability of a weight-bearing lunge measure of ankle dorsi- 56. Dedering A, Roos af Hjelmsater M, Elfving B, et al. Between-days
flexion. Aust J Physiother 1998;44(3):175–80. [Epub 2001/10/26]. reliability of subjective and objective assessments of back extensor
35. Crossley KM, Thancanamootoo K, Metcalf BR, et al. Clinical fea- muscle fatigue in subjects without lower-back pain. J Electromyogr
tures of patellar tendinopathy and their implications for rehabilita- Kinesiol 2000;10(3):151–8. [Epub 2000/05/20].
tion. J Orthop Res 2007;25(9):1164–75. [Epub 2007/05/01]. 57. Latimer J, Maher CG, Refshauge K, et al. The reliability and valid-
36. Gabbe BJ, Finch CF, Wajswelner H, et al. Predictors of lower ity of the Biering-Sorensen test in asymptomatic subjects and sub-
extremity injuries at the community level of Australian football. jects reporting current or previous nonspecific low back pain. Spine
Clin J Sport Med 2004;14(2):56–63. [Epub 2004/03/12]. 1999;24(20):2085–9. [Epub 1999/10/30].
37. Finnoff JT, Peterson VJ, Hollman JH, et al. Intrarater and inter- 58. Mannion AF, Dolan P. Electromyographic median frequency
rater reliability of the Balance Error Scoring System (BESS). PM changes during isometric contraction of the back extensors to
R 2009;1(1):50–4. [Epub 2009/07/25]. fatigue. Spine 1994;19(11):1223–9. [Epub 1994/06/01].
394 PART III  Advances in Clinical Science and Practice

59. Moreland J, Finch E, Stratford P, et al. Interrater reliability of six 66. Hrysomallis C. Injury incidence, risk factors and prevention in
tests of trunk muscle function and endurance. J Orthop Sports Phys Australian rules football. Sports Med 2013;43(5):339–54. [Epub
Ther 1997;26(4):200–8. [Epub 1997/10/06]. 2013/03/27].
60. Simmonds MJ, Olson SL, Jones S, et al. Psychometric characteris- 67. Murphy DF, Connolly DA, Beynnon BD. Risk factors for lower
tics and clinical usefulness of physical performance tests in patients extremity injury: a review of the literature. Br J Sports Med 2003;
with low back pain. Spine 1998;23(22):2412–21. [Epub 1998/12/04]. 37(1):13–29. [Epub 2003/01/28].
61. Adams MA, Mannion AF, Dolan P. Personal risk factors for 68. Gray J, Naylor R. BokSmart: musculoskeletal assessment form.
first-time low back pain. Spine 1999;24(23):2497–505. [Epub 2009. <http://www.sarugby.co.za/boksmart/pdf/BokSmart%20
2000/01/08]. -%20Musculoskeletal%20Assessment%20for%20Rugby%20
62. Biering-Sorensen F. Physical measurements as risk indicators Players.pdf>.
for low-back trouble over a one-year period. Spine 1984;9(2): 69. Gabbe BJ, Finch CF, Bennell KL, et al. How valid is a self reported
106–19. 12 month sports injury history? Br J Sports Med 2003;37(6):
63. Smith J, Laskowski ER. The preparticipation physical examination: 545–7.
Mayo Clinic experience with 2739 examinations. Mayo Clin Proc 70. Kiesel K, Plisky PJ, Voight ML. Can serious injury in professional
1998;73(5):419–29. [Epub 1998/05/15]. football be predicted by a preseason functional movement screen?
64. Bahr R, Holme I. Risk factors for sports injuries – a methodological N Am J Sports Phys Ther 2007;2(3):147–58. [Epub 2007/08/01].
approach. Br J Sports Med 2003;37(5):384–92. [Epub 2003/09/30]. 71. Plisky PJ, Rauh MJ, Kaminski TW, et al. Star Excursion Balance
65. Freckleton G, Pizzari T. Risk factors for hamstring muscle strain Test as a predictor of lower extremity injury in high school basket-
injury in sport: a systematic review and meta-analysis. Br J Sports ball players. J Orthop Sports Phys Ther 2006;36(12):911–19. [Epub
Med 2013;47(6):351–8. [Epub 2012/07/06]. 2006/12/30].

CHAPTER 39.2  ■  WHAT IS OUR BASELINE FOR

MOVEMENT? THE CLINICAL
NEED FOR MOVEMENT SCREENING,
TESTING AND ASSESSMENT
Gray Cook  •  Kyle Kiesel

strength have not been shown to consistently correlate

INTRODUCTION with functional outcomes such as return to previous level
of activity or self-reported participation.2 Additionally,
More than any other health-related problem in the these measures have been shown to be predictive of
United States, the cost of treating musculoskeletal disor- future injury in only small subgroups when considering
ders has risen to become the greatest financial burden.1 specific patho-anatomical diagnosis such as hamstring
Treatment associated with arthritis, back pain and other strain3 or anterior cruciate ligament tears.4
musculoskeletal dysfunction accounted for US$128 Fundamental movement patterns are seen as key mile-
billion in 2012 as compared to US$116 billion for heart stones in human growth and development.5 They are
disease. Unlike approaches to other areas of health systematically used as developmental biomarkers for
care that are often guided by agreed care guidelines, the charting normal acquisition of motor development during
treatment of musculoskeletal disorders continues to be the first 3 or 4 years of life. When these fundamental
dominated by varied patterns of practice and a lack of movement patterns are delayed or compromised, this
standardization. information is used as a trigger to evaluate the systems
The musculoskeletal system is unique among the involved with mobility and motor control. In this popula-
other systems of the human body. Unlike other systems, tion, a compromised movement pattern provides an entry
the traditional approach in musculoskeletal medicine has point for investigation as well as a baseline for the inter-
been to wait for symptoms to appear before treatment is vention progress.
instigated. Understanding that the measurement of individual
In other systems, heath-care providers frequently parts may not yield desired results, some have described
screen for underlying abnormalities, using biomarkers of models that consider more comprehensive systems
elevated risk and dysfunction as part of routine care to of analysis of human movement focused on the motor
prevent more serious conditions from occurring. Exam- control aspect of the musculoskeletal system. Two
ples include blood testing for elevated cholesterol and such approaches are described by Janda and colleagues6
colonoscopy screening for bowel cancer. There has been and the movement systems approach described by
no meaningful approach that has successfully followed Sahrmann.7
this example for the musculoskeletal system. A key component of the Janda and Sahrmann models
is that they consider patterns of movement, that is, how
the parts work together to produce functional movement.
MOVEMENT PATTERNS While these approaches have provided alternative
methods of assessment and management of musculoskel-
Traditional models consider the musculoskeletal system etal pain and dysfunction, there remains a need for stan-
as individual anatomical parts. Basic impairment mea- dardization and the establishment of clinically measurable
sures such as isolated joint range of motion and muscle risk factors that can be utilized in preventative efforts.
 39  Screening 395

Clinicians need to consider that symptom resolution provide a standard operating procedure for screening,
and functional restoration require independent measure- testing and assessment of movement pattern mobility and
ment tools to assess progress and should be used together motor control limitations and asymmetry. In practice,
to demonstrate successful rehabilitation and protection the system is used to categorize risk and provides sug-
against future episodes. Outcomes data from the physi- gested corrective strategies. The system also offers higher
cal therapy literature related to two of the most com- levels of testing when asymmetry and motor control are
monly encountered diagnoses treated, low back pain considered competent with basic screening and to assist
and anterior cruciate ligament reconstruction, suggest with risk assessment. Lastly, the system provides a move-
somewhat disappointing results. Low back pain reoc- ment pattern assessment model for the clinician, when
currence rates remain high, disability associated with treating a patient with known musculoskeletal pain, that
low back pain remains common and at 41 months post- separates asymptomatic and dysfunctional movement
anterior cruciate ligament reconstruction only 63% of patterns from movement patterns that produce symp-
participants have returned to their previous level of toms and may or may not be dysfunctional. Taken
function but 90% demonstrated normal impairment together, the functional movement systems provide a
testing.2,8 These are examples of less than desirable basic screening standard operating procedure, a measure-
outcomes, and regardless of the rehabilitation approach ment and testing standard operating procedure, and a
or programme employed for a given musculoskeletal diagnostic assessment standard operating procedure.
condition, there is arguably a need for standardized Each has its own unique place in prevention and patient
movement pattern screening, testing and assessment care from any entry point into the system from screening
measures that may be applied across the many disciplines for prevention through to discharge at the completion of
of musculoskeletal healthcare providers. In this new rehabilitation
paradigm, where movement pattern screening, testing
and assessment may complement each other, the clini- The Functional Movement Screen – The
cian must understand that patients with the same mus-
culoskeletal presentation will often have unique
Categorization and Predictive System
movement profiles. Because of these differences, the The Functional Movement Screen (FMS) is a reliable
ideal treatment and preventative approaches, particularly (ICC values ranging from 0.76–0.90 and Kappa values
from an exercise perspective, may vary based on the from 0.70–1.0)9–15 screening tool created to rank move-
movement profile of the patient rather than the ortho- ment patterns that are fundamental to normal function.
paedic medical diagnosis. The screen includes movements that require the basic
mobility and motor control needed to complete a major-
ity of fundamental movements utilized routinely by active
FUNCTIONAL MOVEMENT SYSTEMS individuals in daily function and sport. The FMS includes
seven movements: overhead deep squat, hurdle step,
The Functional Movement System (Fig. 39-1) is a series in-line lunge, shoulder mobility, active straight leg raise,
of movement-based measurement tools (screening, trunk stability push up and rotary stability. Each of
testing, assessment) that focus on biomarkers of move- these patterns is graded on a 0–3 ordinal scale where
ment quality. The system has been proposed to establish 0 represents pain with the movement, 1 represents dys-
biomarkers within human movement patterns and to functional movement, 2 represents acceptable movement

Functional Movement Systems

Performance

Skill

Performance Testing + YBT

Patterns
FMS Entry Point
Pain
SFMA – Top tier
FIGURE 39-1  ■  A representation of the Func- Parts
tional Movement System showing the Func- SFMA – Breakouts
tional Movement Screen as the entry point and
pain being an indicator of moving up towards
higher level testing or down towards the Selec-
Impairments
tive Functional Movement Assessment for
rehabilitation purposes. FMS, Functional
Movement Screen; SFMA, Selective Functional
Movement Assessment; YBT, Y Balance Test.
396 PART III  Advances in Clinical Science and Practice

and 3 represents optimal movement. By screening these flexion, multisegmental extension, multisegmental rota-
patterns, movement limitations and asymmetries are tion, single leg stance and the overhead deep squat, and
readily identified and measured. Basic movement pattern is designed to assess fundamental patterns of movement
limitation and asymmetry are thought to reduce the in those with known musculoskeletal pain.26
effects of training and physical conditioning and recent The SFMA is a tool within the complete evaluation
data suggest these factors may be related to future injury. that complements the standard musculoskeletal examina-
One goal of the FMS is to identify the asymptomatic tion in two distinct ways. Firstly, when the clinical assess-
population with movement pattern limitations or asym- ment is initiated from the perspective of the movement
metry so individualized correct exercise can be prescribed pattern, the clinician has the opportunity to identify
to normalize movement prior to an increase in physical meaningful impairments that may be seemingly unre-
training or activity or a competitive sports season. lated to the main musculoskeletal complaint, but contrib-
Research has linked low or asymmetrical scores on the uting to the associated disability. This concept, known as
FMS to injury risk in professional football players,16,17 regional interdependence, is a hallmark of the SFMA that
firefighters,18,19 college athletes20,21 and military per- guides the clinician to the most dysfunctional non-painful
sonal.22,23 Researchers have demonstrated that a standard- movement pattern that is then assessed in detail. Sec-
ized individual programme based on corrective exercise ondly, the SFMA is specifically designed to assist the
does improve dysfunctional movement and asymmetry as clinician in the most effective therapeutic exercise choices
measured by the FMS.24,25 The FMS is a screening tool targeting movement pattern restoration. Manual therapy,
and is designed for those individuals who do not have a such as joint mobilization and manipulation and soft
known musculoskeletal injury or patients who are asymp- tissue treatments such as trigger point and myofascial
tomatic and as part of a standardized discharge pro- releases and stretching, are techniques that may be con-
gramme when patients are returning to active, athletic, sidered to treat the impairment level of motor control;
or tactical situations following rehabilitation.26 however, the musculoskeletal clinician must also consider
strategies to restore motor control through developmen-
The Y Balance Tests – The tal movement patterns and facilitation techniques.
Following the logic in the SFMA, the clinician sepa-
Measurement System rates painful patterns from non-painful patterns. Next,
The Y Balance Tests are clinically reliable27,28 and serve following a systematic approach, the dysfunctional pat-
as both clinical measurement tools and have demon- terns are broken down to identify the root cause of the
strated predictive validity related to injury risk in multiple dysfunction as primarily a mobility deficit or a stability/
populations including high school and college athletes.29–31 motor control deficit. The system accounts for managing
They functionally represent the upper and lower quarters multiple dysfunctional patterns simultaneously and with
of the body and measure how the subject performs at this knowledge a precise intervention may be prescribed
their limits of stability. The test is scored on a continuous to normalize the dysfunctional patterns from a motor
scale where the maximum amount of linear movement control perspective. The SFMA is measured clinically as
produced in each of the three reach directions is normal- each of the seven patterns are categorized into one of the
ized by dividing by the subject’s respective limb length. four following categories:
This provides a measurement that is a percentage of limb 1. Functional and non-painful (FN)
length; researchers have demonstrated that normative 2. Functional and painful (FP)
values on Y Balance Test performance vary based on 3. Dysfunctional and painful (DP)
gender, age and sport played.32 The tests require moder- 4. Dysfunctional and non-painful (DN)
ate to advanced motor control and should be used in Simple criteria for each movement have been established,
asymptomatic situations to accurately measure motor allowing the clinician to quickly determine if the move-
control abilities. The tests can also be used throughout ment is ‘functional’ which is defined as meeting the cri-
the rehabilitation process and provide systematic feed- teria as described. If one or more of the criteria are not
back about the effectiveness of treatment, including ther- met, the pattern is labelled as ‘dysfunctional’. If pain is
apeutic exercise, on motor control and movement pattern present during the movement it is considered painful, if
symmetry. Along with the FMS, the Y Balance Tests are not it is non-painful allowing for categorization in one of
also recommended as part of a standardized discharge the four categories.
protocol for patients returning to an active lifestyle after Once the seven major movement patterns have been
the rehabilitation programme has concluded to ensure categorized, the patterns that were scored as DNs are
that movement pattern risk factors have been appropri- addressed first. By prioritizing DN patterns the clinician
ately managed. is able to address underlying dysfunction in the move-
ment system that is not complicated by pain. Each DN
The Selective Functional Movement pattern is broken down in detail to diagnose the cause of
dysfunction as either a mobility problem or a stability/
Assessment – The Diagnostic System motor control problem. To achieve this diagnosis a sys-
The Selective Functional Movement Assessment (SFMA) tematic ‘breakout examination’ is applied in a logical
is specifically designed for clinical situations where manner. The breakout logic includes assessing movement
movement is complicated by symptoms (Fig. 39-2). The in different conditions to determine the diagnosis. Firstly,
SFMA is a series of seven full-body movements including the influence of the extremities on the movement is
cervical patterns, shoulder patterns, multisegmental reduced (such as placing hands on hips during the
 39  Screening 397

The Selective Functional Movement Assessment

SFMA Scoring FN FP DP DN

Active Cervical Flexion

Active Cervical Extension

Cervical Rotation L
R

Upper Extremity Pattern 1 (MRE) L

R

Upper Extremity Pattern 2 (LRF) L

R

Multisegmental Flexion

Multisegmental Extension

Multisegmental Rotation L
R

FIGURE 39-2  ■  The score sheet for each of the top-

tier movements of the Selective Functional Movement Single Leg Stance L
Assessment. DN, Dysfunctional and non-painful; DP, R
Dysfunctional and painful; FN, Functional and non-
painful; FP, Functional and painful; L, Left; LRF,
Lateral rotation flexion; MRE, Medial rotation exten-
sion; R, Right; SFMA, Selective Functional Movement Overhead Deep Squat
Assessment.

extension movement rather than overhead), next the the movement can now be completed we have our second
movement is assessed in an unloaded condition, and piece of information to help us with the diagnosis. For
finally active versus passive movement is considered. By this example, let us assume that our patient does achieve
applying these breakout principles to each dysfunctional a score of functional on the unloaded movement. This
pattern, a movement-orientated diagnosis is obtained. To demonstrates that the patient has the requisite mobility
capture the breakout logic in a systematic way and to be to complete the pattern (adequate ankle dorsiflexion, hip
sure that no step is missed, the use of the breakout flow- flexion, posterior chain soft tissue mobility and adequate
charts is recommended. The flowcharts take the clinician spinal flexion mobility) but was not able to coordinate the
through each step of the breakout logic in an efficient parts of the movement into a functional pattern.
manner. This is the definition of a ‘stability/motor control dys-
There are 15 total flowcharts that encompass the function’ and is further broken down to determine the
entire SFMA breakout system. Using multisegmental severity of the stability/motor control dysfunction by
flexion (toe-touching pattern) as an example, we will assessing functional rolling patterns. If, for example, the
describe how each part of the logic is applied to obtain a patient would have been unable to complete the unloaded
movement-orientated diagnosis. Firstly, to reduce the toe-touching movement, the logic would have taken us
influence of one lower extremity on the pattern, the to look at each part, that is, active leg raising, followed
patient shifts their weight to bear the majority of their by passive if needed, then to hip flexion mobility and
weight on one side and then repeats the forward bending spinal mobility as indicated. This example provides the
movement. If the pattern can now be completed normally reader with the basic logic and process of how the SFMA
we have our first piece of information to help us with the structure allows for a movement diagnosis to be obtained,
diagnosis. Next, the movement is performed in the allowing for a targeted intervention to be applied. If
unloaded position (sit and reach movement). This is to the patient would have been diagnosed with a stability/
say that the lower extremities are now unloaded and if motor control dysfunction for multisegmental flexion our
398 PART III  Advances in Clinical Science and Practice

intervention would need to be motor control re-training 2. Ardern CL, Taylor NF, Feller JA, et al. Return-to-sport outcomes
rather than mobility or stretching. If our diagnosis ends at 2 to 7 years after anterior cruciate ligament reconstruction
surgery. Am J Sports Med 2012;40(1):41–8.
up as a mobility problem, either joint mobility dysfunc- 3. Opar DA, Williams MD, Shield AJ. Hamstring strain injuries:
tion or a tissue extensibility dysfunction, then mobility factors that lead to injury and re-injury. Sports Med 2012;42(3):
techniques would be indicated prior to the re-establishment 209–26.
of motor control with appropriate exercise. 4. Myer GD, Ford KR, Brent JL, et al. Differential neuromuscular
training effects on ACL injury risk factors in ‘high-risk’ versus
To simplify the process, we are simply looking for ‘low-risk’ athletes. BMC Musculoskelet Disord 2007;8:39.
mobility problems first, and when they are present, they 5. Cech JDMS. Functional Movement Development. 3rd ed.
are treated accordingly prior to movement re-training. If St. Louis Missouri: Elsevaier; 2012.
mobility is considered acceptable, then the treatment can 6. Key J, Clift A, Condie F, et al. A model of movement dysfunction
proceed to movement re-training. An important point provides a classification system guiding diagnosis and therapeutic
care in spinal pain and related musculoskeletal syndromes: a para-
here is that this can only be applied to patterns that are digm shift-Part 2. J Bodyw Mov Ther 2008;12(2):105–20.
non-painful. When a pattern is complicated by pain, 7. Sahrmann SA. Diagnosis and Treatment of Movement Impairment
caution must be utilized, as it is not recommended to Syndromes. St Louis, MO: Mosby; 2002.
provide exercise re-training to a painful pattern because 8. Delitto A, George SZ, Van Dillen LR, et al. Low back pain.
J Orthop Sports Phys Ther 2012;42(4):A1–57.
of the profound unpredictable effects of pain on motor 9. Minick KI, Kiesel KB, Burton L, et al. Interrater reliability of the
control. The approach employed by the SFMA is based functional movement screen. J Strength Cond Res 2010;24(2):
in fundamental movement logic and at the moment is 479–86.
based on experience and clinical observation. There are 10. Teyhen DS, Shaffer SW, Lorenson CL, et al. The functional move-
published reliability and validity studies referred to above ment screen: a reliability study. J Orthop Sports Phys Ther 2012;
42(6):530–9.
indicating that movement patterns may be reliably mea- 11. Gribble PA, Brigle J, Pietrosimone BG, et al. Intrarater reliability
sured and are related to injury risk when using the FMS of the functional movement screen. J Strength Cond Res 2013;
and Y Balance Tests at the screening and testing levels. 27(4):978–81.
The SFMA is designed to manage patients from a move- 12. Frohm A, Heijne A, Kowalski J, et al. A nine-test screening battery
for athletes: a reliability study. Scand J Med Sci Sports 2012;
ment perspective with known musculoskeletal pain but is 22(3):306–15.
not designed as a predictive tool. The system, including 13. Onate JA, Dewey T, Kollock RO, et al. Real-time intersession and
the FMS, Y Balance Tests and SFMA, is presented as a interrater reliability of the functional movement screen. J Strength
whole and recommended to be used together. There are Cond Res 2012;26(2):408–15.
reliability and validity data at the screening and testing 14. Smith C, Chimera N, Wright N, et al. Interrater and intrarater
reliability of the functional movement screen. J Strength Cond Res
levels which are recommended to be performed near dis- 2013;27(4):982–7.
charge from the rehabilitation process. The reliability of 15. Gulgin H, Hoogenboom B. The functional movement screening
the top-tier SFMA has been reported to be substantial to (fms)™: an inter-rater reliability study between raters of varied
almost perfect with Kappa values from 0.72–0.83.33 There experience. JISPT 2014;9(1):14–20.
16. Kiesel K, Plisky PJ, Voight ML. Can serious injury in professional
are no SFMA specific validity data published to date. football be predicted by a preseason functional movement screen?
N Am J Sports Phys Ther 2007;2(3):147–58.
17. Kiesel KB, Butler RJ, Plisky PJ. Limited and asymmetrical funda-
CONCLUSION mental movement patterns predict injury in american football
players. J Sport Rehabil 2013.
18. Butler RJ, Contreras M, Burton LC, et al. Modifiable risk factors
Currently, when managing the musculoskeletal system predict injuries in firefighters during training academies. Work
our opportunity to intervene is largely driven by symp- 2013;46(1):11–17.
toms. Other medical specialties screen for biomarkers 19. Peate WF, Bates G, Lunda K, et  al. Core strength: a new model
that may indicate the development and onset of more for injury prediction and prevention. J Occup Med Toxicol 2007;
2:3.
serious pathology. This may be a direction for musculo- 20. Chorba RS, Chorba DJ, Bouillon LE, et al. Use of a functional
skeletal physiotherapy to evolve and build on the reliable movement screening tool to determine injury risk in female colle-
and validated screens and tests that have been established. giate athletes. N Am J Sports Phys Ther 2010;5(2):47–54.
In addition, evidence is necessary to demonstrate that 21. Lehr ME, Plisky PJ, Butler RJ, et al. Field-expedient screening and
normalizing the screening and testing risk factors does injury risk algorithm categories as predictors of noncontact lower
extremity injury. Scand J Med Sci Sports 2013.
indeed make a meaningful long-term difference to the 22. Lisman P, O’Connor FG, Deuster PA, et al. Functional movement
patient’s disability and may even prevent symptoms from screen and aerobic fitness predict injuries in military training. Med
starting. This evolution in musculoskeletal care moves us Sci Sports Exerc 2013;45(4):636–43.
away from just assessing and treating pain originating 23. O’Connor FG, Deuster PA, Davis J, et al. Functional movement
screening: predicting injuries in officer candidates. Med Sci Sports
from the musculoskeletal system. To move away from a Exerc 2011.
pain-driven model we must become experts at screening, 24. Bodden JG, Needham RA, Chockalingam N. The effect of an
testing and assessing human movement patterns. We intervention program on functional movement screen test scores in
must define dysfunction and relate it to risk where appli- mixed martial arts athletes. J Strength Cond Res 2013.
cable. Previous injury is the number one risk factor for a 25. Kiesel K, Plisky P, Butler R. Functional movement test scores
improve following a standardized off-season intervention in profes-
future injury, and if we become better at managing move- sional football players. Scand J Med Sci Sports 2011;21(2):
ment dysfunction we may influence future risk as well. 287–92.
26. Cook E. Movement. Aptos California: On Target Publishing;
2010.
REFERENCES 27. Plisky PJ, Gorman PP, Butler RJ, et al. The reliability of an instru-
1. Medical Expenditure Panel Survey. 2011. Available from: <http:// mented device for measuring components of the star excursion
meps.ahrq.gov/> [cited 2014]. balance test. N Am J Sports Phys Ther 2009;4(2):92–9.
 39  Screening 399

28. Westrick R, Miller J, Carow S, et al. Exploration of the y-balance 31. Butler RJ, Lehr ME, Fink ML, et al. Dynamic balance performance
test for assessment of upper quarter closed kinetic chain perfor- and noncontact lower extremity injury in college football players:
mance. Int J Sports Phys Ther 2012;7(2):139–47. an initial study. Sports health 2013;5(5):417–22.
29. de Noronha M, Franca LC, Haupenthal A, et al. Intrinsic predic- 32. Gorman PP, Butler RJ, Rauh MJ, et al. Differences in dynamic
tive factors for ankle sprain in active university students: a prospec- balance scores in one sport versus multiple sport high school
tive study. Scand J Med Sci Sports 2012. athletes. Int J Sports Phys Ther 2012;7(2):148–53.
30. Plisky PJ, Rauh MJ, Kaminski TW, et al. Star Excursion Balance 33. Glaws K, Juneau C, Becker L, et al. Intra- and Inter-rater Reli-
Test as a predictor of lower extremity injury in high school basket- ability of the Selective Functional Movement Assessment (SFMA).
ball players. J Orthop Sports Phys Ther 2006;36(12):911–19. Int J of Sports Phys Ther 2014;9(2):195–207.
 CHAPTER 40 

Advanced Roles in Musculoskeletal

Physiotherapy
Jill Gamlin • Maree Raymer • Jeremy Lewis

shortages,20–23 professional interest from physiothera-

INTRODUCTION pists,24–27 and emerging evidence relating to the impact
of new service delivery models. Organizational and polit-
Innovative and cost-effective service models are sought ically driven factors, such as the desire to reduce waiting
to address the challenges of rising demand on health times have been suggested as the dominant factor.27
services and unsustainable growth in health expenditure. In the UK, political directives such as the European
Health service redesign, in which physiotherapists take Working Time Directive that restricted doctors working
on an expanded role and level of responsibility in service hours were a key driving factor.20,21,23 Initial development
provision for patients with musculoskeletal conditions, of advanced practice roles related to local circumstances
has been implemented in many countries, particularly and local innovation; however, this was subsequently sup-
in public sector services. This chapter will provide an ported by Department of Health policy and governance
overview of the development of advanced roles in mus- arrangements and these roles have become a standard
culoskeletal physiotherapy. Current models of practice part of service delivery models.28–31 Advanced roles have
and the evidence for the impact of these roles will also also developed in other countries, predominantly in
be presented, as will key current issues associated public sector services. In Australia, the key driving factors
with advanced practice and the potential for future have been similar to those in the UK, including unsus-
development. tainable demand on public hospital services, resulting in
extended waiting lists and unacceptable waiting times to
access care.16,18,32 In some Australian states a jurisdiction-
wide approach has been taken, while in others, service
BACKGROUND TO DEVELOPMENT developments have occurred at individual facilities.
OF ADVANCED ROLES Advanced practice roles have also developed in response
to medical workforce shortages. For example, Aiken8
Advanced musculoskeletal physiotherapy roles were first describes the development of a collaborative care model
developed in the military in the 1970s.1,2 In the United in Ontario, Canada, in which physiotherapists undertake
Kingdom (UK), advanced practice roles began in the an advanced role in hospital orthopaedic services to
1980s, as an innovative way to address long waiting times manage patients referred to hip and knee arthroplasty
for rheumatology and orthopaedic clinics in secondary clinics.
care services.3,4 A combination of undergraduate and The common feature in service redesign has been
postgraduate education, autonomous practice, mentor- an aim to maximize the value of the knowledge and
ship, vision and close collaboration with medical col- skills of experienced musculoskeletal physiotherapists
leagues, enabled physiotherapists to undertake these and their contribution to streamlined pathways of care
roles. As examples of these service developments began and improved outcomes for patients. Physiotherapists
to appear in the literature, these advanced roles devel- in advanced roles may now be found in diverse settings
oped and flourished across the UK and began to emerge in many countries. The breadth and depth of work
and become embedded in health services in other undertaken has evolved to include independent assess-
countries.5–18 ment, referral for imaging investigations and pathology
tests, diagnosis as the first point of contact in the man-
agement pathway for patients referred for specialist
DRIVERS OF ADVANCED ROLE medical opinion or those presenting to emergency care
DEVELOPMENT settings, case management and clinical consultancy and
discharge decision making. In the UK advanced roles
A range of factors have been associated with the develop- have developed to also include listing for surgery and
ment of advanced roles in musculoskeletal physiotherapy additional therapeutic interventions such as injection
practice. These include unmet and unsustainable demand therapy and ultrasound-guided injections for joints and
on health systems, which is contributed to by the growing soft tissues, hydro-distension for contracted frozen
burden of musculoskeletal conditions and related dis- shoulders and, more recently, independent prescribing
ability worldwide,19 working patterns and workforce of medicines.
400
 40  Advanced Roles in Musculoskeletal Physiotherapy 401

Musculoskeletal conditions are associated with high as in primary care services. Some examples of service
and increasing prevalence rates. They are one of the settings in which advanced roles are found are discussed
major causes of disability worldwide and the demands on in the following sections.
services to provide timely and effective health care are
predicted to increase.19 Advanced roles that capitalize on
the knowledge and skills of experienced musculoskeletal Orthopaedics, Neurosurgery and
physiotherapists are expected to continue to develop to Rheumatology in Hospital-Based
help meet this challenge.
Services
Referrals to an orthopaedic surgeon that are triaged as
DEFINITIONS ‘unlikely to require immediate surgical intervention’ are
directed to a physiotherapy-led service where the phys-
Initially, advanced roles were developed to address local iotherapist is responsible for providing a high level of
needs and requirements. Ad hoc development has resulted diagnostic assessment and management planning.27,34,35
in inconsistent terminology and definition of roles and a In some services where the focus includes optimizing
wide range of nomenclature exists to describe these posi- non-surgical management, the physiotherapist’s role
tions. Titles include advanced physiotherapy practitioner, includes high-level consultancy and in some cases leader-
advanced practice physiotherapist, extended scope prac- ship of a multidisciplinary team.32 Services may be
titioners, orthopaedic physiotherapy practitioners, spe- targeted to manage patients with a broad range of mus-
cialist physiotherapists, highly specialist physiotherapist, culoskeletal conditions, or to specific body regions (e.g.
physiotherapy specialist, Norwegian manual therapist spine/shoulder/knee) or specific diagnoses (e.g.
and consultant physiotherapist. This list is not exhaustive arthritis).4,7,9–18,32
and in different countries different criteria must be met Services have developed to manage an entire episode
to attain these roles. This may vary from completing post of care that may include initial assessment, referral for
graduate qualification(s), undertaking in-house education non-surgical management, monitoring of progression of
and training, demonstrating work-based competency or the condition/disease, listing for surgery when required,
passing an examination defined by a national physio- pre-operative preparation and post-operative rehabilita-
therapy professional body. While titles will vary between tion. There are also examples of physiotherapist-led
organizations, jurisdictions and countries, the develop- fracture follow-up clinics,36 post-operative review clinics37
ment of consistent definitions of advanced scope of prac- and the management of spinal pain referred to neuro-
tice roles would be beneficial to support progress in surgical outpatient services.38 Advanced roles in rheu-
research and professional practice worldwide. matology have developed to include triage and the
While separate descriptions of advanced or extended ongoing management of patients with inflammatory
scope of practice exist,33 perhaps what best defines these conditions.3,39
roles is that they require:
• post graduate education and training beyond initial
qualification standards
Emergency Departments
• significant clinical experience Advanced roles in emergency departments (EDs) involve
• location in an area of specialization and independent assessment, referral for diagnostic tests,
• inclusion of activities and a level of work that may diagnosis, management and discharge of patients pre-
have previously been undertaken by medical or senting with musculoskeletal conditions. Depending
other health-care practitioners. on their scope of practice and jurisdiction in which
The degree of autonomy and accountability may vary they work, ED roles may include independent inter-
between roles but, at the highest level, an individual prac- pretation of imaging findings and prescription and/or
titioner may be totally responsible for the assessment, administration of medications.40–45 In some ED services,
investigation, diagnosis and management of specific physiotherapists also provide primary contact manage-
patient groups across an entire episode of care. The ment of patients with uncomplicated fractures and
development of the consultant physiotherapist role in the dislocations.45
UK, which combines 50% expert practice with dedicated
time for research, teaching and service redesign, gives
the opportunity for further expansion and evaluation of
Primary Care Settings
advanced roles. With many consultants participating in Since the late 1990s, orthopaedic screening services have
local and national advisory bodies, strategic influence also been implemented in primary care settings in the
may be exercised in shaping pathways of care around the UK.46 In these services, physiotherapists provide assess-
needs of patients to achieve improved quality and better ment and management of patients who would otherwise
outcomes. be referred to hospital orthopaedic services for review by
a consultant physician or surgeon. The development of
services that bridge the gap between primary and second-
MODELS OF ADVANCED PRACTICE ary care was a major recommendation of the Musculo­
skeletal Services Framework developed for the United
Patients with musculoskeletal conditions are seen in a Kingdom National Health Service (NHS).47 While
variety of subspecialty services in hospital settings, as well multidisciplinary in nature, community assessment and
402 PART III  Advances in Clinical Science and Practice

treatment services specifically include physiotherapists Diagnostic Accuracy

working in an advanced role and are now in place in the
majority of NHS Primary Care Trusts.48 Orthopaedic Systematic reviews of studies conducted in orthopaedic
physiotherapy screening in primary care is also being and ED settings have concluded that physiotherapists in
trialled in other jurisdictions.5 advanced roles are able to triage, diagnose musculoskeletal
conditions and identify patients requiring surgery with
comparable ability to that of orthopaedic consultants.34,35
OTHER ASPECTS OF ADVANCED
PRACTICE Treatment Effectiveness
Prescribing and administration of medicines for patients A systematic review of the impact of advanced roles in
with musculoskeletal conditions is an example of an EDs reported high-level evidence of improved short-
element of advanced practice that has been undertaken term clinical outcomes for patients managed by physio-
by physiotherapists across both hospital and primary care therapists compared to routine ED care.55 A subsequent
settings. While supplementary prescribing rights for randomized controlled trial concluded that patients
physiotherapists have been in place in the UK since 2005, managed by physiotherapists in advanced roles in EDs
the granting of independent rights is aimed at improving achieve equivalent outcomes compared to care provided
access to care, convenience and choice for patients while by medical staff.56
maximizing the value of physiotherapy workforce A systematic review including studies in both ED and
resources within the NHS.49,50 Physiotherapists in the orthopaedic settings concluded that outcomes of care
UK are the first to be granted independent prescribing provided by physiotherapists in advanced roles may be as
rights under legislation that came into effect in 2013.49 good as, or more beneficial than, usual care.35 A pilot
Prescribing has also been part of advanced roles in other study by Comans et al.32 also suggests that overall treat-
countries in particular circumstances and development ment effectiveness, as measured in quality adjusted life
of competency-based frameworks and nationally consis- years (QALYs) gained, may be higher in physiotherapy-
tent pathways for non-medical prescribing are being led orthopaedic service models than that achieved in tra-
explored.1,2,51–53 ditional models of care. In addition, Chambers et al.57
Physiotherapists in the UK have been performing demonstrated that appropriately educated physiothera-
injections for musculoskeletal conditions since the mid- pists were as accurate as orthopaedic surgeons in per-
1990s. This is another important area of advanced prac- forming landmark-guided subacromial bursal injections
tice as it allows physiotherapists to embed these skills (67% accuracy in both groups), whereas orthopaedic reg-
within an evidence-based package of care for individual istrars demonstrated lower accuracy (48%).
patients with defined musculoskeletal conditions. This
reduces the requirement for additional referrals and
reduces waiting times.54 More recently this practice has
Patient Satisfaction/Experience
evolved further with increasing numbers of physiothera- Patient satisfaction is the most commonly reported
pists performing ultrasound-guided injections to target outcome in the evaluation of new allied health profes-
specific structures. Physiotherapists have also completed sional (AHP) roles and service models.6 Kilner’s system-
education programmes to be able to perform ultrasound- atic review identifies that there is high-level evidence of
guided hydro-distension procedures for conditions such improved patient satisfaction for advanced ED physio-
as contracted frozen shoulders. Audit evidence exists that therapy services.55 In their systematic review of advanced
demonstrates that patients with conditions such as frozen and extended roles, Desmeules et al.35 included seven
shoulder may be entirely managed (assessment, referral studies that evaluated patient satisfaction across a range
for imaging, ultrasound-guided corticosteroid and anal- of practice settings including ED, orthopaedics and rheu-
gesic injections, hydro-distension injections and appro- matology. Satisfaction levels with these services were
priate physiotherapy treatments together with advice and high in all seven studies, with physiotherapy-led care
education) in a cost-effective manner with high levels of resulting in significantly higher levels of satisfaction in
patient satisfaction, without the need for referral to other three studies and equivalent levels of satisfaction to usual
medical/health professionals.54 care in another three studies.

EVALUATION OF ADVANCED Process/Organizational Impacts

PRACTICE ROLES AND IMPACTS Reporting of process-related outcomes, such as waiting
ON HEALTH SERVICES times, is also common and usually indicates reduced
waiting times for patients.6 Emergency and orthopaedic
Advanced roles in musculoskeletal physiotherapy have department waiting times are the subject of key health
rapidly expanded in recent years, but the pace of change service performance targets internationally and the ability
in response to significant service delivery challenges often to impact on waiting times can be a key driver for service
means that robust evaluation of new roles and service model reform. McClellan et al.58 found that streaming
models lags behind their uptake.21 Current evidence patients appropriate to be seen by physiotherapists in
regarding advanced musculoskeletal physiotherapy roles advanced roles can reduce overall ED waiting times, a
is briefly summarized in the following section. finding also supported by the review by Desmeules et al.35
 40  Advanced Roles in Musculoskeletal Physiotherapy 403

In orthopaedic services, many observational and audit pathways that are patient-centred. This process works
studies describe reduced waiting times. The systematic best when all involved in the provision of health care
review by Stanhope et al.34 identified two high-quality construct meaningful pathways, based on care delivered
studies which reported reductions in orthopaedic waiting by the right practitioner, at the right time, in the right
times associated with the introduction of advanced role place and within a cost-effective delivery model.
physiotherapy services. While the current evidence base is promising in rela-
tion to the impacts of advanced roles, it is apparent that
the evidence base lags behind the rate at which these
Health Economic Impacts services have been developed and implemented. Key
While many studies evaluate process measures and stake- criticisms of the majority of published studies include the
holder satisfaction, relatively few analyse the economic small numbers of clinicians involved, single-centre
impacts of new roles.6 The results of early studies that designs, short-term follow-up periods, limited focus on
included economic measures are mixed and hampered by patient-centred outcomes and little direct comparison of
methodological limitations, being criticized for lacking a patient outcomes between physiotherapist-led and
comprehensive description of services provided, how routine care.6,34,35,62 There are also unanswered questions
resources were valued and information relevant to making about cost effectiveness, impacts on the workforce
a purchasing decision.35 and numerous education and training issues. Deficits in
A cost-effectiveness evaluation of a randomized con- knowledge supporting these pathways need to be
trolled trial suggests that physiotherapy-led care in the addressed with further research. Access to suitable educa-
ED is clinically equivalent, but may not be cost saving.59 tion, training and mentorship to support individual
Another study has attempted to address the methodologi- development and longer-term service sustainability is
cal issues associated with previous economic evaluations fundamental to the continual evolution of advanced clini-
of advanced physiotherapy roles in orthopaedic settings.32 cal practice roles.
In this study an economic (Markov) model was con- The aims of these roles are to deliver seamless care to
structed in order to assess the costs, health outcomes, patients in a timely and cost-effective manner and support
value for money and potential cost savings of a optimum use of the skills of the entire health workforce.
physiotherapy-led orthopaedic service in Queensland, It is conceivable that in the future physiotherapists may
Australia. The economic model was populated with ret- take on additional roles as health teams continue striving
rospective, published, administrative and audit data and to streamline pathways of care. These new roles should
indicates the physiotherapy-led service could be consid- be built upon the foundations of physiotherapists’ exist-
ered to be highly cost effective and may be cost saving in ing scope of practice, knowledge and expertise and add
some circumstances. It is expected that the Markov model measurable value to patient outcomes and experiences.
proposed in this preliminary study could be modified to
support robust economic evaluation of other advanced
roles and services in the future. CONCLUSIONS AND
RECOMMENDATIONS
Professional Issues Role and service innovations have become widespread in
Changes to service provision require evaluation to ensure an attempt to address the almost universal burden of
patients are receiving optimal care as well as to under- musculoskeletal conditions on health services. Since the
stand the clinical, financial and psychosocial impact on inception of advanced practice roles, physiotherapists
clinicians involved in the change. Collins et al.60 found have pushed the boundaries of clinical practice in pursuit
that nurses and allied health professionals in innovative of providing seamless, evidence-based care pathways for
roles in the UK generally experienced high levels of job patients, which maximize the value of the knowledge and
satisfaction, which was related to increased freedom and skills of experienced musculoskeletal physiotherapists
autonomy in managing their own caseload and increased and other health professionals to the patient and health
responsibility. They concluded that increased job satis- services. This development in health care has trans-
faction is likely to contribute to retention of experienced formed service delivery in many ways. It aims to provide
professionals within the NHS. Dawson and Ghazi61 access to the right practitioner, at the right time in a cost-
undertook a very small-scale qualitative study to explore effective manner, while maintaining or improving the
the experience of physiotherapists in extended roles in quality of care provided, together with improved out-
orthopaedic services in the UK and concluded that comes and experiences for patients. Current evidence
although advanced roles can be stressful for the clinician, suggests a range of potential benefits for patients and
they are also very satisfying. It is evident, however, that health services. Care provided by physiotherapists in
the workforce and professional impacts of advanced roles, advanced roles may be as beneficial, or more beneficial,
both on the clinician themselves and on other health than traditional service models in terms of access to treat-
professionals, have not been widely explored. ment, diagnostic accuracy and patient satisfaction, and
From a historic perspective the delivery of health care result in more timely provision of care. However, the
is constantly evolving, responding to new knowledge pace of development means there are persistent gaps in
and demands. Advanced roles are best developed in envi- the evidence which indicate that further high-quality,
ronments where knowledge is shared within multidisci- methodologically sound research is required in order to
plinary teams, providing integrated evidence-based explore fully the benefits and impacts of the introduction
404 PART III  Advances in Clinical Science and Practice

of these roles. International consensus on definitions of and Social Work, University of Salford, UK; 2012. Available from:
advanced practice will assist in progressing this research. <http://usir.salford.ac.uk/26989/>; [cited 2013 12/8/13].
24. Durrell S. Expanding the scope of physiotherapy: clinical physio-
therapy specialists in consultants’ clinics. Man Ther 1996;1(4):210–
REFERENCES 13. [Epub 1996/09/01].
1. James JJ, Stuart RB. Expanded role for the physical therapist. 25. Li LC, Westby MD, Sutton E, et al. Canadian physiotherapists’
Screening musculoskeletal disorders. Phys Ther 1975;55(2):121– views on certification, specialisation, extended role practice, and
31. [Epub 1975/02/01]. entry-level training in rheumatology. BMC Health Serv Res
2. Benson CJ, Schreck RC, Underwood FB, et al. The role of army 2009;9:88. [Epub 2009/06/06].
physical therapists as nonphysician health care providers who pre- 26. Robertson VJ, Oldmeadow LB, Cromie JE, et al. Taking charge of
scribe certain medications: observations and experiences. Phys change: a new career structure in physiotherapy. Aust J Physiother
Ther 1995;75(5):380–6. [Epub 1995/05/01]. 2003;49(4):229–31. [Epub 2003/11/25].
3. Langridge JC, Moran CJ. A comparison of two methods of manag- 27. ACT-Health. ACT Health 2008 Physiotherapy Extended Scope
ing patients suffering from rheumatoid arthritis. Physiotherapy Practice: Phase 1 Final Report. Australian Capital Territory (ACT),
1984;70(3):109–13. [Epub 1984/03/01]. Australia: ACT Government Health Directorate, ACT Govern-
4. Byles S, Ling R. Orthopaedic out-patients: a fresh approach. Phys- ment; 2008. Available from: <http://www.health.act.gov.au/
iotherapy 1989;75(7):433–7. professionals/allied-health/allied-health-projects>; [12/8/13].
5. Samsson K, Larsson ME. Physiotherapy screening of patients 28. Modernisation Agency Department of Health UK. 10 High Impact
referred for orthopaedic consultation in primary healthcare – A Changes for Service Improvement and Delivery. A Guide for
randomised controlled trial. Man Ther 2013;[Epub 2013/11/20]. NHS Managers. United Kingdom: UK Department of Health;
6. Comans TA, Clark MJ, Cartmill L, et al. How do allied health 2004. Available from: <http://www.skane.se/Upload/Webbplatser/
professionals evaluate new models of care? What are we measuring Utvecklingscentrum/dokument/10%20bra%20punkter%20
and why? J Healthc Qual 2011;33(4):19–28. [Epub 2011/07/08]. NHS1.pdf>; [01/10/2013].
7. Dunlop B, McLaughlin L, Goldsmith C. Non-physician triage in 29. Department of Health UK. Freedom to Practice: Dispelling the
patients with low back pain, sciatica and spinal stenosis. J Bone Joint Myths. London: United Kingdom UK Department of Health;
Surg Br 2011;93-F(Suppl. IV):584. 2003. Available from: <http://webarchive.nationalarchives.gov.uk/+/
8. Aiken A. Improved use of allied health professionals in the health www.dh.gov.uk/en/Publicationsandstatistics/Publications/
care system: the case of the advanced practice physiotherapist in PublicationsPolicyAndGuidance/DH_4061524>; [01/12/2013].
orthopedic care. World Hosp Health Serv 2012;48(1):28–30. [Epub 30. Department of Health UK. Meeting the Challenge: A Strategy for
2012/09/29]. the Allied Health Professionals. London: United Kingdom
9. Aiken AB, Harrison MM, Atkinson M, et al. Easing the burden UK Department of Health; 2000. Available from: <http://
for joint replacement wait times: the role of the expanded webarchive.nationalarchives.gov.uk/+/www.dh.gov.uk/en/publ
practice physiotherapist. J Healthc Qual 2008;11(2):62–6. [Epub icationsandstatistics/Publications/Publicationspolicyandguidance/
2008/03/26]. DH_4025477>; [01/10/2010].
10. Hockin J, Bannister G. The extended role of a physiotherapist in an 31. Department of Health UK. The NHS Plan – A Plan for Reform
out-patient orthopaedic clinic. Physiotherapy 1994;80(5):281–4. London. UK Department of Health; 2000. Available from: <http://
11. Hourigan P, Weatherley C. The physiotherapist as an orthopaedic webarchive.nationalarchives.gov.uk/+/www.dh.gov.uk/en/publica
assistant in a back pain clinic. Physiotherapy 1995;81(9):546–8. tionsandstatistics/publications/publicationspolicyandguidance/
12. Weale AE, Bannister GC. Who should see orthopaedic outpatients – dh_4002960>; [01/12/2010].
physiotherapists or surgeons? Ann R Coll Surg Engl 1995;77(2 32. Comans T, O’Leary S, Raymer M, et al. Cost-effectiveness of a
Suppl.):71–3. [Epub 1995/03/01]. physiotherapist-led service for orthopaedic outpatients. J Health
13. Daker-White G, Carr AJ, Harvey I, et al. A randomised controlled Serv Res Policy 2014;19(4):216–23.
trial. Shifting boundaries of doctors and physiotherapists in ortho- 33. Association AP. Positions Statement – Scope of Practice. Australia:
paedic outpatient departments. J Epidemiol Community Health Australian Physiotherapy Association; 2009. Available from:
1999;53(10):643–50. [Epub 2000/01/05]. <http://www.physiotherapy.asn.au/DocumentsFolder/Advocacy_
14. Hattam P. The effectiveness of orthopaedic triage by extended Position_Scope_of_Practice_2009.pdf>; [13/08/2013].
scope physiotherapists. Clinical Governance 2004;9(4):244–52. 34. Stanhope J, Grimmer-Somers K, Milanese S, et al. Extended scope
15. Pearse EO, Maclean A, Ricketts DM. The extended scope physio- physiotherapy roles for orthopedic outpatients: an update system-
therapist in orthopaedic out-patients – an audit. Ann R Coll Surg atic review of the literature. J Multidiscip Healthc 2012;5:37–45.
Engl 2006;88(7):653–5. [Epub 2006/11/30]. [Epub 2012/02/24].
16. Oldmeadow LB, Bedi HS, Burch HT, et al. Experienced physio- 35. Desmeules F, Roy JS, MacDermid JC, et al. Advanced practice
therapists as gatekeepers to hospital orthopaedic outpatient care. physiotherapy in patients with musculoskeletal disorders: a system-
Med J Aust 2007;186(12):625–8. [Epub 2007/06/20]. atic review. BMC Musculoskelet Disord 2012;13:107. [Epub
17. Aiken AB, Atkinson M, Harrison MM, et al. Reducing hip and knee 2012/06/22].
replacement wait times: an expanded role for physiotherapists in 36. Moloney A, Dolan M, Shinnick L, et al. A 6 month evaluation of
orthopedic surgical clinics. Healthc Q 2007;10(2):88–91, 6. [ Epub a clinical specialist physiotherapist’s role in a fracture clinic. Phys-
2007/05/12]. iother Irel 2009;30(1):8–15.
18. Blackburn MS, Cowan SM, Cary B, et al. Physiotherapy-led triage 37. Walton MJ, Walton JC, Bell M, et al. The effectiveness of
clinic for low back pain. Aust Health Rev 2009;33(4):663–70. [Epub physiotherapist-led arthroplasty follow-up clinics. Ann R Coll Surg
2010/02/20]. Engl 2008;90(2):117–19. [Epub 2008/03/08].
19. Vos T, Flaxman AD, Naghavi M, et al. Years lived with disability 38. Blackburn M, Cowan S, Cary B, et al. Physiotherapy-led triage for
(YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: low back pain. Aust Health Rev 2009;33(4):663–70.
a systematic analysis for the Global Burden of Disease Study 2010. 39. MacKay C, Veinot P, Badley EM. Characteristics of evolving
Lancet 2012;380(9859):2163–96. [Epub 2012/12/19]. models of care for arthritis: a key informant study. BMC Health
20. Pickersgill T. The European working time directive for doctors in Serv Res 2008;8:147. [Epub 2008/07/16].
training. BMJ 2001;323(7324):1266. [Epub 2001/12/04]. 40. Morris CD, Hawes SJ. The value of accident and emergency based
21. Kersten P, McPherson K, Lattimer V, et al. Physiotherapy extended physiotherapy services. J Accid Emerg Med 1996;13(2):111–13.
scope of practice – who is doing what and why? Physiotherapy [Epub 1996/03/01].
2007;93(4):235–42. 41. Jibuike OO, Paul-Taylor G, Maulvi S, et al. Management of soft
22. Comeau P. Crisis in orthopedic care: surgeon and resource short- tissue knee injuries in an accident and emergency department: the
age. CMAJ 2004;171(3):223. [Epub 2004/08/04]. effect of the introduction of a physiotherapy practitioner. Emerg
23. Suckley J. Core Clinical Competencies for Extended Scope Phys- Med J 2003;20(1):37–9. [Epub 2003/01/21].
iotherapists Working in Musculoskeletal Interface Clinics Based in 42. Bethel J. The role of the physiotherapist practitioner in emergency
Primary Care: A Delphi Consensus Study. Manchester, UK: departments: a critical appraisal. Emerg Nurse 2005;13(2):26–31.
College of Health and Social Care, School of Nursing, Midwifery [Epub 2005/05/26].
 40  Advanced Roles in Musculoskeletal Physiotherapy 405

43. McClellan CM, Greenwood R, Benger JR. Effect of an extended 53. Health Workforce Australia. Health Professionals Prescribing
scope physiotherapy service on patient satisfaction and the outcome Pathway (HPPP) Project Final Report. Australia: Health
of soft tissue injuries in an adult emergency department. Emerg Workforce Australia; 2013. Available from: <http://www.hwa.gov.au/
Med J 2006;23(5):384–7. [Epub 2006/04/22]. sites/default/files/HWA%20HPPP%20final%20report_LR.pdf>;
44. Anaf S, Shepherd L. Physiotherapy as a clinical service in emer- [21/11/2013].
gency departments: a narrative review. Physiotherapy 2007;93: 54. O’Connaire E, Lewis JS. Arthrographic hydrodistension for
243–52. frozen shoulder. A physiotherapy-led initiative in primary care.
45. Ball ST, Walton K, Hawes S. Do emergency department physio- 2011. Available from: <http://www.health.org.uk/media_manager/
therapy practitioners, emergency nurse practitioners and doctors public/75/programme_library_docs/Central%20London%20
investigate, treat and refer patients with closed musculoskeletal -%20Frozen%20Shoulder.pdf>.
injuries differently? Emerg Med J 2007;24(3):185–8. [Epub 55. Kilner E. What evidence is there that a physiotherapy service in
2007/03/14]. the emergency department improves health outcomes? A system-
46. Hattam P. Smeatham A. Evaluation of an orthopaedic screening atic review. J Health Serv Res Policy 2011;16(1):51–8. [Epub
service in primary care. Clin Perform Qual Health Care 2010/12/28].
1999;7(3):121–4. [Epub 2000/06/10]. 56. McClellan CM, Cramp F, Powell J, et al. A randomised trial com-
47. Department of Health UK. The Musculoskeletal Services Frame- paring the clinical effectiveness of different emergency department
work, a Joint Responsibility: Doing Things Differently. United healthcare professionals in soft tissue injury management. BMJ
Kingdom: UK Department of Health; 2006. Available from: Open 2012;2(6):[Epub 2012/11/13].
<http://webarchive.nationalarchives.gov.uk/20130107105354/ 57. Chambers I, Hide G, Bayliss N. An audit of accuracy and efficacy
http:/www.dh.gov.uk/en/Publicationsandstatistics/Publications/ of injections for subacromial impingement comparing consultant,
PublicationsPolicyAndGuidance/DH_4138413>; [23/10/2013]. registrar and physiotherapist. J Bone Joint Surg Supp II Orthop
48. Arthritis and Musculoskeletal Alliance (ARMA). The Musculoskel- Proc 2005;87-B(Suppl. II Orthopaedic Proceedings):160.
etal Map of England. United Kingdom: Arthritis and Musculosk- 58. McClellan C, Cramp F, Powell J, et al. Extended scope physio-
eletal Alliance (ARMA); 2010. Available from: <http://arma.uk.net/ therapists in the emergency department: a literature review. Phys
wp-content/uploads/2014/10/England-Musculoskeletal-map Ther Rev 2010;15:106–11.
-FINAL2.pdf>; [20/10/13]. 59. McClellan CM, Cramp F, Powell J, et al. A randomised trial com-
49. Chartered Society of Physiotherapy. Independent Prescribing Gets paring the cost effectiveness of different emergency department
legal Green Light. United Kingdom: Chartered Society of Physio- healthcare professionals in soft tissue injury management. BMJ
therapy; 2013. Available from: <http://www.csp.org.uk/ Open 2013;3(1):[Epub 2013/01/08].
news/2013/08/20/independent-prescribing-gets-legal-green- 60. Collins K, Jones ML, McDonnell A, et al. Do new roles contribute
light>; [23/10/2013]. to job satisfaction and retention of staff in nursing and professions
50. Department of Health-(UK). Allied health Professions Prescribing allied to medicine? J Nurs Manag 2000;8(1):3–12. [Epub 2000/
and Medicines Supply Mechanisms Scoping Project Report. United 10/03].
Kingdom: Department of Health (UK); 2009. Available from: 61. Dawson LJ, Ghazi F. The experience of physiotherapy extended
<http://webarchive.nationalarchives.gov.uk/+/www.dh.gov scope practitioners in orthopaedic outpatient clinics. Physiotherapy
.uk/en/Publicationsandstatistics/Publications/DH_103948>; 2004;90(4):210–16.
[20/10/2013]. 62. Cramp F. Systematic Review of Literature Evaluating Extended
51. Department of Health Queensland. A Framework for Allied Health Scope of Practice and Advanced Practice Physiotherapy Provision
Professional Prescribing Trials within Queensland Health (Revised within Musculoskeletal Healthcare. United Kingdom: Chartered
April 2013). Queensland, Australia: Queensland Department of Society of Physiotherapy; 2013. Available from: <http://www.esp
Health; 2011. Available from: <http://www.health.qld.gov.au/ -physio.co.uk/?page_id=43>; [23/10/2013].
ahwac/docs/min-taskforce/prescribefwork.pdf>; [21/11/2013]
April 2013.
52. Morris J, Grimmer K. Non medical prescribing by physiothera-
pists: issues reported in the current evidence. Man Ther
2014;19(1):82–6.
This page intentionally left blank
 PA RT I V

OVERVIEW OF
CONTEMPORARY
ISSUES IN PRACTICE

407
This page intentionally left blank
 SECTION 4 . 1

INTRODUCTION

The last 20 years in particular has seen an ever-growing rationale and evidence base. There is now widespread
body of research in the basic and applied clinical and recognition of the patient heterogeneity which is present
behavioural sciences which has shaped and undoubtedly within any ‘diagnostic label’. A major field of clinical
advanced musculoskeletal physiotherapy clinical practice. research in many conditions is addressing this problem
Clinicians, researchers and healthcare funders are seeking of heterogeneity in patient presentation. Perhaps the
research-informed and evidence-based practices to offer field which is most advanced is subgrouping of low back
to patients in their care. Despite considerable advances pain patients to inform/direct therapeutic approaches.
in knowledge of the basic and clinical sciences and The chapter on low back pain has principally been
advances in the art of clinical practice, we are not yet at devoted to the subgrouping approaches developed by
a point where any one scientific or philosophical approach physiotherapists. This is the first edition of Grieve’s
to management for a musculoskeletal disorder has the Modern Musculoskeletal Physiotherapy to include discussion
answers for all individuals. Nor is there strong evidence on musculoskeletal disorders in the extremities. Chapters
for the superiority of a particular treatment approach to in this section present current research and practice
the exclusion of all others. Thus this section has not across a scope of disorders in a particular region. For
attempted to present ‘How to treat’ monologues. Rather example, the chapter dealing with the knee discusses
the aim of this section is to inform the clinician on con­ three prevalent presentations, acute knee injuries, ante­
temporary issues in practice as well as the comprehensive rior knee pain and knee osteoarthrosis, while the chapter
practice of current musculoskeletal physiotherapy. on the shoulder covers the complexity of shoulder assess­
A somewhat eclectic approach has been taken in this ment and discusses a range of shoulder conditions in­
section devoted to clinical practice so that the reader is cluding; rotator cuff tendinopathy, subacromial pain
broadly informed about the state of present-day practice, syndrome, shoulder instability, posterior shoulder tight­
current thinking and research. In some chapters, as for ness and frozen shoulder.
example in the cervical spine, contemporary issues in the This section will hopefully inform and inspire clini­
field have been chosen and discussed. In other regions, cians and researchers towards better practice for patients
such as the thoracic spine and pelvis, there are quite dif­ with musculoskeletal disorders and provide motivation
ferent approaches to management internationally. Thus for further research and innovation to optimize their
clinicians and researchers in the field have presented patients’ quality of life.
overviews of these different approaches, including their

409
 CHAPTER 41 

Cervical Spine:
IDIOPATHIC NECK PAIN
Gwendolen Jull Deborah Falla Shaun O’Leary Christopher McCarthy
● ● ●

The personal and societal burdens of mechanical neck patient-centred management that considers the require-
pain of idiopathic origin are growing and likely reflect ments of the individual.
both contemporary occupational and lifestyle influences Patient presentations are variable. Biological, psycho-
as well as the ageing population internationally.1–6 The logical and social features differ within and between
annual prevalence of neck pain is variably reported as domains and change at various time points within the
between 30% and 50%.7,8 The annual incidence of more course of a patient’s recovery. This suggests that an
bothersome or activity-limiting neck pain is up to 13% optimal management approach is based on gaining a
and is most common in the middle-aged population.7,8 comprehensive profile of the individual patient which
Neck pain is characteristically a recurrent disorder which appreciates the diversity within, the relationships between
underscores the burden of neck pain and its effects on and relative weighting of importance of the biological,
quality of life. Episodes may occur over a lifetime with psychological and social domains in the individual at
variable degrees of recovery between occurrences. Up to initial and progressive time points. This is achieved
85% of those who experience first episode neck pain will through good communication and technical skills within
have a recurrence.9 A Swedish multi-year cohort study a clinical reasoning process. Considerable research over
found that only 11% of women and 14% of men reported the last two to three decades into mechanical neck pain
recovery periods of at least 1 year duration.7 In the USA, across biological, psychological and social domains has
neck pain ranks fourth of the 30 diseases contributing to revealed its many and varied features. This section illus-
years lived with disability.2 These statistics call for effec- trates some of this heterogeneity to support the position
tive primary, secondary and tertiary interventions for for multidimensional profiling of patients with mechani-
people with mechanical neck pain to reduce both the cal neck pain as the basis for best practice management.
personal and societal burdens.
Three distinct contemporary issues have been chosen
for discussion in relation to mechanical neck pain towards
Biological Perspectives
more effective prevention and management: Pain mechanisms are a primary consideration in diagno-
1. patient profiling sis and management of patients with neck pain. They are
2. training variable between people and disorders. For instance,
3. cervical spine mobilization and manipulation. studies investigating primary and secondary mechanical
hyperalgesia and thermal hyperalgesia have demonstrated
that central sensitization (secondary hyperalgesia) may
PROFILING PATIENTS WITH be present, but generally is a less dominant feature of
MECHANICAL NECK PAIN mechanical neck pain when compared to whiplash-
associated disorders.12–14 Nevertheless, there are specific
Patients with neck pain disorders are usually regarded instances which vary from such a generalization. For
within both medical diagnostic10 and biopsychosocial instance, Chua et al.15 demonstrated that a zygapophysial
models. The diagnostic label of mechanical neck pain is joint disorder was associated with primary hyperalgesia
used for disorders where current imaging techniques fail when it was a nociceptive source of a persistent neck pain
to identify a relevant lesion in the cervical structures, disorder. Yet when the zygapophysial joint was a nocicep-
onset is not related to a motor vehicle crash (for which tive source in patients with cervicogenic headache, it was
the term whiplash-associated disorder is used), a cervical also associated with secondary hyperalgesia and central
radiculopathy is not present and there is no evidence that sensitization.15 Pain mechanisms need to be identified in
neck pain comes from a non-musculoskeletal cause.11 the individual patient as they influence treatment deliv-
Over 80% of people with neck pain fall into the mechani- ery. The greater the sensory disturbances, the less any
cal neck pain category. The potential problem with this intervention (manual therapy or exercise) should be pain
one-dimensional term is that it can infer homogeneity in provocative in nature to avoid potential symptom aggra-
patient presentations. Likewise, the term biopsychosocial vation.16 Likewise, when there is evidence that nerve
provides no indication of consideration of the relative tissue mechanosensitivity is contributing to a patient’s
contributions of biological, psychological and social pain syndrome, whether cervicobrachial pain or cervico-
features. The consequence is the potential for prescrip- genic headache,17,18 a similar careful approach to manage-
tive and generic management approaches rather than ment is in order.
410
 41  Cervical Spine 411

The multidimensional and diverse responses to neck Studies of fear avoidance or fear of activity illustrate
pain and pathology are also evident within the senso- the conflicting results and lack of definitive evidence.
rimotor system. There is now clear evidence of a reorga- They exemplify why multidimensional profiling is neces-
nization of cervical motor control strategies. These sary, rather than making any generic assumptions for
include altered coordination between deep and superfi- patients with mechanical neck pain. Some studies have
cial neck muscles,19–21 a loss of muscles’ directional speci- found fear of activity to be a prognostic feature or a
ficity22 and increased co-activation of neck flexor and feature able to explain a reasonable proportion of the
extensor muscles during functional tasks.23,24 There are level of neck pain and disability.40,42,51 In contrast, a study
altered temporal features of muscle activity demonstrated of health workers with neck pain found that fear avoid-
by an increased latency between the onset of the deltoid ance was not a risk factor.41 Other studies have found that
muscle and onset of the neck muscles with rapid arm fear of movement was more evident in patients in the
movement25,26 and delayed activation of the neck muscles acute state but not so evident in patients in the subacute
during full body perturbations.27 People with neck pain phase or in patients with persistent disorders.52–55 In most
display reduced strength and endurance at various con- studies, the scores on the various questionnaires used to
traction intensities and their neck muscles demonstrate examine fear constructs (Fear-Avoidance Beliefs Ques-
increased fatigability.28–30 Patients may present with tionnaire,56 Tampa Scale for Kinesiophobia,57 Pictorial
altered joint position and/or movement sense and control, Fear of Activity Scale-Cervical58) were either quite low
impaired balance and altered oculomotor control particu- or within normal range with few patients exhibiting high
larly when there are complaints of light-headedness scores.48,52–55 In view of such low scores, Cleland et al.59
or unsteadiness in association with neck pain and/or suggested that the experience of idiopathic, mechanical
headache.31–36 In summary, disturbances in sensorimotor neck pain may not provoke the same level or type of fear
function are a common feature of neck pain disorders but as might the experience of low back pain. Thus it would
their presence and magnitude varies considerably between seem that fear avoidance has some role in mechanical
patients.37 This exemplifies the necessity for individual neck pain in the acute stage but may not have a substan-
profiling when prescribing patient-specific exercise tial moderating effect on recovery for the majority of
programmes. patients in the subacute or persistent stages of mechanical
neck disorders.
Features other than fear-avoidance beliefs may con-
Psychological Perspectives tribute to a greater extent to persistent disability in
Pain is an individual sensory and emotional experience. patients with neck pain. Nevertheless it seems that psy-
The adoption of the biopsychosocial model spurred an chological responses are not a major feature in most
increase in research into psychological features. Most patients with mechanical neck pain. For instance, Verha-
research initially concerned low back pain and then inter- gen et al.49 studied patients with mechanical neck pain in
est was directed towards neck pain disorders. Whiplash- primary care. They found that pain severity and catastro-
associated disorders have received the greatest attention, phizing modified treatment success, but catastrophizing
being compensable disorders with some unique psycho- scores were not high. Mercardo et al.45 found that poor
logical reactions (e.g. post-traumatic stress symptoms) coping skills only predicted the 9% of their cohort (n =
identified.38 Here the focus is on findings in persons with 571) with very disabling neck or back pain. More research
idiopathic mechanical neck pain. is required to understand the incidence and role of psy-
Some level of anxiety and depression accompanies chological and behavioural features in mechanical neck
pain regardless of its source.39 Various psychological pain. However, at this point in time, it would seem that
features have been identified in association with the they may have a substantive role in only the minority of
neck pain experience, including fear avoidance, soma- patients, which emphasizes the need for individual
tization, catastrophization, poorer physical health and profiling.
well-being,40–43 as have behavioural factors such as
illness beliefs, coping skills44–46 and pain self-efficacy.47
The moderating effect of various psychological features
Social Perspectives
on the course of recovery of patients with mechani- In considering social perspectives, extensive research has
cal neck pain has received attention.42,45,48,49 A recent been undertaken into work-related neck pain. Generally,
overview of systematic reviews on prognostic factors50 work absenteeism is not as great a problem for persons
found that there was limited evidence of significant with neck disorders as it is in low back pain. Office or
associations, and thus very low confidence in the sedentary workers with mechanical neck pain in the main
risk, between several psychological and behavioural attend work (presenteeism) albeit their neck pain results
features and recovery from mechanical neck pain. in loss of productivity which is a problem in itself.60
The features with more substantive evidence of mod- Several social features have been identified as moderating
erate risk were a history of musculoskeletal disorders work-related mechanical neck pain. They include low
in other body regions and older age. This lack of supervisor support, high job demands, low co-worker
evidence does not necessarily mean that psychological support, poor job satisfaction and low job control as well
features have little role in the course of mechanical as work features (occupation type, manual labour, sustain
neck pain. Rather at this point in time there are work postures, awkward work postures) and poor physi-
too few studies or studies have produced conflicting cal work environment.6,61–65 A recent systematic review65
results. concluded that the most consistent predictors of
412 PART IV  Overview of Contemporary Issues in Practice

occupational neck pain were social factors of high job The information from psychological questionnaires
demands and low levels of supportive leadership and should be used constructively to inform the therapeutic
work features of sustained neck flexion and lifting in approach, rather than be regarded as a negative prognos-
awkward postures. Psychological distress was not a risk tic feature.68 As mentioned above, many of the psycho-
factor, as was also determined by Walton et al.50 Interest- logical features are normal but unhelpful reactions to
ingly, a study of health-care workers did not find associa- pain (Yellow Flags). For instance, fear of movement is a
tions between high job strain, low supervisor support and normal and understandable response when neck pain is
neck pain,41 which again emphasizes the need for indi- in the acute stage. It directs management to include
vidual and multidimensional profiling in assessment and assurance and education about pain and movement along
management of the patient with mechanical neck pain. with interventions to reduce the pain and increase motion.
It is artificial to consider physical, psychological or Fear usually declines as pain resolves.69 It would not be
social features separately. As examples of how they may unusual for the patient to have some anxiety associated
interact, Johnson et al.66 found that high supervisor with a pain state. Good clinician–patient communication
support, decision authority and skill discretion reduced skills, empathy and education can assure the patient and
the impact of several physical risk factors for neck pain help relieve the anxiety often associated with ‘the
in female office workers. Thompson et al.43 determined unknown’ about their pain or disorder. Likewise, it is
that greater catastrophizing and lower pain vigilance and important to understand patients from perspectives of
awareness together, moderated greater pain intensity and coping skills, pain self-efficacy and perceived barriers to
McLean et al.47 found that pain self-efficacy mediated the recovery. Clinicians may need to apply behavioural modi-
relationship between neck pain and disability and upper fication and health coaching skills to optimize recovery,
limb disability. Thus, true to the biopsychosocial model, particularly with regard to concordance to management
the different elements of the model may interact and strategies.
have the potential to positively or negatively influence There will be some patients with neck pain who
neck pain. present with abnormally elevated scores on question-
naires for various psychological behaviours and beliefs or
who demonstrate persisting abnormal illness behaviours,
Patient Profiling in Clinical Practice increasing the weighting of the psychological domain.
Mechanical neck pain needs to be considered from mul- The clinician should endeavour to understand why a
tidimensional perspectives in the context of the biopsy- person, for example is scoring highly on a catastrophiza-
chosocial model. As illustrated, each domain has multiple tion scale, and provide education and implement strate-
dimensions and the weighting of each domain can be gies that may assure or help relieve their distress within
very different between patients. An optimal management the management programme. If issues persist, however,
approach is based on gaining a comprehensive profile referral to a clinician with appropriate advanced skills in
of the individual patient that appreciates the diversity behavioural modification or managing the patient in col-
and weights the biological, psychological and social laboration with an appropriately qualified practitioner
aspects. such as a psychologist may be beneficial. It should be
We propose that from the biological perspective, it is noted that scores from psychological questionnaires
necessary to understand physiological pain mechanisms provide an indication of certain psychological symptoms,
and identify sources of peripheral nociception in the rather than a diagnosis. A diagnosis requires a clinical
articular, neural and muscle systems that might benefit examination by a qualified practitioner such as a psy-
from physical therapies. Likewise it is necessary to fully chologist. The clinician should be alert to abnormally
profile the functional status of these systems in the upper elevated scores on questionnaires. These may be an indi-
quadrant through the assessment of posture, local and cator of, for instance, severe psychological distress (which
regional cervical and thoracic motion, nerve tissue motion may or may not be associated with the neck disorder) or
and neck and axio-scapular muscle function. Clinical a true psychopathology such as depression. In such cir-
assessment of kinaesthetic sense, balance and oculomotor cumstances a timely referral to an appropriate health
control is relevant especially in patients with symptoms professional is required.
of light-headedness or unsteadiness in association with In instances of occupationally related neck pain in
their neck pain.67 Within a clinical reasoning framework particular, the social domain will assume a greater weight-
the relationship between these sensorimotor impair- ing. There is considerable evidence for the association
ments and the patient’s pain and functional complaints as between work-related physical exposures and neck pain.70
well as how the dysfunction in one system relates to or It is vital that any physical aspect of work that is a poten-
moderates function of another system must be under- tial driver or moderator of the neck pain state is identified
stood to profile the patient and prescribe patient-specific and rectified as much as is possible to gain long-term
multimodal management. health benefits for the patient. Likewise, the clinician
The research into psychosocial features of patients must gain an insight into the patient’s work environment
with mechanical neck pain of idiopathic origin indicates with the knowledge that, for example, low supervisor
that in the majority of cases, psychological factors are support, most likely in association with other features,
likely to be a normal illness behaviour and often scores can moderate the course of recovery and outcome. Nego-
on psychological questionnaires are not high. This sug- tiations with workplace personnel and knowledge of
gests that the weighting of this domain may be less than workplace legislation may help modify these effects to
the biological domain for the majority of these patients. achieve desired outcomes.
 41  Cervical Spine 413

Summary Statement strength and endurance,82–84 force steadiness30,73,85 and

acuity of movement.86,87
The biopsychosocial model emphasizes the interactions
between different domains and stresses the importance of
the interaction between domains in a patient’s musculo-
Training for Pain Relief
skeletal pain state. There is no argument that mechanical Similar changes in perceived neck pain and disability have
neck pain is positioned well within the biopsychosocial been observed for various exercise programmes ranging
model and no suggestion that patients present within from low-load training to improve neuromuscular control
only one domain of the model. Rather it is suggested that and posture,88 to high-load training to improve muscular
the weighting of the relative importance of biological, strength and endurance.89,90 Thus various training
psychological and social domains varies between patients approaches may be appropriate for the management of
and that multidimensional profiling of patients is neces- pain. However, patients may respond to different exercise
sary to offer best practice patient-centred care. protocols depending on the stage of their disorder and
their level of pain and disability.71 For instance, gentle
low-load exercise of the neck produces a superior imme-
TRAINING diate hypoalgesic effect compared to higher load exer-
cise91 (Fig. 41-1) and thus may be more appropriate in
Numerous studies support the prescription of exercise for the initial stages of rehabilitation where the focus is on
the clinical management of mechanical neck pain.67,71 In pain relief.
particular, exercise aimed at improving neuromuscular
control of the cervical spine and shoulder girdle has Training to Restore
shown the strongest evidence of effect of all conservative
therapies for mechanical neck pain, particularly when
Neuromuscular Function
combined with manual therapy.72 The prescription of this Therapeutic exercise of the neck has been shown to
form of exercise is justified by the numerous sensorimo- induce alterations in neck muscle behaviour in patients
tor impairments that have been identified in mechanical with mechanical neck pain including changes in the
neck pain including alterations in the timing and ampli- amplitude88,92,93 and specificity94 of neck muscle activity
tude of activation of the neck and axio-scapular muscles (Fig. 41-2), as well as timing of muscle activity during
during tasks of the cervical spine20,22,25,73,74 and upper postural perturbations.92 Changes in the physical struc-
limb,23,75,76 increased muscle fatigability,28,77 physical ture of the neck muscles have also been demonstrated
changes in muscle size,78 and fibre type composition.79–81 following neck exercise programmes including changes
Ultimately, these alterations contribute to impaired at the cellular level,95 as well as improvements in strength
motor output which include deficiencies in contractile and endurance.90,92,93 Although these studies confirm that

Craniocervical flexion Cervical flexion

FIGURE 41-1  ■  (A) Patients with chronic neck

pain were randomized into two training
groups. The craniocervical flexion exercise A
involved a nodding movement of the head
which remained in contact with the support­ 130
ing surface. The flexion motion occurs pre­ Craniocervical flexion
dominantly about the upper cervical motion 125 Cervical flexion
segments. In contrast in the cervical flexion
exercise, the head is lifted off the supporting 120
PPT (kPa)

surface and flexion occurs predominantly

about the lower cervical motion segments.  115
(B) Change in pressure pain threshold re­
corded over the most symptomatic cervical
110
motion segment immediately following one
session (~3 minutes) of exercise. Note the sig­
nificantly increased pressure pain threshold 105
(reduced pain sensitivity) following the cra­
niocervical flexion exercise only. (Reprinted 100
B Pre-intervention Post-intervention
with permission from O’Leary et al.91)
414 PART IV  Overview of Contemporary Issues in Practice

Contol versus Pre–post Pre–post

neck pain Training No intervention
Neck pain Control Pre Post Pre Post
0° 0° 0° 0° 0° 0°
Right sternocleidomastoid

Right sternocleidomastoid

Right sternocleidomastoid
330 30 330 30 330 30 330 30 330 30 330 30
300 60 300 60 300 60 300 60 300 60 300 60

270 90 270 90 270 90 270 90 270 90 270 90

240 120 240 120 240 120 240 120 240 120 240 120

210 150 210 150 210 150 210 150 210 150 210 150
180 180 180 180 180 180

0° 0° 0° 0° 0° 0°
330 30 330 30 330 30 330 30 330 30 330 30
Right splenius capitis

Right splenius capitis

Right splenius capitis

300 60 300 60 300 60 300 60 300 60 300 60

270 90 270 90 270 90 270 90 270 90 270 90

240 120 240 120 240 120 240 120 240 120 240 120

210 150 210 150 210 150 210 150 210 150 210 150
180 180 180 180 180 180

A B C
FIGURE 41-2  ■  (A) Representative directional activation curves obtained from the right sternocleidomastoid and splenius capitis
muscles during a circular contraction performed at 15°N with change in force direction in the range 0–360°, for a control subject
and a patient with chronic neck pain. The directional activation curve represents the modulation in intensity of muscle activity with
the direction of force exertion. Note the defined activation of the sternocleidomastoid and splenius capitis for the control subject
with minimal activity during the antagonist phase of the task. Conversely, the directional activation curves for the patient indicate
more even activation levels of each muscle for all directions. (B) Representative directional activation curves for a patient with
chronic neck pain performing the circular contraction at 15°N at baseline and at week 9, following an 8-week specific training inter­
vention. Note that at baseline the patient shows undefined directional activation curves of their neck muscles largely due to
co-activation of the neck muscles when acting as an antagonist, that is, activation of the sternocleidomastoid muscle during the
extension phase of the contraction and activation of the splenius capitis during the flexion phase of the contraction. However, after
training the patient from the exercise group displays more defined directional activation curves which more appropriately reflect
the anatomical action of the muscle. (C) In contrast, no change in the directional activation curves was observed for a patient assigned
to the control group (no intervention). (Reprinted with permission from Falla et al.94)

motor function can be modified by exercise in mechanical two exercise protocols) or active movement training
neck pain, it is relevant to compare the specific changes (despite an emphasis on correct movement patterns
achieved by different training interventions. In contrast during training)93 (Fig. 41-3). As expected from earlier
to the similar effects on clinical symptoms, neuromuscu- studies,26,97 substantially greater gains in neck muscle
lar changes in response to training are specific to the endurance were acquired by the endurance training
mode of exercise performed. For example, low-load coor- group compared to the other training groups.93 Thus
dination training, but not high-load strength training, is higher load resistance training can be introduced in the
effective in increasing the activation of the deep cervical rehabilitation programme with the aim of inducing mor-
flexor muscles in mechanical neck pain,92 restoring the phological adaptations in order to ameliorate endurance
coordination between the deep and superficial flexors,92 and strength of selected muscles and movements also
enhancing the speed of activation of the deep muscles known to be associated with mechanical neck pain.82–84
when challenged by a postural perturbation92 and improv- Such exercises typically follow later in the rehabilitation
ing the patient’s ability to maintain an upright posture of programme, once more specific changes in motor control
the cervical spine during prolonged sitting.96 In contrast, have been addressed.67
neck exercise programmes utilizing higher load endur-
ance and strength protocols have shown superior gains in
cervical muscle strength, endurance and resistance to
Transfer to Function
fatigue compared to coordination training.93,97 These A primary focus of rehabilitation is retraining capacity to
clinical studies confirm basic studies in exercise physiol- perform daily functional activities that are often work-
ogy which show that specific neuronal98 and muscle related. Specific technique correction of functional activ-
changes99 are dependent on the primary behavioural ities is recommended as a means of normalizing muscle
demand of training undertaken.98–101 behaviour during problematic functional tasks67 such as
Differences in the change in neck muscle behaviour the correction of aberrant scapular orientation during
induced by exercise may even occur when the biome- typing.75 Importantly, optimizing muscle control when
chanical demands of two exercises are similar. A reduc- training a functional task requires specific instruction and
tion in superficial neck flexor muscle activity during a task facilitation. For example, enhanced activation of the
of craniocervical flexion was observed in patients with longus colli/longus capitis and lumbar multifidus muscles
mechanical neck pain after 10 weeks of low-load through- has been shown in patients with mechanical neck pain
range craniocervical flexion (coordination) training, but during a therapist-facilitated postural correction exercise
not following isometric craniocervical flexion endurance compared to independent sitting correction.102 What is
training (despite biomechanical similarities between the unknown at this stage, however, is the degree to which
 41  Cervical Spine 415

10, 26 10, 26
10 10
0.7

0.6

0.5
Normalized RMS

0.4

0.3

0.2

0.1

0.0
22 24 26 28 30 22 24 26 28 30 22 24 26 28 30
Endurance training Coordination training Mobility training
FIGURE 41-3  ■  EMG activity (normalized root mean square) of the sternocleidomastoid muscles during the progressive stages of the
craniocervical flexion test (22–30) for all three training groups at baseline (open circles), and after 10 weeks (grey circles) and 26
weeks (black circles). The brackets denote significant between-group differences for a single stage of the craniocervical flexion test
at 10 weeks (10) and/or 26 weeks (26). Note only the group who performed specific coordination training demonstrated a change
in the coordination measure (reduced superficial muscle activity during the craniocervical flexion test) in response to training.
(Reprinted with permission from O’Leary et al.93)

specific changes in muscle control induced during formal activation of their deep cervical flexors prior to training
exercise of muscle groups are transferred to the perfor- (Fig. 41-4).105 This study also demonstrated that the
mance of functional tasks. While there is some initial degree of improvement in motor control was associated
evidence that specific neck exercise can alter postural with the extent of symptomatic improvement.105 Thus
orientation during functional tasks in sitting,96,103 the although training is relevant to some degree for all
degree of transference of muscle behaviour changes patients with mechanical neck pain, the extent to which
between specific exercise and functional activities is therapeutic exercise will benefit the patient from the
inconclusive. In the reverse scenario, there is some evi- point of view of pain will vary between individuals. These
dence that specific training of posture will improve neck findings suggest that exercise interventions will be most
muscle behaviour and reduce superficial neck flexor effective when targeted to findings of a precise assess-
muscle activity during the craniocervical flexion task.104 ment of the patients’ neuromuscular control and deliv-
These studies collectively support clinical recommenda- ered within a multimodal context in which several
tions to include specific training of problematic func- modalities may be used to address the pain.
tional activities to optimize patterns of muscle behaviour
during rehabilitation.67 Exercise Dosage to Address Recurrence
Neck pain disorders are recurrent in nature.9 Logically,
Variability in Response to Training good neuromuscular control would contribute substan-
There is considerable variability in the extent of impair- tially to primary prevention and especially to secondary
ment in neuromuscular control of the cervical spine and tertiary prevention towards decreasing recurrence
between individuals with mechanical neck pain.23 This rate and slowing disease progression. Impaired neuro-
variability is partially related to the magnitude of the muscular control does not necessarily automatically
patient’s neck pain intensity. For instance, augmented resolve following relief of pain,88,106 which emphasizes
sternocleidomastoid and anterior scalene muscle activity the necessity for adequate rehabilitative exercise to
during repetitive arm movements is greatest in patients restore normal muscle function (Fig. 41-5). At present,
reporting higher levels of pain and disability.23 Further- there is little specific knowledge of what ‘dosage’ of exer-
more, higher levels of pain are associated with greater cise is required to restore ‘normal’ cervical neuromus-
delays in the activation of the deep cervical flexors during cular control and research is required to address this
postural perturbations and lower amplitude of activation issue. Outcomes of exercise in clinical trials are usually
during isometric craniocervical flexion.37 The variability presented as the average changes for the cohort in the
of motor control impairments in patients with mechani- measures of the muscle function under investigation.
cal neck pain partly explains the variable symptomatic This may signify improvement but it does not tell if full
benefit experienced by patients from neck exercise pro- rehabilitation of the impairment was achieved for any or
grammes.88,92 Recent work has shown that specific train- all individuals in the cohort. It would be a step forward
ing of the deep cervical flexor muscles in patients with for outcome data to also be presented in terms of what
chronic neck pain reduces pain and increases the activa- percentage of the group returned to values within, for
tion of these muscles, especially in patients with the least example, the 95% confidence intervals of a healthy
416 PART IV  Overview of Contemporary Issues in Practice

140 4

intensity post-training (VAS)

Change in DCF normalized

Change in average pain

RMS post-training (%)
120
2
100
80 0

60 –2
40
–4
20
0 –6
10 20 30 40 50 60 –10 0 10 20 30 40 50 60
DCF normalized RMS pre-training (%) Change in DCF normalized
A B RMS post-training
FIGURE 41-4  ■  (A) Scatter plot of pre-training normalized deep cervical flexor (DCF) electromyographic (EMG) amplitude (root mean
square [RMS]) and the percentage change in DCF EMG amplitude values after 6 weeks of specific training of the DCF muscles in a
group of patients with chronic neck pain. (B) Scatter plot of post-training normalized DCF EMG amplitude and change in average
neck pain intensity rated on a visual analogue scale (VAS) post training. (Reprinted with permission from Falla et al.105)

0 0 4

Change in pressure (mmHg)

Headache frequency (days)

3
Neck pain index (%)

–4
–1
2
–8
1
–2
–12
0

–16 –3 –1
Pre Post 3 mth 6 mth 12 mth Pre Post 3 mth 6 mth 12 mth Pre Post 3 mth 6 mth 12 mth
A B C

Exercise Manual therapy and exercise Manual therapy Control

FIGURE 41-5  ■  Data from participants with cervicogenic headache randomized into four groups: manual therapy, exercise, manual
therapy combined with exercise, and a control (no intervention) group. Mean values for the (A) Northwick Park Neck Pain Question­
naire, (B) headache frequency and (C) change in pressure on the clinical test of craniocervical flexion recorded at baseline, in the
week immediately after treatment (week 7) and 3, 6 and 12 months (mth) after the intervention. Note that although each intervention
group demonstrated a reduction in neck pain intensity and headache frequency, only the groups that received specific muscle
rehabilitation (exercise or manual therapy combined with exercise) improved their performance on the craniocervical flexion test
(clinical test of deep cervical flexor muscle activation). (Reprinted with permission from Jull et al.88)

population. This would start to provide insight and effects on neck pain and disability, cervical motor
promote further research into dosage parameters (fre- adaptations to training are dependent on the specific
quency, intensity and duration of training) required for behavioural demands of the training tasks. Changes in
‘normalization’ of cervical muscle function. It would also motor behaviour acquired with exercise have question-
inform on whether it is possible to ‘normalize’ muscle able transference to daily functional activities and exer-
function in all persons after an episode of neck pain or cise should incorporate training of cervical/shoulder
whether in some, subclinical pathology may drive a level girdle muscles as well as technique correction of prob-
of dysfunction.107 At present, the costs of health care are lematic functional activities. The outcome of training
a primary consideration of governments and insurers will likely be best when exercise is tailored to the patient’s
around the world. If knowledge of dosage suggests that presenting neuromuscular deficits. Further knowledge is
extended interventions are necessary to ‘normalize’ required about appropriate dosage of exercise.
muscle function, the cost benefits of extended interven-
tions would have to be clearly demonstrable for any
translation in primary or secondary health-care proto- CERVICAL SPINE MOBILIZATION
cols. These would include decreasing recurrence rates AND MANIPULATION
and lifetime costs of neck pain and increasing quality of
life and productivity. There is strong evidence supporting the benefits of
manipulative therapy in the management of mechanical
neck pain, albeit best when combined with exercise. Yet
Summary there is still uncertainty regarding the most appropriate
Exercise is a key element of any rehabilitation pro- application of this therapy particularly with regard to
gramme for patients with mechanical neck pain. Although cervical manipulation. It is difficult to draw clear conclu-
various exercise protocols may have similar beneficial sions regarding the effectiveness of spinal manipulation
 41  Cervical Spine 417

compared to cervical mobilization for mechanical neck use with chronic low back pain.134,135 Combining spinal
pain. The terminologies of mechanical neck pain and manipulation with a neck exercise programme has been
spinal manipulation are ‘catch all’ terms, which make shown to be more effective than the provision of spinal
precise estimates of effect difficult. Cervical mobilization manipulation alone.136,137 The latest Cochrane Review
refers to low-frequency, oscillatory or sustained passive comparing outcomes of manipulation versus mobiliza-
movement typically aiming to encourage movement of tion of the neck concludes there is no difference in pain-
intervertebral segments along the planes of their zyg- relieving effect between the two passive modalities.128
apophysial joints. Spinal manipulation as yet does not Data from Leaver et al.,138 who compared the rate of pain
have a universally accepted definition (see Chapter 29). reduction and recovery of function in acute mechanical
After a review of the mechanisms of the technique, a neck pain, also showed equivalent outcomes for spinal
definition was proposed to facilitate discussion in the manipulation and mobilization. Some authors have
field. The definition suggested is as follows: shown a greater reduction in pain with spinal manipula-
tion compared to mobilization in the very short term,
Spinal manipulation is the application of rapid movement suggesting a greater transient analgesic effect of spinal
to vertebral segments producing joint surface separation, manipulation.139,140 However, the addition of spinal
transient sensory afferent input and reduction in perception manipulation to a course of mobilization treatments does
of pain. Joint surface separation will commonly result in not appear to add any additional clinical benefit.141 There
intra-articular cavitation, which in turn, is commonly is some debate regarding the effect of spinal manipulation
accompanied with an audible pop. Post manipulation on range of cervical movement. One review suggests
reductions in pain perception are influenced by supraspinal there is some increase in range of movement with manip-
mechanisms including expectation of benefit. ulation, compared to sham treatment,113 while other
authors demonstrate equal improvements in cervical
Spinal manipulation is commonly undertaken to reduce range of movement when mobilization and manipulation
patients’ pain and impairment.108 The spine is positioned treatments were compared.112
in a manner such that when rapid passive movement is There has also been a discussion of the validity of the
applied, gapping of spinal joint surfaces occurs.109–111 As assumed need for localization of spinal manipulation
a consequence there may be transient alterations in spinal techniques to particular symptomatic levels, as improve-
biomechanics,111–113 pain perception114–116 and muscle ments in neck pain have been demonstrated with manip-
recruitment,117–120 with the magnitude of effect being ulation techniques applied to the thoracic spine.142–144 In
influenced by the patient’s expectations and other psy- addition, the validity of the passive testing procedures
chological features.121,122 In light of these observations it used to identify symptomatic levels to which spinal
would seem likely that the utilization of manipulative manipulation techniques are targeted, is only moder-
therapy (mobilization or manipulation) could facilitate ate,145 and the application of spinal manipulation tech-
the effectiveness of exercise programmes, designed to niques, targeted to symptomatic levels, provides equivocal
regain cervical motor control. However, many questions pain relief compared to manipulation randomly applied
remain regarding the specific technique selection. The to any level of the cervical spine.146 However, one study
uncertainty regarding the specific objectives of spinal showed superior short-term reduction in neck pain relief
manipulation and the complex interaction of its mecha- for those receiving cervical spinal manipulation com-
nisms suggest that more mixed-methods research is pared to those who received thoracic spinal manipula-
required before we fully understand the rationale behind tion.69 While there are clinical rationale for the benefit
selection, integration and application of this complex of spinal manipulation not specifically applied to cervical
intervention.123 symptomatic levels (i.e. improved mobility to biome-
Controversy and clinician concern regarding the use chanically dependent adjacent regions such as the tho-
of spinal manipulation in the cervical region is magnified racic spine), it would appear that the beneficial effect of
by the small chance of serious neurovascular adverse non-specific spinal manipulation may be due to other
events that have been reported to occur in response to factors. For example, the response also appears to be
cervical manipulation.124,125 Research to establish the mediated by expectation of effect. Those expecting
profile of patients who are most likely to benefit and have improvement have greater pain reduction.147,148 Expecta-
the lowest concomitant risk of serious adverse events, is tion of benefit is one of the predictive features of greater
in its infancy.126,127 However, despite uncertainties within pain relief.126 The therapeutic effects of spinal manipula-
the literature one can have reasonable confidence in the tion may also be widespread due to their known neuro-
assertion that neck pain is reduced with the utilization of physiological effects.
spinal manipulation.128,129 Associated with this are reduc-
tions in neck disability and health costs.130,131 Spinal
manipulation is both clinically and cost effective in the
Neurophysiological Mechanisms of
treatment of mechanical neck pain. Spinal Manipulation

Specific Effectiveness of Cervical A number of studies have demonstrated spinal

manipulation-induced hypoalgesia in accord with
Spinal Manipulation up-regulation of noradrenergic fight-or-flight system
The use of spinal manipulation appears to be equally responses.114 In spinal manipulation-induced hypoalgesia,
effective as the provision of a home exercise programme the periaqueductal grey and rostro-ventromedial medul-
in acute132 and chronic neck pain.133 This is similar to its lary centres of the brain stem are likely to be important
418 PART IV  Overview of Contemporary Issues in Practice

components of the descending pain inhibition systems. There are a number of cardiovascular162 and connec-
These are distinct areas within the periaqueductal grey tive tissue factors127 that increase the chance of spontane-
that mediate transmission of nociceptive information. ous arterial dissection. Thus specific ‘screening’ for these
Afferent stimulation of the dorsal periaqueductal grey risk factors during the patient interview is recommended.
elicits a fight-or-flight reaction, with sympatho-excitation Furthermore, it is recommended that the practitioner
leading to a modulation of pain that is effectively attempts to establish if the patient has a pre-existing arte-
instantaneous.149 rial dissection. This is difficult as an arterial dissection
The potential for spinal manipulation to selectively may mimic common musculoskeletal presentations, with
inhibit C fibre afferent information has been highlighted the typical referral pattern of pain with an arterial dissec-
in recent studies measuring the effect of spinal manipula- tion reported in the neck and head.163 Also, in the early
tion on the extent of dorsal horn wind up (or sensitiza- stages of an arterial dissection, symptoms may be present
tion).116,150 Aδ fibre information appears to be less while signs of brainstem ischaemia may not.163 Thus,
influenced by spinal manipulation than that carried by C neurological examination (including cranial nerve exami-
fibres, suggesting that the thresholds for the Aδ transpor- nation) may be negative.164 Pain of an unusual, throbbing,
tation of instantaneous, ‘protective’ pain is less influenced ‘never experienced anything like it before’ nature are
by manipulation. This may be explained by the fact that features suggested to indicate the early non-ischaemic
simple pain sensations, carried by Aδ fibres, appear to arterial dissection (see Chapter 35).165,166
have less limbic and cortical moderation en route to the
somatosensory cortex, with less need for interpretation
of its value.151 It has been suggested that spinal manipula-
Summary
tion may rapidly adjust the maladaptive cortical inte­ In light of the equivocal effectiveness of spinal manipula-
gration of sensory afferent information,152–154 induce a tion, when compared with mobilization techniques, the
brief inhibition of the spinal motoneuron pool clinician has the option of choosing either. In some
excitability155–157 and facilitate the return of efficient patients, likely to be those with an expectation that spinal
motor control.120,152–154 manipulation will be effective, there may be a superior,
Spinal manipulation may also inhibit pain by reducing short-term improvement in pain. However, there is evi-
inflammatory cytokines in treated tissues and systemi- dence to suggest that in isolation, spinal manipulation is
cally. For example, Teodorczyk-Injeyan et al.158 assessed not superior to other manual or exercise approaches.
inflammatory cytokines in response to a single spinal Currently, we are unable to accurately predict those who
manipulative thrust compared to a sham procedure and should be offered the approach, beyond those who have
a control condition and showed a brief, systemic down- an expectation that it will be beneficial. While the practi-
regulation of pro-inflammatory cytokines. The mecha- cal technique of spinal manipulation is targeted towards
nisms of effect of spinal manipulation are clearly complex individual spinal joints, the specificity of effect is thought
and interactive and thus an understanding of both its to be poor, with the influence of spinal manipulation on
local biomechanical and wider neurophysiological effects pain being systemic in nature. Widespread pain relief and
is necessary so that treatment with spinal manipulation improvement in spinal movement can follow the applica-
can be utilized effectively. Recently a thorough discussion tion of cervical spinal manipulation. How to best opti-
and proposal of a mechanistic model of spinal manipula- mize these effects, and reduce the small risk of serious
tion was proposed by Bialosky and colleagues.147 While adverse events, requires further biomechanical, vascular
complex, the model does provide the clinician with some and neurophysiological investigation.
guidance regarding the aims and objectives of spinal
manipulation (see Chapter 29 for more detail).
REFERENCES
1. Farioli A, Mattioli S, Quaglieri A, et al. Musculoskeletal pain in
Risks of Cervical Spinal Manipulation Europe: the role of personal, occupational, and social risk factors.
Scand J Work Environ Health 2014;40:36–46.
Recently the International Federation of Orthopaedic 2. US Burden of Disease Collaborators. The state of US health,
Manipulative Physical Therapists, a subgroup of the 1990–2010. Burden of diseases, injuries, and risk factors. JAMA
World Congress of Physical Therapy, produced a docu- 2013;310:597–608.
ment discussing the screening of patients prior to cervical 3. Son K, Cho N, Lim S, et al. Prevalence and risk factor of neck
manual therapy.127 The document reflects the need to pain in elderly Korean community residents. J Korean Med Sci
2013;28:680–6.
clinically reason the individual weighting of risk and 4. Steinmetz A, Scheffer I, Esmer E, et al. Frequency, severity
benefit before selecting spinal manipulation, in light and predictors of playing-related musculoskeletal pain in profes-
of the common minor adverse reactions to spinal manip- sional orchestral musicians in Germany. Clin Rheumatol
ulation (treatment soreness for 24 hours)159,160 and the 2014;doi:10.1007/s10067-013-2470-5; [Epub ahead of print].
5. Long M, Bogossian F, Johnston V. The prevalence of work-related
rare serious neurovascular adverse events associated with neck, shoulder, and upper back musculoskeletal disorders among
dissection of a cervical artery.159 The reported risk of midwives, nurses, and physicians: a systematic review. Workplace
vertebral artery dissection associated with recent spinal Health Saf 2013;61:223–9.
manipulation is estimated to be in the order of 1.3 in 6. Carroll LJ, Hogg-Johnson S, Cote P, et al. Course and prognostic
100 000 patients under the age of 45 (interestingly, not factors for neck pain in workers. Spine 2008; 33:S93–100.
7. Skillgate E, Magnusson C, Lundberg M, et al. The age- and sex-
observed in the over-45-years age group).161 Neverthe- specific occurrence of bothersome neck pain in the general popu-
less, it is important to remember that this point estimate lation – results from the Stockholm public health cohort. BMC
is not necessarily the individual patient’s level of risk. Musculoskelet Disord 2012;13:185.
 41  Cervical Spine 419

8. Hogg-Johnson S, van der Velde G, Carroll LJ, et al. The burden 32. Woodhouse A, Vasseljen O. Altered motor control patterns in
and determinants of neck pain in the general population – results whiplash and chronic neck pain. BMC Musculoskelet Disord
of the bone and joint decade 2000–2010 task force on neck pain 2008;9:90.
and its associated disorders. Spine 2008;33:S39–51. 33. Chen X, Treleaven J. The effect of neck torsion on joint position
9. Carroll L, Hogg-Johnson S, van der Velde G, et al. Course and error in subjects with chronic neck pain. Man Ther 2013;18:
prognostic factors for neck pain in the general population. Spine 562–7.
2008;33:S75–82. 34. Tjell C, Rosenhall U. Smooth pursuit neck torsion test: a specific
10. Gellhorn A, Katz J, Suri P. Osteoarthritis of the spine: the facet test for cervical dizziness. Am J Otol 1998;19:76–81.
joints. Nat Rev Rheumatol 2013;9:216–24. 35. Yahia A, Ghroubi S, Jribi S, et al. Chronic neck pain and vertigo:
11. Acute Musculoskeletal Pain Guidelines Group Australia. Evidence is a true balance disorder present? Ann Phys Rehabil Med
Based Management of Acute Musculoskeletal Pain. Brisbane: Aus- 2009;52:556–67.
tralian Academic Press; 2004. 36. Jørgensen M, Skotte J, Holtermann A, et al. Neck pain and pos-
12. Chien A, Sterling M. Sensory hypoaesthesia is a feature of chronic tural balance among workers with high postural demands – a
whiplash but not chronic idiopathic neck pain. Man Ther 2010; cross-sectional study. BMC Musculoskelet Disord 2011;12:176.
15:48–53. 37. Falla D, O’Leary S, Farina D, et al. Association between intensity
13. Johnston V, Jimmieson NL, Jull G, et al. Quantitative sensory of pain and impairment in onset and activation of the deep cervical
measures distinguish office workers with varying levels of neck flexors in patients with persistent neck pain. Clin J Pain
pain and disability. Pain 2008;137:257–65. 2011;27:309–14.
14. Scott D, Sterling M, Jull G. A psychophysical investigation of pain 38. Sterling M, Hendricks J, Kenardy J. Developmental trajectories
processing mechanisms in chronic neck pain. Clin J Pain of pain/disability and PTSD symptoms following a whiplash
2005;21:175–81. injury. Pain 2010;150:22–8.
15. Chua N, van Suijlekom H, Vissers K, et al. Differences in sensory 39. Ligthart L, Gerrits M, Boomsma D, et al. Anxiety and depression
processing between chronic cervical zygapophysial joint pain are associated with migraine and pain in general: an investigation
patients with and without cervicogenic headache. Cephalalgia of the interrelationships. J Pain 2013;14:363–70.
2011;31:947–57. 40. Feleus A, van Dalen T, Bierma-Zeinstra1 S, et al. Kinesiophobia
16. Sterling M. A proposed new classification system for whiplash in patients with non-traumatic arm, neck and shoulder complaints:
associated disorders – implications for assessment and manage- a prospective cohort study in general practice. BMC Musculosk-
ment. Man Ther 2004;9:60–70. elet Disord 2007;8:117.
17. Nee R, Vicenzino B, Jull G, et al. Neural tissue management 41. Hoe V, Kelsall H, Urquhart D, et al. Risk factors for musculosk-
provides immediate clinically relevant benefits without harmful eletal symptoms of the neck or shoulder alone or neck and shoul-
effects for patients with nerve-related neck and arm pain: a ran- der among hospital nurses. Occup Environ Med 2012;69:
domised trial. J Physiother 2012;58:23–31. 198–204.
18. Zito G, Jull G, Story I. Clinical tests of musculoskeletal dysfunc- 42. Karels C, Bierma-Zeinstra S, Burdorf A, et al. Social and psycho-
tion in the diagnosis of cervicogenic headache. Man Ther logical factors influenced the course of arm, neck and shoulder
2006;11:118–29. complaints. J Clin Epidem 2007;60:839–48.
19. Cagnie B, Dolphens M, Peeters I, et al. Use of muscle functional 43. Thompson D, Urmston M, Oldham J, et al. The association
magnetic resonance imaging to compare cervical flexor activity between cognitive factors, pain and disability in patients with
between patients with whiplash-associated disorders and people idiopathic chronic neck pain. Disabil Rehabil 2010;32:1758–67.
who are healthy. Phys Ther 2010;90:1157–64. 44. Hurwitz E, Goldstein M, Morgenstern H, et al. The impact of
20. Falla DL, Jull GA, Hodges PW. Patients with neck pain demon- psychosocial factors on neck pain and disability outcomes among
strate reduced electromyographic activity of the deep cervical primary care patients: results from the UCLA Neck Pain Study.
flexor muscles during performance of the craniocervical flexion Disabil Rehabil 2006;28:1319–29.
test. Spine 2004;29:2108–14. 45. Mercado A, Carroll L, Cassidy J, et al. Passive coping is a risk
21. Jull G, Kristjansson E, Dall’Alba P. Impairment in the cervical factor for disabling neck or low back pain. Pain 2005;117:51–7.
flexors: a comparison of whiplash and insidious onset neck pain 46. Stenberg G, Fjellman-Wiklund A, Ahlgren C. ‘I am afraid to make
patients. Man Ther 2004;9:89–94. the damage worse’ – fear of engaging in physical activity among
22. Lindstrom R, Schomacher J, Farina D, et al. Association between patients with neck or back pain – a gender perspective. Scand J
neck muscle co-activation, pain, and strength in women with neck Caring Sci 2014;28:146–54.
pain. Man Ther 2011;16:80–6. 47. McLean S, Klaber Moffett J, Sharp D, et al. An investigation to
23. Falla D, Bilenkij G, Jull G. Patients with chronic neck pain dem- determine the association between neck pain and upper limb dis-
onstrate altered patterns of muscle activation during performance ability for patients with non-specific neck pain: a secondary analy-
of a functional upper limb task. Spine 2004;29:1436–40. sis. Man Ther 2011;16:434–9.
24. Johnston V, Jull G, Souvlis T, et al. Neck movement and muscle 48. Pool J, Ostelo R, Knol D, et al. Are psychological factors prog-
activity characteristics in office workers with neck pain. Spine nostic indicators of outcome in patients with sub-acute neck pain?
2008;33:555–63. Man Ther 2010;15:111–16.
25. Falla D, Jull G, Hodges PW. Feedforward activity of the cervical 49. Verhagen A, Karels C, Schellingerhout J, et al. Pain severity and
flexor muscles during voluntary arm movements is delayed in catastrophising modify treatment success in neck pain patients in
chronic neck pain. Exp Brain Res 2004;157:43–8. primary care. Man Ther 2010;15:267–72.
26. Jull G, Falla D, Vicenzino B, et al. The effect of therapeutic 50. Walton D, Carroll L, Kasch H, et al. An overview of systematic
exercise on activation of the deep cervical flexor muscles in people reviews on prognostic factors in neck pain: results from the Inter-
with chronic neck pain. Man Ther 2009;14:696–701. national Collaboration on Neck Pain (ICON) Project. Open
27. Boudreau S, Falla D. Chronic neck pain alters muscle activation Orthop J 2013;7:494–505.
patterns to sudden movements. Exp Brain Res 2014;232: 51. Saavedra-Hernández M, Castro-Sánchez A, Cuesta-Vargas A,
2011–20. et al. The contribution of previous episodes of pain, pain intensity,
28. Falla D, Rainoldi A, Merletti R, et al. Myoelectric manifestations physical impairment, and pain-related fear to disability in patients
of sternocleidomastoid and anterior scalene muscle fatigue in with chronic mechanical neck pain. Am J Phys Med Rehabil
chronic neck pain patients. Clin Neurophysiol 2003;114:488–95. 2012;91:1070–6.
29. Edmondston S, Björnsdóttir G, Pálsson T, et al. Endurance and 52. Äng BO. Impaired neck motor function and pronounced pain-
fatigue characteristics of the neck flexor and extensor muscles related fear in helicopter pilots with neck pain – a clinical approach.
during isometric tests in patients with postural neck pain. Man J Electromyogr Kinesiol 2008;18:538–49.
Ther 2011;16:332–8. 53. Edmond S, Cutrone G, Werneke M, et al. Association between
30. O’Leary S, Jull G, Kim M, et al. Cranio-cervical flexor muscle centralization and directional preference; and functional and pain
impairment at maximal, moderate, and low loads is a feature of outcomes in patients with neck pain. J Orthop Sports Phys Ther
neck pain. Man Ther 2007;12:34–9. 2014;44:68–75.
31. Beinert K, Taube W. The effect of balance training on cervical 54. Hanney W, Kolber M, George S, et al. Development of a prelimi-
sensorimotor function and neck pain. J Mot Behav 2013;45:271–8. nary clinical prediction rule to identify patients with neck pain that
420 PART IV  Overview of Contemporary Issues in Practice

may benefit from a standardized program of stretching and muscle scapular dysfunction. J Manipulative Physiol Ther 2012;35:
performance exercise: a prospective cohort study. Int J Sports Phys 346–53.
Ther 2013;8:756–76. 77. Falla D, Farina D. Muscle fiber conduction velocity of the
55. Osborn W, Jull G. Patients with non-specific neck disorders upper trapezius muscle during dynamic contraction of the upper
commonly report upper limb disability. Man Ther 2013;18: limb in patients with chronic neck pain. Pain 2005;116:
492–7. 138–45.
56. Waddell G, Newton M, Henderson I, et al. Fear-Avoidance 78. Elliott JM, Pedler AR, Jull GA, et al. Differential changes in
Beliefs Questionnaire (FABQ) and the role of fear-avoidance muscle composition exist in traumatic and nontraumatic neck
beliefs in chronic low back pain and disability. Pain 1993;52: pain. Spine 2014;39:39–47.
157–68. 79. Uhlig Y, Weber BR, Muntener DGM. Fiber composition and
57. Kori S, Miller R, Todd D. Kinisophobia: a new view of chronic fiber transformations in neck muscles of patients with dysfunction
pain behavior. Pain Manag 1990;Jan/Feb:35–43. of the cervical spine. J Orthop Res 1995;13:240–9.
58. Turk D, Robinson J, Sherman J, et al. Assessing fear in patients 80. Kadi F, Waling K, Ahlgren C, et al. Pathological mechanisms
with cervical pain: development and validation of the Pictorial implicated in localized female trapezius myalgia. Pain 1998;78:
Fear of Activity Scale-Cervical (PFActS-C). Pain 2008;139: 191–6.
55–62. 81. Lindman R, Hagberg M, Angqvist KA, et al. Changes in muscle
59. Cleland JA, Fritz J, Childs J. Psychometric properties of the fear- morphology in chronic trapezius myalgia. Scand J Work Environ
avoidance beliefs questionnaire and Tampa scale of kinesiophobia Health 1991;17:347–55.
in patients with neck pain. Am J Phys Med Rehabil 2008;87: 82. Falla D, Jull G, Edwards S, et al. Neuromuscular efficiency of the
109–17. sternocleidomastoid and anterior scalene muscles in patients with
60. Collins J, Baase C, Sharda C, et al. The assessment of chronic neck pain. Disabil Rehabil 2004;26:712–17.
health conditions on work performance, absence, and total eco- 83. Jordan A, Mehlsen J, Ostergaard K. A comparison of physical
nomic impact for employers. J Occup Environ Med 2005;47: characteristics between patients seeking treatment for neck pain
547–57. and aged-matched healthy people. J Manipulative Physiol Ther
61. Bugajska J, Zołnierczyk-Zreda D, Jędryka-Góral A, et al. Psycho- 1997;20:468–75.
logical factors at work and musculoskeletal disorders: a one year 84. Watson DH, Trott PH. Cervical headache: an investigation of
prospective study. Rheumatol Int 2013;33:2975–83. natural head posture and upper cervical flexor muscle perfor-
62. Carroll L, Hogg-Johnson S, van der Velde G, et al. Course and mance. Cephalalgia 1993;13:272–84.
prognostic factors for neck pain in the general population. Spine 85. Muceli S, Farina D, Kirkesola G, et al. Force steadiness in women
2008;33:S75–82. with neck pain and the effect of short term vibration. J Electro-
63. De Loose V, Burnotte F, Cagnie B, et al. Prevalence and risk myogr Kinesiol 2011;21:283–90.
factors of neck pain in military office workers. Mil Med 86. Kristjansson E, Dall’Alba P, Jull G. A study of five cervicocephalic
2008;173:474–9. relocation tests in three different subject groups. Clin Rehabil
64. Larsman P, Kadefors R, Sandsjö L. Psychosocial work conditions, 2003;17:768–74.
perceived stress, perceived muscular tension, and neck/shoulder 87. Sjolander P, Michaelson P, Jaric S, et al. Sensorimotor distur-
symptoms among medical secretaries. Int Arch Occup Environ bances in chronic neck pain – range of motion, peak velocity,
Health 2013;86:57–63. smoothness of movement, and repositioning acuity. Man Ther
65. Sterud T, Johannessen H, Tynes T. Work-related psychosocial and 2008;13:122–31.
mechanical risk factors for neck/shoulder pain: a 3-year follow-up 88. Jull G, Trott P, Potter H, et al. A randomised controlled trial of
study of the general working population in Norway. Int Arch exercise and manipulative therapy for cervicogenic headache.
Occup Environ Health 2014;87:471–81. Spine 2002;27:1835–43.
66. Johnston V, Jull G, Souvlis T, et al. Interactive effects from self- 89. Andersen LL, Jorgensen MB, Blangsted AK, et al. A randomized
reported physical and psychosocial factors in the workplace on controlled intervention trial to relieve and prevent neck/shoulder
neck pain and disability in female office workers. Ergonomics pain. Med Sci Sports Exerc 2008;40:983–90.
2010;53:502–13. 90. Ylinen J, Takala EP, Nykanen M, et al. Active neck muscle training
67. Jull G, Sterling M, Falla D, et al. Whiplash, Headache and Neck in the treatment of chronic neck pain in women: a randomized
Pain: Research Based Directions for Physical Therapies. Edin- controlled trial. JAMA 2003;289:2509–16.
burgh: Elsevier UK; 2008. 91. O’Leary S, Falla D, Hodges P, et al. Specific therapeutic exercise
68. Stewart J, Kempenaar L, Lauchlan D. Rethinking yellow flags. of the neck induces immediate local hypoalgesia. J Pain 2007;8:
Man Ther 2011;16:196–8. 832–9.
69. Puentedura E, Landers M, Cleland J, et al. Thoracic spine thrust 92. Jull GA, Falla D, Vicenzino B, et al. The effect of therapeutic
manipulation versus cervical spine thrust manipulation in patients exercise on activation of the deep cervical flexor muscles in people
with acute neck pain: a randomized clinical trial. J Orthop Sports with chronic neck pain. Man Ther 2009;14:696–701.
Phys Ther 2011;41:208–20. 93. O’Leary S, Jull G, Kim M, et al. Training mode-dependent
70. Mayer J, Kraus T, Ochsmann E. Longitudinal evidence for the changes in motor performance in neck pain. Arch Phys Med
association between work-related physical exposures and neck Rehabil 2012;93:1225–33.
and/or shoulder complaints: a systematic review. Int Arch Occup 94. Falla D, Lindstrom R, Rechter L, et al. Effectiveness of an 8-week
Environ Health 2012;85:587–603. exercise programme on pain and specificity of neck muscle activity
71. O’Leary S, Falla D, Elliott JM, et al. Muscle dysfunction in cervi- in patients with chronic neck pain: a randomized controlled study.
cal spine pain: implications for assessment and management. Eur J Pain 2013;17:1517–28.
J Orthop Sports Phys Ther 2009;39:324–33. 95. Mackey AL, Andersen LL, Frandsen U, et al. Strength training
72. Gross AR, Goldsmith C, Hoving JL, et al. Conservative manage- increases the size of the satellite cell pool in type I and II fibres of
ment of mechanical neck disorders: a systematic review. J Rheumat chronically painful trapezius muscle in females. J Physiol 2011;
2007;34:1083–102. 589:5503–15.
73. Falla D, Lindstrom R, Rechter L, et al. Effect of pain on the 96. Falla D, Jull G, Russell T, et al. Effect of neck exercise on sitting
modulation in discharge rate of sternocleidomastoid motor units posture in patients with chronic neck pain. Phys Ther 2007;87:
with force direction. Clin Neurophysiol 2010;121:744–53. 408–17.
74. O’Leary S, Cagnie B, Reeve A, et al. Is there altered activity of 97. Falla D, Jull G, Hodges P, et al. An endurance-strength training
the extensor muscles in chronic mechanical neck pain? A func- regime is effective in reducing myoelectric manifestations of cervi-
tional magnetic resonance imaging study. Arch Phys Med Rehabil cal flexor muscle fatigue in females with chronic neck pain. Clin
2011;92:929–34. Neurophysiol 2006;117:828–37.
75. Wegner S, Jull G, O’Leary S, et al. The effect of a scapular pos- 98. Adkins DL, Boychuk J, Remple MS, et al. Motor training induces
tural correction strategy on trapezius activity in patients with neck experience-specific patterns of plasticity across motor cortex and
pain. Man Ther 2010;15:562–6. spinal cord. J Appl Physiol 2006;101:1776–82.
76. Zakharova-Luneva E, Jull G, Johnston V, et al. Altered trapezius 99. Coffey VG, Hawley JA. The molecular bases of training adapta-
muscle behavior in individuals with neck pain and clinical signs of tion. Sports Med 2007;37:737–63.
 41  Cervical Spine 421

100. Fluck M. Functional, structural and molecular plasticity of mam- 123. Dieppe P. Complex interventions. Musculoskelet Care 2004;2:
malian skeletal muscle in response to exercise stimuli. J Exp Biol 180–6.
2006;209:2239–48. 124. Cassidy JD, Boyle E, Cote P, et al. Risk of vertebrobasilar stroke
101. Gabriel DA, Kamen G, Frost G. Neural adaptations to resistive and chiropractic care: results of a population-based case-control
exercise: mechanisms and recommendations for training practices. and case-crossover study. Spine 2008;33:S176–83.
Sports Med 2006;36:133–49. 125. Kerry R, Taylor AJ, Mitchell J, et al. Manual therapy and cervical
102. Falla D, O’Leary S, Fagan A, et al. Recruitment of the deep cervi- arterial dysfunction, directions for the future: a clinical perspec-
cal flexor muscles during a postural correction exercise performed tive. J Man Manip Ther 2008;16:39–48.
in sitting. Man Ther 2007;12:139–43. 126. Puentedura EJ, Cleland JA, Landers MR, et al. Development of a
103. Lee MH, Park SJ, Kim JS. Effects of neck exercise on high- clinical prediction rule to identify patients with neck pain likely
school students’ neck-shoulder posture. J Phys Ther Sci 2013;25: to benefit from thrust joint manipulation to the cervical spine.
571–4. J Orthop Sports PhysTher 2012;42:577–92.
104. Beer A, Treleaven J, Jull G. Can a functional postural exercise 127. Rushton A, Rivett D, Carlesso L, et al. International framework
improve performance in the cranio-cervical flexion test?–a pre- for examination of the cervical region for potential of cervical
liminary study. Man Ther 2012;17:219–24. arterial Dysfunction prior to orthopaedic manual therapy inter-
105. Falla D, O’Leary S, Farina D, et al. The change in deep cervical vention. Man Ther 2014;19:222–8.
flexor activity after training is associated with the degree of pain 128. Gross A, Miller J, D’Sylva J, et  al. Manipulation or mobilisa-
reduction in patients with chronic neck pain. Clin J Pain 2012;28: tion for neck pain: a Cochrane review. ManTher 2010;15:
628–34. 315–33.
106. Sterling M, Jull G, Vicenzino B, et al. Development of motor 129. Millan M, Leboeuf-Yde C, Budgell B, et al. The effect of spinal
dysfunction following whiplash injury. Pain 2003;103:65–73. manipulative therapy on experimentally induced pain: a systematic
107. Lee H, Nicholson LL, Adams RD. Cervical range of motion literature review. Chiropr Man Therap 2012;20:26.
associations with subclinical neck pain. Spine 2003;29:33–40. 130. Haldeman S, Carroll L, Cassidy JD, et al. The bone and joint
108. Bialosky JE, Simon CB, Bishop MD, et al. Basis for spinal manip- decade 2000–2010 task force on neck pain and its associated dis-
ulative therapy: a physical therapist perspective. J Electromyogr orders: executive summary. Spine 2008;33:S5–7.
Kinesiol 2012;22:643–7. 131. Michaleff ZA, Lin CW, Maher CG, et al. Spinal manipulation
109. Cramer GD, Cambron J, Cantu JA, et al. Magnetic resonance epidemiology: systematic review of cost effectiveness studies.
imaging zygapophyseal joint space changes (gapping) in low back J Electromyogr Kinesiol 2012;22:655–62.
pain patients following spinal manipulation and side-posture posi- 132. Bronfort G, Evans R, Anderson AV, et  al. Spinal manipulation,
tioning: a randomized controlled mechanisms trial with blinding. medication, or home exercise with advice for acute and subacute
J Manipulative Physiol Ther 2013;36:203–17. neck pain: a randomized trial. Ann Intern Med 2012;156:
110. Evans DW, Breen AC. A biomechanical model for mechanically 1–10.
efficient cavitation production during spinal manipulation: pre- 133. Martel J, Dugas C, Dubois JD, et al. A randomised controlled trial
thrust position and the neutral zone. J Manipulative Physiol Ther of preventive spinal manipulation with and without a home exer-
2006;29:72–82. cise program for patients with chronic neck pain. BMC Musculo-
111. Herzog W. The biomechanics of spinal manipulation. J Bodyw skelet Disord 2011;12:41.
Mov Ther 2010;14:280–6. 134. Bronfort G, Maiers MJ, Evans RL, et al. Supervised exercise,
112. Cassidy JD, Lopes AA, Yong-Hing K. The immediate effect of spinal manipulation, and home exercise for chronic low back pain:
manipulation versus mobilization on pain and range of motion in a randomized clinical trial. Spine J 2011;11:585–98.
the cervical spine: a randomized controlled trial. J Manipulative 135. Ernst E. Chiropractic spinal manipulation for neck pain: a system-
Physiol Ther 1992;15:570–5. atic review. J Pain 2003;4:417–21.
113. Millan M, Leboeuf-Yde C, Budgell B, et al. The effect of spinal 136. Bronfort G, Evans R, Nelson B, et al. A randomized clinical trial
manipulative therapy on spinal range of motion: a systematic lit- of exercise and spinal manipulation for patients with chronic neck
erature review. Chiropr Man Therap 2012;20:23. pain. Spine 2001;26:788–97.
114. Coronado RA, Gay CW, Bialosky JE, et al. Changes in pain sen- 137. Evans R, Bronfort G, Nelson B, et al. Two-year follow-up of a
sitivity following spinal manipulation: a systematic review and randomized clinical trial of spinal manipulation and two types of
meta-analysis. J Electromyogr Kinesiol 2012;22:752–67. exercise for patients with chronic neck pain. Spine 2002;27:
115. Fernandez-de-las-Penas C, Alonso-Blanco C, Cleland JA, et al. 2383–9.
Changes in pressure pain thresholds over C5–C6 zygapophyseal 138. Leaver AM, Maher CG, Herbert RD, et al. A randomized con-
joint after a cervicothoracic junction manipulation in healthy sub- trolled trial comparing manipulation with mobilization for recent
jects. J Manipulative Physiol Ther 2008;31:332–7. onset neck pain. Arch Phys Med Rehabil 2010;91:1313–18.
116. George SZ, Bishop MD, Bialosky JE, et al. Immediate effects of 139. Cassidy JD, Quon JA, LaFrance LJ, et al. The effect of manipula-
spinal manipulation on thermal pain sensitivity: an experimental tion on pain and range of motion in the cervical spine: a pilot
study. BMC Musculoskelet Disord 2006;7:68. study. J Manipulative Physiol Ther 1992;15:495–500.
117. Dishman JD, Bulbulian R. Comparison of effects of spinal manip- 140. Dunning JR, Cleland JA, Waldrop MA, et al. Upper cervical and
ulation and massage on motoneuron excitability. Electromyogr upper thoracic thrust manipulation versus nonthrust mobilization
Clin Neurophysiol 2001;41:97–106. in patients with mechanical neck pain: a multicenter randomized
118. Dunning J, Rushton A. The effects of cervical high-velocity low- clinical trial. J Orthop Sports PhysTher 2012;42:5–18.
amplitude thrust manipulation on resting electromyographic 141. Boyles RE, Walker MJ, Young BA, et al. The addition of cervical
activity of the biceps brachii muscle. Man Ther 2009;14: thrust manipulations to a manual physical therapy approach in
508–13. patients treated for mechanical neck pain: a secondary analysis.
119. Fernandez-Carnero J, Fernandez-de-las-Penas C, Cleland JA. J Orthop Sports PhysTher 2010;40:133–40.
Immediate hypoalgesic and motor effects after a single cervical 142. Cleland JA, Childs JD, McRae M, et al. Immediate effects of
spine manipulation in subjects with lateral epicondylalgia. thoracic manipulation in patients with neck pain: a randomized
J Manipulative Physiol Ther 2008;31:675–81. clinical trial. Man Ther 2005;10:127–35.
120. Haavik TH, Murphy B. The effects of spinal manipulation on 143. Cross KM, Kuenze C, Grindstaff TL, et al. Thoracic spine thrust
central integration of dual somatosensory input observed after manipulation improves pain, range of motion, and self-reported
motor training: a crossover study. J Manipulative Physiol Ther function in patients with mechanical neck pain: a systematic
2010;33:261–72. review. J Orthop Sports PhysTher 2011;41:633–42.
121. Bialosky JE, Bishop MD, George SZ, et al. Placebo response to 144. Krauss J, Creighton D, Ely JD. Podlewska-Ely J. The immediate
manual therapy: something out of nothing? J Man Manip Ther effects of upper thoracic translatoric spinal manipulation on cervi-
2011;19:11–19. cal pain and range of motion: a randomized clinical trial. J Man
122. Bialosky JE, Bishop MD, Robinson ME, et al. The influence of Manip Ther 2008;16:93–9.
expectation on spinal manipulation induced hypoalgesia: an exper- 145. Triano JJ, Budgell B, Bagnulo A, et al. Review of the methods used
imental study in normal subjects. BMC Musculoskelet Disord by Chiropractors to determine the site for applying manipulation.
2008;9:19. Chiropr Man Therap 2013;21:36.
422 PART IV  Overview of Contemporary Issues in Practice

146. Haas M, Groupp E, Panzer D, et al. Efficacy of cervical endplay 157. Dishman JD, Weber KA, Corbin RL, et al. Understanding inhibi-
assessment as an indicator for spinal manipulation. Spine 2003; tory mechanisms of lumbar spinal manipulation using H-reflex
28:1091–6. and F-wave responses: a methodological approach. J Neurosci
147. Bialosky JE, Bishop MD, Price DD, et al. The mechanisms of Methods 2012;210:169–77.
manual therapy in the treatment of musculoskeletal pain: a com- 158. Teodorczyk-Injeyan JA, Injeyan HS, Ruegg R. Spinal manipula-
prehensive model. Man Ther 2009;14:531–8. tive therapy reduces inflammatory cytokines but not substance P
148. Bishop MD, Mintken PE, Bialosky JE, et al. Patient expectations production in normal subjects. J Manipulative Physiol Ther
of benefit from interventions for neck pain and resulting influence 2006;29:14–21.
on outcomes. J Orthop Sports Phys Ther 2013;43:457–65. 159. Cagnie B, Vinck E, Beernaert A, et al. How common are side
149. Wright A. Hypoalgesia post-manipulative therapy: a review of effects of spinal manipulation and can these side effects be pre-
a potential neurophysiological mechanism. Man Ther 1995;1: dicted? Man Ther 2004;9:151–6.
11–16. 160. Carnes D, Mars TS, Mullinger B, et al. Adverse events and
150. Bialosky JE, Bishop MD, Robinson ME, et al. Spinal manipulative manual therapy: a systematic review. Man Ther 2010;15:355–63.
therapy has an immediate effect on thermal pain sensitivity in 161. Miley ML, Wellik KE, Wingerchuk DM, et al. Does cervical
people with low back pain: a randomized controlled trial. Phys manipulative therapy cause vertebral artery dissection and stroke?
Ther 2009;89:1292–303. Neurologist 2008;14:66–73.
151. Rolls ET. The functions of the orbitofrontal cortex. Brain Cogn 162. Debette S, Leys D. Cervical-artery dissections: predisposing
2004;55:11–29. factors, diagnosis, and outcome. Lancet Neurol 2009;8:668–78.
152. Dishman JD, Dougherty PE, Burke JR. Evaluation of the effect 163. Kerry R, Taylor AJ. Cervical arterial dysfunction: knowledge and
of postural perturbation on motoneuronal activity following reasoning for manual physical therapists. J Orthop Sports Phys-
various methods of lumbar spinal manipulation. Spine J 2005; Ther 2009;39:378–87.
5:650–9. 164. Kerry R, Taylor AJ, Mitchell J, et al. Cervical arterial dysfunction
153. Haavik H, Murphy B. The role of spinal manipulation in address- and manual therapy: a critical literature review to inform profes-
ing disordered sensorimotor integration and altered motor sional practice. Man Ther 2008;13:278–88.
control. J Electromyogr Kinesiol 2012;22:768–76. 165. Kerry R, Taylor AJ. Cervical arterial dysfunction assessment and
154. Haavik-Taylor H, Murphy B. Cervical spine manipulation alters manual therapy. Man Ther 2006;11:243–53.
sensorimotor integration: a somatosensory evoked potential study. 166. Taylor AJ, Kerry R. Neck pain and headache as a result of internal
Clin Neurophysiol 2007;118:391–402. carotid artery dissection: implications for manual therapists. Man
155. Dishman JD, Ball KA, Burke J. Central motor excitability changes Ther 2005;10:73–7.
after spinal manipulation: a transcranial magnetic stimulation
study. J Manipulative Physiol Ther 2002;25:1–9.
156. Dishman JD, Burke J. Spinal reflex excitability changes after cervi-
cal and lumbar spinal manipulation: a comparative study. Spine J
2003;3:204–12.
 CHAPTER 42 

Whiplash-Associated Disorders
Michele Sterling  •  Tze Siong Ng  •  David Walton  •  Ashley Smith

despite conventional imaging usually not being able to

INTRODUCTION detect such tissue damage.9 Evidence for the presence of
peripheral tissue damage stems from a combination of
Whiplash-associated disorders (WAD) are a controversial cadaveric dissection, animal and biomechanical studies,
condition associated with substantial personal and eco- together with recent studies documenting the presence
nomic costs. Most individuals with WAD incur the injury of inflammatory biomarkers in individuals with persistent
as a result of a road traffic collision but the symptoms can moderate to severe symptoms.10,11 However, the impor-
arise from other traumatic events such as sporting inci- tance of patho-anatomical lesions and underlying sources
dents. Consistent international data indicate that up to of nociception is debatable in regard to their significance
50% of those injured will not fully recover, with approxi- and relevance for the initiation and/or maintenance of
mately 30% reporting ongoing moderate to severe pain whiplash pain. This section will summarize the mecha-
and disability.1 Mental health problems are also associ- nisms of injury and symptom production following whip-
ated with the whiplash condition,2 with disorders such as lash injury, including tissue lesions that have been
post-traumatic stress disorder, depression and anxiety identified, and whether modulation of nociception
being common.3,4 The predominant symptom of WAD arising from these lesions results in improved clinical
is neck pain, but headaches, arm pain, neck stiffness, diz- outcomes.
ziness and paraesthesia/anaesthesia in the upper quadrant
are also frequently reported. Evidence Supporting the Presence
Whiplash is a controversial condition, most likely due
to it being a compensable injury where a clinical diagno-
of Tissue Damage
sis of tissue damage or lesion in the neck cannot usually Mechanisms of whiplash injury have been demonstrated
be made.5 Some still doubt the veracity of patients’ com- using high-speed cineradiography in human volunteers,12
plaints and deny it as a legitimate condition.6 This is cadaveric experiments13 and computer models.14 Essen-
despite much research data in recent years demonstrating tially, energy from the road traffic collision is transferred
the presence of both physical and psychological manifes- from the collision to the body, resulting in a cervical
tations including psychophysical indictors of augmented acceleration/deceleration motion, as the inertia of the
central nociceptive processing, movement loss, altered head reacts to this energy.15 These forces are non-
muscle recruitment patterns, morphological muscle physiological in nature16 and could theoretically result in
changes, post-traumatic stress symptoms, psychological injury to various tissues in the cervical spine. Engineers
distress, fear of movement and pain catastrophizing have responded to results of these studies, by developing
amongst others. car seats to minimize the forces individuals are exposed
It is not the aim of this chapter to discuss these changes to with whiplash trauma.17,18 As a result, neck injury rates
and for interested readers, more in-depth detail of these have reduced significantly.19 Given that the injury rates
factors and their implications for physiotherapy assess- have fallen in response to these lower forces, it can be
ment and management of WAD is available elsewhere.7 presumed that injuries to neck tissues are associated with
Rather, this chapter will focus on some current unre- whiplash symptoms.
solved issues surrounding the whiplash condition; the Supporting evidence for the presence of potential
research evidence base around these issues and their tissue damage identified in engineering studies can be
implications for the management of the whiplash condi- found from post-mortem dissection studies of non-
tion. Specifically the chapter will discuss four main issues: survivors of road traffic collisions who presumably have
(a) is there tissue damage in WAD and what is the clinical more serious injuries.20–23 Multiple injuries have been
relevance of this?; (b) is WAD a culturally dependent demonstrated, including disruption to the facet joints,
condition?; (c) the clinical relevance of outcome predic- spinal ligaments, vertebral arteries, dorsal root ganglia
tion; and (d) what needs to be done in the area of treat- and muscle tissue. Detection of these lesions has proven
ment in order to improve health outcomes? difficult, likely due to insensitivity of current radiological
imaging techniques,23,24 but has been demonstrated utiliz-
ing techniques such as cryomicrotomy (frozen sectioning
THE ROLE OF TISSUE DAMAGE IN and detailed microscopic investigation) where lesions
WHIPLASH-ASSOCIATED DISORDERS involving the capsule, ligaments and discs can be
detected.25
It is generally presumed that individuals sustain a periph- Clinical studies are also available to support the pres-
eral injury to the neck following whiplash trauma,5,8 ence of tissue damage in chronic WAD. These studies
423
424 PART IV  Overview of Contemporary Issues in Practice

have utilized diagnostic injections to provide a diagnosis Cold Pain Thresholds vs. Time
of cervical facet joint pathology and have determined that 25
the cervical facet joint is probably the most common
tissue lesion contributing to chronic WAD symptoms.26,27 20

Degrees Celcius
Injuries to the cervical facet joint are proposed to arise
from synovial fold impingement or capsular distension,8 15
and facet joint capsules are rich with nociceptors.28
In vivo animal experiments demonstrate a relationship 10
between capsular distension and altered collagen fibre
organization,29 afferent fibre sensitization,30,31 dorsal root 5
ganglion sensitization and spinal cord metabolite
changes,32,33 and behavioural sensitivity (pain)34 under 0
t(1) t(2) t(3) t(4)
experimental conditions similar to those observed in
FIGURE 42-1  ■  Changes in cold pain thresholds over time prior
simulated whiplash.35 A treatment for cervical facet joint to and following radiofrequency neurotomy of the cervical facet
dysfunction is available. Radiofrequency neurotomy joints. t(1), one month after initial preliminary cervical facet joint
(RFN) is a neuroablative technique directed at the medial blockade; t(2), immediately prior to radiofrequency neurotomy
branch of the dorsal rami of the cervical facet joints,27 of cervical facet joints; t(3), one month following radiofrequency
providing 7–14 months relief of pain,36 together with neurotomy; t(4), three months following radiofrequency
neurotomy.
resolution of psychological distress.37 The procedure can
successfully be repeated when pain returns.36
Thus convergent data from cadaveric, biomechanical and pain catastrophization.44 These changes were evident
and clinical studies indicate that tissue damage, in some within 1 month of receiving RFN and remained stable at
form, is likely following whiplash injury. 3 months. Physical measures returned to values similar
to those of a healthy control cohort. No changes were
observed in post-traumatic stress symptoms.44 Upon
The Relationship of Tissue Damage to return of pain, these findings reversed, with increased
the Clinical Presentation of Whiplash- central hyperexcitability and deterioration of neck range
of movement, pain catastrophizing and psychological dis-
Associated Disorders tress.45 Measures were not significantly different to those
The inability of current diagnostic imaging modalities to present prior to undergoing RFN.
accurately detect tissue damage in individual patients fol- Hence, these data indicate that neck tissue pathology
lowing whiplash injury presents a dilemma. However, contributes to the physical and psychological manifesta-
caution also needs to be applied when possible tissue tions of chronic WAD. However, RFN did not result in
damage is identified to determine if it is relevant to the complete resolution of pain and disability.43 This is not
patient’s symptoms and whether effective treatment for surprising, as many factors are likely responsible for
such damage is available. Magnetic resonance imaging symptom persistence, including psychological factors,
has demonstrated possible pathology of the cranioverte- the social context of the patient,46,47 compensation-related
bral ligaments38–40 in people with whiplash. However, factors,48 beliefs and expectations.49
similar ‘pathologic’ changes in these ligaments were Clinically, it is evident that individuals with chronic
observed in asymptomatic, age- and gender-matched WAD presenting with a combination of physical and
individuals and individuals with non-traumatic neck psychological manifestations may also have peripheral
pain.41 Moreover, even when detected by magnetic reso- tissue pathology. Consideration for referral for diagnostic
nance imaging, correlation with clinical symptoms is facet joint injection can be made in patients not respond-
questionable,41 and outcomes did not differ significantly ing to conservative physiotherapy treatment. These indi-
between those with high signal changes of the alar and viduals may be identified by a positive response to each
transverse ligaments compared to those without these of the following clinical tests: extension–rotation test,
changes.42 segmental tenderness and provocation of familiar neck
Moreover, evidence suggests that nociception from pain upon manual spinal examination.50 Unfortunately, at
the cervical facet joint contributes to other physiological the present time it is not possible to anaesthetize other
and psychological manifestations of the whiplash condi- cervical tissues in order to determine their role in
tion. In a recent series of studies, individuals with chronic whiplash symptoms. Until then, as in other conditions
WAD (3–4 years post-road traffic collision) underwent characterized by persistent pain, treatment directed at
RFN following successful response to diagnostic facet mechanisms and impairments underlying the disorder
joint injections. Individuals were assessed on two occa- need to be addressed.51
sions prior to undergoing the procedure (10 months
apart) and then at 1 and 3 months post-procedure as well
as at a subsequent time point upon the return of pain.
Summary
Prior to receiving RFN, no changes were measured in Convergent evidence suggests that peripheral pathology
any physical or psychological manifestations.43 Following is evident in individuals following whiplash injury. Lack
RFN, pain, disability and central hyperexcitability of diagnostic imaging evidence does not preclude the
decreased (Fig. 42-1) with concomitant increases in neck presence of a lesion, with most evidence currently
range of movement43 and reduced psychological distress supporting cervical facet joint involvement. Successful
 42  Whiplash-Associated Disorders 425

treatment of a tissue lesion demonstrated significant This was consistent with findings of sensory hypersensi-
improvements in physical and psychological manifesta- tivity found in patients with chronic WAD in Australia,
tions, but future research needs to consider other lesions Europe, Canada and the United States of America.43,70–72
and treatment options. A recent study found mechanical and thermal pain
thresholds were not significantly different between white
Australians and Asian Singaporeans with WAD when
both groups were compared directly using the same
IS WHIPLASH-ASSOCIATED DISORDER research methodology (Ng et al., unpublished data).
A CULTURALLY DEPENDENT There were differences in cold pressor pain threshold and
CONDITION? tolerance, with Singaporean patients demonstrating
lower pain thresholds and tolerance than Australian
Chronic WAD has been proposed to be a culturally patients with the cold pressor test. This was consistent
dependent condition. In Western countries such as with studies which reported higher cold pressor pain sen-
Australia, Canada and the United Kingdom, the propor- sitivity in Asian than white patients.68 Due to previous
tion of people who develop chronic WAD following a reports of lower WAD prevalence in Singapore, the find-
whiplash injury is as high as 50%.1,52 The condition is ings that Singaporeans were more pain sensitive than
purported to be less prevalent in countries such as Lithu- Australians was not expected.
ania and Germany.53–55 There has been little research on It is clear that various psychological factors including
WAD in Asian countries but an early study reported the post-traumatic stress symptoms, pain catastrophizing and
prevalence as being low in Singapore.56 While there are general distress amongst others are common in patients
no more recent data available for WAD, the prevalence with WAD.73 The lifetime prevalence of psychological
of chronic pain in general would seem to be lower in disorders of post-traumatic stress disorder, anxiety and
Singapore ranging from 9–16%57,58 compared to 19–50% depression is higher in Western than Asian countries.74–76
in Australia.59–61 Psychological factors of post-traumatic stress disorder
The prevalence of WAD may be affected by the com- symptoms and depression have also been shown to be
pensation and social systems in each society. In the prov- correlated with neck disability in patients with WAD.77,78
ince of Saskatchewan in Canada, the incidence of WAD The higher prevalence of psychological disorders in
was 417 per 100 000 persons under a fault-based motor Western than Asian countries may have implications on
insurance system and decreased to 300 per 100 000 the cross-cultural presentation of chronic WAD. A pre-
persons under a no-fault system.48 The prevalence of liminary study that compared psychological factors
chronic WAD in Brisbane, Australia, is believed to be between Australian and Singaporean patients with chronic
higher than in Singapore.56,62 Brisbane and Singapore WAD revealed no statistically significant difference in
both have a fault-based motor insurance system. Public post-traumatic stress symptom severity, depression sever-
health care is universal and the permanently disabled ity, self-efficacy, catastrophizing and fear-avoidance
receive some form of social support in both cities. beliefs between both groups (Ng et al., unpublished data).
However, unemployment social benefits are provided in However, Australian patients reported lower perceived
Brisbane while in Singapore there is an emphasis on injustice and held more positive illness perceptions. This
employment benefits and unemployment benefits are not is contrary to expectations of poorer psychological pre-
provided.63 The culture and social systems may be factors sentation in Australians given the previously reported
which affect the cross-cultural prevalence of WAD. greater prevalence of chronic WAD and chronic pain.
The cross-cultural difference in prevalence of WAD The relatively few social benefits for Singaporean patients
could also be related to cultural differences in pain per- with WAD who may have difficulty seeking employment
ception and psychological responses to pain.64–66 In the post injury could contribute to their higher level of per-
United States, African-Americans with chronic neck and ceived injustice and more negative illness perceptions.
back pain have reported greater pain and disability when However, this cultural difference between Australians
compared to Caucasians with similar conditions.64,67 A and Singaporeans did not reflect the higher prevalence of
systematic review revealed white patients generally exhib- WAD in Brisbane.
ited higher pain thresholds and pain tolerances than The social–cognitive model suggests that expectations
African-American and Asian patients in studies that used of health outcomes are shaped both by beliefs and the
experimental pain models to assess pain sensitivity,68 and sociocultural context.79 Another possible reason for the
this may explain the greater levels of pain and disability difference in WAD prevalence between various countries
in African-American patients with chronic pain condi- may be related to different beliefs and expectations about
tions. Investigation of cultural responses to pain and WAD and its recovery. There is strong evidence showing
injury in WAD is scant but recent investigation has been that health-care professionals’ beliefs are known to influ-
undertaken to directly compare chronic WAD in Singa- ence both their clinical management as well as their
pore and Australia. The results of these recent studies are patients’ beliefs about their condition.80,81 With respect to
briefly described in this section. WAD, the beliefs and expectations of the injured person
Singapore is a multiracial Asian society comprising of have been shown to predict health outcomes with studies
three major ethnic groups: Chinese, Malay and Indian. in Canada and Sweden showing that patients with acute
Singaporean patients with chronic WAD demonstrated WAD who reported more pessimistic expectations of
lowered cold and mechanical pain threshold as well as recovery had slower recovery82 and higher disability levels
cold pain tolerance, when compared to healthy controls.69 6 months post injury.83 A comparison of physiotherapists’
426 PART IV  Overview of Contemporary Issues in Practice

whiplash beliefs in Brisbane and Singapore found physio- physiotherapist prognosis is rarely about survival of the
therapists in both cities generally held beliefs that were patient. Rather, outcomes we most commonly consider
positive and consistent with clinical practice guidelines important include pain or other symptoms, function and
for WAD. However, a higher proportion of physiothera- disability, work status (or role participation), and global
pists in Singapore than Brisbane believed in a psycho- satisfaction or well-being. Such outcomes pose a unique
genic origin of WAD and also believed in more positive challenge for prognostic research, in that it is rare that
recovery for a patient vignette depicting chronic WAD.84 they can be easily dichotomized as good/bad, alive/dead,
It is unclear whether this stronger belief in a psychogenic recovered/not recovered, etc. The continuous nature of
origin of chronic WAD and more positive expectation of many clinical physiotherapy outcomes has forced
long-term outcome of chronic WAD has any relationship researchers in the area into rather difficult and sometimes
with the prevalence of chronic WAD in Singapore. arbitrary decisions about the outcomes to be predicted,
A few studies have investigated expectations about what constitutes a ‘good’ or ‘bad’ outcome, and what
WAD and its recovery on non-injured laypersons, namely early variables can and should be captured that may
employees from local utilities companies. The results predict them. WAD offers an interesting context from
indicate that Canadians hold more negative expectations which to conduct such research, as chronic problems are
than Lithuanian,85 Greek,86 and German people.87 These relatively common,1 gross structural lesions are often
studies suggest that in countries like Canada with a higher unable to explain the problems,5 and it often occurs
prevalence of chronic WAD, there is expectation of worse within a highly litigious medico-legal context that
long-term outcomes. Using the whiplash beliefs ques- requires some degree of defensibility of complaints. This
tionnaire, a recent study compared whiplash beliefs in section will summarize the current state of evidence in
laypersons in Brisbane, Australia and Singapore. There the area of whiplash prognosis, will briefly describe some
is a presumably higher prevalence of chronic WAD in of the caveats and pitfalls of research in this area, and will
Brisbane than Singapore56,62 but laypersons’ expectations offer some concrete suggestions for applying the current
of recovery and beliefs about WAD in Brisbane and Sin- evidence in clinical practice.
gapore were generally similar and mostly positive.88 The
equivocal evidence suggests that laypersons’ beliefs may
not reflect the cross-cultural differences in prevalence of
Predisposed Does Not Mean Predestined
chronic WAD. It is beyond the scope of this text to offer a comprehen-
In summary, the proposal of chronic WAD being cul- sive description of the characteristics of good prognostic
turally dependent is debatable. In Brisbane and Singa- research. Fortunately, such accounts can easily be found
pore, which have similar fault-based motor insurance on the internet, including that of Kamper and col-
systems but different social benefits for the unemployed, leagues,89 and the statement of the ‘strengthening the
patients with chronic WAD were largely similar in their reporting of observational studies in epidemiology
physical and psychological presentation. Laypersons, and (STROBE)’ group (http://www.strobe-statement.org).
physiotherapists’ whiplash beliefs in these two cities were Briefly, there are key caveats of prognostic research of
also generally similar. The cultural differences in cold which clinicians must be aware in order to make prudent
pressor pain sensitivity, perceived injustice and illness and judicious use of the evidence. Arguably the most
perceptions did not seem to reflect the higher prevalence important is an awareness of the nature of cause and
of WAD in Brisbane. Further studies are needed to more effect. In 1965, Sir Austin Bradford-Hill offered nine
accurately determine the current prevalence of chronic criteria for causality that still hold relevance today.90 The
WAD in Asian countries. Nevertheless, the largely similar criteria are presented in Table 42-1. At best, purely
physical and psychological presentation of patients with observational prognostic research, where potential pre-
chronic WAD in Brisbane and Singapore indicated that dictors are measured early and then analysed for their
clinicians may treat patients with WAD similarly in dif- association with a later outcome, can only provide evi-
ferent cultures, regardless of patients’ country, ethnicity dence for strength of association, temporality, possibly
or jurisdiction. Clinicians in Asia may adopt the recom- dose–response relationships, indirect or theoretical evi-
mendations of clinical practice guidelines written for dence for biologic plausibility, and then independent
patients with WAD in Western populations. verification could offer consistency. Therefore, while
good prospective ‘prognostic’ research can offer support
for some of the Bradford-Hill criteria, it cannot support
all of them. In practical terms this means that clinicians
THE CLINICAL RELEVANCE OF need to be willing to look critically at the evidence before
OUTCOME PREDICTION them, and decide whether a variable reported in a research
paper is in fact a causative factor.
The ability to establish a prognosis for clinical conditions As an example of the above comments, Hill and col-
is being increasingly recognized as a vital skill for clini- leagues91 conducted a large prospective study of 786
cians. When the prognosis is favourable, clinicians may people with neck pain of varying cause and duration, fol-
opt for less-intensive interventions, reassurance, advice lowing them for a period of 1 year to determine who
and education. When the prognosis is unfavourable, the continued to complain of neck pain for at least 1 day over
astute clinician will attempt to identify specific targets for the past month. Of the significant risk factors they identi-
intervention in an effort to mitigate the risk of poor fied, one was cycling. That is, those who indicated they
outcome. Unlike many medical conditions, for the cycle at least sometimes were at significantly greater risk
 42  Whiplash-Associated Disorders 427

TABLE 42-1  Criteria for Cause and Effect

Criterion Description
Strength of association The magnitude of the association (e.g. correlation, effect size) should be strong enough to
provide confidence that the cause and effect are in fact connected
Consistency of findings The association should be consistent across different samples, contexts, designs and
research groups
Specificity of the relationship In current terms, this refers to the degree to which an association is real, and not influenced
by confounders or other variables that may be related to both cause and effect but are
actually driving the association. If the cause is associated with a specific set of effects
(very specific symptoms for example, rather than a broad range of symptoms), this
criterion is satisfied
Temporality The cause MUST always occur before the effect
Dose–response relationship In most cases, more (or less) of exposure to the cause should lead to more (or less) effect.
Note however that in some conditions, the mere presence of the cause is enough to
trigger the effect so this criterion is not inherently critical in all cases
Plausibility The association between cause and effect should make sense. The burden of this criterion
falls largely on the authors who should make the case for at least a theoretical connection
between cause and effect
Coherence Refers to a more general coherence of findings between large-scale population-based or
epidemiological research and lab-based basic science research. In other words, if the
relationship exists in the lab, does it also exist in the field? If it exists in the field, can it be
reproduced in the laboratory?
Experimental evidence In the current era of evidence-informed practice, this criterion seems almost superfluous,
but as Bradford-Hill put it: ‘Occasionally it is possible to appeal to experimental evidence’
Causation through analogy A sort of ‘pre-scientific’ criterion which is probably the weakest of the bunch. Analogy and
clinical observation form the basis of most scientific research, in that someone,
somewhere, has observed and related the apparent association. An example here might
be an observation that whiplash is a result of car accidents, but not all car accidents result
in whiplash. Empirical scientific evidence is then required to clarify that relationship
Reversibility Not part of Bradford-Hill’s initial criteria, but a logical addition for conditions that are
reversible. If the presence of a factor (e.g. high catastrophic thinking) is in fact a cause of
an outcome (e.g. chronic pain-related disability), then removing the cause should reduce
or abolish the effect

Adapted from Bradford-Hill (see text).90

(2.4 times greater) of belonging to the ‘persistent pain’ newer and more complex risk algorithms that consider
group than those who stated they never cycle. If cycling multiple factors average around 70–80% classification
were in fact a cause of persistent neck pain, then clinicians accuracy at best.92,93 Many univariate analyses provide
should routinely recommend that their patients not cycle, things like odds ratios or relative risk, which in most cases
and when a new patient enters their practice who states can be interpreted as the increase in odds that a person
they even occasionally ride a bike, the clinician should falls into the high-risk group, rather than any definitive
immediately become concerned about the risk of long- dooming of the person to developing chronic pain.
term problems. But clearly (and encouragingly), this does Finally, it potentially becomes a self-fulfilling prophecy
not appear to be the case. The question then becomes: is when risk is ascribed to an individual if there’s nothing
cycling in fact a cause of chronic neck pain? Or could to be done about it. Sex, age, educational attainment or
there be something else about those who cycle compared socioeconomic status; these are all factors for which at
to those who never cycle that could explain this finding least some evidence exists to suggest they may be useful
(a question of specificity)? Is it biologically reasonable? to identify those at risk of a poor outcome. However,
Are those who cycle more at greater risk than those who their clinical usefulness is questionable considering, at
cycle less (dose–response)? If cyclists stopped cycling, least as of today, there is nothing that can easily be done
would they be more likely to improve (reversibility)? Is to address them.
it possible that this is a chance finding, a risk that increases With these caveats in mind, the next section provides
with increasing comparisons performed? Is the outcome a summary of the current evidence (updated to the end
(at least 1 day of neck pain in the preceding month) of of 2012) for or against the prognostic factors that have
importance for your clinical population? All of these are been examined to date.
questions that clinicians should consider before imple-
menting such evidence into practice. Summary of Current Evidence – What
One additional important point to be made before
moving to the summary of evidence is with respect to the
are Risk Factors, What are Not?
title of this subsection: predisposed does not mean pre- For the purposes of this chapter, and with space limita-
destined. It is extremely rare that a predictor variable is tions in mind, only those factors for which the evidence
able to perfectly classify all people into those that will provides adequately compelling evidence for or against
develop chronic problems and those that will not. Even their status as risk factors for a poor outcome exists, are
428 PART IV  Overview of Contemporary Issues in Practice

discussed. An issue that has yet to be resolved in this field problems despite the recent focus on psychosocial
is the best definition and operationalization of a ‘poor’ factors.70,98,99 As clinical and observational evidence con-
outcome.94 While this is problematic on many levels, tinues to mount, a true biopsychosocial understanding of
meta-analytic procedures have so far not found a consis- the factors that drive the onset and maintenance of
tent difference in the predictive capacity of a variable chronic post-WAD problems is likely to emerge.
based on the outcome it was predicting, as long as those
outcomes were at least reasonably similar.95,96 With this
caveat in mind, Box 42-1 presents those prognostic vari-
Summary
ables for which the current balance of evidence provides The science of predicting the future is growing in the
the greatest confidence in their status as either predictors whiplash field, due largely to the recognition that chronic
or non-predictors of a poor outcome. The box has been WAD is notoriously difficult to treat in the majority of
adapted from that of Walton and colleagues.95,96 Of par- cases. The balance of evidence currently suggests that
ticular note, high neck pain intensity (‘high’ can be con- high initial neck pain intensity, high self-reported dis-
fidently considered as 6/10 or higher) is the most ability, indicators of central hyperexcitability, and psy-
consistent predictor of a poor outcome, but as per a pre- chological distress are the strongest predictors of poor
vious comment, may not be the most valuable clinical medium- to long-term outcome. The challenge for aca-
decision aid. High neck-related disability, most com- demics and clinicians is to unravel the meaning and
monly assessed using the Neck Disability Index (NDI),97 mechanisms underlying these factors, and to identify
is likely most prognostic when neck-related disability is additional areas in which intervention may mitigate the
also the outcome being predicted. On balance, there is risk of chronicity. The field is still relatively young by
considerably greater evidence for the risk posed by strong most standards, and continues to struggle with inconsis-
psychological distress (catastrophizing, post-traumatic tent methods and operationalization of key variables.
stress) than for physical or clinical signs such as range of However, current evidence syntheses provide at least
motion or neck strength. Similarly, mechanisms of the some guidance for clinicians hoping to identify the ‘at
event itself, including direction or speed of impact and risk’ patient in their practice, and may offer useful
seating position of the victim, appear to have little impact windows through which to view the best targets for
on the likelihood of a smooth recovery. However, caution intervention.
must be observed when interpreting these findings: it is
rare that a valid, systematic approach to evaluating clinical
or diagnostic signs or parameters of the event has been THE TREATMENT OF WHIPLASH-
employed in research, which leads to under-representation ASSOCIATED DISORDERS
of such findings in systematic reviews. Evidence is slowly
mounting that biological processes may well play an The most recent systematic reviews conclude that activity
important role in the development of long-term = and/or exercise-based interventions are the most effec-
tive conservative treatments for acute and chronic WAD
but that effects are modest and the relative effectiveness
of various exercise regimens is not clear.100,101 Since these
BOX 42-1  Factors for Which the Current reviews in 2010, further randomized controlled trials
Balance of Evidence (to May 2012) have been conducted and these demonstrate only small,
Provides Confidence in Their if any, effects with physical rehabilitation approaches.
Status as Either Risk Factors of a
Poor Outcome, or as Having No
Association with Outcome Acute Whiplash-Associated Disorders
In acute WAD, a recent randomized trial conducted in
STRONG OR MODERATE CONFIDENCE OF AN
ASSOCIATION WITH A POOR OUTCOME
emergency departments of UK hospitals demonstrated
that six sessions of physiotherapy (a multimodal approach
High pain intensity of exercise, manual therapy) was only slightly more
High neck-related disability
Post-traumatic stress symptoms at inception
effective, but not cost effective, than a single session
Catastrophizing of advice from a physiotherapist.102 However, only
Cold hyperalgesia/hypersensitivity 45–50% of participants in either treatment group
reported their condition as being ‘much better’ or
STRONG OR MODERATE CONFIDENCE IN NO ‘better’ at short- (4 months) and long-term follow-up
ASSOCIATION WITH A POOR OUTCOME (12 months) – a low recovery rate that is little different
Angular deformity of the neck (scoliosis, flattened to the usual natural recovery following the injury.4 In
cervical lordosis) view of the physical and psychological factors shown
Impact direction to be present in acute WAD,103 it could be surmised
Seating position that a physiotherapy approach alone would not be suf-
Aware of impending collision
Head-rest in place
ficient to address these factors. For this reason another
Older age recent randomized controlled trial investigated if the
Vehicle stationary when hit early targeting of these factors would provide better
outcomes than usual care.104 Participants with acute
Adapted from Walton et al.95 WAD (≤4 weeks duration) were assessed using measures
 42  Whiplash-Associated Disorders 429

of pain, disability, sensory function and psychological treatment comprising advice, assurance, together with
factors including general distress and post-traumatic simple exercises may be most effective for this group,
stress symptoms. Treatment was tailored to the findings although this proposal requires formal testing. Those
of this baseline assessment and could range from a mul- patients at medium or high risk of poor recovery will
timodal physiotherapy approach of advice, exercise and likely need additional treatments to the basic advice/
manual therapy for those with few signs of central activity/exercise approach. This may include medication
hyperexcitability and psychological distress to an inter- to target pain and nociceptive processes as well as methods
disciplinary intervention comprising medication (if pain to address early psychological responses to injury. As can
levels were greater than moderate and signs of central be seen in a recent trial by Jull et al.,104 this approach may
hyperexcitability were present) and cognitive behavioural not be straightforward. The participants of this trial not
therapy delivered by a clinical psychologist (if scores only found the side effects of medication unacceptable
on psychological questionnaires were above threshold). but also were less compliant with attendance to a clinical
This pragmatic intervention approach was compared to psychologist (46% of participants attended fewer than
usual care where the patient could pursue treatment as four of ten sessions) compared to attendance with the
they normally would. Analysis revealed no significant physiotherapist (12% attended fewer than four sessions
differences in frequency of recovery (defined as Neck over 10 weeks).104 The reasons for non-compliance are
Disability Index <8%) between pragmatic and usual care not clear but the burden of attending numerous health-
groups at 6 months (OR 0.55, 95% CI 0.23 to 1.29) care visits with different practitioners may have played a
or 12 months (OR 0.65, 95% CI 0.28 to 1.47). There role. An alternative approach, currently being evaluated,
was no improvement in non-recovery rates at 6 months is to train physiotherapists to deliver psychological inter-
(64% for pragmatic care and 49% for usual care), indi- ventions and to play more of a ‘gatekeeper’ role in the
cating no advantage of the early interdisciplinary inter- early assessment, risk stratification and triaging of patients
vention.104 Several possible reasons for these results were with acute WAD. This approach has been investigated in
proposed. The design of the trial may have been too mainly chronic conditions such as arthritis106 as well as in
broad and not sensitive enough to detect changes in acute low back pain105 with results showing some early
subgroups of patients, suggesting better outcomes would promise. This is not to say that patients with a diagnosed
be achieved by specifically selecting patients at high psychopathology such as depression or post-traumatic
risk of poor recovery. Additionally, 61% of participants stress disorder should be managed by physiotherapists
in the trial found the medication (low-dose opioids and/ and of course, these patients will require referral to an
or adjuvant agents) to be unacceptable due to side effects appropriately trained professional.
such as dizziness and drowsiness and did not comply
with the prescribed dose,104 indicating that more accept-
able medications need to be evaluated. Compliance with
Chronic Whiplash-Associated Disorders
attending sessions with the clinical psychologist was less The most recent systematic review of treatments for
than compliance with physiotherapy, perhaps indicating chronic WAD identified only 22 randomized trials that
patient preference for physiotherapy. met the criteria for inclusion and only 12 were of good
The results of the above-mentioned trial should not quality.101 The authors concluded that exercise pro-
mean that attempts to address and target potentially grammes are effective at relieving pain, although it does
modifiable risk factors in the early injury stage be aban- not appear that these gains are maintained over the long
doned. There were, as outlined, several methodological term.101 It is also not clear if one form of exercise is more
issues that may have influenced the results. It is recog- effective than another. Since this review further trials
nized that the risk factors for chronic pain development investigating exercise approaches for chronic WAD have
following whiplash injury are not necessary causally been conducted and shown only small to modest effects
related, it still remains logical that further studies inves- of the interventions. In one trial, a specific motor and
tigate the targeting of factors such as pain, central hyper- sensorimotor retraining programme for the cervical spine
excitability, catastrophizing and post-traumatic stress combined with manual therapy107 resulted in just clini-
symptoms. Such an approach has been explored in the cally relevant decreases in pain-related disability com-
area of low back pain where stratified care was provided pared to usual care. Similar effects were demonstrated
to patients depending upon their risk of developing in another trial of graded functional exercise and advice
chronic pain and disability with results showing some compared to advice alone where small improvements in
promise.105 Recently a clinical prediction rule including pain, bothersomeness and functional ability were found
some of these factors was developed to identify both at short-term follow-up.108 In a recent subsequent large
chronic moderate/severe disability and full recovery at 12 randomized controlled trial,109 these two forms of exer-
months post injury with good specificity and adequate cise were combined to a comprehensive exercise inter-
sensitivity.93 Whether or not the use of a stratified vention that first focused on improving cervical motor
pathway of care for whiplash can improve recovery and postural control before progressing to more func-
remains to be seen. tional higher load activities. Aerobic exercise was also
In addition to identifying patients at risk of poor performed by the participants throughout the 12-week
recovery, an important aspect of such clinical prediction treatment period. The results were disappointing with
rules is also the identification of patients with good the comprehensive exercise programme being no more
potential for recovery (low-risk patients). These patients effective than advice in reducing pain (the primary
will likely require less-intensive interventions and outcome). At 14 weeks the treatment effect was 0.0 (95%
430 PART IV  Overview of Contemporary Issues in Practice

CI −0.7 to 0.7), 6 months 0.2 (−0.5 to 1.0) and at 12 showed initial promise as moderators of treatment effec-
months −0.1 (−0.8 to 0.6). Some of the effects on sec- tiveness107 have not stood up to further scrutiny109 and the
ondary outcomes were statistically significant but none investigation of additional or different factors requires
were sufficiently large to be considered clinically thought.
worthwhile. With respect to acute WAD, an important goal of
Two studies have investigated factors that may moder- treatment should be to prevent the development of
ate the effects of predominantly exercise-based interven- chronic pain and disability. The time period for this to
tions. In an earlier trial, participants with both cold and be achieved appears to be short – within about 2–3
mechanical hyperalgesia did not respond to a specific months of injury.4 Physiotherapists play a vital role in this
cervical muscle retraining as those without these fea- stage of the injury and as such may need to take a greater
tures107 but this analysis was performed post-hoc and the role in the overall care plan of the patient. This would
study was not powered to specifically detect any modera- mean having expertise in the assessment of risk factors
tion effects. In the recent larger trial, the sample size was and an understanding of when additional treatments such
increased in order to be able to evaluate the possible as medication and psychological interventions are
moderation effects of factors such as measures of central required. While this has traditionally been the role of
hyperexcitability, post-traumatic stress symptoms, pain general practitioners, it is difficult to see how the busy
catastrophizing and symptom duration.109 None of these structure of medical primary care will allow for the
factors were shown to moderate the effect of the exercise appropriate assessment of patients to first identify those
programme. So at present it remains unclear which at risk, develop a treatment plan, follow the patient’s
patients will respond to exercise interventions. progress and modify treatment as necessary. Physiothera-
In accordance with the biopsychosocial model of pists are well-placed to take on a coordination or ‘gate-
chronic pain, it may be expected that physical keeper’ role in the management of WAD and research
rehabilitation-only approaches for chronic WAD will into health services models that include physiotherapists
not be sufficient. Few trials of interdisciplinary in such a role is also needed.
approaches have been conducted in a chronic WAD
group and these approaches have been varied, from
physiotherapists delivering psychological-type interven- REFERENCES
tions in addition to physiotherapy to psychological 1. Carroll L, Holm L, Hogg-Johnson S, et al. Course and prognostic
interventions alone. In their systematic review, Teasell factors for neck pain in whiplash-associated disorders (WAD).
et  al.101 concluded that although the majority of studies Results of the bone and joint decade 2000–2010 task force on neck
suggest that interdisciplinary interventions are beneficial, pain and its associated disorders. Spine 2008;33:583–92.
it is difficult to formulate conclusions given the het- 2. Wilson S, Derrett S, Cameron I, et al. Prevalance of poor out-
comes soon after injury and their association with the severity of
erogeneity of the interventions. Since that review, addi- injury. Inj Prev 2014;20(1):57–61.
tional trials have investigated psychological approaches 3. Mayou R, Bryant B. Psychiatry of whiplash neck injury. Br J Psy-
for chronic WAD. Dunne and colleagues showed that chiatry 2002;180:441–8.
trauma-focused cognitive behavioural therapy provided 4. Sterling M, Hendrikz J, Kenardy J. Developmental trajectories of
pain/disability and PTSD symptoms following whiplash injury.
to individuals with chronic WAD and post-traumatic Pain 2010;150:22–8.
stress disorder led to decreased psychological symptoms 5. Curatolo M, Bogduk N, Ivancic P, et al. The role of tissue damage
of post-traumatic stress disorder, anxiety and depression, in whiplash associated disorders. Spine 2011;36:S309–15.
as well as decreased pain-related disability.110 Although 6. Schiltenwolf M, Beckmann C. letter to the editor: whiplash dis-
this was a small preliminary study, the results suggest order – is it a valid disease definition? Pain 2013;154(10):2235.
7. Sterling M. Physiotherapy management of whiplash associated
that psychological interventions may be useful to disorders (WAD). J Physiother 2014;60(1):5–12.
improve not only psychological symptoms but also pain- 8. Siegmund G, Winkelstein B, Ivancic P, et al. The anatomy and
related disability. biomechanics of acute and chronic whiplash injury. Traffic Inj
Prev 2009;10:101–12.
9. Haldeman S, Carroll L, Cassidy D, et al. The bone and joint
Future Directions decade 2000–2010 task force on neck pain and its associated dis-
orders executive summary. Spine 2008;33:S5–7.
We are at cross-roads in the research and clinical man- 10. Linman C, Appel L, Fredrikson M, et al. Elevated (11C)-D-
agement of acute and chronic WAD. The evidence is deprenyl uptake in chronic whiplash associated disorder suggests
demonstrating that the usual ‘traditional’ treatment persistent musculoskeletal inflammation. PLoS ONE 2011;6:
e19182.
approaches that comprise predominantly of physical 11. Sterling M, Elliott J, Cabot P. The course of serum inflammatory
rehabilitation are offering only small effects. This is not biomarkers following whiplash injury and their relationship to
to say that exercise-based interventions should not be sensory and muscle measures: a longitudinal cohort study. PLoS
provided to people with WAD as exercise and activity is ONE 2013;8(10):e77903.
12. Kaneoka K, Ono K, Inami S, et al. Motional analysis of cervical
important for their long-term general health. It may be vertebrae during whiplash loading. Spine 1999;24:763–70.
that activity/exercise is combined with other treatments 13. Panjabi M, Paerson A, Ito S, et al. Cervical spine curvature during
such as psychological approaches, educational approaches simulated whiplash. Clin Biomech 2004;19:109.
and medication. The optimal combination and dosage of 14. Stemper B, Yoganandan N, Pintar F. Gender- and region-
such approaches will need to be determined. The results dependent local facet joint kinematics in rear impact: implications
in whiplash injury. Spine 2004;29:1764–71.
of the randomized controlled trials also indicate that 15. McConnell W, Howard R, Guzman H, et al. Analysis of human
some people respond to physical rehabilitation, but our test subject kinematic response to low velocity rear end impacts.
ability to recognize these patients is lacking. Factors that SAE Tech Pap 1993;21–30.
 42  Whiplash-Associated Disorders 431

16. Grauer J, Panjabi M, Cholewicki J, et al. Whiplash produces 42. Vette N, Krakenes J, Eide G, et al. Are MRI high-signal changes
S-shaped curvatures of the neck with hyperextension at lower of alar and transverse ligaments in acute whiplash injury related
levels. Spine 1997;22:2489–94. to outcome? BMC Musculoskelet Disord 2011;11.
17. Jakobsson L, Lundell B, Norin H, et al. WHIPS–Volvo’s Whip- 43. Smith A, Jull G, Schneider G, et al. Cervical radiofrequency neu-
lash Protection Study. Acc Anal Prevent 2000;32:307–91. rotomy reduces central hyperexcitability and improves neck move-
18. Viano D, Olseon S. The effectiveness of active head restraint in ment in individuals with chronic whiplash. Pain Med 2014;
preventing whiplash. J Trauma 2001;51:959–69. 15(1):128–41.
19. Farmer C, Wells J, Lund A. Effects of head restraint and seat 44. Smith A, Jull G, Schneider G, et al. Cervical radiofrequency neu-
redesign on neck injury risk in rear-end crashes. J Spinal Disord rotomy reduces psychological distress and pain catastrophization,
2003;4:251–63. but not post-traumatic stress in individuals with chronic WAD.
20. Jonsson H, Cesarini K, Sahlstedt B, et al. Findings and outcome Pain Res Manag 2013;18:e13.
in whiplash-type neck distortions. Spine 1994;19:2733–42. 45. Smith A, Jull G, Schneider G, et al. Modulation of cervical facet
21. Taylor J, Taylor M. Cervical spinal injuries: an autopsy study of joint nociception and pain attenuates physical and psychological
109 blunt injuries. J Musculoskeletal Pain 1996;4:61–79. features of chronic whiplash: a prospective study. Pain Manage
22. Taylor J, Twomey L. Acute injuries to cervical joints. Spine Res 2015;accepted.
1993;18:1115–22. 46. Carroll L, Cassidy D, Cote P. The role of pain coping strategies
23. Uhrenholt L, Grunnet-Nilsson N, Hartvigsen J. Cervical spine in prognosis after whiplash injury: passive coping predicts slowed
lesions after road traffic accidents. a systematic review. Spine recovery. Pain 2006;124:18–26.
2002;27:1934–41. 47. Sterling M, Jull G, Kenardy J. Physical and psychological predic-
24. Davis S, Teresi L, Bradley W, et al. Cervical spine hyperextension tors of outcome following whiplash injury maintain predictive
injuries: MR findings. Radiology 1991;180:245–51. capacity at long term follow-up. Pain 2006;122:102–8.
25. Yoganandan N, Cusick J, Pintar F, et al. Whiplash injury deter- 48. Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating com-
mination with conventional spine imaging and cryomicrotomy. pensation for pain and suffering on the outcome of insurance
Spine 2001;26:2443–8. claims for whiplash injury. N Engl J Med 2000;20:1179–213.
26. Barnsley L, Lord S, Bogduk N. Comparative local anaesthetic 49. Bostick G, Ferrari R, Carroll L, et al. A population-based survey
blocks in the diagnosis of cervical zygapophyseal joint pain. Pain of beliefs about neck pain from whiplash injury, work-related neck
1993;55:99–106. pain, and work-related upper extremity pain. Europ J Pain
27. Lord S, Barnsley L, Wallis B, et  al. Chronic cervical zygapophy- 2009;13:300–4.
sial joint pain after whiplash: a placebo-controlled prevalence 50. Schneider G, Jull G, Thomas K, et al. Derivation of a clinical
study… including commentary by Derby R Jr. Spine 1996;21: decision guide in the diagnosis of cervical facet joint pain. Arch
1737–45. Phys Med Rehabil 2014;95:1695–701.
28. McLain R. Mechanoreceptors endings in human cervical facet 51. Jensen T, Baron R. Translation of symptoms and signs into mech-
joints. Spine 1994;19:495–501. anisms in neuropathic pain. Pain 2003;102:1–8.
29. Quinn K, Winkelstein B. Detection of altered collagen fiber align- 52. Rebbeck T, Sindhausen D, Cameron I. A prospective cohort study
ment in the cervical facet capsule after whiplash-like joint retrac- of health outcomes following whiplash associated disorders in an
tion. Ann Biomed Eng 2011. Australian population. Inj Prev 2006;12:86–93.
30. Lee K, Thinnes J, Gokhin D, et al. A novel rodent neck pain 53. Ferrari R, Pieschl S. An examination of coping styles and expecta-
model of facet-mediated behavioral hypersensitivity: Implications tions for whiplash injury in Germany: comparison with Canadian
for persistent pain and whiplash injury. J Neurotrauma data. Clin Rheumatol 2011;30:1209–14.
2004;137:151–9. 54. Obelieniene D, Schrader H, Bovim G, et al. Pain after whiplash:
31. Quinn K, Winkelstein B. Cervical facet capsular ligament yield a prospective controlled inception cohort study. J Neurol Neuro-
defines the threshold for injury and persistent joint-mediated neck surg Psychiatry 1999;66:279–93.
pain. J Biomechanics 2007;40:2299–306. 55. Richter M, Ferrari R, Otte D, et al. Correlation of findings, col-
32. Dong L, Odeleye A, Jordan-Sciutto K, et al. Painful facet joint lision parameters and psychological factors in the outcome of
injury induces neuronal stress activation in the DRG: implications whiplash associated disorders. J Neurol Neurosurg Psychiatry
for cellular mechanisms of pain. Neurosci Lett 2008;443:90–4. 2004;75.
33. Dong L, Winkelstein B. Simulated whiplash modulates expression 56. Balla J. The late whiplash syndrome: a study of an illness in Aus-
of the glutamatergic system in the spinal cord suggesting spinal tralia and Singapore. Cult Med Psychiatry 1982;6:191–210.
plasticity is associated with painful dynamic cervical facet loading. 57. Subramaniam M, Abdin E, Vaingankar J, et al. Impact of psychi-
Neurotrauma 2011;27:163–74. atric disorders and chronic physical conditions on health-related
34. Winkelstein B, Santos D. An intact facet capsular ligament modu- quality of life: Singapore Mental Health Study. J Affect Disord
lates behavioral sensitivity and spinal glial activation produced by 2013;147.
cervical facet joint tension. Spine 2008;33:856–62. 58. Yeo S. Pain prevalence in Singapore. Ann Acad Med Singapore
35. Winkelstein BA, Nightingale RW, Richardson WJ, et al. The 2009;38:937–42.
cervical facet capsule and its role in whiplsh injury. Spine 59. Blyth F, March L, Brnabic A, et al. Chronic pain in Australia: a
2000;25:1238–46. prevalence study. Pain 2001;89:127–34.
36. McDonald G, Lord S, Bogduk N. Long-term follow-up of 60. Harstall C, Ospina M. How prevalent is chronic pain. Pain Clin
patients treated with cervical radiofrequency neurotomy for Updates 2003;XI:1–4.
chronic neck pain. Neurosurgery 1991;45:61–7. 61. Henderson J, Harrison C, Britt H, et al. Prevalence, causes, sever-
37. Wallis B, Lord S, Bogduk N. Resolution of psychological distress ity, impact, and management of chronic pain in Australian general
of whiplash patients following treatment by radiofrequency neu- practice patients. Pain Med 2013;14:1346–61.
rotomy: a randomised, double-blind, placebo controlled trial. Pain 62. MAIC. Motor Accident Insurance Commission Annual Report
1997;73:15–22. 2009–10. Queensland Government 2010.
38. Krakenes J, Kaale B. Magnetic resonance imaging assessment of 63. <www.mof.gov.sg/budget_2011/pd.html>; 2012. (Accessed May
craniovertebral ligaments and membranes after whiplash trauma. 2013.).
Spine 2006;31:2820–6. 64. Campbell C, Edwards R. Ethnic differences in pain and pain
39. Krakenes J, Kaale B, Moen G, et al. MRI assessment of the alar management. Pain Manag 2012;2:219–30.
ligaments in the late stage of whiplash injury – a study of structural 65. Lasch K. Culture and pain. Pain Clin Updates 2002;X.
abnormalities and observer agreement. Neuroradiology 2002;44: 66. Rahim-Williams B, Riley JL III, Herrera DG, et al. Ethnic iden-
617–24. tity predicts pain sensitivity in African Americans and Hispanics.
40. Krakenes J, Kaale B, Moen G, et al. MRI of the tectorial and Pain 2007;129:177–84.
posterior atlanto-occipital membranes in the late stage of whiplash 67. Carey T, Freburger J, Holmes G, et al. Race, care seeking, and
injury. Neuroradiology 2003;44:637–44. utilization for chronic back and neck pain: population perspec-
41. Myran R, Zwart J, Kvistad K, et al. Clinical characteristics, pain, tives. J Pain 2010;11:343–50.
and disability in relation to alar ligament MRI findings. Spine 68. Rahim-Williams B, Riley J, Williams A, et al. A quantitative
2008;36:E862–7. review of ethnic group differences in experimental pain response:
432 PART IV  Overview of Contemporary Issues in Practice

do biology, psychology, and culture matter? Pain Med 2012; 90. Bradford Hill A. The environment and disease: association or
13:522–40. causation? Proc Royal Soc Med 1965;58:6.
69. Ng T, Pedler A, Vicenzino B, et al. Less efficacious conditioned 91. Hill J, Lewis A, Papageorgiou K, et al. Predicting persistent neck
pain modulation and sensory hypersensitivity in chronic whiplash- pain: a 1-year follow-up of a population cohort. Spine
associated disorders in Singapore. Clin J Pain 2014;30(5): 2004;29:1648–54.
436–42. 92. Kasch H, Kongsted A, Qerama E, et al. A new stratified risk
70. Stone A, Vicenzino B, Lim E, et al. Measures of central hyperex- assessment tool for whiplash injuries developed from a prospective
citability in chronic whiplash associated disorder – a systematic observational study. BMJ Open 2013;3.
review and meta-analysis. Man Ther 2012;18:111–17. 93. Ritchie C, Hendrikz J, Kenardy J, et al. Development and valida-
71. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, et al. Central tion of a screening tool to identify both chronicity and recovery
hypersensitivity in chronic pain after whiplash injury. Clin J Pain following whiplash injury. Pain 2013;154:2198–206.
2001;17:306–15. 94. Walton D. A review of the definitions of ‘recovery’ used in prog-
72. Elliott J, Sterling M, Noteboom T, et al. The clinical presentation nostic studies on whiplash using an ICF framework. Disabil
of chronic whiplash and the relationship to findings of MRI fatty Rehabil 2009;31:943–57.
infiltrates in the cervical extensor musculature: a preliminary 95. Walton D, Macdermid J, Giorgianni A, et al. Risk factors for
investigation. Eur Spine J 2009;18:1371–8. persistent problems following acute whiplash injury: update of a
73. Williamson E, Williams M, Gates S, et al. A systematic review of systematic review and meta-analysis. JOSPT 2013;43:31–42.
psychological factors and the development of late whiplash syn- 96. Walton D, Pretty J, MacDermid J, et al. Risk factors for persistent
drome. Pain 2008;135:20–30. problems following whiplash injury: results of a systematic review
74. Chen C, Wong J, Lee N, et al. The Shatin community mental and meta-analysis. JOSPT 2009;39:334–50.
health survey in Hong Kong. II. Major findings. Arch Gen Psy- 97. Vernon H, Mior S. The neck disability index: a study of reliability
chiatry 1993;50:125–33. and validity. J Manipulative Physiol Ther 1991;14:409–15.
75. Chong S, Abdin E, Vaingankar J, et al. A population-based survey 98. Borstov A, Smith L, Diatchenko L, et al. Polymorphisms in the
of mental disorders in Singapore. Ann Acad Med Singapore glucocorticoid receptor co-chaperone FKBP5 predict persistent
2012;41:49–66. musculoskeletal pain after traumatic stress exposure. Pain
76. Kenardy J, Dunne R. Traumatic injury and traumatic stress. Spine 2013;154:1419–26.
2011;36:S233–7. 99. Elliott J, Pedler A, Kenardy J, et al. The temporal development
77. Merrick D, Stalnacke B. Five years post whiplash injury: symp- of fatty infiltrates in the neck muscles following whiplash injury:
toms and psychological factors in recovered versus non-recovered. an association with pain and posttraumatic stress. PLoS ONE
BMC Res Notes 2010;3. 2011;6:e21194.
78. Sterling M, Hendrikz J, Kenardy J. Similar factors predict dis- 100. Teasell R, McClure J, Walton D, et al. A research synthesis of
ability and PTSD trajectories following whiplash injury. Pain therapeutic interventions for whiplash-associated disorder (WAD):
2011;152:1272–8. part 2 – interventions for acute WAD. Pain Res Manag
79. Janzen J, Silvius J, Jacobs S, et al. What is a health expectation? 2010;15:295–304.
Developing a pragmatic conceptual model from psychological 101. Teasell R, McClure J, Walton D, et al. A research synthesis of
theory. Health Expect 2006;9:37–48. therapeutic interventions for WAD: part 4 – non invasive inter-
80. Darlow B, Fullen B, Dean S, et al. The association between health ventions for chronic WAD. Pain Res Manag 2010;15:313–22.
care professional attitudes and beliefs and the attitudes and beliefs, 102. Lamb S, Gates S, Williams M, et al. Emergency department treat-
clinical management, and outcomes of patients with low back pain: ments and physiotherapy for acute whiplash: a pragmatic, two-
a systematic review. Eur J Pain 2012;16:3–17. step, randomised controlled trial. Lancet 2013;381:546–56.
81. Parsons S, Harding G, Breen A, et al. The influence of patients’ 103. Sterling M, Jull G, Vicenzino B, et al. Characterisation of acute
and primary care practitioners’ beliefs and expectations about whiplash associated disorders. Spine 2004;29:182–8.
chronic musculoskeletal pain on the process of care: a systematic 104. Jull G, Kenardy J, Hendrikz J, et al. Management of acute whip-
review of qualitative studies. Clin J Pain 2007;23:91–8. lash: a randomized controlled trial of multidisciplinary stratified
82. Carroll L, Holm L, Ferrari R, et al. Recovery in whiplash- treatments. Pain 2013;154:1798–806.
associated disorders: do you get what you expect. J Rheumatol 105. Hill J, Whitehurst D, Lewis M, et al. Comparison of stratified
2009;36:1063–70. primary care management for low back pain with current best
83. Holm L, Carroll L, Cassidy D, et al. Expectations for recovery practice (STarT Back): a randomised controlled trial. Lancet
important in the prognosis of whiplash injuries. PLoS Med 2011;378:1560–71.
2008;5:e105. 106. Hunt M, Keefe F, Bryant C, et al. A physiotherapist-delivered,
84. Ng T, Pedler A, Vicenzino B, et al. Physiotherapists’ beliefs about combined exercise and pain coping skills training intervention for
whiplash injury: a cross-cultural comparison between Singapore individuals with knee osteoarthritis: a pilot study. Knee 2013;
and Queensland. Physiother Res Int 2014;in press. 20:106–12.
85. Ferrari R, Obelieniene D, Russell A. A cross-cultural comparative 107. Jull G, Sterling M, Kenardy J, et al. Does the presence of sensory
study between Canada and Lithuania. Med Sci Monitor 2002;8. hypersensitivity influence outcomes of physical rehabilitation for
86. Ferrari R, Constantoyannis C, Papadakis N. Laypersons’ expecta- chronic whiplash? – A preliminary RCT. Pain 2007;129:28–34.
tion of the sequelae of whiplash injury: a cross-cultural compara- 108. Stewart M, Maher C, Refshauge K, et al. Randomised controlled
tive study between Canada and Greece. Med Sci Monitor trial of exercise for chronic whiplash associated disorders. Pain
2003;9:CR120–4. 2007;128:59–68.
87. Ferrari R, Lang C. A cross-cultural comparison between Canada 109. Michaleff Z, Maher C, Lin C, et al. Comprehensive physiotherapy
and Germany of symptom expectation for whiplash injury. J Spinal exercise program or advice alone for chronic whiplash (PROMISE):
Disord Tech 2005;18:92–7. a pragmatic randomised controlled trial. Lancet 2014;384:
88. Ng T, Bostick G, Pedler A, et al. Laypersons’ expectations of 133–41.
recovery and beliefs about whiplash injury: a cross-cultural com- 110. Dunne R, Kenardy J, Sterling M. A randomised controlled trial
parison between Australians and Singaporeans. Eur J Pain of cognitive behavioural therapy for the treatment of PTSD in the
2013;17(8):1234–42. context of chronic whiplash. Clin J Pain 2012;28:755–65.
89. Kamper S, Hancock M, Maher C. Optimal designs for prediction
studies of whiplash. Spine 2011;36:s268–74.
 CHAPTER 43 

Temporomandibular Disorders:
Neuromusculoskeletal
Assessment and Management
Harry von Piekartz

to assess the neuromusculoskeletal domain of the TMJ

INTRODUCTION to determine its role and relevance to the individual
patient’s presenting orofacial complaint.
Orofacial pain with headache is common in society. Its Figure 43-1 presents a modified flowchart (based on
prevalence ranges from 8–15% for women and from the second Research Diagnostic Criteria for Temporo-
3–10% for men.1,2 The American Academy of Orofacial mandibular Disorders (RCD/TMD) classification) of the
Pain uses orofacial pain as a collective term for a number clinical diagnostic process. The RCD/TMD) classifica-
of dysfunctions and sensory complaints associated with tion is divided into three sub-classifications.9,11 The neu-
the temporomandibular joint (TMJ), the masticatory rogenic classification has been added to the original
muscles and associated structures.3 It encompasses terms version by the author. AXIS I represents the physical dis-
such as Costen syndrome, temporomandibular disorders orders and AXIS II represents psychosocial factors such
(TMDs), craniomandibular disorders and mandibular as altered mood, context and beliefs, which are particu-
dysfunction. This chapter focuses on TMDs. It presents larly important in the chronic situation. AXIS III repre-
a discussion of clinical patterns and possible contributing sents clinical considerations or contributing factors,
factors for different myogenic, arthrogenous and neuro- which may maintain the patient’s complaints. In 2013 the
genic TMDs and highlights aspects of assessment and RCD/TMD Taxonomy was reviewed by different profes-
management. sional societies resulting in a proposed expanded TMD
taxonomy; the Diagnosed Criteria of TMD (DC/
TMD).9,11 New recommendations include short and
DO TEMPOROMANDIBULAR DISORDERS simple screenings instruments for Axis I and II focused on
HAVE THEIR OWN ENTITY? structural diagnosis with a more patient-centred approach.
It is relevant to investigate the characteristics of myo-
The diagnosis ‘TMD’ is based on signs and symptoms genic, arthrogenic and neurogenic categories of TMDs.
produced during movements of the mandible. Move-
ment can affect both masticatory muscles and joint
structures. Signs include changes in the range and
Myogenic Temporomandibular Disorders
quality of mandibular movements such as an opening Muscle dysfunction is common in craniomandibular dys-
shift (deviation) and TMJ sounds. Symptoms include kinesia during orofacial activities such as chewing, swal-
headache, vertigo, tinnitus or swallowing impairments.4 lowing, sucking, speaking and facial expression.2 Pain
Clinical and research reports indicate that head and from the masticatory system is difficult to localize. It is
orofacial pain around the TMJ may or may not be characterized by dull pressure, pulling sensations and
related to TMJ neuromusculoskeletal dysfunctions.5 feelings of stiffness.12 It may be referred from other facial
TMD pain may overlap with other headaches types regions such as the teeth, eyes, sinuses and middle
such as migraine, tension and cervicogenic headache. ear.13 Myofascial TMD pain is often described as pain
Glaros et  al.6 demonstrated that there were more com- around the TMJ without reference to a particular patho-
plaints of headache in patients with TMD than without physiological mechanism.14 TMD pain is related to a
TMD, and Ballenberger et  al.1 suggest that migraine variety of biomedical, neurobiomedical and psychological/
and tension-type headache could be risk factors for emotional factors.14 Other sub-factors such as dental
the development of TMD. Likewise a recent study occlusion, hormones and stress may also be related to
concluded that cervicogenic headache was often associ- chronic TMD pain. Thus myofascial TMD pain is con-
ated with TMD pain with 44% of patients having sidered as a phenomenon related to multiple factors.15,16
clear TMD signs.7,8 Thus there is evidence to support Risk factors influencing muscle activity at rest include
the involvement of TMD in orofacial and cervical pain dental occlusion, neuroendocrine and genetic factors and
and dysfunction, but there may be overlap with other parafunctional activities, but recent research has chal-
headache types. It is important for the physiotherapist lenged some factors.
433
434 PART IV  Overview of Contemporary Issues in Practice

Axis I Pain head/neck

Mandibular ROM impairment

Axis II Psychosocial status

Non-TMDs TMDs Pain-related limitations
impact (ICF)

Other diagnosis: Non-specific TMDs (axis I) Specific

Referred pain: dental musculoskeletal
Pathology: pharynx, Specific TMDs (axis I) diagnosis:
salivary glands; Neoplasm, inflammatory, growth Osteochondroma, RA,
neurological; psychiatry, disturbance, systemic coronoid process
medically unexplained hypertrophy,
physical complaints hyperuricaemia

Muscular Articular Neurogenic Muscular/Articular

Disc displacement Axon Axis III Prognosis

Myofascial dominance Expansion (local/spread)
pain Temporal (acute/chronic)
Osteoarthrosis/-itis Course (normal/abnormal)
Nerve trunk Type (nociceptive/neuropathic)
Arthralgia dominance Treatment without success
(no/yes)
Myofascial pain with Pain medication
limited jaw opening Adhesion/ankylosis (adequate/inadequate)
Comorbidity (no/yes)
Hypermobility,
dislocation

FIGURE 43-1  ■  A modified flowchart of the clinical diagnosis process during subjective and physical examination based on the revised
RCD/TMD.9,10 ICF, International Classification of Function; RA, Rheumatoid arthritis; ROM, Range of motion; TMD, Temporomandibu-
lar disorder.

Dental Occlusal Factors evidence of their contribution to headache and orofacial

pain.23–25 The neurobiological relationship between para-
It was assumed for decades that changes in dentition functions and myofascial pain is still debated.23 Parafunc-
directly influence movement patterns, neuromuscular tional habits seem to be associated with postural habits
imbalance and masticatory pain.17 Recent evidence refutes such as the forward head posture and bracing. The latter
this view.18 In a systematic review, Türp and Greene16 may cause TMD pain, headache and joint strain.26 In
concluded that occlusal factors were overestimated in assessment, different orofacial motor functions and habits
models of myofascial TMD and pain. Nevertheless, ques- may be noticed that might support the role of parafunc-
tions about altered motor activity and pain during orofa- tional activities. Motor control deficits may be observed
cial activity in relation to a history of occlusal interference in oral habits (chewing, nail biting), linguistic activities
are still included in the examination to determine any (speech, singing) or functions such as swallowing and
direct relationships. sucking.
Parafunctional activities such as bruxism are charac-
terized by clenching and grinding of the teeth during the
Neuroendocrine and Genetic Factors
night or day, and bracing or thrusting the mandible.27
The incidence of TMD muscle pain is more prevalent in Terminologies such as bruxomania (grinding during the
women than men. This may reflect the influence of day) and bracing (diurnal teeth pressing without vertical
female reproductive hormones on orofacial pain.19 Oes- teeth movement) are no longer distinguished because of
trogen in particular has a strong influence on nerve their overlap and blurring of the underlying pathobio-
growth factor and hence depolarization of nociceptors, logical mechanism.27 Clinically, bruxism and bracing are
which may play an important role in the genesis of TMD related to different clinical patterns, which have to be
pain, allodynia and increased muscle activity.20,21 This is distinguished as they require different (neuromusculosk-
even more important when genetic factors play a role eletal) management strategies.28 Table 43-1 presents the
such as enzyme polymorphism.22 different clinical patterns.

Parafunctions Increased Muscle Activity During Rest

Parafunctional activities (abnormal oral habits) are not Increased resting activity of the jaw muscles is found in
directly associated with TMD pain but there is some orofacial pain patients,29,30 but it is unclear if pain increases
 43  Temporomandibular Disorders: Neuromusculoskeletal Assessment and Management 435

It is characterized by restriction in mouth opening, pain,

TABLE 43-1  Manifestation of Dominant
no clicking sounds but usually a history of clicking in the
Bruxism and Bracing Patterns
TMJ. If the disc displacement becomes chronic, mouth
Bruxism Bracing opening improves and active and end-range movements
are less painful. Joint crepitation with (minor) inflamma-
a.m. masticatory stiffness, a.m. no masticatory
symptoms stiffness, symptoms
tion may persist.34–36
Eases during the day Increases during the day
It must be noted that approximately 33% of the
Not really conscious of Conscious of mechanism
general population have moderate to severe disc derange-
mechanism ment37,38 and there is no correlation between disc position
Sleep disturbances No sleep disturbances and TMD pain.39 Although disc displacements may, in
(superficial sleep) the long-term, lead to degeneration, there is no correla-
Abrasion* Less abrasion* tion between degenerative changes and pain.39,40 Imaging
Unilateral muscular signs Bilateral muscular signs techniques are promoted as gold standard tests for assess-
and symptoms and symptoms ment of disc–condyle position. However, they do not
Restricted opening Restricted opening guarantee the correct diagnosis of the type of disc
(muscular related) (muscular related) displacement.41–43 Thus the clinician has to interpret the
Note: Clinically, an overlap is often seen with one pattern being results of imaging in line with clinical diagnostic tests and
dominant. ask the question: do the results fit?
*Abrasion: the loss of tooth structure by mechanical forces.
Modified after von Piekartz28 and Lobbezoo et al.27
Hypermobility and Dislocation
muscle activity or vice versa.31 Factors such as changes of Hypermobility and dislocation are strongly related to
head position1 neuropathic pain and local ischaemic disc instabilities. TMJ hypermobility is characterized by
changes in the muscle fibres may deregulate the motor increased condylar anterior glide during mouth opening.44
end-plates. This might maintain a neural loop of sensory In dislocations the condyle is subluxed out of the fossa
afferent information and consequently sustain abnormal behind the crest of the articular eminence, which restricts
motor and autonomic afferents. In turn this may result mouth closure.44,45 Hypermobility is often seen in (young)
in myofascial trigger points.31 people with general hypermobility and/or after a (small)
trauma to the mandible.46 Functionally, neuromusculo­
Arthrogenic Temporomandibular skeletal contributing factors include reduced muscular
control especially with excessive pterygoid muscle activ-
Disorders ity,47 stiffness in the opposite TMJ, craniocervical posture
Arthrogenic TMDs include disc displacements, arthral- changes48 and occlusal interference. Orofacial functions
gia, hypermobility/dislocation, osteoarthrosis/itis adhe- such as chewing, talking and singing may be affected.
sion and ankylosis.3 The discussion in this chapter is During the assessment of the TMJ the clinician aims to
limited to the non-specific arthrogenic disorders such identify possible contributing factors, which might main-
as disc derangements, hypermobility, dislocation and tain the hypermobility or (minor) dislocation.
arthralgia, which are commonly seen by physiotherapists.
Arthralgia
Disc Displacements
Arthralgic pain is not a single pathological entity. It is
Disc displacements or derangements are characterized by non-specific articular TMD (see Fig. 43-1) and is classi-
an abnormal condyle–disc relationship, which is classified fied by clinical characteristics and clinical tests.49 An
into displacement with or without reduction or posterior arthralgia is diagnosed when pain is present around the
displacement. The usual direction of displacement is ear, provoked by mandibular movements, which are
anterior and anteriomedial.10 The aetiology of disc dis- restricted. Palpation of masticatory structures can provoke
placements is not established. Anatomical research has the familiar pain.3 Pain mapping (structural diagnosis of
shown that the capsule around the head of the mandibu- TMJ pain by joint palpation and in combination with
lar and ligaments attaching the disc to the condyle are passive TMJ movements50) may help the clinician dif-
elongated. This allows increased movement of the disc, ferentiate pain dominantly from a peripheral sensitized
often found in disc displacements, trophic changes, local structure or from a more central mechanism. This
impairment and osteoarthritis.32,33 decision has important consequences for further assess-
The most common disc dysfunction is disc displacement ment and treatment.
with reduction (unstable relationship between the disc and
condyle), characterized by a clicking or popping sound Neurogenic Temporomandibular
during mouth opening and closing (closing often pro-
duces less sound than opening). Opening of the mouth is
Disorders
slightly restricted with a shift usually towards the other Neuropathic orofacial pain is classified in the RCD/
side. The disc hurts or starts to click during correction TMD II as non-TMD and is sub-classified as episodic or
of the mandible. In contrast, disc displacement without continuous neuropathic pain with diagnoses such as tri-
reduction is due to malposition (anterior position) of the geminal, laryngeal and glossopharyngeal neuralgia.3 It is
disc in front of the condyle during habitual teeth contact. characterized by unpredictable episodic sharp, stabbing
436 PART IV  Overview of Contemporary Issues in Practice

face pain with different triggers such as temperature presents a proposed classification of nerve dysfunction
changes, emotional and mechanical stress and hormone and pain caused by the axon or the nerve trunk com-
changes.51 In the more peripheral part of the trigeminal piled from literature and from patients presenting
nerve (distal to the trigeminal ganglion), spontaneous clinically.61–64
demyelination may occur after a traumatic event, such as
teeth extractions, mandibular trauma, or long-term
minor pressure on branches of the mandibular nerve (e.g.
long-term pressure of the pterygoid muscle on the lingual
ASSESSMENT
branch). Trauma and pain onset may not be obviously Subjective Examination
linked. In many cases the aetiology is unknown.
An underestimated cause of head and orofacial pain A systematic subjective examination provides a hypoth-
may be neurogenic dysfunction where the signs and esis for the type of TMD, possible pain mechanisms, the
symptoms come from the nerve trunk and the mechani- patient’s activity and participation level, as well as possi-
cally or chemically sensitized nociceptors in the connec- ble Yellow and Red Flags. It forms the basis for planning
tive tissue sheaths of the nervous system (i.e. nervi the physical examination.65 The standardized taxonomy
nervorum).52–54 For example, the trigeminal branches research diagnostic criteria for temporomandibular dis-
may be predisposed to nerve trunk pain by: orders (RCD/TMD) is recommended for research pur-
• Long-term minor pressure on the intracranial blood poses as well as multidisciplinary practice.66 For a detailed
vessels in the pontine angle at the entry zone of the description of a subjective examination, the reader is
trigeminal nerve from craniocervical postures and referred to existing literature.3,67,68
movement.55,56
• Compression phenomena around the foramen
rotundum and oval foramen (entry zone to the skull
Physical Examination
floor) during neck movements, particularly during The physical examination of the TMJ includes observa-
lateral flexion.57,58 tion and analysis of posture, assessment of active and
• Long-term pressure on the alveolar nerve by man- passive movement as well as muscle testing, which
dibular implants.59 includes an evaluation of endurance, strength and length
• Intermittent compression, traction and friction on and palpation for muscle tightness. This provides infor-
the mandibular nerve during mouth opening in mation on the general function of the masticatory
patients with an anterior disc displacement. The system. It must be appreciated that the findings may
mandibular nerve moves by an average distance of not be directly related to the aetiology of the dysfunc-
4–5 mm towards the disc.60 tion and the clinician has to consider possible
A set of clinical diagnostic tests may support a hypoth- contributing/risk factors, which might support and
esis of peripheral neurogenic TMD pain. Table 43-2 maintain TMD pain.

TABLE 43-2  Proposed Features of Neurogenic Facial Dysfunction and Pain

Qualities Axon Dominance Nerve Trunk Dominance
Pathogenesis Axonal destruction, emerging of AIGS Trophic changes in connective tissue

Subjective Examination
Pain description Burning, itching, raw, electric Dragging, dull, searing, aching/sore
muscles, background pain
History Spontaneous, first episode Several small traumas in the same nerve
region
Exacerbation Stress, temperature changes, immunologic Moving and stretching, palpation
dysfunctions, tissue stretch
Relief Rest Rest and posture changes

Clinical Examination
Nerve palpation Delayed symptoms. Pain has a ‘shooting’ Slow increase and spread of symptoms
character during palpation
No obvious nerve swelling Obvious swelling of the nerve, less
Transverse movements possible transverse movements possible
Neurological examination Neurological signs evident in cranial nerve No neurological signs or rapid
(e.g. strength, reflexes, innervation improvement after short trial of
sensitivity) treatment of the nerve and its
environment
Cranial neurodynamic No obvious resistance. Pain behaviour/ Resistant-pain behaviour during tests/
tests latent pain reaction possible sensitizing movement positive
Protective spasm without pain during the Protective spasm without pain during the
test may persist test may persist
Electromyogram Delayed or absence of conductivity No obvious disturbance of conductivity
 43  Temporomandibular Disorders: Neuromusculoskeletal Assessment and Management 437

The Relationship between an Altered

Posture of the Head and
Temporomandibular Disorders
There is strong evidence for a neurophysiological, bio- Canthus
mechanical and functional connection between the cervi-
cal spine and the TMJ.68 Nevertheless, there is still debate ETHA
regarding whether or not head posture is directly related Tragus
to TMD and orofacial pain. Two reviews68,69 found several
studies reporting a relationship between head posture
and the stomatognathic system; however, the evidence PTC7A
was inconclusive for the functional relationship between Pogonion
head posture, jaw posture and occlusion. On the other
hand, a recent study found that different head postures,
especially the forward head posture, changed mouth TC7SA C7
opening and decreased pressure pain thresholds over the
TMJ and masticatory muscles.70 Even though evidence at
present is somewhat inconclusive, it is still recommended
that the clinician assesses the influence of the individual Upper middle point
patient’s head posture on their condition. If changing shoulder
head posture improves a patient’s complaints, it may be
reasoned that it has a role in the TMD pain or associated
symptoms. Furthermore, a measure of posture can be
used as an outcome measure to evaluate the effect of any
head posture muscle control exercises. A simple, cheap FIGURE 43-2  ■  Head posture measurements as proposed by
and safe method to (re)assess the posture of the head is Armijo-Olivo et al.77 ETHA, Eye(Canthus)–Tragus–Horizontal
photometry. Van Niekerk71 compared photometry and Angle; PTC7A, Pogonion–Tragus–C7 Angle; TC7SA, Tragus–C7–
radiographic measures and found a good to moderate Shoulder Angle
correlation between body angles and a moderate to good
reliability for repeated photographs (intraclass correla-
tion coefficient ranging from 0.78 to 0.99). Armijo-Olivo et al.77 found a clear difference between
patients with TMD and healthy persons for the eye–
tragus–horizontal angle and all measures showed excel-
Measurement of Head Position
lent intra- and inter-rater reliability (intraclass correlation
The craniocervical angle is the most common angle of coefficient 0.996–0.998). Studies are in progress adding
interest. It is usually measured with photometry which extra lines/angles to better depict forward head posture
has moderate to good validity when compared to radio- and posterior rotation of the head (upper cervical exten-
graphs.68,72–74 The role of the craniocervical angle in sion).78 The challenge with these studies is the marked
headache and TMD is still controversial.4,72–75 The head individual variability in postures which makes clear (clini-
can also be forced into rotation about the sagittal plane, cal) significance between groups difficult to determine.
described as a posterior rotation of the cranium/head.50
This is often observed in individuals who have a mouth-
breathing pattern, in persons with an angle class II and
those with an anterior atlas tilt position.76 Including face Clinical Diagnostic Testing of
reference points in measurement of the head position Temporomandibular Disorders
may provide indicators of anteroposterior or posterior Quality of Clinical Tests
rotation of the head.
A system for the measurement of head position has In general, results of single clinical tests have limited
been proposed by Armijo-Olivo et al.77 (Fig. 43-2): value due to large variations in values.79 Clustering of
• Eye–tragus–horizontal angle: the angle between a relevant tests related to symptoms and multi-test scores
line connecting the midpoint of the lateral corner (MTS) stand to increase the diagnostic value of clinical
of the eye with the tragus of the ear and the hori- tests. For example, if TMJ ‘noises’ are provoked during
zontal line starting at the level of the tragus. active movements AND an additional test such as a static
• Pogonion–tragus–C7 angle: the angle between a test is positive, then one can conclude that the applied
line connecting the pogonion (the most forward MTS is positive. Table 43-3 presents the results of the
projecting point on the anterior surface of the chin) inter-examiner reliability of MTS for most cardinal
with the tragus and a line connecting the tragus to symptoms of TMD: pain, ‘noise’ and movement restric-
the C7 vertebra. tion.49 It may be possible to confirm the hypothesized
• Tragus–C7–shoulder angle: the angle formed by the clinical pattern or diagnosis using clustered MTS and this
intersection between the upper middle point of the will be the starting point for management.
shoulder with the C7 vertebra and the line connect- The combination of symptoms and a clinical test,
ing the tragus with the C7 vertebra. which has a moderate to high reliability (k-values >0.4),
438 PART IV  Overview of Contemporary Issues in Practice

TABLE 43-3  Inter-Examiner Reliability for Multi-Test Scores (MTS) of Test Combinations for the
Three Main Symptoms of Temporomandibular Disorders
MTS Categories Agreement % K Signs/Symptoms Present %
Pain
During active movements 65 0.3 49
During additional tests (passive opening, joint play, 6 0.4 59
compression static pain)
During function (active movements and/or additional tests) 89 0.7 69
During function and palpation 96 0.8 91

Noises
During active movements 80 0.6 55
During additional tests 68 0.3 32
During function 77 0.5 60

Restriction of Movement
During active movements 92 0.6 10
During active movements and/or joint play tests 75 0.4 29

K = Cohen’s Kappa statistic in a TMD patient group (n = 79).

Modified after Steenks et al.49

assists the clinician to sub-classify the patient’s presenta- combination of movements (craniocervical flexion, upper
tion into arthrogenic, myogenic or neurogenic TMD. cervical lateroflexion, mouth opening (depression) and/
Steenks et al.49 using a stepwise logistic regression, clas- or contralateral laterotrusion of the mandible) are more
sified a sample of TMD patients (n = 160) by different sensitive than accessory movements to the ipsilateral
tests and test combinations into myogenic (n = 69) and mandibular head. Alternatively, the longitudinal caudal
arthrogenic groups (n = 91). movement together with anteroposterior movement and
laterotrusion may be stiff and locally painful on the symp-
tomatic side. When palpation of the temporal muscle
Which Clinical Neuromusculoskeletal Tests
provokes the same pain and craniocervical flexion and
Should be Chosen for Assessing
lateroflexion do not change the pain, then the TMD may
Temporomandibular Disorders?
have myogenic characteristics.
The aim of the examination is to sub-classify signs and
symptoms of TMD pain to identify its source as more Additional Tests
arthrogenic, myogenic or neurogenic. Physiological and
accessory movements, together with structural differen- Muscle Testing.  An indication of myogenic TMD is
tiation, in general give a good overview of the cardinal often obtained from the five physiological movements
signs which may be confirmed by additional tests. (active and/or passive) and static muscle tests.82 In myo-
genic TMD, the typical pattern is that, in restricted
Physiological and Accessory Movements.  A combina- mouth opening, overpressure beyond the active range
tion of active and passive movements (mouth opening, results in more mouth opening (10–15  mm), mostly
laterotrusion, retrusion and protrusion) related to the without noises, and restriction of laterotrusions or pro-
MTS provides a sense of TMD and its sub-classifications. trusion. Additional tests such as lengthening tests (a
Accessory movements, as longitudinal caudal, cranial, combination of physiological and accessory movement)
medial and lateral transverse, anteroposterior, posteroan- and palpation of muscle tenderness or trigger points
terior glides and variations (angulation and combina- may support the hypothesis of myogenic TMD. It is
tions) are used for testing peri- and intra-articular appropriate to implement pressure pain threshold tests
structures. Accessory movements contribute to a test to gain another parameter of the patient’s pain experi-
battery, which can distinguish between the sub- ences. Pressure pain threshold tests can also be used
classifications arthrogenic and myogenic, but the end- to test for trigeminal or extratrigeminal sensitivity to
feel/stiffness, especially of the caudal longitudinal support the classification of a TMD pain mechanism
movement is not structure-specific.80,81 or for assessment of treatment effectiveness.83,84 Recent
studies indicate the presence of both local and wide-
Structural Differentiation of Temporomandibular spread mechanical hypersensitivity in persons with
Disorder Pain Associated with Peripheral Nerve TMD.83–86
Sensitization.  When there is clear (long-term) nocicep-
tive pain in the TMJ area, structural differentiation by Nervous System.  A battery of quantitative sensory tests
physiological and accessory movement might support can be performed to suggest (cranial) nervous system
sub-classifications of TMD. For example if the mandibu- involvement in pain mechanisms. Cranial neural tissue
lar branch of the trigeminal nerve is involved, a testing will inform on the function of nerves.
 43  Temporomandibular Disorders: Neuromusculoskeletal Assessment and Management 439

• Quantitative sensory testing includes the reaction to symptoms and mandibular movement between a
vibration, thermal, electrical, and mechanical whiplash and control group.65
stimuli.87,88 Quantitative sensory testing is not a At the conclusion of the examination, the clinician is
diagnostic test for a particular disease entity but a positioned to make a reasoned functional statement from
tool for helping in the mechanism-based diagnosis the cardinal signs (pain, noises and range of movement)
of pain.89 Quantitative sensory testing has been used and additional tests (muscle, joint or neural tests). The
in the diagnosis of neurogenic TMD.90–92 results may confirm the sub-classification of pain arising
• Cranial neural tissue testing: Assessment of cranial from arthrogenous, myogenic or neurogenic TMD.
neural tissue consists of several modalities: conduc-
tion tests, palpation and neuromechanical sensitiv-
ity. Discussion will focus on the mandibular branch MANAGEMENT
(V3) of the trigeminal nerve as this nerve innervates
the temporomandibular region. During the last decade physiotherapy has become increas-
• Conduction tests: Tests include sensory features of ingly viable as a treatment option for TMD. There is
discriminative touch, simple touch, pain, tempera- growing consensus on management strategies between
ture, motor function and the mandibular jaw jerk or different care-providers who work in the domain of head,
reflex. These tests may confirm a peripheral lesion neck and orofacial pain.49
or dysfunction of the mandibular branch.93 Persisting head and orofacial pain is a complex entity
• The mandibular jaw jerk (a small tap on the chin which can have different sources and multiple contributing/
on a slightly opened mouth) is, in contrast to a risk factors. This chapter has focused on TMD in persis-
spinal reflex, multisegmental in origin. It is altered tent head-orofacial pain in full recognition that this is one
in sensorimotor disturbances of the trigeminal of many possible pathological sources. The clinician has
nerve. It may be used to differentiate extreme to decide which temporomandibular, craniofacial, cranio-
central pathologies when clonus or trismus is neural and/or craniocervical region(s) are dominant in
detected.94 the patient’s pain and functional limitation.
• Nerve trunk palpation: Provocation of symptoms
does not necessarily identify the site of nerve tissue Evidence for Physiotherapy in
injury, because the entire tract can become mechan-
ically sensitive after injury61,86,95 (e.g. toothache or
Temporomandibular Disorders
pain around implants). The mental branch (in In the TMD literature, physiotherapy is reputed to
the mental foramen on the chin) and the auriculo- relieve musculoskeletal pain and restore normal function,
temporal nerve can be palpated.62,96 Mandibular reduce local inflammation and promote regeneration of
branches, including the lingual, interior alveolar, TMJ tissue. It is usually used as an addition to other
mental and auriculotemporal nerves, are readily pal- treatments.3 In 2006, two systematic reviews concluded
pable. Together with results from the other cranial that, despite the criticisms about reliability, validity,
neural tissue testing, nerve palpation can provide outcome measurements and inclusion and exclusion cri-
indicators of pain from neurogenic TMD. teria for TMD, exercises, manual therapy, electrotherapy,
• Neurodynamic testing. In the temporomandibular relaxation training and biofeedback seem to have the best
region, the ovale foramen of the skull floor, outcomes in TMD treatment.102,103 Nevertheless contem-
the head of the mandible, the lateral and medial porary evidence is inconclusive. Two recent randomized
pterygoid muscles are all in direct contact with controlled trials investigating the long-term effect of
the mandibular nerve.93,97 A preliminary study98 physiotherapy on TMD muscle pain and disc displace-
of movement of cranial nerve tissue, using MRI ment without reduction, did not prove the effectiveness
scans, found that the spinomedullar angle changes of these treatments. In contrast, two studies using a clini-
from 6° to 32° when the cervical spine is moved cal reasoning approach for the treatment of TMD in a
from neutral to upper cervical flexion, confirm- chronic cervical headache population determined posi-
ing Breig’s108 report that lateral flexion of the tive outcomes.7,8 Patients complaining of chronic cervical
head challenges the excursion of the trigeminal headache received orofacial manual therapy in addition
nerve. Mouth opening and contralateral laterotru- to usual care. The patients’ symptoms, as well as the
sion load the lingual and inferior alveolar temporomandibular and craniocervical physical out-
branches.99,100 Neck flexion and longitudinal move- comes, were significantly better at 3 and 6 months in the
ment of the mandible move the auriculotemporal group receiving therapy including orofacial treatment
nerve.101 The proposed examination sequence for when compared with the group receiving usual care only.
the mandibular nerve is a combination of cra- Further randomized controlled trials are required into
niocervical flexion, contralateral lateroflexion in treatment effectiveness.
about 25  mm mouth opening. It is proposed A home exercise regimen has been found to be effec-
that this moves the mandibular nerve maximally tive in improving the range of mouth opening.104,105
towards the other side (laterotrusion) without Importantly, the combination of manual therapy and
extreme stress on the intra-articular TMJ tissue.65 home exercise individualized to patient’s needs has been
Research into this test is in its infancy, but a shown to have superior outcomes.106 Eight motor control
study using the mandibular neurodynamic test tests are proposed as an option for the basis of an exercise
displayed differences in spread and intensity of programme, based on impairments found in the
440 PART IV  Overview of Contemporary Issues in Practice

individual patient’s performance. The tests can be easily • Test 7: Controlled protrusion of the mandible with
transformed into exercises (Fig. 43-3). controlled head position (‘dog follows boss’) (Fig.
Each test is associated with a cue, which may facilitate 43-3G).
the movement • Test 8: Static stabilization test in 20 mm mouth
• Test 1: Thoracic extension. The thoracic spine opening in the laterotrusion direction without facial
follows the person’s hand without associated activity muscle and craniocervical activity. (‘stay there’) (Fig.
of the orofacial and cervical region (‘the arrow’) 43-3H).
(Fig. 43-3A). Tests 1 to 4 have a general motor control character; tests
• Test 2: Craniocervical extension is performed 5 to 8 are orientated to mandibular activity. They tend
without increased activity of the mandible, which in to be more difficult and may be used as a progression.
turn is controlled by the patient themself with her/ Stoltz et al.107 found inter-tester reliability (kappa) for
his own hand (‘sky viewer’) (Fig. 43-3B). these tests ranged from 0.28–0.74. Seven out of eight
• Test 3: Isolated controlled protrusion of the man- tests showed substantial reliability (k > 0.6). Intra-tester
dible without associated movement of the facial reliability ranged between K 0.48–0.91. Of particular rel-
muscles and the craniocervical region (‘rain collec- evance, the tests distinguished chronic from non-chronic
tor’) (Fig. 43-3C). TMD (five out of seven tests) but not between a TMD
• Test 4: Protrusion of the tongue. Isolated anterior and a control group.
tongue movement while controlling the hyoid bone
without associated activity of the lips and ventral
neck muscles (‘tongue relaxer’) (Fig. 43-3D). SUMMARY
• Test 5: Mouth opening (hinge movement) without
shift or sound controlled by the person’s own tacti- Non-specific TMD pain may be defined as a separate
cal feedback (‘breathing fish’) (Fig. 43-3E). entity, strongly associated with biomedical, psychosocial
• Test 6: Laterotrusion of the mandible. Isolated and pathophysiological (risk) factors. Screening of these
movement of the mandible without excessive facial risk factors is part of a systematic examination and the
and neck activity (‘side bite’) (Fig. 43-3F). cardinal signs (pain, noises and range of movement) have

A B C D

E F G H

FIGURE 43-3  ■  Motor control tests for the orofacial region. The tests may be used as a basis for further management.
 43  Temporomandibular Disorders: Neuromusculoskeletal Assessment and Management 441

to be proven through clinical tests. These must comply 20. Svensson P, Cairns B, Wang K, et al. Injection of nerve growth
with the principles of MTS. In order to decide on man- factor into human masseter muscle evokes long-lasting mechanical
allodynia and hyperalgesia. Pain 2003;104:241–7.
agement strategies, trigeminal pain has to be distin- 21. Cairns B, Svensson P, Wang K, et al. Ketamine attenuates
guished. Further, the RCD/TMD axis has to be classified glutamate-induced mechanical sensitization of the masseter
before choosing the main neuromusculoskeletal inter- muscle in human males. Exp Brain Res 2006;169:467–72.
vention and/or other (pain) management or (facial) reha- 22. Zubieta JK, Heitzeg MM, Smith Y, et al. COMT val158met geno-
type affects mu-opioid neurotransmitter responses to a pain
bilitation modalities. stressor. Science (New York, NY) 2003;299:1240–3.
23. Lobbezoo F, Lavigne G. Do bruxism and temporomandibular
disorders have a cause-and-effect relationship? J Orofac Pain
1997;11:15–23.
REFERENCES 24. Svensson P, List T, Hector G. Analysis of stimulus-evoked pain in
1. Ballenberger N, von Piekartz H, Paris-Alemany A, et al. Influence patients with myofascial temporomandibular pain disorders. Pain
of different upper cervical positions on electromyography activity 2001;92:399–409.
of the masticatory muscles. J Manipulative Physiol Ther 25. Glaros AG, Owais Z, Lausten L. Reduction in parafunctional
2012;35:308–18. activity: a potential mechanism for the effectiveness of splint
2. Nilsson I-M, List T, Drangsholt M. Headache and co-morbid therapy. J Oral Rehabil 2007;34:97–104.
pains associated with TMD pain in adolescents. J Dent Res 26. Mense S, Schiltenwolf M. Fatigue and pain; what is the connec-
2013;92:802–7. tion? Pain 2010;148:177–8.
3. De Leeuw R, Klasser G. Orofacial Pain. Guidelines for Assess- 27. Lobbezoo F, Ahlberg J, Glaros A. Bruxism defined and graded: an
ment, Diagnosis and Management. 5th ed. Quintessence Chicago: international consensus. J Oral Rehabil 2013;40:2–4.
The American Academy of Orofacial Pain; 2013. 28. Von Piekartz H. Management of parafunctional activities and
4. Okeson J. Temporomandibular pains in bells. Orofac Pain Bruxism. In: Selvararnam P, Nier K, Zuluaga M, editors. Head-
2014;6:329–81. ache, Orofacial Pain and Bruxism. Churchill Livingstone; 2009.
5. Marklund S, Wänman A. Incidence and prevalence of temporo- p. 261–77.
mandibular joint pain and dysfunction. A one-year prospective 29. Manfredini D, Cocilovo F, Favero C, et al. Surface electromyog-
study of university students. Acta Odontol Scand 2007;65: raphy of jaw muscles and kinesiographic recordings: diagnostic
119–27. accuracy for myofascial pain. J Oral Rehabil 2011;38:791–9.
6. Glaros AG, Williams K, Lausten L. Diurnal variation in pain 30. Castroflorio T, Falla D, Wang K, et al. Effect of experimental
reports in temporomandibular disorder patients and control sub- jaw-muscle pain on the spatial distribution of surface EMG activ-
jects. J Orofac Pain 2008;22:115–21. ity of the human masseter muscle during tooth clenching. J Oral
7. Von Piekartz H, Hall T. Orofacial manual therapy improves cervi- Rehabil 2012;39:81–92.
cal movement impairment associated with headache and features 31. McPartland J, Simons D. Myofascial Trigger Points: translating
of temporomandibular dysfunction: a randomized controlled trial. molecular theory into Manual Therapy. In: Dommerholft J, Hui-
Man Ther 2013;18:345–50. jbregts P, editors. Myopfascial Trigger Points. Pathophysiology
8. Von Piekartz H, Lüdtke K. Effect of treatment of temporoman- and Evidence Informed Diagnosis and Management. Boston:
dibular disorders (TMD) in patients with cervicogenic headache: Jones and Bartlett Publishers; 2011.
a single-blind, randomized controlled study. Cranio 2011;29: 32. Stegenga B, de Bont L, Boering G, et al. Tissue responses to
43–56. degenerative changes in the temporomandibular joint: a review.
9. Peck C, Goulet JP, Lobbezoo F, et al. Expanding the taxonomy of J Oral Maxillofac Surg 1991;49:1079–88.
the diagnostic criteria for temporomandibular disorders. J Oral 33. Nitzan D. Friction and adhesive forces. Possible underlying causes
Rehabil 2014;1:2–23. for temporomandibular joint internal derangement. Cells Tissues
10. Schiffman E, Ohrbach R, Truelove EL, et al. The Research Diag- Organs 2003;174(1-2):6–16.
nostic Criteria for Temporomandibular Disorders. V: methods 34. Delcanho R. Temporomandibular joint arthroscopy. Aust Dent J
used to establish and validate revised Axis I diagnostic algorithms. 2000;45:143.
J Orofac Pain 2010;24:63–78. 35. Minakuchi H, Kuboki T, Matsuka Y, et al. Randomized controlled
11. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic Criteria evaluation of non-surgical treatments for temporomandibular
for Temporomandibular Disorders (DC/TMD) for Clinical and joint anterior disk displacement without reduction. J Dent Res
Research Applications: Recommendations of the International 2001;80:924–8.
RDC/TMD Consortium Network and Orofacial Pain Special 36. Balasubramaniam R, Ram S. Orofacial movement disorders. Oral
Interest Group. J Oralfac Pain Headache 2014;28:6–27. Maxillofac Surg Clin North Am 2008;20:273–85.
12. Benoliel R, Svensson P, Heir GM, et al. Persistent orofacial 37. Greene C, Laskin D. Long-term status of TMJ clicking in patients
muscle pain. Oral Dis 2011;17(Suppl. 1):23–41. with myofascial pain and dysfunction. J Am Dent Assoc
13. Wright EF. Referred craniofacial pain patterns in patients with 1988;117:461–5.
temporomandibular disorders. J Am Dent Assoc 2000;131: 38. Larheim T. Role of magnetic resonance imaging in the clinical
1307–15. diagnosis of the temporomandibular joint. Cells Tissues Organs
14. Schindler H, Svensson P, Türp J, et al. Myosfascial Temporoman- 2005;180:6–21.
dibular Disorder Pain. Pathophysiology and Management. The 39. Schiffman E, Anderson G, Fricton J, et al. The relationship
Puzzle of Orofacial Pain. Basel: Karger; 2007. between level of mandibular pain and dysfunction and stage of
15. De Boever JA, Carlson GE. Etiology and differential diagnosis. temporomandibular joint internal derangement. J Dent Res
In: Zarb GA, Garlsson GE, Sessle BH, et al., editors. Temporo- 1992;71:1812–15.
mandibular Joint and Masticatory Muscle Disorders. Munkgaard: 40. Luder H, Bobst P, Schroeder H. Histometric study of synovial
Copenhagen; 1994. p. 171–87. cavity dimensions of human temporomandibular joints with
16. Türp J, Greene C, Strub J. Dental occlusion: a critical reflection normal and anterior disc position. J Oral Rehabil 1993;7:
on past, present and future concepts. J Oral Rehabil 2008;35: 263–74.
446–53. 41. Westesson P, Bronstein S, Liedberg J. Internal derangement of
17. McCarroll R, Naeije M, Kim Y, et al. Short-term effect of a sta- the temporomandibular joint: morphologic description with cor-
bilization splint on the asymmetry of submaximal masticatory relation to joint function. Oral Surg Oral Med Oral Pathol
muscle activity. J Oral Rehabil 1989;16:171–6. 1985;59:323–31.
18. Michelotti A, Farella M, Gallo L, et al. Effect of occlusal interfer- 42. Davant T, Greene C, Perry H, et al. A quantitative computer-
ence on habitual activity of human masseter. J Dent Res 2005; assisted analysis of disc displacement in patients with internal
84:644–8. derangement using sagittal view magnetic resonance imaging.
19. LeResche L, Saunders K, Von Korff M, et al. Use of exogenous J Oral Maxillofac Surg 1993;51:974–9, discussion 979–81.
hormones and risk of temporomandibular disorder pain. Pain 43. Santos K, Dutra M, Warmling L, et al. Correlation among
1997;69:153–60. the changes observed in temporomandibular joint internal
442 PART IV  Overview of Contemporary Issues in Practice

derangements assessed by magnetic resonance in symptomatic 67. Langendoen J. Management of craniomandibular disorders. In:
patients. J Oral Maxillofac Surg 2013;71:1504–12. Hengeveld E, Banks K, editors. Maitland’s Peripheral Manipula-
44. De Leeuw J, Ros WJ, Steenks MH, et al. Multidimensional evalu- tion, 5th ed. Management of neuromusculoskeletal disorders, vol.
ation of craniomandibular dysfunction. II: pain assessment. J Oral 2. Churchill Livingston; 2013. p. 88–142.
Rehabil 1994;21:515–32. 68. Armijo Olivo S, Magee D, Parfitt M. The association between the
45. Kavuncu V, Sahin S, Kamanli A, et al. The role of systemic hyper- cervical spine, the stomatognathic system, and craniofacial pain: a
mobility and condylar hypermobility in temporomandibular joint critical review. J Orofac Pain 2006;20:271–87.
dysfunction syndrome. Rheumatol Int 2006;26:257–60. 69. Manfredini D, Castroflorio T, Perinetti G, et al. Dental occlusion,
46. Huddleston Slater J, Lobbezoo F, Onland-Moret N, et al. Ante- body posture and temporomandibular disorders: where we are
rior disc displacement with reduction and symptomatic hypermo- now and where we are heading for. J Oral Rehabil 2012;39:
bility in the human temporomandibular joint: prevalence rates and 463–71.
risk factors in children and teenagers. J Orofac Pain 2007;21: 70. La Touche R, París-Alemany A, von Piekartz H, et al. The influ-
55–62. ence of cranio-cervical posture on maximal mouth opening and
47. De Leeuw R. Post MVA TMD patients endorse more general pressure pain threshold in patients with myofascial temporoman-
symptoms than nontrauma TMD patients. J Evid Based Dent dibular pain disorders. Clin J Pain 2011;27:48–55.
Pract 2008;8:246–8. 71. Van Niekerk SM, Louw Q, Vaughan N, et al. Photographic mea-
48. Faralli M, Calenti C, Ibba M, et al. Correlations between posturo- surement of upper body sitting posture of high school students:
graphic findings and symptoms in subjects with fractures of the a reliability and validity study. BMC Musculoskelet Disord
condylar head of the mandible. Eur Arch Otorhinolaryngol 2008;9:113–19.
2009;266:565–70. 72. Watson DH, Trott PH. Cervical headache: an investigation of
49. Steenks M, Hugger A, De Wijer A. Painful Arthrogenous Tem- natural head posture and upper cervical flexor muscle perfor-
poromandibular Disorders. Pathophysiology, diagnosis, manage- mance. Cephalalgia 1993;13:272–84.
ment and prognosis. In: Türp J, Sommer C, Hugger A, editors. 73. Raine S, Twomey L. Head and shoulder posture variation in 160
The Puzzle of Orofacial Pain. Basel: Karger; 2007. p. 124– asymptomatic women and men. Arch Phys Med Rehabil 1997;
53. 78:1215–23.
50. Rocabado Seaton M, Iglarsh ZA. Musculoskeletal evaluation of 74. Visscher C, Boer W, Lobbezoo F, et al. Is there a relationship
the maxillofacial region. In: Musculoskeletal Approach to Maxil- between head posture and craniomandibular pain? J Oral Rehabil
lofacial Pain. New York: Lippincott Company; 1991. p. 11–117. 2002;29:1030–6.
51. Haanpää M, Attal N, Backonja M, et al. New PSIG guidelines on 75. Fernández-de-Las-Peñas C, Coppieters M, Cuadrado M, et al.
neuropathic pain assessment. Pain 2011;152:14–27. Patients with chronic tension-type headache demonstrate
52. Asbury A, Fields H. Pain due to peripheral nerve damage: a increased mechano-sensitivity of the supra-orbital nerve. Head-
hypothesis. Neurology 1984;34:1587–90. ache 2008;48:570–7.
53. Hromada J. Current concepts on the spinal nerves with reference 76. Archer S, Vig P. Effects of head position on intraoral pressures in
to their function and reparative processes. Acta Chir Orthop Trau- Class I and Class II adults. Am J Orthond 1985;87:311–18.
matol Cech 1963;30:14–23. 77. Armijo-Olivo S, Rappoport K, Fuentes J. Head and cervical
54. Gadient P, Smith J. The neuralgias: diagnosis and management. posture in patients with temporomandibular disorders. J Orofac
Curr Neurol Neurosci Rep 2014;14:459–65. Pain 2011;25:199–209.
55. Janetta P. Microsurgical approach to the trigeminal nerve for tic 78. Lorenz P, von Piekartz H. Profile head measurement of patients
douloureux. In: Krayenbühl HP, Maspes E, Sweet W, editors. with a TMJ in comparison with a control group. Is there a differ-
Progress in Neurological Surgery, vol. 7. Basel: Karger; 1976. ence? Manuelle Therapie, Thieme (in press).
p. 180. 79. Haas M. Interexaminer reliability for multiple diagnostic test regi-
56. Yuguang L, Chengyuan W, Meng L, et al. Neuroendoscopic mens. J Manipulative Physiol Ther 1991;14:95–103.
anatomy and surgery of the cerebellopontine angle. J Clin Neu- 80. Hesse J, Naeije M, Hansson T. Craniomandibular stiffness in
rosci 2005;12:256–60. myogenic and arthrogenous CMD patients and control subjects:
57. Barba D, Alksne JF. Success of microvascular decompression with a clinical and experimental investigation. J Oral Rehabil
and without prior surgical therapy for trigeminal neuralgia. J Neu- 1996;23:379–85.
rosurg 1984;60:104. 81. Okeson J, Leeuw R. Differential diagnosis of temporomandibular
58. Jannetta P, Bissonette D. Management of failed patient with tri- disorders and other orofacial pain disorders. Dent Clin North Am
geminal neuralgia. Clin Neurosurg 1985;32:334–47. 2011;55:105–20.
59. Renton T, Dawood A, Shah A, et al. Post-implant neuropathy of 82. Anderson G, John MT, Ohrbach R, et al. Influence of headache
the trigeminal nerve. A case series. Br Dent J 2012;212:E17. frequency on clinical signs and symptoms of TMD in subjects with
60. Pedullà E, Meli GA, Garufi A. Neuropathic pain in temporoman- temple headache and TMD pain. Pain 2011;152:765–71.
dibular joint disorders: case-control analysis by MR imaging. Am 83. Alonso-Blanco C, Fernández-de-las-Peñas C, de-la-Llave-Rincón
J Neuroradiol 2009;30:1414–18. A, et al. Characteristics of referred muscle pain to the head from
61. Hall T, Elvey R. Nerve trunk pain: physical diagnosis and treat- active trigger points in women with myofascial temporomandibu-
ment. Man Ther 1999;4:63–73. lar pain and fibromyalgia syndrome. J Headache Pain 2012;13:
62. Murayama R, Stuginski-Barbosa J, Moraes N, et al. Toothache 625–37.
referred from auriculotemporal neuralgia: case report. Int Endod 84. Von Piekartz H, Mohr G. Reduction of head and face pain by
J 2009;42:845–51. challenging lateralization and basic emotions: a proposal for future
63. Cavicchi O, Caliceti U, Fernandez I, et al. Laryngeal neuromoni- assessment and rehabilitation strategies. J Man Manip Ther 2014;
toring and neurostimulation versus neurostimulation alone in 22:25–35.
thyroid surgery: a randomized clinical trial. Head Neck 2012; 85. Türp J, Kowalski C, Stohler C. Pain descriptors characteristic of
34:141–5. persistent facial pain. J Orofac Pain 1997;11:285–90.
64. Fingleton C, Dempsey L, Smart K, et al. Intraexaminer and inter- 86. Fernández-Pérez A, Villaverde-Gutiérrez C, Mora-Sánchez A,
examiner reliability of manual palpation and pressure algometry et al. Muscle trigger points, pressure pain threshold, and cervical
of the lower limb nerves in asymptomatic subjects. J Manipulative range of motion in patients with high level of disability related to
Physiol Ther 2014;37:97–104. acute whiplash injury. J Orthop Sports Phys Ther 2012;42:
65. Von Piekartz H. Guidelines for Assessment of Craniomandibular 634–41.
and Craniofacial Region in Craniofacial Pain, Neuromusculosk- 87. Hansson P, Backonja M, Bouhassira D. Usefulness and limitations
eletal Assessment, Treatment and Management. Butterworth- of quantitative sensory testing: clinical and research application in
Heinemann, Elsevier; 2007. p. 59–83. neuropathic pain states. Pain 2007;129:256–9.
66. Dworkin S, Sherman J, Mancl L, et al. Reliability, validity, and 88. Fernández-de-Las-Peñas C, Arendt-Nielsen L, Svensson P. Tri-
clinical utility of the research diagnostic criteria for Temporoman- geminal and extra-trigeminal hypersensitivity in orofacial pain
dibular Disorders Axis II Scales: depression, non-specific physical patients: what are the consequences for further assessment and
symptoms, and graded chronic pain. J Orofac Pain 2002;16: treatment? In: von Piekartz H, editor. Craniofacial Assessment
207–20. and Treatment. Stuttgart: Thieme; 2014 [Chapter 5] (in press).
 43  Temporomandibular Disorders: Neuromusculoskeletal Assessment and Management 443

89. Butler D. The Sensitive Nervous System. Adelaide, Australia: 100. Kumar Potu B, Jagadeesan S, Bhat K, et al. Retromolar foramen
Noigroup Publications; 2000. and canal: a comprehensive review on its anatomy and clinical
90. Eliav E, Gracely RH, Nahlieli O, et al. Quantitative sensory applications. Morphologie: Bulletin de l’Ass des Anat 2013;97:
testing in trigeminal nerve damage assessment. J Orofac Pain 31–7.
2004;18:339–44. 101. Schroër M, von Piekartz H, Stark W. Movement behaviour of the
91. List T, Leijon G, Svensson P. Somatosensory abnormalities auriculotemporal nerve during physiological movements of the
in atypical odontalgia: a case-control study. Pain 2008;139: mandible and cervical spine pilot study using sonographic diagno-
333–41. sis. Man Ther 2012;16:181–90.
92. Baad-Hansen L, Pigg M, Ivanovic S. Intraoral somatosensory 102. Medlicott MS, Harris SR. A systematic review of the effectiveness
abnormalities in patients with atypical odontalgia: a controlled of exercise, manual therapy, electrotherapy, relaxation training,
multicentre qualitative sensory testing study. Pain 2013;154: and biofeedback in the management of temporomandibular disor-
1287–94. ders. Phys Ther 2006;86:955–73.
93. Johansson A, Isberg A, Isacsson GA. Radiographic and histologic 103. McNeely ML, Armijo Olivo S, Magee D. A systematic review of
study of the topographic relations in the temporomandibular joint the effectiveness of physical therapy interventions for temporo-
region: implications for a nerve entrapment mechanism. J Oral mandibular disorders. J Phys Ther 2006;86:710–25.
Maxillofac Surg 1990;48:953–61, discussion 96. 104. Michelotti A, de Wijer A, Steenks M, et al. Home-exercise
94. Minami I, Akhter R, Luraschi J, et al. Jaw-movement smoothness regimes for the management of non-specific temporomandibular
during empty chewing and gum chewing. Eur J Oral Sci disorders. J Oral Rehabil 2005;32:779–85.
2012;120:195–200. 105. Zeno E, Griffin J, Boyd C, et al. The effects of a home exercise
95. Novak C, Mackinnon S. Evaluation of nerve injury and nerve program on pain and perceived dysfunction in a woman with
compression in the upper quadrant. J Hand Surg 2005;18: TMD: a case study. Cranio 2001;19:279–88.
230–40. 106. Tuncer AB, Ergun N, Tuncer AH, et al. Effectiveness of manual
96. Shankland W. Atypical trigeminal neuralgia of the mental nerve: therapy and home physical therapy in patients with temporoman-
a case study. Cranio 2009;27:19–23. dibular disorders: a randomized controlled trial. J Bodyw Mov
97. Isberg A, Isacsson G, Williams W, et al. Lingual numbness and Ther 2013;17:302–8.
speech articulation deviation associated with temporomandibular 107. Stotz E, Ballenberger N, von Piekartz H. The reliability of oro-
joint disk displacement. Oral Surgery Oral Medicine Oral Pathol- facial motor function exercises in TMD versus no TMD. Is there
ogy 1987;64:9–14. a difference? 2014 (manuscript in preparation).
98. Doursounian L, Alfonso JM, Iba-Zizen M, et al. Dynamics of the 108. Breig A. Pathologic biomechanics of the cord. In: Breig A, editor.
junction between the medulla and the cervical spinal cord: an in Biomechanics of the Central Nervous System. Stockholm:
vivo study in the sagittal plane by magnetic resonance imaging. Almqvist & Wiksell; 1960. p. 120–6.
Surg Radiol Anat 1989;11:313–22.
99. Benninger B, Kloenne J, Horn J. Clinical anatomy of the lingual
nerve and identification with ultrasonography. Br J Oral Maxil-
lofac Surg 2013;51:541–4.
 CHAPTER 44 

Thoracic Spine: Models of

Assessment and Management

CHAPTER OUTLINE

Editor’s Introduction Ch 44.3  Management of the Thoracic Spine in

Patients with COPD  455
Ch 44.1  Clinical Examination and Targeted
Management of Thoracic Musculoskeletal Nicola Heneghan
Pain  444
Quentin Scott
Ch 44.2  The Thoracic Ring Approach™ – A Whole
Person Framework to Assess and Treat the
Thoracic Spine and Ribcage  449
Linda-Joy Lee

EDITOR’S INTRODUCTION

The thoracic region is a complex region volume of research into management methods
consisting of five sets of joints for most thoracic for thoracic spine disorders is likewise limited.
segments. It is uniquely encased by ribs, and Nevertheless clinicians and researchers are
their attachment to the sternum makes it a working in the field. In this chapter, authors
stable structure. It can project its influence have been asked to present an overview of two
regionally, for example in breathing or in the quite different approaches to management of
way its postural angle influences cervical thoracic spine disorders that highlight the
posture. The research into thoracic spine diversity which exists in this field. This chapter
musculoskeletal disorders is scant in comparison also brings into discussion the interest and
with that undertaken into low back and neck research, particularly over the last decade,
pain disorders. This probably reflects the lower into the relationship between the thoracic
incidence of thoracic pain when compared to the spine from the musculoskeletal perspective
two other regions but this paucity of research and respiratory function. The diversity in
should not lessen the importance or impact of scope within this chapter provides directions
thoracic pain disorders on the individual. The for future enquiry.

CHAPTER 44.1  ■  CLINICAL EXAMINATION AND

TARGETED MANAGEMENT OF
THORACIC MUSCULOSKELETAL PAIN
Quentin Scott

Thoracic spine and chest wall pain (TSP) requires accu- pleura and thoracic aorta that can mimic musculoskeletal
rate diagnosis for safe and effective management. The pain conditions. Thoracic spine function has a significant
clinician must diagnose the presence of a mechanical influence on cervical, lumbar and extremity disorders.
musculoskeletal movement disorder and exclude other Thoracic musculoskeletal pain is common across all age
possible causes including disorders of the heart, lungs, groups1 and requires thorough and precise clinical
444
 44  Thoracic Spine: Models of Assessment and Management 445

examination to ensure accurate diagnosis. This will Further exploration of aggravating activities may be
provide a framework for targeted management address- required to understand the mechanisms involved in the
ing specific impairments. presenting disorder, for example:
• thoracic rotation on pelvis due to computer place-
ment in workplace
• habitual leg crossing driving asymmetrical weight
ANATOMICAL AND BIOMECHANICAL bearing and spinal side bent position
CONSIDERATIONS • stroke versus bow side rowing
• dominant arm with overhead sporting activities.
The thoracic spine can be divided into discrete regions
based upon vertebral body dimension,2,3 zygapophyseal
joint orientation or rib joint articulations.4 The thoracic
spine is commonly divided into upper, middle and lower
History
regions based upon anatomy and differences in range of A detailed history of the presenting complaint is impor-
movement and coupled movement patterns.5 Assessment tant to substantiate the mechanisms involved in the
of thoracic spine movement requires knowledge of zyg- onset of pain and progression of symptoms. TSP is
apophyseal joint orientation and biomechanics and the often associated with concurrent musculoskeletal symp-
corresponding rib articulations with their influence on toms.1,12,13 Information regarding other musculoskeletal
thoracic movement patterns. pain assists the clinician to identify contributing factors,
An in-depth understanding of the normal range of for example, chronic low back pain with altered trunk
movement and biomechanics throughout the thorax will muscle activation patterns leading to reduced thoracic
allow the clinician to identify faulty movement patterns. spine mobility and TSP. The history should include
The dominant movement of the thoracic spine is axial details of any treatment of the presenting complaint as
rotation that mostly occurs in the upper and middle this will determine possible future assessment, modes
regions.5–7 Movement studies show greater flexion/ of treatment and the appropriateness of continued
extension range of movement and reduced axial rotation management.
in the lower thoracic spine.5,6
Specific Spinal Pathologies
The clinician needs to be aware of specific patholo-
ASSESSMENT AND DIAGNOSIS OF TSP gies that can influence posture and movement, for
example:
Subjective Examination • Scheuermann’s disease
• Ankylosing spondylitis
Area of Symptoms
• deformity due to osteoporotic vertebral compres-
A detailed description of the area of pain and associated sion fracture (Fig. 44-1)
symptoms is the first step in identifying potential sources • scoliosis.
of nociception. Thoracic pain is commonly referred from The presence of these and other conditions will play a
the cervical spine and both the abdominal and thoracic role in the differential diagnosis of TSP disorders.
viscera.8,9 In addition, the thoracic spine can refer to the
posterior shoulder region, rib cage, anterolateral abdomi- Red Flags
nal wall and iliac crest region.10,11
Red flags are indicators of serious pathology requiring
medical referral or further investigations. Inquiries
Behaviour of Symptoms
regarding the patient’s general health and specific screen-
The behaviour of symptoms will further differentiate ing questions (such as smoking, history of heart disease,
potential sources of pain, help determine whether the unexplained weight loss) may be necessary to exclude
symptoms are mechanical in origin and identify driving non-musculoskeletal pathology. Questioning for red
mechanisms. Identification of aggravating and easing flags, information regarding behaviour of symptoms
factors will allow the clinician to explore the relationship (such as consistency and severity) and knowledge of
between movement behaviour and symptomatology. potential sources of thoracic spine and chest wall pain is
Aggravating factors for thoracic spine disorders often required to assist identification of presentations that are
encompass one or a combination of the following not mechanical musculoskeletal in origin, for example,
activities: the thoracic spine is a common region for metastatic
• thoracic movement, especially rotation and disease. Detailed discussion regarding red flag recogni-
extension tion and presentations is beyond the scope of this section
• upper limb movements, especially into elevation or and the reader is directed elsewhere.14
sustained upper limb activity
• sustained postural load, usually sitting Yellow Flags
• cervical motion
• respiration Yellow flags are indicators of psychosocial factors associ-
• repetitive lower limb activities. ated with poor recovery from injury. Psychosocial risk
446 PART IV  Overview of Contemporary Issues in Practice

FIGURE 44-2  ■  Increased thoracolumbar extension with poor

mid-thoracic, scapula and low lumbar correction in sitting.
FIGURE 44-1  ■  Increased thoracic kyphosis due to osteoporotic
vertebral compression fracture.
thoracolumbar junction extension with poor mid-thoracic
and scapula correction (Fig. 44-2).
factors have been reported in TSP15 and therefore thera- Altered thoracic postures are usually linked to postural
pists should be able to identify the presence of yellow faults in other spinal regions, for example, in sitting,
flags that will influence management strategies and increased thoracic kyphosis is often associated with
prognosis. forward head posture and protracted scapulae while
decreased kyphosis or flat thoracic spine is seen with
increased lumbar flexion (Fig. 44-3). A thoracic posture
Physical Examination assessment should also include observation of scapula
Information gained in the subjective examination on the position and cervical and lumbopelvic regions. Therapist-
behaviour of symptoms will guide physical examination. assisted correction of posture and reassessment of
The clinician should conduct specific postural, func- symptomatology will allow further analysis of postural
tional, movement and muscle activation assessment to involvement.
determine faulty movement patterns and motor control An understanding of the effects of age and specific
strategies. pathologies on the thoracic spine anatomy and resultant
thoracic curvature will assist in determining the revers-
ibility of the adopted posture and related movement
Posture
patterns.
Altered thoracic spine posture has been linked to painful
movement impairments,16 reduced shoulder elevation,17,18 Motion Assessment
altered scapula kinematics,17 altered rib cage motion19,20
and altered chest wall shape.19 Thoracic spine active movement assessment will concen-
Assessment of thoracic spine posture focuses on sagit- trate on the range and symmetry of thoracic rotation and
tal plane orientation (increased kyphosis vs lordosis), the range of sagittal plane movement. Careful analysis of
transverse plane orientation (thoracic rotation) and movement patterns is required throughout the cervical,
coronal plane orientation (scoliosis). Assessment of the thoracic and lumbar spines and more specifically between
adopted resting posture and how the patient attempts to the regions of the thoracic spine.
correct this posture will provide information regarding When assessing thoracic spine rotation, it is important
proprioceptive deficits and possible faulty movement pat- to observe the pattern of movement, where the move-
terns. A common postural correction fault is increased ment is occurring and the relationship to pain. It is
 44  Thoracic Spine: Models of Assessment and Management 447

$ %

FIGURE 44-3  ■  (A) Increased thoracic kyphosis with forward head posture and protracted scapulae. (B) Flat thoracic spine with
increased lumbar flexion.

possible that restriction in one region of the thorax can BOX 44-1  Diagnosis and Classification of
lead to increased strain through another region. Thoracic TSP Disorders
extension can be assessed with bilateral shoulder flexion.
The range and pattern of thoracic extension will be Pathobiological processes
linked to postural findings. Increased thoracic kyphosis Source of nociception
results in reduced thoracic extension range and possible Pain mechanisms
compensatory patterns in the regions above and below. Patho-anatomical processes
Altered thoracic posture can influence the range and Exclusion of non-mechanical thoracic pain or serious mus-
pattern of movement coupling.21 Correction of faulty culoskeletal pathology
postural and movement patterns and reassessment of Presence of structural pathology
Understanding of faulty thoracic movement and postural
symptomatology and movement behaviour assist identi-
patterns
fication of driving mechanisms. A common example is Muscle system impairment
reassessment of thoracic rotation following correction of Psychosocial involvement
the thoracolumbar position.

Muscle System Assessment

TSP disorders can occur as a result of sub-optimal mus- altered relationship between the abdominal muscles,
cular control of movement leading to increased tissue diaphragm and rib cage. Asymmetry in the length
strain.16 Assessment of muscle function related to the and recruitment of the trunk muscles will influence
thoracic spine will involve analysis of posture, functional movement of the thoracic spine and rib cage.16 Different
movement, specific movement tests and specific muscle thoracolumbar postures can influence trunk muscle
activation and length tests. recruitment across the three regions of the spine.23,24 This
Assessment of the trunk, hip and axioscapula muscle has the potential to influence thoracic movement
system (which potentially influence the thoracic spine patterns.
and rib cage) will be determined by the behaviour of
symptoms and observation of altered movement patterns. Manual Examination
Axioscapula muscle control should be assessed when the
behaviour of thoracic symptoms involves upper limb or Manual examination of the thoracic spine, rib cage, cervi-
postural activities. Hip muscle control will be important cal spine and scapula play an important role in assessment
to assess when the patient reports symptoms with func- of relative motion and provocation of symptoms in TSP
tional activities involving standing and repetitive lower disorders.
limb movement.
Assessment of breathing patterns will assist in identify- Diagnosis
ing the adopted motor strategy in many TSP disorders.
Reduced rib cage mobility has been shown in a low back Diagnosis and classification of TSP disorders (Box 44-1)
pain population.22 This is argued to be the result of the should encompass the possible source of nociception and
448 PART IV  Overview of Contemporary Issues in Practice

more importantly the underlying mechanisms to direct example, specific mobilization of mid-thoracic rotation
the clinician on specific management. can improve the overall rotation pattern of movement
and reduce lower thoracic strain.
Improving thoracic spine range of motion is also
MANAGEMENT OF THORACIC important in the management of cervical spine, lumbar
MUSCULOSKELETAL PAIN DISORDERS spine and upper limb disorders. Movement dissociation
between the different spinal regions will be linked to
Specific management of thoracic musculoskeletal pain proprioceptive deficits and the retraining of these aspects
disorders is dependent upon accurate diagnostics allow- will go hand in hand. Restoring improved thoracic spine
ing a targeted approach. The emphasis in the manage- range and pattern of movement may not occur unless
ment will depend on the outcome of the physical postural deficits in other regions are addressed in
examination. Thoracic musculoskeletal pain can result conjunction.
from other mechanisms rather than movement restric-
tion. Thoracic musculoskeletal pain disorders make up a
heterogeneous group that requires specific treatment
Optimize Muscle Function
approaches to address the presenting impairments. Goals should be focused on:
The main aspects of management will involve a com- • Facilitation of improved thoracic erector spinae
bination of the following. endurance and strength. This is indicated in cases
of increased thoracic spine kyphosis.
• Facilitation of improved thoracic spine motion
Postural Correction control. Improved control may be required either
Correction of the thoracic spine and other regional pos- into thoracic rotation, flexion or extension.
tural and proprioceptive impairments is an important Facilitation of motion control may be specific to a region
starting point in management. Correction of thoracic of the thoracic spine and not to the entire thoracic spine.
spine posture should occur in conjunction with cervical Addressing impairments in thoracic motion control
spine, scapula, lumbar spine and hip correction, for cannot be achieved without first observing the movement
example, correction of the lumbar spine into neutral patterns of the regions above and below the thoracic
posture will be essential before correction of the thoracic spine. Often addressing lumbar spine, cervical spine and
spine is possible. scapula muscle function greatly improves thoracic spine
Correction of postural asymmetry in the coronal and muscle impairments.
transverse planes to ensure no spinal/thoracic rotation or
shifting is required in conjunction with correction of
sagittal plane postures (Fig. 44-4).
Address Contributing Impairments
1. Restore normal lumbopelvic and cervical postural
and movement patterns. This will assist normaliza-
Improve Thoracic Spine Mobility tion of trunk musculature that will potentially affect
Optimal thoracic spine function requires the restoration thoracic spine and rib cage mobility.
of symmetrical and adequate rotation and appropriate 2. Breathing control to address the relationship
thoracic spine sagittal plane motion. This may be depen- between the abdominal muscles, diaphragm and rib
dent upon factors such as age, degree of thoracic kyphosis cage. This will involve:
and reversibility of the thoracic posture. • facilitation of improved abdominal muscle activa-
Manual therapy directed at both the zygapophyseal tion and control
joint and rib joint articulations may be required to restore • retraining normal breathing patterns
normal movement in cases of restricted segmental • improving lateral rib cage mobility.
motion. Improving movement at one region of the tho- 3. Axioscapula muscle control. Facilitation of im-
racic spine will often reduce stress at another region, for proved axioscapula motor control should occur

$ %

FIGURE 44-4  ■  Correction of right thoracic rotation in conjunction with sagittal plane postural correction.
 44  Thoracic Spine: Models of Assessment and Management 449

together with thoracic spine postural and move- 10. Fukui S, Ohseto K, Shiotani M. Patterns of pain induced by
ment retraining. distending the thoracic zygapophyseal joints. Reg Anesth
1997;22(4):332–6.
4. Hip muscle control. Facilitation of optimal hip 11. Feinstein B, Langton JN, Jameson RM, et al. Experiments on pain
extensor and abduction strength and endurance in referred from deep somatic tissues. J Bone Joint Surg Am 1954;
weight-bearing activities is essential to allow appro- 36-A(5):981–97.
priate trunk muscle activation strategies during 12. Murphy S, Buckle P, Stubbs D. A cross-sectional study of self-
reported back and neck pain among English schoolchildren and
function. This works to prevent adverse effects on associated physical and psychological risk factors. Appl Ergon
thoracic movement and loading patterns. 2007;38(6):797–804.
13. Wedderkopp N, Leboeuf-Yde C, Andersen LB, et al. Back pain
Precise examination of the thoracic spine will allow the reporting pattern in a Danish population-based sample of children
clinician to differentiate thoracic mechanical musculosk- and adolescents. Spine 2001;26(17):1879–83.
14. Giles IGF, Singer KP, editors. Clinical Anatomy and Management
eletal from non-mechanical sources. Knowledge of tho- of Thoracic Spine Pain. Oxford: Butterworth Heinemann; 2000.
racic anatomy, biomechanics, normal range of motion, 15. Briggs AM, Bragge P, Smith AJ, et al. Prevalence and associated
postures and other regional influences, enables identifica- factors for thoracic spine pain in the adult working population: a
tion of the thoracic movement disorder and underlying literature review. J Occup Health 2009;51(3):177–92.
16. Spitznagle T, Ivens R. Movement system syndromes of the thoracic
mechanisms. This results in a more targeted approach to spine. In: Sahrmann SA, editor. Movement System Impairment
management. Syndromes of the Extremities, Cervical and Thoracic Spines. St
Louis: Elsevier Mosby; 2011.
REFERENCES 17. Kebaetse M, McClure P, Pratt NA. Thoracic position effect on
shoulder range of motion, strength, and three-dimensional scapular
1. Briggs AM, Smith AJ, Straker LM, et al. Thoracic spine pain in the kinematics. Arch Phys Med Rehabil 1999;80(8):945–50.
general population: prevalence, incidence and associated factors in 18. Crawford HJ, Jull G. the influence of thoracic posture and move-
children, adolescents and adults. A systematic review. BMC Mus- ment on range of arm elevation. Physiother Theory Pract 1993;
culoskelet Disord 2009;10:77. 9:143–8.
2. Edmondston SJ. Clinical biomechanics of the thoracic spine includ- 19. Lee LJ, Chang AT, Coppieters MW, et al. Changes in sitting
ing the rib cage. In: Boyling JD, Jull GA, editors. Grieve’s Modern posture induce multiplanar changes in chest wall shape and motion
Manual Therapy The Vertebral Column. 3rd ed. Edinburgh: with breathing. Respir Physiol Neurobiol 2010;170(3):236–44.
Churchill Livingstone; 2004. 20. Culham EG, Jimenez HA, King CE. Thoracic kyphosis, rib mobil-
3. Panjabi MM, Takata K, Goel V, et al. Thoracic human vertebrae. ity, and lung volumes in normal women and women with osteopo-
Quantitative three-dimensional anatomy. Spine 1991;16(8): rosis. Spine 1994;19(11):1250–5.
888–901. 21. Edmondston SJ, Aggerholm M, Elfving S, et al. Influence of
4. Lee D. The Thorax: An Integrated Approach. Britsih Columbia: posture on the range of axial rotation and coupled lateral flexion of
Diane G. Lee Physiotherapist Corporation; 2003. the thoracic spine. J Manipulative Physiol Ther 2007;30(3):
5. Willems JM, Jull GA, Ng JKF. An in vivo study of the primary and 193–9.
coupled rotations of the thoracic spine. Clin Biomech (Bristol, 22. Scott QJ, Deeg T, Richardson CA, editors. The Effect of Low Back
Avon) 1996;11(6):311–16. Pain on Lateral Rib Cage Mobility. Brisbane: MPA Conference;
6. White A. Analysis of the mechanics of the thoracic spine in man: 2005.
an experimental study of autopsy specimens. Acta Orthop Scand 23. Caneiro JP, O’Sullivan P, Burnett A, et al. The influence of differ-
1969;127(Suppl.):1–105. ent sitting postures on head/neck posture and muscle activity. Man
7. Edmondston SJ, Singer KP. Thoracic spine: anatomical and bio- Ther 2010;15(1):54–60.
mechanical considerations for manual therapy. Man Ther 1997; 24. O’Sullivan PB, Dankaerts W, Burnett AF, et al. Effect of different
2(3):132–43. upright sitting postures on spinal-pelvic curvature and trunk muscle
8. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain activation in a pain-free population. Spine 2006;31(19):E707–12.
patterns. I: a study in normal volunteers. Spine 1990;15(6):453–7.
9. Goodman CC, Snyder TK. Differential Diagnosis for Physical
Therapists: Screening for Referral. 5th ed. United States: Elsevier;
2012.

CHAPTER 44.2  ■  THE THORACIC RING APPROACH™ –

A WHOLE PERSON FRAMEWORK TO
ASSESS AND TREAT THE THORACIC
SPINE AND RIBCAGE
Linda-Joy Lee

Clinicians have long recognized that the thoracic spine spine treatment is limited and provides conflicting insight
can be the silent but underlying cause, or ‘driver’, for into when treatment will improve outcomes; while some
problems elsewhere in the body. Most commonly, the subjects show improvements, others report aggravation
hypothesis is that a stiff thorax creates excessive forces of symptoms.1,2 Clinical experiences can be similarly
and pain in adjacent areas such as the lumbar spine, neck ambiguous. Furthermore, treatment to the thorax may
and shoulder girdle.1–3 cause adverse experiences such as nausea and sympathetic
A challenge for clinicians is how to determine when nervous system symptoms.
treatment to the thorax will resolve symptoms either To make wise clinical decisions regarding when and
locally or distally. Research on the benefits of thoracic how to treat the thorax, the thoracic spine needs to be
450 PART IV  Overview of Contemporary Issues in Practice

viewed with a broader lens. Firstly, the thoracic spine

needs to be assessed and treated within the context of the
three-dimensional ‘thoracic ring’.4–8 Secondly, the thorax
needs to be assessed within the context of the whole
person and whole body function. That is, in order to
determine whether or not treatment to the thorax will
positively impact a patient’s problem, it is necessary to
understand and assess the connections between the thorax
and the rest of the body. Thirdly, treatment to the thorax A
needs to expand beyond techniques that aim to increase
mobility, to incorporate training optimal neuromuscular
control and muscle balance for optimal movement, load
transfer and respiration.

CONNECTING THE THORACIC SPINE

AND RIBCAGE AS A SERIES OF
‘THORACIC RINGS’
In both research and clinical realms the thoracic spine is
commonly considered in isolation from the ribs and B
ribcage, with separate assessment and treatment tech-
niques for each.9–12 However, anatomical13 and recent
biomechanical data14,15 support that where there are ante-
rior attachments, the true functional spinal unit of the
thorax is the ‘thoracic ring’.4,8 For example, the fifth tho-
racic ring is comprised of the right and left fifth ribs, their
anterior attachments to the sternum, the T4–T5 thoracic
vertebrae and the T4–T5 intervertebral disc.4–8,10 There-
fore there is a need for manual assessment and treatment
techniques for the entire thoracic ring.
Thoracic Ring Approach™16,17 techniques employ pal-
pation points and forces applied around the anterior,
C
lateral and posterior ribcage to assess and treat the three-
dimensional thoracic rings.4–7,16–18 Due to the strong ana- FIGURE 44-5  ■  (A) Two ‘thoracic rings’, with the upper thoracic
tomical connections between the ribs and thoracic spine, ring depicting the osteokinematics that occur with right rotation.
motion detected at the lateral ribs reflects vertebral During right rotation, the vertebra rotates right, the right rib
posteriorly rotates and the left rib anteriorly rotates,10 and there
motion, and forces applied to the side of the ring impact is a left (contralateral) translation of the thoracic ring that can
the vertebral segment as well as the ribs (i.e. the entire be palpated at the lateral aspect of the ring.4,5 (B) ‘Stacked’ tho-
ring).19 Thoracic ‘ring palpation’4–7,17 is applied farthest racic rings – when neuromuscular forces are balanced around
from the axis of rotation of the thoracic segment and and between the thoracic rings, optimal alignment is supported
and provides a base from which to initiate movement. There is
where there is greater amplitude of motion to detect sufficient space between the thoracic rings. Although not all
compared to palpation points centrally at the vertebra. muscles are depicted here, optimal alignment of the thoracic
Thoracic ring techniques facilitate assessment of inter- rings is supported by balance between the deep and superficial
ring (segmental) motion and control during functional muscles attaching to the rings. Note that the top vertebra is
tasks, as well as analysis of multiple rings and inter- missing from the superior thoracic ring. If this figure depicts
rings 3, 4 and 5, the related vertebral segments include T2–T5.
regional relationships simultaneously (Fig. 44-5). Fur- Less muscle bulk over the sides of the rings compared to the
thermore, thoracic ring palpation and ‘thoracic ring posterior aspect of the ring facilitates more accurate analysis of
correction’ techniques4,5,6,16,17 provide a method to evalu- ring motion during functional tasks. (C) ‘Unstacked’ thoracic
ate the connections between a dysfunctional thoracic ring rings – when force vectors around the thoracic rings are unbal-
anced, there are multiple patterns of thoracic ring dysfunction
and whole body function.5,6,17,20 that can occur. This figure depicts one potential pattern of non-
optimal inter-ring relationships. Compression between the
upper and lower rings on the right creates left translation of the
CONNECTING THE THORAX TO WHOLE middle ring, which is coupled with right rotation. Compression
of the rings also creates side bending, which is coupled with
BODY FUNCTION: DETERMINING IF THE rotation. These inter-ring relationships can be assessed simul-
THORACIC RINGS ARE THE ‘DRIVER’ taneously using thoracic ring palpation techniques. Findings
from manual assessment of the posterior joints of the thoracic
FOR THE PATIENT’S PROBLEM spine and ribcage need to be interpreted in reference to the
position and behaviour of the related thoracic ring. (Reproduced
with permission from Linda-Joy Lee Physiotherapist Corp.)
Understanding the role of the thorax in whole body func-
tion facilitates more effective clinical reasoning to decide
 44  Thoracic Spine: Models of Assessment and Management 451

when treatment to the thoracic rings will result in best biomechanics and other first principles, several biologi-
outcomes. The ultimate goal of treatment is to change cally plausible mechanisms have been proposed6,16,17
the way that patients experience their bodies and to create (Table 44-1).
more optimal strategies for posture, movement and per- Thus, a patient with a dysfunctional thorax can present
formance. Therefore, when considering any area of the with a wide variety of symptoms and functional problems.
body, the relationship of regional dysfunction to whole Location of pain or tissue changes does not always cor-
body function needs to be assessed and determined. relate to the primary underlying cause of the problem.
There are multiple mechanisms by which dysfunction ‘Meaningful Task Analysis (MTA)’ was initially proposed
of the thoracic rings, whether painful or not, can drive as a whole body assessment framework to determine
distal problems as diverse as incontinence, groin pain, whether or not dysfunction in the thorax was the under-
Achilles tendinopathy and shoulder impingement. It is lying cause, or ‘driver’, of the patient’s problem.20 MTA
not possible to describe these mechanisms in depth here, incorporates not only the biomechanical features of a
but based on evidence from anatomy, neurophysiology, task, but also the emotional, cognitive, social and

TABLE 44-1  Connections Between the Thorax and the Rest of the Body – Examples of Biologically
Plausible Mechanisms as to how the Thoracic Rings can Drive Distal Pain and Problems
Anatomical Connections/Role of Possible Mechanisms by Which Dysfunction of the
the Thorax Thoracic Rings can Drive Distal Problems
Direct muscular/myofascial connections Hypertonicity of specific fascicles related to a thoracic ring alters forces
between thoracic rings and other at specific segments in the lumbar spine, cervical spine, pelvis and
regions bones of the shoulder girdle
Provides a foundation for shoulder girdle Rotation/side-bending dysfunction of any thoracic rings creates an
and head/neck function asymmetrical foundation for muscle function and load transfer, poor
control of thoracic rings results in loss of a stable base for the
shoulder girdle, neck and head
Centre of trunk rotation Altered rotational control of the thorax creates altered forces/loads at
other rotational centres in the body (e.g. atlanto-axial joint, hips,
subtalar joints)
Closely related to the brachial plexus and Twists anywhere in the thorax can create compensatory rotations of the
subclavian vessels first ring and clavicle, reducing space in the thoracic outlet
Fascial and neural connections to the Connect the thoracic rings internally to the neck, cranium, abdominal
visceral system cavity – for example the pleura of the lungs has connections into the
deep cervical fascia; innervation of many viscera comes from thoracic
segments → altered neural drive creates gastrointestinal symptoms
such as bloating, ‘irritable bowel syndrome’
Diaphragm – costal attachments (lower Altered alignment of multiple thoracic rings changes tension through the
two ribs and lowest four rings) muscle fibres and fascia of the diaphragm → alters breathing patterns
and can change the shape of apertures for oesophagus, aorta, inferior
vena cava → changes blood flow to lower extremity, contributes to
oesophageal reflux
Sympathetic trunks run anterior to the Tensioning of the sympathetic trunk can occur across multiple levels due
heads of the ribs to multiple ‘unstacked’ rings and contribute to sensitization of the
sympathetic system and symptoms such as hyperhidrosis, flushing
and agitation
Innervation of all abdominal muscles ‘Unstacked’ thoracic rings create asymmetrical abdominal muscle
from T7–L1/2 nerve roots, thoracic rings recruitment due to altered neural drive, altered position of muscle
provide attachment/origin for attachments, or as a compensatory strategy for non-optimal rotational
abdominal muscles control in the upper thoracic rings → impacts lumbopelvic control,
indirect effect on pelvic floor muscle and lumbar paraspinal muscle
function
Relationship between intrathoracic and Excessive superficial muscle activity in the thorax increases IAP →
intra-abdominal pressure (IAP) ‘pressure belly’ creates excessive loads on pelvic floor fascia
(contributes to pelvic organ prolapse), or creates sustained increases
in pelvic floor muscle activity (contributes to incontinence/pain).
Thoracic drivers commonly create asymmetrical patterns of pressure
and altered pelvic floor activity due to rotational role
Contributes to control of postural Poorly controlled thoracic rings, or rings held in one movement pattern
equilibrium, especially in the coronal create altered loading of lower-extremity structures, especially
and transverse planes, because thoracic medial–lateral forces, changes left–right leg weight bearing → alters
rings can segmentally and activation of lower extremity muscles → hip impingement and
multisegmentally move into lateral osteoarthritis, Achilles tendinopathy, metatarsal stress fractures,
translation and rotation to provide increased risk for knee ligament injuries21
control of the centre of mass over the
base of support
’Stacked’ thoracic rings provide a Loss of space between thoracic rings decreases ability to dissipate loads
shock-absorbing ‘spring’ for the trunk in the trunk → increased loads to the low back on heel strike
452 PART IV  Overview of Contemporary Issues in Practice

contextual features related to a specific problematic or meaningful complaint/ symptoms and (c) optimizes
goal-related movement. Meaningful tasks are determined transfer of loads through other areas of the body, then
from the patient’s story and direct the choice of tasks there is support for the hypothesis of a thoracic ring
analysed in the objective assessment. driver. To further strengthen the hypothesis, manual cor-
The clinical decision as to whether or not the thorax rections are also applied to other areas of the body and
should be treated, and which specific thoracic rings to the impact compared to the thoracic ring correction. In
treat, is determined by assessing and manually modifying the case of a thoracic ring driver, corrections to other
thoracic ring behaviour during screening tasks related to areas either have a negative effect or not as positive an
the patient’s meaningful task. For example, for a runner effect as the thoracic ring correction.4,5,16,17,20 This clinical
who experiences lateral foot pain on the push-off phase reasoning framework is a key feature of the Thoracic
of gait, a relevant screening task is a step forward (Fig. Ring Approach™16,17 and the Integrated Systems Model
44-6). If non-optimal alignment, biomechanics or control for Pain and Disability.22
of any thoracic rings occurs during the task, a ‘thoracic Therefore the indication to treat the thorax, and
ring correction’ is performed, whereby optimal thoracic specific levels of the thorax, is that the thorax is shown
ring alignment, movement and control is provided to be a ‘driver’ in MTA. This provides a clinical ratio-
through gentle but specific manual facilitation at the spe- nale to support that treatment to the thoracic rings will
cific ring level.4,5,16,17,20 If this ‘thoracic ring correction’ result in positive clinical outcomes for whole body
positively changes (a) ease of task performance, (b) function.

$ % &

FIGURE 44-6  ■  Meaningful Task Analysis (MTA).20 To find the driver for the patient’s foot pain related to push-off during running, a
step forward task is used as a screening task. Multiple areas of non-optimal alignment, biomechanics and/or control (non-optimal
load transfer [NOLT]) are identified during the task. (A) During left step forward, the right foot demonstrates lateral weight bearing
on push-off, with valgus forces at the ankle. At initiation of the step forward, the fourth thoracic ring is felt to translate left, creating
a segmental right rotation. Optimally the upper thorax should rotate left, and therefore the movement of the fourth thoracic ring is
non-optimal. The resultant left shift of the thorax over the base of support requires the compensatory valgus at the ankle to neutral-
ize the centre of mass over the base of support. Inset: a close-up of the impact of the early left translation of the fourth thoracic ring
on the right foot. (B) Correction of the fourth thoracic ring during the left step forward task results in optimal weight bearing through
the right ankle and foot during push-off, and reduction of the patient’s symptoms. Commonly, the starting position of the thoracic
rings needs to be corrected by ‘stacking’ them into optimal inter-ring relationships, then optimal movement and control is manually
facilitated during the task. The thorax can drive distal problems in the hip, knee, ankle and foot because of rotational mechanisms
and the effect that lateral translation of the thorax has on the centre of mass relative to the base of support. Inset: a close-up of the
right foot in push-off in response to the fourth thoracic ring correction. Note the significantly improved position. Application of
thoracic ring correction techniques during functional movement analysis allows evaluation of the potential impact that treating
specific levels of the thorax will have on symptoms, task performance, and other problematic areas in the kinetic chain. (C) The
impact of corrections to other areas of NOLT (upper panel: pelvis, and lower panel: foot) is assessed and compared to the impact
of the thoracic ring correction. The thoracic ring correction resulted in the best change in task performance, the most positive change
on all areas of NOLT, and optimized load transfer through the right foot (area of symptoms). (Reproduced with permission from Linda-
Joy Lee Physiotherapist Corp.)
 44  Thoracic Spine: Models of Assessment and Management 453

manipulation can be successful in addressing these

TREATMENT OF THE THORACIC impairments. However, often multiple vectors are present.
RING DRIVER A novel treatment technique, ‘thoracic ring stack and
breathe’,32 simultaneously releases multiple vectors
Effective treatment will address the underlying impair- around and between the thoracic rings, and can be pro-
ments of the thoracic rings. Although it is widely held gressed to dynamic contexts to combine release and neu-
that the most common impairment in the thorax is stiff- romuscular training (Fig. 44-7).
ness, due to the presence of the ribcage,3,23,24 minimal data Notably, it is common to find strong vectors from
support this belief. The intact thorax is mobile in all hypertonicity of muscles positioned laterally and anteri-
planes, and in contrast to the limited rotation of the orly around the thoracic rings (e.g. intercostals, serratus
lumbar segments, the primary motion of the thorax is anterior, pectoralis minor, oblique abdominals, dia-
rotation, followed by lateral bending.25–27 Taken as a phragm). In these cases, if treatment techniques are
whole, the evidence supports that the thorax is inherently focused only posteriorly (e.g. to the erector spinae or
flexible in nature.8 posterior articular structures), there is potential to
The capacity for movement within and between the increase imbalances around the thoracic ring and create
segments of the thorax, along with the requirements for more dysfunction, even if those levels are the underlying
control of upright posture and respiration, requires driver. When intercostal hypertonicity is present, assess-
complex coordination of muscle activity by the central ment and treatment of the two related sequential thoracic
nervous system to meet the demands of stability and rings is essential. If treatment is focused to just one of the
movement. Differential control of the deep and superfi- thoracic rings, there is potential to make the other ring
cial thoracic paraspinal muscles occurs in the transverse more dysfunctional. This highlights the importance of
plane, where the thorax has the greatest movement, for assessing force vectors around the entire thoracic ring.
control of opposite rotational perturbations.28–30 Evaluation of neuromuscular strategies for the thorax
Clinically, multiple patterns of non-optimal sequenc- needs to include: segmental control (intra-ring and inter-
ing, force modulation, and synergy between the muscles ring), inter-regional control and control of postural equi-
around the thoracic ring, between the ten thoracic rings librium.8,33 Exercise prescription is based on control
and between the rings and other regions of the body impairments found on assessment. Based on anatomical
have been observed.4,6,16,17 These non-optimal neuromus- attachments and research from other areas of the spine,
cular forces create the appearance of ‘stiffness’ that is it has been proposed that the deep segmental muscles
not related to true articular restriction. This proposal is such as thoracic multifidus and intercostals are architec-
consistent with studies that demonstrate that mobiliza- turally suited to control intra-ring and inter-ring motion.18
tion and manipulation techniques effect change via neu- Imagery, visualization and sensory cues combined with
rophysiological mechanisms that alter muscle tone and specific thoracic ring taping are used to recruit the deep
activity.31 ring control muscles, and this skill is integrated with
Therefore an essential aim of treatment is to create more complex movement patterns to train synergistic
more optimal patterns of muscle recruitment and func- patterns with superficial, multisegmental muscles con-
tion related to the thoracic rings. This is addressed necting the thoracic rings to other regions.4,7,16–18,20
through a multimodal treatment program, ensuring If dysfunction has been present for any significant
that any cognitive and/or emotional components are period of time, alterations in strength and synergies of
addressed along with physical impairments. An effective muscles between the driving thoracic rings and con-
treatment program includes concurrent: nected regions will be present. For example, if the upper
1. addressing impairments such as hypertonic muscles thoracic rings have functioned in left translation/right
creating non-optimal force vectors on the thoracic rotation, muscles on both sides of the shoulder girdle will
rings (remove the old strategy) and have adapted. As old non-optimal patterns are removed,
2. training new patterns of neuromuscular activity, weakness in specific shoulder girdle muscles will become
balancing muscular synergies and building capacity evident and need to be addressed. Exercises that train
(strength, endurance) for more optimal control of maintenance of thoracic ring control with shoulder girdle
the thorax. Specific thoracic ring taping supports dissociation, both in open and closed chain progressions,
the exercise process. provide an intermediate step to more complex move-
Non-optimal force vectors on thoracic rings can arise ments. Discussion of specific thoracic ring exercise pro-
from multiple structures attaching externally or inter- gressions and program design is beyond the scope of
nally anywhere around the three-dimensional ring. Most this section; however, a brief outline is provided in
common are neuromuscular vectors, but impairments Table 44-2.
related to the visceral system, myofascial system and
articular system are also possible. ‘Thoracic ring vector
analysis’32 assesses the location and type of system vectors. SUMMARY
The driving rings (usually two sequential thoracic rings)
are corrected and ‘stacked’ into optimal alignment and Shifting from the paradigm that the thorax is stiff and
the location and quality of the resistance to the correction requiring mobilization to one where the thorax is flexible
are evaluated. Specific treatment to the structures and requiring optimal neuromuscular control provides
identified as creating the resistance can then be applied. greater insight into why the thorax can drive distal prob-
Tools such as specific myofascial and neuromuscular lems. This moves away from conceptualizing the thorax
release, dry needling, muscle energy, mobilization and as a static, stiff box to being a dynamic stack of ten rings,
454 PART IV  Overview of Contemporary Issues in Practice

$ % &

FIGURE 44-7  ■  ‘Thoracic ring stack and breathe’.32 This technique can be performed by the therapist in combination with specific
muscle releases (such as the serratus anterior), or taught to patients as a self-release technique. The driving thoracic rings are cor-
rected and manually controlled while different breathing patterns and movements of the trunk and extremities are used to tension
different vectors acting on the rings. Over multiple cycles of deep breaths and through movement, the relevant vectors are released,
creating a platform to train new muscle recruitment patterns. (A) Thoracic ring stack and breathe of rings 3/4 while moving through
child’s pose to release vectors between the shoulder girdle/arms and the driving thoracic rings. (B) Self-stack and breathe of rings
3/4 – the patient self-corrects two sequential thoracic rings on opposite sides, and over several breath cycles moves the pelvis/hips
into rotation to release vectors between the driving thoracic rings and the lumbopelvic–hip region. (C) Dynamic thoracic ring stack
and breathe – the driving thoracic rings are corrected while the patient moves into a functional task and breathes in different pat-
terns. The therapist can modify this to become a training exercise for thoracic ring control by modulating the degree of support and
correction provided, giving primarily sensory input and less manual correction support so that the patient actively controls the
thoracic rings during movement. (Reproduced with permission from Linda-Joy Lee Physiotherapist Corp.)

TABLE 44-2  Categories to Consider for Thoracic Ring Exercise Progressions and Program Design
Segmental control Intra-ring and inter-ring Deep muscles; optimal recruitment evidenced by change in
ring position and control in response to verbal cues and
without superficial muscle activity
Inter-regional control Thoracic rings – head Maintain neutral thoracic ring stacking and dissociate from
Thoracic rings – shoulder girdle head movement, shoulder girdle movement (e.g. head
Include open and closed chain rotation, supine horizontal shoulder abduction)
Inversion postures are key to train Maintain neutral trunk position
vertical loading capacity in thorax → during lower extremity challenges (e.g. squats, split
(e.g. downward dog modified with squats)
knees bent → wall handstands → → during upper extremity challenges (e.g. wall push-ups,
handstand push-ups on wall) bench push-ups)
Thoracic rings – lumbopelvic/hip → combined upper/lower extremity challenges (e.g. front
(trunk control) medicine ball throws)
Dissociate thoracic ring control in rotation/side-bending
patterns – both congruent and incongruent from other
regions (e.g. bow and arrow with pulley, lateral medicine
ball throws, walking lunges with contralateral trunk rotation)
Postural equilibrium Thoracic rings – feet (base of Use challenges to postural equilibrium and trunk control in
support) coronal plane (lateral perturbations) while ensuring optimal
thoracic ring alignment and control (e.g. deep lateral lunges,
star lunges, lateral hops)
Thoracic spring Ensure thoracic ring control while Jump squats, lateral hops, skipping
maintaining vertical space and
without bracing or rigidity

much like a ‘slinky’ or a shock-absorbing spring. When multiple connections between the thorax and other
there is loss of optimal sequencing, force modulation, and regions of the body. Patients present with non-optimal
synergy between the muscles around the thoracic ring, strategies for their meaningful task that are linked to
between the ten thoracic rings and between the rings and non-optimal experiences of their body. In thorax-driven
other regions of the body, there are many possible con- cases, treating the thoracic ring(s) in the context of a
sequences throughout the whole body. biopsychosocial model provides the pathway to change
The Thoracic Ring Approach™16,17 incorporates these non-optimal strategies and create a positive experi-
current research on the thorax and provides innovative ence of movement, reconceptualize pain and support
clinical assessment and treatment skills for the thorax, as optimal strategies for function and performance for the
well as a clinical reasoning framework that considers the whole person.
 44  Thoracic Spine: Models of Assessment and Management 455

REFERENCES 17. Lee LJ. The Essential Role of the Thorax in Whole Body Function
and the ‘Thoracic Ring Approach’, Assessment & Treatment
1. Bergman GJD, Winters JC, van der Heijden GJMG, et al. Gron- Videos. Linda-Joy Lee Physiotherapist Corp; 2012 <www.ljlee.ca>.
ingen Manipulation Study. The effect of manipulation of the struc- 18. Lee LJ. Chapter 7: Restoring force closure/motor control of the
tures of the shoulder girdle as additional treatment for symptom thorax. In: Lee DG, editor. The Thorax An Integrated Approach.
relief and for prevention of chronicity or recurrence of shoulder White Rock, BC: Diane G. Lee Physiotherapist Corporation;
symptoms. Design of a randomized controlled trial within a com- 2003b.
prehensive prognostic cohort study. J Manipulative Physiol Ther 19. Keene C. Some experiments on the mechanical rotation of the
2002;25(9):543–9. normal spine. J Bone Joint Surg 1906;s2–4(1):69–79.
2. Cleland JA, Glynn P, Whitman JM, et al. Short-term effects of 20. Lee LJ. The essential role of the thorax in restoring optimal func-
thrust versus nonthrust mobilization/manipulation directed at the tion. Keynote presentation at the 2008 Orthopaedic Symposium of
thoracic spine in patients with neck pain: a randomized clinical trial. the Canadian Physiotherapy Association. Montreal, Canada: 2008.
Phys Ther 2007;87(4):431–40. 21. Zazulak BT, Hewett TE, Reeves NP, et al. Deficits in neuromus-
3. McConnell J. The use of taping for pain relief in the management cular control of the trunk predict knee injury risk: a prospective
of spinal pain. In: Boyling JD, Jull GA, et al., editors. Grieve’s biomechanical-epidemiologic study. Am J Sports Med 2007;35(7):
Modern Manual Therapy: The Vertebral Column. 3rd ed. Edin- 1123–30.
burgh: Elsevier Churchill Livingstone; 2005. p. 433–42. 22. Lee LJ, Lee DG. Chapter 7: Clinical practice – the reality for clini-
4. Lee LJ. Thoracic Stabilization & the Functional Upper Limb: cians. In: Lee DG, editor. The Pelvic Girdle. Elsevier; 2011.
Restoring Stability with Mobility. Vancouver, BC: Course Notes; p. 255–82.
2003. 23. Geelhoed MA, McGaugh J, Brewer PA, et al. A new model to
5. Lee LJ. A clinical test for failed load transfer in the upper quadrant: facilitate palpation of the level of the transverse processes of the
how to direct treatment decisions for the thoracic spine, cervical thoracic spine. J Orthop Sports Phys Ther 2006;36(11):876–81.
spine, and shoulder complex. Proceedings of the 2005 Orthopaedic 24. Takeuchi T, Abumi K, Shono Y, et al. Biomechanical role of the
Symposium of the Canadian Physiotherapy Association. London, intervertebral disc and costovertebral joint in stability of the tho-
Ontario, Canada: 2005. racic spine. A canine model study. Spine (Phila Pa 1976) 1999;
6. Lee LJ. The Role of the Thorax in Pelvic Girdle Pain. Presented 24(14):1414–20.
at the 6th Interdisciplinary World Congress on Low Back and 25. Gregersen GG, Lucas DB. An in vivo study of the axial rotation of
Pelvic Pain. Barcelona, Spain: 2007 November 7–10. the human thoracolumbar spine. J Bone Joint Surg Am 1967;49(2):
7. Lee LJ, Lee DG. An integrated multimodal approach to the tho- 247–62.
racic spine and ribs. In: Magee DJ, et al., editors. Pathology and 26. Lovett R. The mechanism of the normal spine and its relation to
Intervention in Musculoskeletal Intervention. Elsevier; 2008. scoliosis. Boston Med Surg J 1905;153:349–58.
8. Lee LJ. Motor Control and Kinematics of the Thorax in Pain-Free 27. Watkins R 4th, Watkins R 3rd, Williams L, et al. Stability provided
Function. Australia: University of Queensland; 2013. by the sternum and rib cage in the thoracic spine. Spine (Phila Pa
9. Giles LGF, Singer KP. The Clinical Anatomy and Management of 1976) 2005;30(11):1283–6.
Thoracic Spine Pain, the Clinical Anatomy and Management of 28. Lee L-J, Coppieters MW, Hodges PW. Differential activation of
Back Pain Series. Oxford: Butterworth-Heinemann; 2000. the thoracic multifidus and longissimus thoracis during trunk rota-
10. Lee DG. Manual Therapy for the Thorax. 1st ed. DOPC, British tion. Spine 2005;30:870–6.
Columbia: Diane G. Lee Physiotherapist Corp.; 1994. 29. Lee L-J, Coppieters MW, Hodges PW. Anticipatory postural
11. Maitland GD. Vertebral Manipulation. London: Butterworths; adjustments to arm movement reveal complex control of paraspinal
1964. muscles in the thorax. J Electromyogr Kinesiol 2009;19(1):46–54.
12. Mitchell FL, Mitchell PKG. The Muscle Energy Manual – Evalu- 30. Lee L-J, Coppieters MW, Hodges PW. En bloc control of deep
ation and Treatment of the Thoracic Spine, Lumbar Spine & Rib and superficial thoracic muscles in sagittal loading and unloading
Cage. 2nd ed. East Lansing, Michigan: MET press; 2002. of the trunk. Gait Posture 2011;33(4):588–93.
13. Standring S. Gray’s Anatomy: The Anatomical Basis of Clinical 31. Bialosky JE, Bishop MD, Price DD, et al. The mechanisms of
Practice. 40th ed. Edinburgh: Churchill Livingstone; 2008. manual therapy in the treatment of musculoskeletal pain: a com-
14. Molnar S, Mano S, Kiss L, et al. Ex vivo and in vitro determination prehensive model. Man Ther 2009;14(5):531–8.
of the axial rotational axis of the human thoracic spine. Spine (Phila 32. Lee LJ. Discover the Thorax – Level 1: Inter-ring Rotational
Pa 1976) 2006;31(26):E984–91. Control for Optimal Trunk Function. Vancouver, BC: Course
15. Lee L-J, Chang AT, Coppieters MW, et al. Changes in sitting Notes; 2009.
posture induce multiplanar changes in chest wall shape and motion 33. Hodges PW. Neuromechanical control of the spine. Department
with breathing. Respir Physiol Neurobiol 2010;170(3):236–44. of Neuroscience. Stockholm, Sweden: Karolinska Institutet; 2003.
16. Lee LJ. Discover the Role of the Thorax in Total Body Function:
Introduction to the Thorax ‘Ring Approach’. Bergen, Norway:
Course Notes; 2011.

CHAPTER 44.3  ■  MANAGEMENT OF THE THORACIC

SPINE IN PATIENTS WITH COPD
Nicola Heneghan

Chronic obstructive pulmonary disease (COPD) is a It is conceivable that some of these co-morbidities may
common progressive, preventable and treatable disease, themselves adversely affect pulmonary function, when
characterized by persistent airflow limitation and associ- viewing the respiratory system as a ‘whole’ (i.e. lungs and
ated with an enhanced chronic inflammatory response. related musculoskeletal structures). Collagen degrada-
Primarily a disease of the lungs, the impact on other body tion or vertebral fractures, which are prevalent in COPD,
systems, including the musculoskeletal system, is now are likely detrimental to pulmonary function due to pain
widely reported, contributing to functional impairments and thoracic cage restriction.4 Likewise hyperinflation, a
and increased mortality.1–3 common feature of COPD, results in the ribs adopting a
456 PART IV  Overview of Contemporary Issues in Practice

more horizontal orientation, which in turn may contrib- concluded that spinal stiffness contributes to pulmonary
ute to chest wall rigidity and impair inspiratory muscle dysfunction, with structural abnormalities leading to
action.5 reduced lung volume, impaired rib movement and altered
Evidence-based non-pharmacological management of respiratory muscle mechanics. Harrison et al.15 concluded
stable COPD is currently limited to smoking cessation from a systematic review of four case-control studies that
and pulmonary rehabilitation.3 Pulmonary rehabilitation osteoporosis-related kyphosis was associated with impair-
combines education, psychosocial support and physical ment of pulmonary function. Furthermore, the observed
exercise, with the latter of these being thought to afford pulmonary dysfunction appeared related to the number
the greatest benefit.3,6 Generally, physical exercise in pul- of vertebral fractures and kyphosis with one study report-
monary rehabilitation aims to develop physiological ing a moderately strong negative association between
capacity through activities such as stair climbing or kyphosis angle and FEV1.
walking, rather than promote ‘flexibility’. A number of Altered respiratory biomechanics and pulmonary
authors have postulated that interventions aimed at dysfunction is also evident in older adults. While multi-
increasing chest wall flexibility through ‘active therapeu- factorial in nature, musculoskeletal changes are highly
tic exercise’ or ‘passive hands-on manual therapy’ may be prevalent and include costal cartilage calcification, costo-
beneficial to reduce the work of breathing.7–11 vertebral joint degeneration and decrease in interverte-
bral space with disc degeneration and respiratory muscle
fibre changes.16–18 Collectively these changes may restrict
ANATOMY AND BIOMECHANICS lung expansion and/or partly explain the observed reduc-
tion in total lung capacity seen in older adults.19 This
There are over 112 muscles with attachments directly or ‘restrictive’ pulmonary disorder is in contrast to the
indirectly to the thoracic rib cage and through their ana- airflow obstruction found in COPD, where reduced
tomical relations, likely have a role in supporting respira- airflow is secondary to inflammation in the airways.
tory function under normal or abnormal conditions.
Grazzini et al.12 propose an overall shift in the relative
contribution that respiratory muscles make to pulmonary SYMPTOMATIC FEATURES OF COPD
function with advancing COPD and a greater involve-
ment of the rib cage; a consequence of physiological and While dyspnoea is the main symptomatic feature of
structural diaphragmatic insufficiency. Activation of the COPD, cervicothoracic pain has also been recently
accessory respiratory muscles may result in clinically reported in this patient population,20 perhaps as a conse-
observed postural changes, including a forward head quence of musculoskeletal structural changes and dys-
posture and protracted and elevated shoulder girdles.5,13 function. Recent work by Bentsen et al.21 reported that
While secondary or beneficial for ventilation in the short prevalence of pain (predominantly neck, shoulders and
term, these musculoskeletal adaptations may alter cervi- chest), a common feature of musculoskeletal conditions,
cothoracic biomechanics, resulting in musculoskeletal was notably higher in patients with COPD (45%) com-
pathologies and pain.5 It is therefore conceivable that pared to the general population (34%). This is unsurpris-
these changes may themselves adversely affect respiratory ing given the observed use of accessory respiratory
function. muscles in COPD relating to dyspnoea20,21 and the adop-
The thoracic spine provides support posteriorly, and tion of a forward neck posture to open the airways.5
an anchorage for the ribs, thus facilitating respiration in Interestingly though, Bentsen et al.21 reported that many
healthy subjects. With the ribs being inextricably linked COPD subjects had used transcutaneous electrical nerve
to the thoracic spine via the costovertebral and costo- stimulation/acupuncture to assist in pain management as
transverse joints, it is conceivable that abnormalities in opposed to other forms of physiotherapy, such as manual
spinal motion or posture may exert some influence on therapy or therapeutic exercise.
pulmonary function. Although in theory it appears rea-
sonable to suppose that changes to musculoskeletal struc-
tures such as bones, joints, posture and muscles in the MANAGEMENT OF COPD TO IMPROVE
thoracic region have the potential to influence pulmonary
function through mechanical alterations, little attention
FLEXIBILITY
has been given to evaluating this. Manual Therapy: Passive Interventions
There are a number of studies describing the use of
RELATIONSHIP BETWEEN THE manual therapy techniques for the management of
MUSCULOSKELETAL SYSTEM AND COPD, mainly from the osteopathic and chiropractic
PULMONARY FUNCTION literature.7,8,22–25 Advocates of manual therapy propose
that passive techniques, aimed at increasing thoracic
Most of what is known of this relationship has emerged mobility, may work to reduce the work of breathing
from research demonstrating reduced pulmonary func- through enhanced oxygen transport and lymphatic
tion in idiopathic spinal scoliosis14 and osteoporosis.15 return.7–11 While this theory has not been systematically
Leong et al.14 investigated spinal stiffness and compared investigated in COPD, a myofascial release technique
chest cage motion in young healthy individuals compared did affect heart rate variability (a measure of autonomic
to those with scoliosis during a deep breath. They activity) in healthy subjects.26 Henley et  al.26 propose
 44  Thoracic Spine: Models of Assessment and Management 457

that manual therapy induces autonomic activity result- While RMSG studies used small sample sizes (n = 12
ing in vasodilation, smooth muscle relaxation and for each), these small pre–post32 and randomized con-
increased blood flow. It is proposed that these neuro- trolled trial31 studies demonstrate that RMSG may afford
physiological effects may then facilitate muscle length some therapeutic benefit in COPD management.
gains, decrease in pain perception and/or change in Performance-based measures, including the 6-minute
tissue tension. walking test, improved significantly with RMSG, with
A systematic review of the evidence for the effects of studies reporting a statistically significant increase in dis-
passive manual therapy interventions on pulmonary func- tance covered.31,32 Patient-reported measures of effect
tion in subjects with COPD identified that there is little also improved with a reduction in dyspnoea at the end of
evidence to currently support or refute the use of manual the 6-minute walk32 and improvements in quality of life
therapy interventions in the management of COPD.27 were also reported for the RMSG intervention.32
Key problems with the included studies were poor meth- Research of exercise to improve pulmonary function
odological quality of both reporting and conduct of in ankylosing spondylitis may provide some support for
studies; heterogeneity of study type, population, inter- its inclusion in COPD management.33,34 Two studies
ventions and outcomes; and inadequate statistical analysis compared usual care with a 3-month home-based pro-
and inadequate length of follow-up. Additionally the gramme of spinal flexibility exercises33,34 and, in the case
focus on performance-based measures did not allow for of Aytekin et al.,34 they also had a third trial arm that
patient-reported measures of well-being such as quality comprised a Global Postural Re-education (GPR®) pro-
of life or breathlessness to be evaluated. The findings gramme. Both studies found significant improvements in
from this review are similar to reviews in asthma, which pulmonary function, pain and flexibility in the interven-
report that there is insufficient evidence to support or tion groups.33,34 Aytekin et al.34 reported even more
refute use of manipulative therapy in asthma.9,28 favourable results for the GPR® programme compared
with the conventional spinal flexibility programme.
GPR® is a physical therapy method developed by
Exercise: Active Interventions Philippe-Emmanuel Souchard (France). The rationale
Respiratory muscle stretch gymnastics (RMSG) is a series being that fascia exerts an influence on individual muscles
of five therapeutic active exercises or ‘patterns’ of move- that operate concurrently in body regions to facilitate
ment (see Box 44-2 and Fig. 44-8) which aims to reduce functional movement, also known as ‘kinetic chains’.
dyspnoea through increased chest wall flexibility of These chains comprise partly of non-contractile tissues
muscles directly or indirectly related to respiration.29–31 and are therefore susceptible to adaptive shortening.35,36
The aim of GPR® programmes is to stretch the short-
ened kinetic chains using 15–20-minute stretch holds in
one of eight therapeutic postures; it uses the principles
BOX 44-2  Respiratory Muscle Stretch of creep, a property of viscoelastic tissue. This is in con-
Gymnastics trast to a more conventional stretching programme,
which targets muscles in isolation, using a timed period
Respiratory Muscle Stretch Gymnastics to be performed in counted in seconds. To minimize the development of
order four times a day31
postural asymmetry, contraction of the antagonist muscles
Pattern 1. Elevating and pulling back the shoulders:
As you slowly breathe in through your nose, gradually is incorporated into the programme. Evaluation of the
elevate and pull back both shoulders. After taking a deep content of the GPR® programme would suggest the pro-
breath, slowly breathe out through your mouth, relax and gramme may be suitable for enhancing pulmonary func-
lower your shoulders. tion through the inclusion of specific strengthening and
Pattern 2. Stretching the upper chest: Place both flexibility exercises of ‘shortened’ muscles, postural
hands on your upper chest. Pull back your elbows and pull muscles, respiratory muscles and trunk muscles.35 Aside
down your chest while lifting your chin and inhaling a deep from differences in the programme content and stretch
breath through your nose. Expire slowly through your duration, GPR® does share similarities to RMSG. Teodori
mouth and relax. et al.36 concluded from a systematic review of the avail-
Pattern 3. Stretching the back muscle: Hold your
hands in front of your chest. As you slowly breathe in
able evidence that GPR® may enhance respiratory muscle
through your nose, move your hands front wards and down, strength and chest wall mobility, although no studies of
and stretch your back. After deep inspiration, slowly breathe GPR® in patients with respiratory disease or dysfunction
out and resume the original position. have yet been identified.
Pattern 4. Stretching the lower chest: Hold the ends There are several research reports evaluating the
of a towel with both hands outstretched at shoulder height. effectiveness of pulmonary rehabilitation in clinically
After taking a deep breath, move your arms up while breath- diagnosed restrictive lung disease.37–39 While results on
ing out slowly. After deep expiration, lower your hands and the whole were favourable and comparable to results of
breathe normally. pulmonary rehabilitation in COPD, recruitment was
Pattern 5. Elevating the elbow: Hold one hand behind principally based on a restrictive pattern of ventilation
your head. Take a deep breath through your nose. While
slowly exhaling through your mouth, stretch your trunk by
from spirometry testing.38,39 Consequently, there is con-
raising your elbow as high as is easily possible. Return to the siderable sample heterogeneity across studies, ranging
original position while breathing normally. Repeat the from interstitial lung disease (pulmonary fibrosis) to non-
process using the alternate hand behind the head. fibrotic restrictive lung diseases of musculoskeletal origin.
This limits the strength of conclusions that can be made
458 PART IV  Overview of Contemporary Issues in Practice

$ %

FIGURE 44-8  ■  Respiratory muscle stretch gymnastics. Pattern 5. (A) Subject places hand behind head and take a deep breath through
the nose. (B) While slowly exhaling through the mouth, the subject stretches their trunk by raising the right elbow as high as pos-
sible. Subject holds this position and then returns to the original position while breathing normally. This is then repeated for the
opposite side.

when discussing restrictive lung diseases of differing aeti- COPD. Management of such dysfunction, asymptomatic
ology and mechanism. Common across all studies and, in or symptomatic, may complement current approaches to
line with other pulmonary rehabilitation studies, the pulmonary rehabilitation where development of physio-
exercise component was focused on developing physio- logical capacity is the main focus.
logical capacity.37–39 Justification for rehabilitation being
‘solely’ focused on developing physiological capacity is REFERENCES
questionable given the majority of the sample in one 1. Cooper CB, Dransfield M. The COPD patient in primary care –
study had restriction of musculoskeletal origin (n = 20 part 4: understanding the clinical manifestations of a progressive
from a total sample of 31 had chest wall disease, such as disease. Am J Med 2008;121:S33–44.
kyphoscoliosis).39 Naji et al.37 did, however, differentiate 2. Barnes PJ, Celli BR. Systemic manifestations and comorbidities of
COPD. Eur Respir J 2009;33:1165–85.
between subjects with interstitial lung disease and skeletal 3. Global Strategy for the Diagnosis, Management and Prevention of
abnormalities, although, with small numbers in each COPD, Global Initiative for Chronic Obstructive Lung Disease
group (n = 11, n = 4, respectively) and high attrition, they (GOLD). 2011 <http://www.goldcopd.org/>; [Accessed 4/1/12].
concluded there was much still to be learned, including 4. Patel ARC, Hurst JC. Extrapulmonary comorbidities in chronic
a question linked to appropriateness of one programme obstructive pulmonary disease: state of the art. Expert Rev Respir
Med 2011;5(5):647–61.
for both groups. 5. Courtney R. The functions of breathing and its dysfunction and
There is a small body of evidence that has sought to their relationship to breathing therapy. Int J Osteopath Med
evaluate the adjunctive use of a flexibility exercise pro- 2009;12:78–85.
gramme in promoting respiratory biomechanics in the 6. American Thoracic Society, European Respiratory Society (ATS/
ERS) statement on pulmonary rehabilitation. Am J Respir Crit
form of RMSG in COPD and GPR® in healthy subjects. Care Med 2006;173:1390–413.
While COPD is primarily an obstructive lung disease 7. Miller WD. Treatment of visceral disorders by manipulative
there appears sufficient evidence to support further therapy. In: Goldstein M, editor. The Research Status of Spinal
research into interventions which promote flexibility of Manipulative Therapy. Bethesda: Dept. HEW; 1975. p. 295–301.
the thoracic cage. 8. Masarsky CS, Weber M. The influence of vertebral manipulation in
the management of patients with COPD. JMPT 1988;11:505–10.
With growing evidence of co-morbid musculoskeletal 9. Hondras MA, Linde K, Jones AP. Manual Therapy for Asthma
changes, manual therapy, in the broadest sense may (Review) 2008. The Cochrane Collaboration. Issue 3 <http://
afford some therapeutic benefit to individuals with www.cochrane.org/>; [Accessed 4/5/2011].
 44  Thoracic Spine: Models of Assessment and Management 459

10. Putt MT, Watson M, Seale H, et al. Muscle stretching technique disease: a case series. J Manipulative Physiol Ther 2011;34(6):
increases vital capacity and range of motion in patients with chronic 413–17.
obstructive pulmonary disease. Arch Phys Med Rehabil 2008;89(6): 26. Henley CE, Ivins D, Mills M. Osteopathic manipulative treatment
1103–7. and its relationship to autonomic nervous system activity as dem-
11. Noll DR, Johnson JC, Baer RW, et al. The immediate effect of onstrated by heart rate variability; a repeated measures study.
individual manipulation techniques on pulmonary function mea- Osteopath Med Prim Care 2008;2(7):1–8.
sures in persons with COPD. Osteopath Med Prim Care 27. Heneghan NR, Balanos GM, Adab P, et al. Manual therapy for
2009;3(9):1–12. chronic obstructive airways disease: a systematic review of current
12. Grazzini M, Stendardi L, Gigliotti F, et al. Pathophysiology of evidence. Man Ther 2012;17(6):507–18.
exercise dyspnoea in healthy subjects and in patients with chronic 28. Ernst E. Spinal manipulation for asthma: a systematic review of
obstructive pulmonary disease (COPD). Respir Med 2005;99: randomised clinical trials. Respir Med 2009;103(12):1791–5.
1403–12. 29. Ito M, Kakizaki F, Tsuzura Y, et al. Immediate effect of respiratory
13. Chaitow L, Gilbert C, Bradley D. Multidisciplinary Approaches to muscle stretch gymnastics and diaphragmatic breathing on respira-
Breathing Pattern Disorders. Churchill Livingstone; 2002. tory pattern. Respiratory Muscle Conditioning Group. Intern Med
14. Leong JCY, Lu WW, Luk KDK, et al. Kinematics of the chest cage 1999;38(2):126–32.
and spine during breathing in healthy individuals and in patients 30. Kakizaki F, Shibuya M, Yamazaki T, et al. Preliminary report on
with adolescent idiopathic scoliosis. Spine 1999;24(13):1310–15. the effects of respiratory muscle stretch gymnastics on chest wall
15. Harrison RA, Siminoski K, Vethanayagam D, et al. Osteoporosis- mobility in patients with chronic obstructive pulmonary disease.
related kyphosis and impairments in pulmonary function: a system- Respir Care 1999;44:409–14.
atic review. J Bone Miner Res 2007;22(3):447–57. 31. Minoguchi H, Shibuya M, Miyagawa T, et al. Cross-over compari-
16. Nathan H, Weinberg G, Robin GC, et al. The costovertebral son between respiratory muscle stretch gymnastics and inspiratory
joints, anatomical – clinical observations in arthritis. Arthritis muscle training. Intern Med 2002;41:805–12.
Rheum 1964;7:228–40. 32. Yamada M, Kakizaki F, Sibuya M, et al. Clinical effects of four
17. Edmondston SJ, Singer KP. Thoracic spine: anatomical and bio- weeks of respiratory muscle stretch gymnastics in patients with
mechanical considerations for manual therapy. Man Ther chronic obstructive pulmonary disease. Nihon Kyobu Shikkan
1997;2(3):132–43. Gakkai Zasshi 1996;34(6):646–52.
18. Britto RR, Zampa CC, de Oliveira TA, et al. (2007) Effects of the 33. Durmuş D, Alayli G, Uzun O, et al. Effects of two exercise inter-
aging process on respiratory function. Gerontology 1997;55: ventions on pulmonary functions in the patients with ankylosing
505–10. spondylitis. Joint Bone Spine 2009;76(2):150–5.
19. Scarlata S, Costanzo L, Giua R, et al. Diagnosis and prognostic 34. Aytekin E, Caglar NS, Ozgonenel L, et al. Home-based exercise
value of restrictive ventilatory disorders in the elderly: a systematic therapy in patients with ankylosing spondylitis: effects on pain,
review of the literature. Exp Gerontol 2012;47:281–9. mobility, disease activity, quality of life, and respiratory functions.
20. Lohne V, Heer HC, Andersen M, et al. Qualitative study of pain Clin Rheumatol 2012;31(1):91–7.
of patients with chronic obstructive pulmonary disease. Heart Lung 35. Global Postural Re-education/ Rééducation Posturale Globale®
2010;39(3):226–34. (RPG®). 2012 <https://sites.google.com/site/rpguk123/home>;
21. Bentsen SB, Rustøen T, Miaskowski C. Prevalence and character- [Accessed 20/08/12].
istics of pain in patients with chronic obstructive pulmonary disease 36. Teodori RM, Negri JR, Cruz MC, et al. Global postural
compared to the Norwegian general population. J Pain 2011;12(5): re-education: a literature review. Rev Bras Fisioter 2011;15(3):
539–45. 185–9.
22. Howell RK, Allen TW, Kappler RE. The influence of osteopathic 37. Naji NA, Connor MC, Donnelly SC, et al. Effectiveness of pulmo-
manipulative therapy in the management of patients with chronic nary rehabilitation in restrictive lung disease. J Cardiopulm Rehabil
obstructive lung disease. JAOA 1975;74(8):757–60. 2006;26(4):237–43.
23. Witt PL, MacKinnon J. Trager psychophysical integration (TPI); 38. Kagaya H, Takahashi H, Sugawara K, et al. Effective home-based
A method to improve chest mobility of patients with chronic lung pulmonary rehabilitation in patients with restrictive lung diseases.
disease. Phys Ther 1986;66(2):214–17. Tohoku J Exp Med 2009;218(3):215–19.
24. Noll DR, Degenhardt BF, Johnson JC, et al. Immediate effects of 39. Salhi B, Troosters T, Behaegel M, et al. Effects of pulmonary reha-
osteopathic manipulative treatment in elderly patients with chronic bilitation in patients with restrictive lung diseases. Chest 2010;
obstructive pulmonary disease. JAOA 2008;108(5):251–9. 137(2):273–9.
25. Dougherty PE, Engel RM, Vemulpad S, et al. Spinal manipulative
therapy for elderly patients with chronic obstructive pulmonary
 CHAPTER 45 

Lumbar Spine
CHAPTER OUTLINE

Editor’s Introduction Ch 45.3  Treatment-Based Classification

System  470
Ch 45.1  The McKenzie Method of Mechanical
Diagnosis and Therapy – an Overview  460 Julie Fritz
Stephen May  •  Helen Clare Ch 45.4  Movement System Impairment Syndromes
of The Low Back  474
Ch 45.2  Multidimensional Approach for the
Targeted Management of Low Back Pain  465 Shirley Sahrmann  •  Linda Van Dillen
Peter O’Sullivan • Wim Dankaerts  •  Ch 45.5  The Role of Motor Control Training  482
Kieran O’Sullivan  •  Kjartan Fersum Paul Hodges

EDITOR’S INTRODUCTION

The topic of low back pain is enormous and clinician they present four different and relatively
numerous books have been written discussing distinct subgrouping approaches whose
assessment and a wide range of management development has been based on differing criteria.
approaches. The contemporary issue that has Despite the differences, the research base for
been chosen for discussion in this text recognizes each subgrouping approach is growing, which
the field of clinical research addressing the suggests that all have some merit. The
problem of heterogeneity in the presentation of physiotherapists who have developed or who are
patients with musculoskeletal disorders. international leaders in these approaches were
Subgrouping of patients has been advocated as a invited to provide a chapter section that offers a
method to address this heterogeneity. In theory brief overview of the respective subgrouping
and practice, patients who share similarities in approach. This allows the reader to better
presentation are grouped by predetermined understand, appraise and appreciate the
criteria. The aim of this grouping is to better differences and synergies in the approaches and
inform and direct specific therapeutic approaches look to current and future research proving the
deemed suitable for this group. Most distinct benefit of subgrouping to low back pain
development and research into subgrouping has patients and their outcomes. Another
occurred in relation to low back pain patients. contemporary issue is training impairments in
This chapter on low back pain presents four sensorimotor control that may accompany low
subgrouping approaches to guide conservative back pain and how this is approached. Thus a
management that have all been developed by chapter section explores current thinking and
physiotherapists from different areas of the evidence about the role of motor control training
world. However, from the perspective of the in relation to low back pain.

CHAPTER 45.1  ■  THE McKENZIE METHOD OF

MECHANICAL DIAGNOSIS AND
THERAPY – AN OVERVIEW
Stephen May  •  Helen Clare

INTRODUCTION and spinal musculoskeletal problems. Robin McKenzie

first described the method for lumbar spine problems,1
The McKenzie method of mechanical diagnosis and and then to address cervical and thoracic problems.2 The
therapy is a unique system of assessment and manage- original texts have recently been updated and augmented,
ment, which can be used in the assessment of extremity with the addition of a book introducing the application
460
 45  Lumbar Spine 461

of the method to patients with extremity musculoskeletal BOX 45-1  Operational Definitions for
problems.3–5 Mechanical Syndromes and
The method uses repeated movements while symp- ‘Other’4,5
tomatic and mechanical responses are being monitored
as the key source of information in the physical examina- DERANGEMENT
tion, and then uses these responses to classify patients • Centralization or progressive abolition of distal pain
into mechanical subgroups. The subgroups determine in response to therapeutic loading
the management strategy, and are classified as derange- • Each progressive abolition retained over time until all
ment, dysfunction or postural syndrome. Patients not symptoms are abolished
meeting the operational definitions for these syndromes • Back pain is also abolished
can generally be classified in one of the ‘other’ syndromes. • Changes in pain remain better
These concepts will be explored more fully below, and • Accompanied by changes in mechanical presentation,
then the evidence for their use as a mechanism for deter- such as increase in range of movement
mining management strategy will be discussed. ARTICULAR DYSFUNCTION
• Local pain only
• Intermittent pain only
ASSESSMENT • At least one movement is restricted and restricted
movement consistently produces concordant pain at
It is important to emphasize that mechanical diagnosis end-range
and therapy is not just a system of management, it is • No rapid reduction or abolition of symptoms
primarily a system of assessment and classification. • No lasting production or peripheralization of
The history component of the assessment follows the symptoms.
usual format including questions about the patient, their CONTRACTILE DYSFUNCTION
problem, its site, whether symptoms are constant or
• Intermittent pain only
intermittent, the history of the problem, what makes • Concordant pain reproduced with resisted movement
symptoms better or worse, any previous problems or • Active movements may also be painful
treatments, medication history and questions about Red
Flags, perhaps indicating serious spinal pathology that is POSTURAL SYNDROME
not suitable for mechanical therapy. • Local pain only
For lumbar spine problems, the physical examination • Intermittent pain only
commences with observing posture, and in particular, • Concordant pain with static loading
noting the effect of posture correction on symptoms. If • Abolition of pain with postural correction
appropriate a neurological examination would be done as • No pain with repeated movements
• No loss of range of movement
part of the baseline assessment. Single movements of
• No pain during movement
flexion, extension and side-gliding are assessed and any
pain noted. Side-gliding is assessed as this focuses move- OPERATIONAL DEFINITIONS FOR ‘OTHER’
ment on the lower lumbar spine. The baseline measures Spinal Stenosis
from the history and the physical examination are reas- • Leg symptoms when walking, eased in flexion
sessed by the therapist to judge response to management. • Minimal extension
The key part of the physical examination is the use of • Sustained extension provokes leg symptoms
repeated movements. A number of repeated movements
could be selected: flexion in standing or lying, extension ISTHMIC SPONDYLOLISTHESIS
in standing or lying and side-gliding in standing. • Sports-related injury in adolescence
However, all of these movements would not be tested in • Worse with static loading
one session; the therapist’s clinical decision making deter- HIP
mines which movements are examined. In general it will
• Pain on walking, eased with sitting
be sagittal movements first as the majority of responses
• Specific pain pattern
occur in this plane, especially extension. The exception • Positive hip tests
to this is a patient who presents with an acute-onset
lateral deformity, which would be addressed first. Sets of SACROILIAC JOINT
about ten repeated movements can be repeated four or • Three or more positive sacroiliac joint pain provoca-
five times to determine the response, before another tion tests
movement might be examined. Operational definitions
MECHANICALLY INCONCLUSIVE
are provided in Box 45-1.
• Inconsistent response to loading strategies
• No obstruction to movement

Repeated Movements CHRONIC PAIN

• Persistent widespread pain
Before the repeated movements are commenced the state • Aggravation with all activity
of the patient’s symptoms are recorded, especially the • Exaggerated pain behaviour
most distal. After each set of repeated movements, • Inappropriate beliefs and attitudes about pain
patient’s symptoms are monitored again. A series of terms
462 PART IV  Overview of Contemporary Issues in Practice

are used during and after the movements to describe the remarkable consistency. Some 80% or more of these
symptom response; the emphasis and decision making is spinal patients were classified into one of the mechanical
based on the latter. syndromes of derangement, dysfunction or postural syn-
The mechanical diagnosis and therapy assessment is drome, with by far the largest group being those with
initially based on patient exercises only, but both the derangement. It is to this classification subgroup that
assessment and the management process allow for force there is the wealth of evidence regarding the prognostic
progressions, which happen in the following order: patient value of centralization and directional preference (see
forces early through to end-range, patient forces end- next section). Thus the largest mechanical syndrome sub-
range with patient overpressure, patient forces with group has the most evidence supporting its use in assess-
therapist overpressure, and therapist mobilization. As ment and management.
indicated above the overpressures are only used if initial
patient-generated forces have been inadequate to gener- Evidence Regarding Prognosis
ate a clear response. The therapist might choose to test
patient overpressures over a 24–48-hour assessment Distal or leg pain can come or go during the natural
period prior to progressing forces. The initial mechanical history of a back pain episode. This is not the same as
diagnosis and therapy assessment is usually conducted in centralization or directional preference, which must be
standing, but force alternatives include repeated move- demonstrated during repeated movements. Directional
ments in lying, and frontal plane movements, with side- preference includes centralization but also a decrease in
gliding or rotation. symptoms and/or an increase in a restricted movement
in response to therapeutic loading. The distinction
between natural history and something which is clinically
Evidence About the Assessment Process induced is important as the positive evidence about these
A systematic review of 48 reliability studies on physical clinical phenomena has been derived from their clinically
examination procedures for non-specific low back pain driven nature.
conducted on patient populations revealed that most pro- Within physiotherapy examination procedures, no
cedures had limited reliability.6 With an upper threshold other finding has the prognostic power of centralization,
of kappa/intra-class correlation coefficient of 0.85, most which is defined as the abolition of distal pain in response
procedures demonstrated either conflicting evidence or to therapeutic loading. A systematic review of 22 articles
moderate to strong evidence of low reliability. When a assessed the prognostic value of examination procedures.
lower threshold was used (i.e. a kappa/intra-class correla- The only evidence for an examination procedure to
tion coefficient of 0.70), which is still regarded as good, inform management was for changes in pain location
only the procedure of pain response to repeated and/or intensity with repeated spinal movements.10
movements demonstrated moderate evidence for high A recent systematic review located 54 articles regard-
reliability. ing centralization and eight for directional preference.11
Pain responses to repeated movements, as used when Centralization had a prevalence rate of 44% in 4745
testing for directional preference and centralization, patients, with a higher rate in acute (74%) than subacute
demonstrated reasonably good levels of reliability, and or chronic back pain (42%). The prevalence rate of direc-
therefore constitute a valid method of determining man- tional preference was 70% in 2368 patients. In other
agement strategies. Four studies examined the reliability words, these phenomena are commonly encountered
of the McKenzie classification system itself; three clinically. Of 23 studies investigating the prognostic
reported kappa values of 0.7 or greater, one reported validity of centralization, 21 demonstrated a positive
poor kappa values, but the therapists involved had limited effect in those patients who demonstrated centralization,
knowledge of the classification system.6 There is thus compared to those who did not. For both centralization
reasonable evidence for the reliability of the system and directional preference, seven out of eight studies
among therapists trained in the method. provided evidence that they are useful treatment effect
Several surveys involving over 1500 patients have been modifiers. This means that these assessment procedures
conducted with McKenzie-trained therapists to deter- are evidence-based ways of assessing appropriate man-
mine the proportions of patients classified in the different agement strategies based on these responses.
mechanical syndromes.7–9 For lumbar spinal patients the
most common classifications were derangement, range
67–75%; dysfunction, 4–6%; postural syndrome, 0–1%; MANAGEMENT
and other, 8–18%. In the derangement category extension
(70%), flexion (6%) and lateral movements (24%) cen- The classification determines the management. For
tralized, decreased or abolished symptoms, respectively. derangement, the patient performs exercises every 2 to 3
The findings were very similar for the 111 cervical spine hours that centralize, decrease or abolish their symptoms.
patients where 81% were classified with derangement, At the same time they avoid any sustained provocative
1% as irreducible derangement, 8% with dysfunction, 3% positions. For instance, an extension responder might be
with postural syndrome and 7% with other. Treatment advised to interrupt sitting every hour by standing and
directions for the derangements were also similar: exten- stretching backwards. For dysfunction, the patient per-
sion (72%), flexion (9%) and lateral movements (19%).8 forms exercises every 2 to 3 hours that reproduce their
These data were gathered with very diverse methods symptoms, but leaves them no worse afterwards. Clear
and from various geographical sites, yet they showed a advice needs to be given about the reason for doing the
 45  Lumbar Spine 463

exercises (i.e. to remodel ‘scar’ tissue, the expected

response, the need not to be worse after exercising and THE ‘OTHER’ SYNDROMES
the need to continue the exercise for many weeks to see
an improvement). For a postural syndrome, the patient As alluded to already, it is recognized that not every
is advised that it is their sustained, usually sitting posture patient can be classified into one of the mechanical syn-
that is the cause of their symptoms, and that they must dromes, and the ability to classify patients is also a reflec-
interrupt this on a regular basis and should, when sitting, tion of a therapist’s experience and training in the method.
maintain a neutral lumbar posture. Box 45-1 presents a list of what is included in an ‘other’
Management is closely linked to the assessment category. As can be seen they tend to be more specific
process; the patient is given one exercise to perform on classifications. In one survey of 607 patients, 101 (17%)
a regular basis, with clear reasoning about why they need were classified as ‘other’ in the following ways: mechani-
to do that exercise or make that adjustment to their cally inconclusive 6%, chronic pain state <4%, post-
posture; and management is very patient-centred. The surgery <2%, and Red Flags, stenosis, sacroiliac joint,
therapist plays the role of an assessor and advisor, the trauma and spondylolisthesis all around 1% each.7
patient is the main player in their recovery. The therapist
equips them with an appropriate exercise, the mechanical
therapy component, and also clear reasoning for the exer-
cise, the educational component.
APPLICATION OF MECHANICAL
DIAGNOSIS AND THERAPY IN THE
Evidence Regarding Management CERVICAL SPINE
When evaluating treatment efficacy the ideal study design The principles outlined above apply in exactly the same
is the randomized controlled trial, with systematic reviews way with patients with cervical and thoracic problems. As
being used to analytically summarize this evidence. A in the lumbar spine, baseline measures of range of move-
number of systematic reviews are relevant in this context ment and neurological status, if appropriate, are taken
(Table 45-1). All are largely supportive of the McKenzie prior to repeated movements. Again repeated movements
approach or classification-based approaches, though tend to start with sagittal plane movements, especially
effect sizes are relatively small. extension, with the key distinction being the importance

TABLE 45-1  Conclusions from Systematic Reviews Regarding Evidence for the McKenzie Method
and Classification Systems
Reference Number of RCTs Remit Conclusions
12
Clare et al. 2004 6 Use of McKenzie principles Short term 8.6% greater reduction in
Meta-analysis of data pain, 5.4% greater reduction in
disability than controls
Cook et al. 200513 5, high quality Therapeutic exercises with Four out of five significantly better
(PEDro) patients classified using than control group
symptom responses
Machado et al. 200614 11, mostly high McKenzie method Short term 4.2% greater reduction in
quality Meta-analysis of data pain, 5.2% greater reduction in
disability than controls
Slade and Keating 200715 6, high quality Unloaded exercises; four out Short term mean difference favoured
of six McKenzie exercises McKenzie for pain 0.36–0.63 and for
function 0.45–0.47
Fersum et al. 201016 5 Sub-classification systems Sub-classification systems
and matched interventions significantly better reduction in
for manual therapy and pain (p = 0.004) and disability
exercise (p = 0.0005) short term, long
term for pain (p = 0.001)
Kent et al. 201017 4, high quality Targeted manual therapy or One study showed McKenzie method
exercise therapy had significantly better effects short
term
Slater et al. 201218 7, grade quality of Sub-classification systems Significant treatment effects favoured
evidence low and matched intervention the classification-based treatment
for manual therapy compared to controls in pain and
disability short and medium term
Surkitt et al. 201219 6–5, high quality Management using Moderate evidence that DP
(GRADE) directional preference (DP) significantly more effective than
controls at short and long term

RCT, Randomized controlled trial.

464 PART IV  Overview of Contemporary Issues in Practice

of retraction and protraction. Retraction involves end- 3. McKenzie RA, May S. The Human Extremities Mechanical Diag-
range upper cervical flexion and lower cervical exten- nosis and Therapy. New Zealand: Spinal Publications; 2000.
4. McKenzie RA, May S. The Lumbar Spine Mechanical Diagnosis
sion,20 and therefore is regarded as an essential precursor and Therapy. New Zealand: Spinal Publications; 2003.
to regaining extension in the cervical spine. Protraction 5. McKenzie RA, May S. The Cervical and Thoracic Spine Mechani-
involves end-range upper cervical extension and lower cal Diagnosis and Therapy. New Zealand: Spinal Publications; 2006.
cervical flexion. As this tends to be the common posture 6. May S. Classification by McKenzie mechanical syndromes: a survey
of McKenzie-trained faculty. J Manipulative Physiol Ther 2006;29:
assumed during slouched sitting, it is often a symptom 637–42.
provocative position. Repeated movement testing for the 7. May S, Littlewood C, Bishop A. Reliability of procedures used in
cervical spine is most commonly done in sitting in an the physical examination of non-specific low back pain: a systematic
upright sitting posture. In acute or very severe cases, review. Aust J Physiother 2006;52:91–102.
repeated movements might need to be conducted in 8. Hefford C. McKenzie classification of mechanical spinal pain:
profile of syndromes and directions of preference. Man Ther
lying. In patients failing to regain extension, manual trac- 2007;13:75–81.
tion in lying might also be used. Home exercises are 9. Werneke MW, Hart D, Oliver D, et al. Prevalence of classification
conducted in sitting or lying position, depending on the methods for patients with lumbar impairments using the McKenzie
physical examination findings. syndromes, pain pattern, manipulation and stabilization clinical
prediction rules. J Man Manip Ther 2010;18:197–210.
Regarding frontal plane movements in the cervical 10. Chorti AG, Chortis AG, Strimpakos N, et al. The prognostic value
spine; two movements are considered: lateral flexion and of symptom responses in the conservative management of spinal
rotation. The latter is theoretically more associated with pain. A systematic review. Spine 2009;34:2686–99.
upper cervical problems, and lateral flexion with lower 11. May S, Aina A. Centralization and directional preference: a system-
cervical problems. In essence both movements are con- atic review. Man Ther 2012;17:497–506.
12. Clare HA, Adams R, Maher CG. A systematic review of efficacy of
sidered with all problems especially if it has been decided McKenzie therapy for spinal pain. Aust J Physiother 2004;50:
lateral rather than sagittal plane forces are needed. 209–16.
There is much less relevant literature for the cervical 13. Cook C, Hegedus EJ, Ramey K. Physical therapy exercise interven-
spine compared to the lumbar spine. However, it has tion based on classification using the patient response method: a
systematic review of the literature. J Man Manip Ther 2005;13:
been noted already that derangement and centralization 152–62.
are commonly found in the cervical spine.8,21 14. Machado LAC, de Souza MvS, Ferreira PH, et al. The McKenzie
Method for low back pain. A systematic review of the literature with
a meta-analysis approach. Spine 2006;31:E254–62.
CONCLUSIONS 15. Slade SC, Keating J. Unloaded movement facilitation exercise com-
pared to no exercise or alternative therapy on outcomes for people
with non-specific chronic low back pain: a systematic review.
The assessment process of mechanical diagnosis and J Manipulative Physiol Ther 2007;30:301–11.
therapy is indicated for all patients with musculoskeletal 16. Fersum KV, Dankaets W, O’Sullivan PB. Integration of sub-
symptoms, many of whom will have mechanical syn- classification strategies in RCTs evaluating manual therapy treat-
ment and exercise therapy for non-specific chronic low back pain:
dromes and can be managed with the exercises described a systematic review. Br J Sports Med 2010;44:1054–62.
in the system. Patients with serious spinal pathology are 17. Kent P, Mjosund HL, Petersen DHD. Does targeting manual
screened and referred for specialist consultation. Patients therapy and/or exercise improve patient outcomes in nonspecific
with other syndromes are assessed and if they do not meet low back pain? A systematic review. BMC Med 2010;8:22.
the criteria of the mechanical syndromes, they will require 18. Slater SL, Ford JJ, Richards MC, et al. The effectiveness of sub-
group specific manual therapy for low back pain: a systematic
another evidence-based approach. review. Man Ther 2012;17:201–12.
The research base for mechanical diagnosis and 19. Surkitt LD, Ford JJ, Hahne AJ, et al. Efficacy of directional prefer-
therapy is substantial and continues to grow. For a fuller ence management for low back pain: a systematic review. Phys Ther
reference list go to www.mckenziemdt.org. 2012;92:652–65.
20. Ordway NR, Seymour RJ, Donelson RG, et al. Cervical flexion,
extension, protrusion, and retraction. A radiographic segmental
REFERENCES analysis. Spine 1999;24:240–7.
1. McKenzie RA. The Lumbar Spine Mechanical Diagnosis and 21. Werneke M, Hart DL, Cook D. A descriptive study of the centralisa-
Therapy. New Zealand: Spinal Publications; 1981. tion phenomenon. A prospective analysis. Spine 1999;24:676–83.
2. McKenzie RA. The Cervical and Thoracic Spine Mechanical Diag-
nosis and Therapy. New Zealand: Spinal Publications; 1990.
 45  Lumbar Spine 465

CHAPTER 45.2  ■  MULTIDIMENSIONAL APPROACH FOR

THE TARGETED MANAGEMENT OF
LOW BACK PAIN
Peter O’Sullivan  •  Wim Dankaerts  • 
Kieran O’Sullivan  •  Kjartan Fersum

increased risk of LBP,20 they have a high prevalence in

THE FAILURE OF CURRENT PRACTICE pain-free populations, are not strongly predictive of
future LBP and correlate poorly with levels of pain and
The biomedical approaches to managing low back pain disability.21–23 The adverse effects of early magnetic reso-
(LBP) have led to an exponential increase in health-care nance imaging for LBP highlight the risk of iatrogenic
costs, with a concurrent increase in disability and chro- disability if spinal imaging is not used sparingly and com-
nicity.1,2 It has been proposed that this is due in part to municated carefully.24–26 In the presence of specific
the lack of person-centred management based on a vali- pathologies, consideration of all other relevant bio­
dated approach to deal with heterogeneity in the LBP psychosocial domains should also be part of the examina-
population, and the failure to adopt a biopsychosocial tion and management process.
framework based on contemporary evidence.3 Time course of the disorder: Differentiating acute
LBP where there is a clear mechanism of injury and
inflammatory component, from LBP related to other
MULTIDIMENSIONAL CLINICAL biopsychosocial factors causing tissue sensitization is
REASONING FRAMEWORK FOR LBP important for targeted management (see Fig. 45-1). Fre-
quently, LBP represents a recurrent disorder. Persistent
While many classification systems have been advocated LBP (PLBP) occurs when pain lasts beyond natural
in order to deal with the heterogeneity of LBP and healing time (8–12 weeks), where pathology (for a small
enhance treatment matching, few have been validated group), peripheral and central pain mechanisms and mal-
and tested in randomized trials.4 Most classification adaptive cognitions, psychosocial factors and behaviours
systems are criticized for being unidimensional and may perpetuate the pain state.
failing to reflect the biopsychosocial and heterogenous Neurophysiological factors: Pain characteristics
nature of LBP, thereby limiting the individualization of reported by patients can range from mechanically to non-
care.5 In response to these limitations, a clinical reasoning mechanically provoked pain and may reflect different under-
framework (CRF) has been developed6 that includes lying pain mechanisms, providing important directions
patient triage and incorporates a contemporary biopsy- for targeted rehabilitation and in some cases pharmacol-
chosocial understanding of LBP in order to identify ogy.27 There is growing evidence that both peripheral
modifiable and non-modifiable factors associated with a (bottom up) and central (top down) pain mechanisms are
person’s disorder, to target person-centred care. The associated with LBP.28,29 For example LBP that is local-
CRF has evolved over time from the O’Sullivan classifi- ized, mechanically provoked and linked to maladaptive
cation system which initially focused more on movement functional and lifestyle behaviours, resulting in abnormal
control mechanisms,7 to the CRF which incorporates a tissue loading, may be associated with nociceptive and
biopsychosocial clinical examination combined with inflammatory pain features such as localized heat and
screening questionnaires for prognostic risk factors8,9 and pressure hyperalgesia.30,31 In contrast, ‘insidious’ pain
review of radiological and medical investigations where flares or PLBP linked to other pain and health
appropriate. A strong therapeutic alliance underpins this co-morbidities and high levels of psychosocial and life-
process.10 The different dimensions of the CRF have style stresses, is often widespread and non-mechanical in
been published in detail previously,11 including a detailed nature. This may present with either an absence of clini-
appendix in the randomized trial publication.12 An outline cal signs or be associated with exaggerated pain responses
of the different dimensions within the CRF is provided to minor mechanical triggers with localized allodynia
(Fig. 45-1). and/or widespread cold hyperalgesia.30,32,33 While for
Triage: On initial assessment, triage of patho- some their pain characteristics appear clearly defined,
anatomical factors is required to identify the minority LBP for many presents as a mixed picture reflecting a
(1–2%) of people with LBP related to serious or systemic combination of both peripheral and central pain mecha-
Red Flag pathology.13 For another 5–10%, their LBP is nisms (see Fig. 45-1).6
associated with specific pathology with or without radicu- PLBP has also been associated with brain changes
lar features.14 The remaining 85–90% of people with such as a loss of grey matter, increased resting brain state,
LBP demonstrate no specific pathology (non-specific changes in the sensorimotor cortex (i.e. body schema
LBP), and present with their own unique contributing alterations) and loss of endogenous pain inhibition.34
factors across cognitive, psychosocial, physical and life- These factors may contribute to tissue sensitization, as
style domains.15–19 While patho-anatomical factors such well as altered motor output and movement disturbances,
as advanced disc degeneration are associated with an highlighting the important role of the central nervous
466 PART IV  Overview of Contemporary Issues in Practice

Clinical reasoning framework for targeted management of LBP

In the context of a strong therapeutic relationship which emphasizes person-centred care, utilizing
motivational communication approach

Investigate Red flag disorders Triage process

and medical
management
where pain is Mixed
disabling, Specific LBP diagnosis profile Non-specific LBP diagnosis
distressing and Consider adaptive vs maladaptive responses Consider maladaptive responses
behaviours are
adaptive
Time course of disorder: acute, sub-acute, persistent, recurrent

Assess risk profile: based on prognostic indicators from clinical assessment integrated with screening questionnaires
(i.e. StartBack or Ørebro)

Mixed
Pain with non-mechanical behaviour profile associated with Pain with mechanical behaviour profile associated with
profile
predominantly central pain mechanisms predominantly peripheral nociceptive pain mechanisms
(Risk profile more likely to be moderate to high) (Risk profile more likely to be low to moderate)

Factors to be considered as Factors to be considered as Factors to be considered as Factors to be considered as

potential non-modifiable potential modifiable drivers of potential non-modifiable potential modifiable drivers of
drivers of central central sensitization and drivers of peripheral peripheral sensitization and
sensitization and associated behaviours: sensitization and associated disability:
associated behaviours: associated disability:
Cognitive and psychological factors i.e. Cognitive and psychological factors
Social factors i.e. early life stress negative beliefs, fear, depression, anxiety, Patho-anatomical factors i.e. disc i.e. negative beliefs regarding pain,
exposures, +/- socio-economic catastrophising, hyper-vigilance, stress degeneration, disc protrusion, posture and movement, fear of
status, +/- contemporary work/ sensitivity, low pain self efficacy, mal- spondylolysis, spondylolisthesis, movement and pain, coping style that
home/social stressors, adaptive coping, anger, perceived stenosis promotes tissue loading (i.e.
+/- cultural factors injustice endurance coper)
Genetic factors–influencing
Psychological factors i.e. trait Social factors i.e. +/- life stressors (work, ligamentous laxity, patho- Mal-adaptive postural and movement
anxiety, negative affect, family, social, financial etc.) anatomy and spinal structure patterns (linked to body schema)
personality type integrity
Lifestyle factors i.e. sleep impairments, Lifestyle factors loading and postural
Genetic/epigenetic factors– inactivity, obesity, smoking, drug use factors linked to home/work/sport
influencing pain thresholds and biomechanical demands and volume,
central pain processing Maladaptive movement and pain ergonomic factors, obesity
communicative behaviours
(body schema)

Other factors requiring consideration: health comorbidities, vitality, energy, educational levels, cultural factors, seeking financial compensation, health
literacy, goals, values, expectations, treatment and activity preferences, readiness for change, level of acceptance, learning capacity and style

Cognitive functional therapy (CFT)

Flexible multidimensional intervention that directs care at the modifiable drivers of pain and disability in order to deliver targeted person-centred care
Four components are targeted based on the various levels of the CRF and linked to the patient’s goals
1. cognitive – bio-psycho-social understanding of pain, cognitive reframing, developing adaptive pain coping strategies
2. functional training – training body schema, functional postural and movement behaviours and abolishing pain behaviours specific where present
3. functional integration - integrate new behaviours into activities of daily living +/- targeted conditioning
4. lifestyle change as indicated

CFT targeted to reduce central sensitization CFT targeted to reduce peripheral sensitization
1. Explain the role cognitive, psychological, social, behavioural and lifestyle 1. Explain factors linked to peripheral sensitization, address beliefs
factors play in setting up vicious cycle of central sensitization and disability, 2. Address maladaptive functional behaviours (postures and movement
develop adaptive pain coping strategies, pacing, mindfulness, fear reduction, Mixed patterns) based on movement classification, linked with primary functional
stress management, acceptance where indicated profile impairments and pain provocation. Manual therapies may be integrated
2. Body relaxation +/- body scanning/mindfulness integrated into provocative where movement impairments provides a barrier for behaviour change
functional tasks, address maladaptive functional and pain communicative 3. New functional behaviours are incorporated into activities of daily living,
behaviours if present, pacing, exposure training if high levels of fear sports, work and social settings previously reported to be provocative.
avoidance Ergonomic adjustments are made where necessary to facilitate new
3. Activity pacing, general conditioning, social, work and home engagement behaviour. Targeted conditioning and pacing of activity/loading is
4. Sleep hygiene, activity levels, sedentary behaviours, diet, smoking, alcohol integrated where appropriate
and drug use etc. 4. Address lifestyle factors such as activity, sedentary behaviours and
Integrated with medical and psychological management where indicated weight loss where they are linked to increased spinal loading
Integrated with medical management where indicated

FIGURE 45-1  ■  Clinical reasoning framework for assessment and targeted management of low back pain (LBP). This framework pro-
vides an understanding of the clinical reasoning process which directs management towards the modifiable factors linked to the
disorder based on prognostic risk factors and underlying pain mechanisms while taking into consideration non-modifiable factors
and individual patient characteristics.
 45  Lumbar Spine 467

system in PLBP.34,35 For health-care practitioners, gaining PLBP (in the absence of pathology) and in some cases
insight into pain mechanisms can be achieved through non-traumatic acute LBP.62 They correlate with pain
careful clinical examination, quantitative sensory testing catastrophizing, providing opportunities for targeted
and validated questionnaires.27,36 behavioural management.63
Cognitive factors such as negative LBP beliefs, cata- There is also growing evidence to support the role
strophizing and fear of movement are predictive of dis- genetic factors have on patho-anatomical (i.e. disc degen-
ability and are linked to PLBP.37–40 Many of these negative eration and prolapse) and pain vulnerability in specific
beliefs gain their origins from health-care practitioners populations.64 While genetic testing is not currently
and can have a devastating impact on LBP trajectories.24,41 available, family history should be considered in the CRF
Psychological factors such as anxiety and depressed examination process.
mood are also commonly comorbid with PLBP.42 These
factors may act to reinforce maladaptive movement and
lifestyle behaviours, enhancing sensitization and disabil-
ity levels.43 They may also lead to dysregulation of the
CLINICAL REASONING FRAMEWORK
hypothalamic–pituitary–adrenal axis, altering central FOR TARGETED MANAGEMENT OF LOW
pain processing and immune and neuroendocrine func- BACK PAIN
tion, promoting central sensitization.44,45 Screening for,
and addressing, these factors is essential for targeted Rather than representing a rigid subgrouping system, the
management.8,9 CRF provides a flexible framework, providing direction
Social and cultural factors, although often non- for person-centred clinical assessment and management
modifiable, may have an influence on pain beliefs, coping as outlined in Figure 45-1. Indeed, many of these factors
and stress load and must be considered in the manage- coexist, are not mutually exclusive and have the potential
ment of LBP.43 Work-related factors should be investi- to both peripherally and centrally sensitize spinal struc-
gated where a person is seeking compensation for pain tures, reinforcing disability behaviours in the presence or
or where work absenteeism or presenteeism are associ- absence of spinal pathology. Some of these factors are
ated with the disorder.46 Numerous lifestyle factors are modifiable while others are not. Consideration of the
modifiable and may contribute to both peripheral (via relative contribution of the different factors is important
mechanical loading) and central pain mechanisms.47 for targeted management (in some cases multidisci-
There is also evidence of the importance of health and plinary) as well as realistic prognosis and goal setting.
pain co-morbidities with LBP and their role in influ-
encing disability levels, general health status and chronic-
ity, as well as providing barriers to management that
require special consideration.15,48,49 Individual factors
COGNITIVE FUNCTIONAL THERAPY FOR
such as the patient goals, preferences, health literacy, THE TARGETED MANAGEMENT OF LOW
levels of acceptance, expectations and readiness for BACK PAIN DISORDERS
change are important when providing person-centred
care in the assessment, management and prognosis of Cognitive functional therapy (CFT) was specifically
people with LBP.39,43,50–53 developed as an approach for targeting treatment in
LBP disorders are frequently associated with pain- patients with LBP where (based on the CRF) maladaptive
related functional behaviours such as altered postures and and modifiable cognitive, psychosocial, functional and
movement patterns linked to impairments of control, lifestyle behaviours are considered provocative of their
movement and loading.17 Growing evidence suggests that disorder (Fig. 45-1). The implementation of CFT is
these behaviours are often maladaptive and provocative adapted to the risk and clinical profile of the patient in
in PLBP.17,30 This is like a ‘limp’ for a sprained ankle that order to target both peripheral and central pain drivers
may be adaptive in the acute phase of a traumatic injury; of the disorder and associated disability. The primary
however, when it persists past natural tissue healing time aims of CFT are to provide a person-centred, biopsycho-
it becomes maladaptive and provocative. These behav- social understanding of pain, enhance pain-coping strate-
iours are commonly associated with high levels of trunk gies through cognitive restructuring, stress and threat
muscle co-contraction (excessive ‘stability’), are not ste- reduction, pain control via targeted functional training
reotypical17,30 and are linked with proprioceptive defi- and lifestyle change. The functional training is based on
cits54,55 and altered body schema.56–58 There is growing the movement classification and discouraging pain behav-
evidence that they can be characterized based on the iours if present, in order to promote pain self-efficacy and
presence of functional impairments and directional pain confidence by normalizing movements and resuming
sensitization, providing an opportunity for targeted activities previously avoided or reported as provocative.
interventions.36,59 Deconditioning may also occur sec- These are integrated into activities of daily living with
ondary to activity avoidance, sedentary lifestyles and physical activation (based on patient preference) in a
habitual postures, and may act to reinforce maladaptive graduated manner while addressing lifestyle and social
movement behaviours associated with the disorder.37,60 factors (such as work) considered to contribute to the
In contrast, endurance copers may present as over- disorder. CFT can be integrated with medical manage-
conditioned through ‘over activity’.61 Pain communica- ment where pain levels dominate and/or psychological
tive behaviours (overt facial and body expressions of management where comorbid mental health disorders
pain) are also considered maladaptive in the context of are a significant barrier to behavioural change.
468 PART IV  Overview of Contemporary Issues in Practice

Underpinning research has assessed the inter-tester behaviourally orientated approach to targeted care for
reliability of different aspects of the CRF and shown patients with LBP, shifting the focus away from treating
substantial agreement between trained health-care pro- the symptom of pain to providing clear targets for behav-
fessionals.36,59 The efficacy of CFT in patients with PLBP, ioural change, enhancing pain coping and positive adap-
has been compared with physiotherapy-led exercise and tation. It utilizes screening questionnaires and therefore
manual therapy in a randomized trial, in primary care, permits integration with other stratification approaches
demonstrating long-term benefits.12 Further research is and can be combined with other treatments where
underway to assess CFT in different care and geographi- indicated. Further research is required, and is ongoing,
cal settings. to further test the validity and clinical utility of this
The potential mechanisms underlying the therapeutic approach.
effect of CFT are likely to be multidimensional. Media-
tion analyses of the data from a randomized trial12
show that reductions in pain intensity, improvements
REFERENCES
in mood and reductions in fear of work were associated
with decreased disability. Qualitative data support these 1. Deyo RA, Mirza SK, Turner JA, et al. Overtreating chronic back
pain: time to back off? J Am Board Fam Med 2009;22:62–8.
findings with people undergoing CFT reporting a 2. Dagenais S, Caro J, Haldeman S. A systematic review of low back
changed mind set towards a biopsychosocial understand- pain cost of illness studies in the United States and internationally.
ing of pain, pain controllability and enhanced self- Spine J 2008;8:8–20.
efficacy to achieve lifestyle goals.65 It is likely that both 3. Borkan J, Van Tulder M, Reis S, et al. Advances in the field of low
back pain in primary care: a report from the fourth international
specific and non-specific treatment effects underpin this forum. Spine 2002;27:E128–32.
process. 4. Foster NE, Hill JC, Hay EM. Subgrouping patients with low back
pain in primary care: are we getting any better at it? Man Ther
2011;16:3–8.
5. Karayannis NV, Jull GA, Hodges PW. Physiotherapy movement
SKILLS REQUIRED TO IMPLEMENT THE based classification approaches to low back pain: comparison of
MULTIDIMENSIONAL APPROACH FOR subgroups through review and developer/expert survey. BMC Mus-
culoskelet Disord 2012;13(1):24.
INDIVIDUALIZED CARE 6. O’Sullivan P. It’s time for change with the management of
non-specific chronic low back pain. Br J Sports Med 2012;46:
224–7.
While the CRF lends itself to any health-care profes- 7. O’Sullivan P. Lumbar segmental instability: clinical presentation
sional managing patients with LBP, CFT requires spe- and specific stabilizing exercise management. Man Ther 2000;5:
cific skills across a number of domains. The utilization of 2–12.
motivational interviewing techniques allows for the 8. Hill JC, Dunn KM, Lewis M, et al. A primary care back pain
development of a strong therapeutic alliance within a screening tool: identifying patient subgroups for initial treatment.
Arthritis Care Res 2008;59:632–41.
biopsychosocial framework while identifying and target- 9. Hockings RL, McAuley JH, Maher CG. A systematic review of the
ing barriers for behavioural change. Diagnostic, observa- predictive ability of the Orebro Musculoskeletal Pain Question-
tional and interpretive skills are required to triage patients naire. Spine 2008;33:E494–500.
and analyse functional and pain behaviours in order to 10. Hall AM, Ferreira PH, Maher CG, et  al. The influence of
the therapist-patient relationship on treatment outcome in
determine adaptive from maladaptive behaviours. Tar- physical rehabilitation: a systematic review. Phys Ther 2010;90:
geted management requires clinicians to communicate 1099–110.
effectively,66 teach body relaxation strategies,67 normalize 11. O’Sullivan P. A classification based cognitive functional approach
functional movement patterns and discourage pain to managing nonspecific chronic low back pain. J Orthop Sports
behaviours,68 utilizing mindfulness69 and motivational70 Phys Ther 2012;24:A17–21.
12. Vibe Fersum K, O’Sullivan P, Skouen J, et al. Efficacy of classifica-
principles for behavioural change. Feedback (visual, tion based cognitive functional therapy in patients with non-specific
sensory and verbal)71,72 and activity pacing73 are compo- chronic low back pain – A randomized controlled trial. Eur J Pain
nents of this process. The biggest obstacle of adopting 2013;17:916–28.
this approach is often casting off strongly held views that 13. Henschke N, Maher CG, Refshauge KM, et al. Prevalence of and
screening for serious spinal pathology in patients presenting to
LBP reflects a purely structural problem of the spine, primary care settings with acute low back pain. Arthritis Rheum
while confidently confronting pain behaviours in patients 2009;60:3072–80.
with pain. In the randomized trial an average of 100 14. Koes BW, van Tulder M, Lin CW, et al. An updated overview of
hours of training including patient assessments and man- clinical guidelines for the management of non-specific low back
agement was reported for experienced physiotherapists pain in primary care. Eur Spine J 2010;19:2075–94.
15. Tschudi-Madsen H, Kjeldsberg M, Natvig B, et al. A strong asso-
to reliably implement this approach.12 Supporting publi- ciation between non-musculoskeletal symptoms and musculoskel-
cations, clinical workshops with patients and web-based etal pain symptoms: results from a population study. BMC
resources (www.pain-ed.com) are available to assist this Musculoskelet Disord 2011;12:285.
process. 16. Carroll LJ, Cassidy JD, Côté P. Depression as a risk factor for onset
of an episode of troublesome neck and low back pain. Pain
2004;107:134–9.
17. Dankaerts W, O’Sullivan P, Burnett A, et al. Discriminating healthy
SUMMARY controls and two clinical subgroups of nonspecific chronic low back
pain patients using trunk muscle activation and lumbosacral kine-
The CRF provides a multidimensional framework in matics of postures and movements: a statistical classification model.
Spine 2009;34:1610–18.
order to diagnose LBP disorders to better target care. 18. Hayes C, Naylor R, Egger G. Understanding chronic pain in a
The strengths of the CRF, and CFT intervention, lifestyle context the emergence of a whole-person approach. Am J
approach are that it provides a multidimensional, Lifestyle Med 2012;6:421–8.
 45  Lumbar Spine 469

19. Crombez G, Vlaeyen JWS, Heuts PHTG, et  al. Pain-related 43. Gatchel RJ, Peng YB, Peters ML, et al. The biopsychosocial
fear is more disabling than pain itself: evidence on the role of approach to chronic pain: scientific advances and future directions.
pain-related fear in chronic back pain disability. Pain 1999;80: Psychol Bull 2007;133:581–624.
329–39. 44. Campbell CM, Edwards RR. Mind-body interactions in pain: the
20. Cheung KM, Karppinen J, Chan D, et al. Prevalence and pattern neurophysiology of anxious and catastrophic pain-related thoughts.
of lumbar magnetic resonance imaging changes in a population Transl Res 2009;153:97–101.
study of one thousand forty-three individuals. Spine 2009;34: 45. Ren K, Dubner R. Interactions between the immune and nervous
934–40. systems in pain. Nat Med 2010;16:1267–76.
21. Carragee EJ, Alamin TF, Miller JL, et al. Discographic, MRI and 46. Shaw WS, Van der Windt DA, Main CJ, et al. Early patient screen-
psychosocial determinants of low back pain disability and remis- ing and intervention to address individual-level occupational factors
sion: a prospective study in subjects with benign persistent back (“blue flags”) in back disability. J Occup Rehabil 2009;19:64–80.
pain. Spine J 2005;5:24–35. 47. Bjorck-van Dijken C, Fjellman-Wiklund A, Hildingsson C. Low
22. Chou R, Fu R, Carrino JA, et al. Imaging strategies for low-back back pain, lifestyle factors and physical activity: a population-based
pain: systematic review and meta-analysis. Lancet 2009;373: study. J Rehabil Med 2008;40:864–9.
463–72. 48. Hestbaek L, Leboeuf-Yde C, Manniche C. Is low back pain part of
23. Jarvik JG, Hollingworth W, Heagerty PJ, et al. Three-year inci- a general health pattern or is it a separate and distinctive entity? A
dence of low back pain in an initially asymptomatic cohort: clinical critical literature review of comorbidity with low back pain.
and imaging risk factors. Spine 2005;30:1541–8. J Manipulative Physiol Ther 2003;26:243–52.
24. Lin IB, O’Sullivan PB, Coffin JA, et al. Disabling chronic low back 49. Schneider S, Mohnen SM, Schiltenwolf M, et al. Comorbidity of
pain as an iatrogenic disorder: a qualitative study in Aboriginal low back pain: representative outcomes of a national health study
Australians. BMJ Open 2013;3(4), doi:10.1136/bmjopen-2013- in the Federal Republic of Germany. Eur J Pain 2007;11:387–97.
002654. 50. Hayes C, Hodson FJ. A whole-person model of care for persistent
25. Webster BS, Cifuentes M. Relationship of early magnetic reso- pain: from conceptual framework to practical application. Pain Med
nance imaging for work-related acute low back pain with disability 2011;12:1738–49.
and medical utilization outcomes. J Occup Environ Med 2010;52: 51. Iles RA, Davidson M, Taylor NF, et al. Systematic review of the
900–7. ability of recovery expectations to predict outcomes in non-chronic
26. Sloan TJ, Walsh DA. Explanatory and diagnostic labels and per- non-specific low back pain. J Occup Rehabil 2009;19:25–40.
ceived prognosis in chronic low back pain. Spine 2010;35:E1120–5. 52. Strand EB, Kerns RD, Christie A, et al. Higher levels of pain readi-
27. Smart KM, Blake C, Staines A, et al. The discriminative validity of ness to change and more positive affect reduce pain reports–a weekly
“nociceptive,” “peripheral neuropathic,” and “central sensitization” assessment study on arthritis patients. Pain 2007;127:204–13.
as mechanisms-based classifications of musculoskeletal pain. Clin J 53. Kalauokalani D, Cherkin DC, Sherman KJ, et al. Lessons from a
Pain 2011;27:655–63. trial of acupuncture and massage for low back pain: patient expecta-
28. Üçeyler N, Zeller D, Kahn A-K, et al. Small fibre pathology in tions and treatment effects. Spine 2001;26:1418–24.
patients with fibromyalgia syndrome. Brain 2013;136:1857–67. 54. Sheeran L, Sparkes V, Caterson B, et al. Spinal position sense and
29. Woolf CJ. Central sensitization: Implications for the diagnosis and trunk muscle activity during sitting and standing in non-
treatment of pain. Pain 2010;152:S2–15. specific chronic low back pain: classification analysis. Spine
30. O’Sullivan P. Diagnosis and classification of chronic low back pain 2012;37:E486–95.
disorders: maladaptive movement and motor control impairments 55. O’Sullivan K, Verschueren S, Van Hoof W, et al. Lumbar reposi-
as underlying mechanism. Man Ther 2005;10:242–55. tioning error in sitting: healthy controls versus people with sitting-
31. Smart KM, Blake C, Staines A, et al. Mechanisms-based classifica- related non-specific chronic low back pain (flexion pattern). Man
tions of musculoskeletal pain: part 3 of 3: symptoms and signs of Ther 2013;18:526–32.
nociceptive pain in patients with low back (+/−leg) pain. Man Ther 56. Luomajoki H, Moseley G. Tactile acuity and lumbopelvic motor
2012;17:352–7. control in patients with back pain and healthy controls. Br J Sports
32. O’Sullivan P, Waller R, Wright A, et al. Sensory Characteristics of Med 2011;45:437–40.
Chronic Non-Specific Low Back Pain: A Subgroup Investigation. 57. Bray H, Moseley GL. Disrupted working body schema of the trunk
Austalian Physiotherapy Association Conference; October 17–20; in people with back pain. Br J Sports Med 2011;45:168–73.
Melbourne 2013. 58. Moseley GL, Gallagher L, Gallace A. Neglect-like tactile dysfunc-
33. Smart KM, Blake C, Staines A, et al. Mechanisms-based classifica- tion in chronic back pain. Neurology 2012;79:327–32.
tions of musculoskeletal pain: part 1 of 3: symptoms and signs of 59. Dankaerts W, O’Sullivan P, Straker L, et al. The inter-examiner
central sensitisation in patients with low back (±leg) pain. Man reliability of a classification method for non-specific chronic low
Ther 2012;17:336–44. back pain patients with motor control impairment. Man Ther
34. Wand B, Parkitny L, O’Connell N, et al. Cortical changes in 2006;11:28–39.
chronic low back pain: current state of the art and implications for 60. Smeets RJ, Wittink H, Hidding A, et al. Do patients with chronic
clinical practice. Man Ther 2011;16:15–20. low back pain have a lower level of aerobic fitness than healthy
35. Moseley GL. Pain, brain imaging and physiotherapy–opportunity controls?: are pain, disability, fear of injury, working status, or level
is knocking. Man Ther 2008;13:475–7. of leisure time activity associated with the difference in aerobic
36. Vibe Fersum K, O’Sullivan P, Kvåle A, et al. Inter-examiner reli- fitness level? Spine 2006;31:90–7.
ability of a classification system for patients with non-specific low 61. Hasenbring MI, Hallner D, Rusu AC. Fear-avoidance and
back pain. Man Ther 2009;14:555–61. endurance-related responses to pain: development and validation
37. Vlaeyen J, Linton S. Fear-avoidance model of chronic musculosk- of the Avoidance-Endurance Questionnaire (AEQ). Eur J Pain
eletal pain: 12 years on. Pain 2012;153:1144–7. 2009;13:620–8.
38. Sullivan M, Thibault P, Andrikonyte J, et al. Psychological influ- 62. Koho P, Aho S, Watson P, et al. Assessment of chronic pain behav-
ences on repetition-induced summation of activity-related pain in iour: reliability of the method and its relationship with perceived
patients with chronic low back pain. Pain 2009;141:70–8. disability, physical impairment and function. J Rehabil Med 2001;
39. Briggs AM, Jordan JE, Buchbinder R, et al. Health literacy and 33:128–32.
beliefs among a community cohort with and without chronic low 63. Martel M, Thibault P, Sullivan M. The persistence of pain behav-
back pain. Pain 2010;150:275–83. iors in patients with chronic back pain is independent of pain and
40. Woby SR, Urmston M, Watson PJ. Self-efficacy mediates the rela- psychological factors. Pain 2010;151:330–6.
tion between pain-related fear and outcome in chronic low back 64. Battié MC, Videman T, Parent E. Lumbar disc degeneration: epi-
pain patients. Eur J Pain 2007;11:711–18. demiology and genetic influences. Spine 2004;29:2679–90.
41. Darlow B, Fullen BM, Dean S, et al. The association between 65. Bunzli S, McEvoy S, O’Sullivan P, et al. A Qualitative Investigation
health care professional attitudes and beliefs and the attitudes and of Pathways through Cognitive Functional Therapy for Chronic
beliefs, clinical management, and outcomes of patients with low Low Back Pain. Australian Physiotherapy Association Conference;
back pain: a systematic review. Eur J Pain 2012;16:3–17. October 17–20; Melbourne 2013.
42. Reichborn-Kjennerud T, Stoltenberg C, Tambs K, et al. Back–neck 66. Darlow B, Dowell A, Baxter GD, et al. The enduring impact of
pain and symptoms of anxiety and depression: a population-based what clinicians say to people with low back pain. Ann Fam Med
twin study. Psychol Med 2002;32:1009–20. 2013;11:527–34.
470 PART IV  Overview of Contemporary Issues in Practice

67. Hoffman BM, Papas RK, Chatkoff DK, et al. Meta-analysis of 71. Wand B, Tulloch V, George P, et al. Seeing it helps: movement-
psychological interventions for chronic low back pain. Health related back pain is reduced by visualization of the back during
Psychol 2007;26:1–9. movement. Clin J Pain 2012;28:602–8.
68. Dankaerts W, O’Sullivan P, Burnett A, et al. The use of a 72. Van Hoof W, Volkaerts K, O’Sullivan K, et al. Comparing lower
mechanism-based classification system to evaluate and direct man- lumbar kinematics in cyclists with low back pain (flexion pattern)
agement of a patient with non-specific chronic low back pain and versus asymptomatic controls–field study using a wireless posture
motor control impairment – A case report. Man Ther monitoring system. Man Ther 2012;17:312–17.
2007;12:181–91. 73. Macedo LG, Smeets RJEM, Maher CG, et al. Graded activity and
69. Chiesa A, Serretti A. Mindfulness-based interventions for chronic graded exposure for persistent nonspecific low back pain: a system-
pain: a systematic review of the evidence. J Altern Complement atic review. Phys Ther 2010;90:860–79.
Med 2011;17:83–93.
70. Jones KD, Burckhardt CS, Bennett JA. Motivational interviewing
may encourage exercise in persons with fibromyalgia by enhancing
self efficacy. Arthritis Care Res 2004;51:864–7.

CHAPTER 45.3  ■  TREATMENT-BASED

CLASSIFICATION SYSTEM
Julie Fritz

What has come to be known as the treatment-based clas- information gathered from the history and physical
sification (TBC) system was originally disseminated in a examination to place a patient into one of four basic clas-
publication in 1995 authored by Delitto and colleagues.1 sification categories: manipulation, specific exercise
The timing of this original publication is relevant to its (flexion, extension and lateral shift patterns), stabilization
structure and purpose. The mid-1990s corresponded to and traction. The signs and symptoms originally pro-
an overall emphasis on evidence-based practice across all posed as the criteria for placing a patient into one of these
dimensions of health care, and the burgeoning of a body categories are listed in Table 45-2, and the intervention
of literature and randomized trials specific to physical procedures originally proposed for each category are
therapy treatments for patients with low back pain listed in Table 45-3. The system was based on clinical
(LBP).2,3 The situation then was much as it is today – experience evidence available at the time of its develop-
several treatments commonly used by physical therapists ment. Since that time additional research has resulted in
for patients with LBP seem to show some effects, perhaps various modifications. The original principles guiding
superior to doing nothing, but overall effect sizes tend to the development of the TBC continued to inform
be modest at best.4,5 A key consideration in interpreting ongoing research including the necessity of creating a
this literature both then and now was the concern that decision-making system that can be adapted into clinical
study designs were essentially taking a ‘magic bullet’ practice as broadly as possible and the focus on the ulti-
approach to LBP treatment.6 In other words, a presump- mate goal of improving patient-centred outcomes.
tion underlying the design of most randomized trials was
that a treatment would either ‘succeed’ or ‘fail’ for nearly
anyone with LBP regardless of clinical presentation. This OVERVIEW OF THE TREATMENT-BASED
presumption contradicted the experience of expert clini-
cians working with patients with LBP who described
CLASSIFICATION CATEGORIES
patterns of clinical findings that were presumed to define Manipulation Classification
subgroups of patients with LBP who would preferentially
respond to a particular type of treatment. Many such Spinal manipulation remains one of the most common
expert-based symptoms had been described by physical treatments used for patients with LBP. The TBC system
therapists by the mid-1990s, but none had been trans- originally proposed to identify patients likely to benefit
lated into an ongoing research agenda.7–12 Questions from manipulation based on clinical characteristics
about optimal strategies for subgrouping patients with grounded in the predominant, biomechanically orien-
LBP and improving patient-centred outcomes remain to tated paradigms most popular in the mid-1990s. A great
this day,13 but it is certain that the TBC system has con- deal of research since that time has raised questions about
tributed significantly to this conversation in the years the validity of these theories explaining the mechanisms
since its introduction. of spinal manipulation,16 and it is therefore not surprising
The TBC system in its original description was that subsequent research has questioned traditional ways
intended for patients with acute or an acute exacerbation of determining which patients with LBP are most likely
of LBP causing substantial pain and limitations in daily to respond to spinal manipulation. The manipulation
activities. The relevance of considering chronicity in the classification of the TBC system was the first to be evalu-
application of the TBC system has been highlighted by ated from a more probabilistic research approach that
subsequent research documenting worse treatment out- sought to identify clusters of findings that predicted
comes and increased difficulty classifying patients whose response to spinal manipulation regardless of the align-
symptoms are chronic.14,15 After screening patients for ment of the findings with expert-based paradigms and
any medical Red Flags, the system proposed using the clinical dogma.17 The goal of the prediction rule resulting
 45  Lumbar Spine 471

TABLE 45-2  Signs and Symptoms Originally Proposed as the Criteria for Placing a Patient into a
Particular Classification and Revised Criteria Based on Updated Evidence
Manipulation Asymmetrical lateral flexion range of No symptoms distal to the knee
motion (i.e. capsular pattern of Recent onset of symptoms (<16 days)
motion restriction) Low levels of fear-avoidance beliefs (FABQW <19)
Unilateral low back pain without Hypomobility of the lumbar spine
symptoms into the lower extremities Hip internal rotation range of motion (ROM) (>35° for at
Asymmetrical bony landmarks of the least one hip)
pelvis
Positive sacroiliac dysfunction tests (i.e.
supine-long sit test, prone knee bend
test, standing flexion test)
Stabilization Frequent recurrent episodes of LBP Younger age (<40 years)
with minimal perturbation Greater general flexibility (post-partum, average SLR ROM
Hypermobility of the lumbar spine >91°)
Previous history of lateral shift ‘Instability catch’ or aberrant movements during lumbar
deformity with alternating sides flexion/extension ROM
Frequent prior use of manipulation with Positive findings for the prone instability test
dramatic but short-term results For patients who are post-partum:
Trauma, pregnancy or use of oral Positive posterior pelvic pain provocation (P4), active
contraceptives straight leg raise (ALSR) and modified Trendelenburg
Relief with immobilization (e.g. bracing) tests
Pain provocation with palpation of the long dorsal
sacroiliac ligament or pubic symphysis
Specific exercise
  Extension Symptoms centralize with lumbar Symptoms distal to the buttock
extension Symptoms centralize with lumbar extension
Symptoms peripheralize with lumbar Symptoms peripheralize with lumbar flexion
flexion Directional preference for extension
  Flexion Symptoms centralize with lumbar Older age (>50 years old)
flexion Directional preference for flexion
Symptoms peripheralize with lumbar Imaging evidence of lumbar spinal stenosis
extension
Diagnosis of lumbar spinal stenosis
  Lateral shift Visible frontal plane deviation of the Visible frontal plane deviation of the shoulders relative to
shoulders relative to the pelvis the pelvis
Asymmetrical side-bending active ROM Directional preference for lateral translation movements of
Painful and restricted extension active the pelvis
ROM
Traction Signs and symptoms of nerve root Signs and symptoms of nerve root compression
compression No movements centralize symptoms
No movements centralize symptoms

TABLE 45-3  Intervention Procedures Originally Proposed for Each Classification and Revised
Interventions Based on Updated Evidence
Classification Original Treatments Proposed by TBC Updated Treatment Considerations
Manipulation Manipulation or mobilization techniques Manipulation of the lumbopelvic region
targeted to the sacroiliac or lumbar Active ROM exercises
region
Active range of motion (ROM) exercises
Stabilization Trunk strengthening and stabilization Promoting isolated contraction and co-contraction of the
exercises deep stabilizing muscles (multifidus, transversus
Advice to avoid end-range movements abdominus)
and positions Strengthening of large spinal stabilizing muscles (erector
Bracing for more severe cases spinae, oblique abdominals)
Specific exercise
  Extension End-range extension exercises End-range extension exercises
Avoidance of flexion activities Mobilization to promote extension
Avoidance of flexion activities
  Flexion End-range flexion exercises Mobilization or manipulation of the spine and/or lower
Mechanical traction performed in flexion extremities
Avoidance of extension activities Exercise to address impairments of strength or flexibility
Body-weight-supported treadmill ambulation
  Lateral shift Exercises to correct lateral shift Exercises to correct lateral shift
Mechanical or autotraction Mechanical traction
472 PART IV  Overview of Contemporary Issues in Practice

from this research was to identify patients who were trunk movement in the sagittal plane and the prone insta-
likely to receive rapid, pronounced benefit from spinal bility test.27,28 Other findings specific to pregnancy-
manipulation, not to exclude the potential that other related LBP have also been proposed.29
patients could not also benefit from the treatment.17,18 A persistent challenge with the stabilization subgroup
The results, supported by a multi-site randomized trial,19 of patients is the optimal treatment strategy. Various
indicate that manipulation may be most specifically ben- motor control exercise programmes have been evaluated,
eficial for patients between the ages of 18–60 years with but effect sizes continue to be modest, even among
no contraindications and an acute onset or exacerbation patients believed to fit the stabilization subgroup.26,28,30,31
(about 2 weeks or less) whose symptoms do not extend Additional research to better understand the needs of
distal to the knee. The pragmatism and simplicity of this patients in this subgroup is needed.
prediction rule are appealing not just within physical
therapy practice, but as an opportunity to communicate
with physicians about the optimal patients to send rapidly
Specific Exercise Classification
to physical therapy.20 The existence of subgroups of patients who preferentially
Another important lesson learned about the manipula- respond to repeated, end-range movements was popular-
tion TBC category relates to generalizability of specific ized by McKenzie in the decades preceding the original
manipulation techniques. Biomechanically focused para- TBC system description.12 Consistent with principles of
digms for identifying patients likely to benefit from McKenzie, the TBC system identified that the presence
manipulation traditionally placed great emphasis on the of the centralization phenomenon was the primary exam-
specificity of the manipulation technique. Recent research ination criterion for inclusion in a specific exercise clas-
suggests the choice of a specific manipulation technique sification, and the movement producing centralization
may not be as relevant as previously thought as long as a determined the specific direction of exercise required for
thrust manipulation procedure is used.21,22 Attempts to the patient. Centralization, defined as a situation in which
extend the prediction rule for manipulation to non-thrust spinal movement or positioning results in movement of
mobilization procedures have not been successful.21,23 symptoms from a distal to a more proximal/midline loca-
The need to consider thrust manipulation and non- tion, has continued to be shown as an important prog-
thrust mobilization as separate treatment modalities is nostic factor for patients with LBP.32,33 A related but
highlighted by this research and is consistent with distinct finding or directional preference, which occurs
more recent theories on the mechanisms of spinal when symptoms are diminished, abolished or central-
manipulation.16 ized,34 may also be useful for identifying the subgroup of
patients likely to respond to directional exercises.
There are some studies that lend support to the
Stabilization Classification hypothesis that patients who demonstrate centralization
The idea of a subgroup of patients with LBP related to and/or directional preference will preferentially respond
spinal instability has been described for decades, but was to repeated, directional exercises;35,36 however, a random-
initially described as a mechanical condition related to ized trial that directly addresses this treatment matching
excessive movement between adjacent vertebrae that hypothesis by evaluating the interaction between direc-
likely required immobilization or surgical stabiliza- tional exercise treatment and these particular examina-
tion.24,25 The original TBC system reflected this per­ tion findings with long-term outcomes has not been
spective, labelling this subgroup ‘immobilization’ and conducted. An interesting finding that has emerged from
recommending examination criteria and interventions recent investigations is a degree of overlap between
designed to manage patients who were presumed to have patients who fit both the manipulation and specific exer-
excessive segmental movement (see Tables 45-2 and 45- cise criteria for extension-orientated treatment.37 Optimal
3). Subsequent research has provided a different perspec- treatment strategies and sequencing for these patients has
tive by emphasizing the importance of spinal muscles in not been evaluated.
maintaining and restoring spinal stability, shifting the
focus of rehabilitation from ‘immobilization’ to ‘stabiliza-
tion’ or ‘motor control’.26
Traction Classification
The original classification criteria for a stabilization Although there was no evidence to support the conten-
subgroup focused on identifying patients presumed to tion at the time, the original TBC system hypothesized
have excessive segmental movements of the spine (see that a subset of patients with LBP existed who were
Table 45-2) such as recurrent LBP episodes, frequent likely to benefit from mechanical traction. The exami-
manipulation or self-manipulation with short-term relief, nation criteria defining this subgroup was proposed to
trauma, pregnancy, oral contraceptive use, and positive be the presence of lower-extremity symptoms and signs
response to immobilization of the spine. Shifting para- of nerve root compression and the absence of central-
digms on spinal ‘instability’ and research that employed ization with movement testing. Systematic reviews have
probabilistic designs to identify patients with LBP likely universally rejected mechanical traction as a potentially
to respond to exercises designed to improve trunk beneficial treatment for patients with LBP,38,39 despite
strength and motor control have resulted in rather dif- support for the treatment by at least some physical
ferent criteria to define this subgroup. The two most therapists.40 The research studies used heterogeneous
important clinical findings appear to be aberrant move- samples of patients with LBP, often with no leg symp-
ment suggestive of poor motor control during active toms whatsoever as the basis for the recommendation
 45  Lumbar Spine 473

against using mechanical traction.41–43 The original TBC 11. Van Dillen LR, Sahrmann SA, Norton BJ, et al. Reliability of
system acknowledged that if a traction subgroup did physical examination items used for classification of patients with
low back pain. Phys Ther 1998;78:979–88.
exist, it would include a relatively small proportion of 12. McKenzie RA. The Lumbar Spine: Mechanical Diagnosis and
patients with LBP. The mismatch between the TBC Therapy. Waikanae, NZ: Spinal Publications New Zealand Ltd.;
system conceptualization of a traction subgroup and 1981.
existing research prompted a randomized trial to evalu- 13. Henschke N, Maher CG, Refschauge KM, et al. Low back pain
research priorities: a survey of primary care practitioners. BMC
ate specific subgrouping factors that may define a trac- Fam Pract 2007;8:40.
tion subgroup.44 The results suggested that patients 14. Apeldoorn AT, Ostelo RW, van Helvoirt H, et al. A randomized
with LBP and leg symptoms who fail to centralize controlled trial on the effectiveness of a classification-based system
with the physical examination and demonstrate a crossed for sub-acute and chronic low back pain. Spine 2012;[Epub ahead
straight leg raise sign may preferentially benefit from of print].
15. Stanton TR, Hancock MJ, Apeldoorn AT, et al. What characterizes
mechanical traction.44 Additional research is needed to people who have an unclear classification using a treatment-based
further evaluate the validity of these criteria and if classification algorithm for low back pain? A cross-sectional study.
appropriate define optimal treatment parameters for Phys Ther 2013;93:345–55.
mechanical traction. 16. Bialosky JA, Bishop MD, Price DD, et al. The mechanisms of
manual therapy in the treatment of musculoskeletal pain: a com-
prehensive model. Man Ther 2009;14:531–8.
17. Flynn T, Fritz J, Whitman J, et  al. A clinical prediction rule for
CONCLUSION classifying patients with low back pain who demonstrate short
term improvement with spinal manipulation. Spine 2002;27:
If any classification system is to be useful for clinical 2835–43.
18. Fritz JM, Childs JD, Flynn TW. Pragmatic application of a clinical
practice it must lead to the identification of specific sub- prediction rule in primary care to identify patients with low back
groups of patients from data that can be collected during pain likely to respond quickly to spinal manipulation. BMC Fam
the initial history and physical examination which in turn Pract 2005;6:29.
guided the selection of optimal intervention strategies. 19. Childs JD, Fritz JM, Flynn TW, et al. Validation of a clinical pre-
diction rule to identify patients with low back pain likely to benefit
The ultimate determination of the value of a classification from spinal manipulation. Ann Intern Med 2004;141:920–8.
system is whether or not it improves patient-centred out- 20. Kramer CD, Koch WH, Fritz JM. Development and outcomes of
comes. Evidence that has emerged since the original a program to translate the evidence for spinal manipulation into
description of the TBC system indicates that it may be physical therapy practice. J Man Manip Ther 2013;21:177–86.
able to accomplish these objectives for at least some 21. Cleland JA, Fritz JM, Kulig K, et al. Comparison of the effective-
ness of three manual physical therapy techniques in a subgroup of
patients with LBP.14,19,45,46 As with any scientific endeav- patients with low back pain who satisfy a clinical prediction rule: a
our, the process of developing and refining a classification randomized clinical trial. Spine 2009;34:2720–9.
system is a dynamic and iterative process that should 22. Sutlive TG, Mabry LM, Easterling EJ, et al. Comparison of short-
result in continuous adjustments and improvements. term responses to two manipulation techniques for patients with
low back pain in a military benficiary population. Mil Med
2009;174:750–6.
23. Hancock MJ, Maher CG, Latimer J, et al. Independent evaluation
REFERENCES of a clinical prediction rule for spinal manipulative therapy: a ran-
1. Delitto A, Erhard RE, Bowling RW. A treatment-based classifica- domised controlled trial. Eur Spine J 2008;17:936–43.
tion approach to low back syndrome: identifying and staging 24. Fryberg O. Lumbar instability: a dynamic approach by traction-
patients for conservative management. Phys Ther 1995;75: compression radiography. Spine 1987;12:119–29.
470–89. 25. Kirkaldy-Willis WH, Farfan HF. Instability of the lumbar spine.
2. Sackett DL. A primer on the precision and accuracy of the clinical Clin Orthop 1982;165:110–23.
examination. JAMA 1992;267:2638–44. 26. Macedo LG, Maher CG, Latimer J, et al. Motor control exercise
3. Sackett DL, Richardson WS, Rosenberg W, et al. Evidence-Based for persistent, nonspecific low back pain: a systematic review. Phys
Medicine: How to Practice and Teach EBM. New York: Churchill Ther 2009;89:9–25.
Livingstone; 2000. 27. Hicks GE, Fritz JM, Delitto A, et al. Preliminary development of
4. Chou R, Atlas SJ, Stanos SP, et al. Nonsurgical interventional a clinical prediction rule for determining which patients with low
therapies for low back pain: a review of the evidence for an american back pain will respond to a stabilization exercise program. Arch
pain society clinical practice guideline. Spine 2009;34:1078–93. Phys Med Rehabil 2005;86:1753–62.
5. Chou R, Huffman LH. Nonpharmacologic therapies for acute and 28. Rabin A, Shashua A, Pizem K, et al. A clinical prediction rule to
chronic low back pain: a review of the evidence for an American identify patients with low back pain who are likely to experience
Pain Society/American College of Physicians clinical practice short-term success following lumbar stabilization exercises: a ran-
guideline. Ann Intern Med 2007;147:492–504. domized controlled validation study. J Orthop Sports Phys Ther
6. Delitto A. Research in low back pain: time to stop seeking the 2014;44:6–13.
elusive “magic bullet”. Phys Ther 2005;85:206–8. 29. Stuge B, Laerum E, Kirkesola G, et al. The efficacy of a treatment
7. Atlas SJ, Deyo RA, Patrick DL, et al. The Quebec Task Force clas- program focusing on specific stabilizing exercises for pelvic girdle
sification for Spinal Disorders and the severity, treatment, and pain after pregnancy: a randomized controlled trial. Spine
outcomes of sciatica and lumbar spinal stenosis. Spine 1996; 2004;29:351–9.
21:2885–92. 30. Costa LOP, Maher CG, Latimer J, et al. Motor control exercise
8. Binkley J, Finch E, Hall J, et al. Diagnostic classification of patients for chronic low back pain: a randomized placebo-controlled trial.
with low back pain: report on a survey of physical therapy experts. Phys Ther 2009;789:1275–86.
Phys Ther 1993;73:138–50. 31. Ferreira ML, Ferreira PH, Latimer J, et  al. Comparison of general
9. Buchbinder R, Goel V, Bombardier C, et al. Classification systems exercise, motor control exercise and spinal manipulative therapy
of soft tissue disorders of the neck and upper limb: do they satisfy for chronic low back pain: a randomized trial. Pain 2007;131:
methodological guidelines? J Clin Epidemiol 1996;49:141–9. 31–7.
10. Riddle DL. Classification and low back pain: a review of the litera- 32. Skytte L, May S, Petersen P. Centralization: its prognostic value in
ture and critical analysis of selected systems. Phys Ther 1998;78: patients with referred symptoms and sciatica. Spine 2005;30:
708–37. E293–9.
474 PART IV  Overview of Contemporary Issues in Practice

33. Werneke MW, Hart DL, Resnik L, et al. Centralization: preva- therapists in the United Kingdom. Arch Phys Med Rehabil
lence and effect on treatment outcomes using a standardized opera- 2005;86:1164–9.
tional definition and measurement method. J Orthop Sports Phys 41. Schimmel JJ, de Kleuver M, Horsting PP, et al. No effect of trac-
Ther 2008;38:116–25. tion in patients with low back pain: a single centre, single blind,
34. Werneke MW, Hart DL, Cuttrone G, et al. Association between randomized controlled trial of Intervertebral Differential Dynamics
directional preference and centralization in patients with low back Therapy. Eur Spine J 2009.
pain. J Orthop Sports Phys Ther 2011;41:22–31. 42. van der Heijden GJ, Beurskens AJ, Dirx MJ, et al. Efficacy of
35. Browder DA, Childs JD, Cleland JA, et al. Effectiveness of an lumbar traction: A randomised clinical trial. Physiother 1995;81:
extension oriented treatment approach in a subgroup of patients 29–35.
with low back pain: a randomized clinical trial. Phys Ther 43. Werners R, Pynsent PB, Bulstrode CJK. Randomized trial compar-
2007;87:1608–18. ing interferential therapy with motorized lumbar traction and
36. Long AL, Donelson R. Does it matter which exercise? A ran­ massage in the management of low back pain in a primary care
domized trial of exercise for low back pain. Spine 2004;29: setting. Spine 1999;24:1579–84.
2593–602. 44. Fritz JM, Lindsay W, Matheson JW, et al. Is there a subgroup of
37. Stanton TR, Fritz JM, Hancock MJ, et al. Evaluation of a treatment- patients with low back pain likely to benefit from mechanical trac-
based classification algorithm for low back pain: a cross-sectional tion? Results of a randomized clinical trial and subgrouping analy-
study. Phys Ther 2011;91:496–509. sis. Spine 2007;32:E793–800.
38. Gay RE, Brault JS. Evidence-based management of chronic low 45. Brennan GP, Fritz JM, Hunter SJ, et al. Identifying sub-groups of
back pain with traction therapy. Spine J 2008;8:234–42. patients with “non-specific” low back pain: results of a randomized
39. Harte AA, Baxter GD, Gracey JH. The efficacy of traction for back clinical trial. Spine 2006;31:623–31.
pain: a systematic review of randomized controlled trials. Arch Phys 46. Fritz JM, Delitto A, Erhard RE. Comparison of a classification-
Med Rehabil 2003;84:1542–53. based approach to physical therapy and therapy based on clinical
40. Harte AA, Gracey JH, Baxter GD. Current use of lumbar traction practice guidelines for patients with acute low back pain: a random-
in the management of low back pain: results of a survey of physio- ized clinical trial. Spine 2003;28:1363–72.

CHAPTER 45.4  ■  MOVEMENT SYSTEM

IMPAIRMENT SYNDROMES
OF THE LOW BACK
Shirley Sahrmann  •  Linda Van Dillen

MOVEMENT SYSTEM: tenet is that ‘because movement in the joint occurs too
INCLUSION NOT EXCLUSION readily and is imprecise, it hurts’. The factors contribut-
ing to the painful movement need to be identified to
Classification of patients with low back pain (LBP) has guide treatment. The movement causing the pain is
been a major focus of researchers for more than 15 attributed to accessory motion hypermobility in both the
years.1–9 Classification immediately highlights the issue of range and frequency of occurrence. Accessory arthro-
diagnosis and labels used by physical therapists and the kinematic motion is defined as motions between articular
overall context for these diagnoses. Clearly the name of surfaces of roll, glide and spin.16 The premise for the
the profession, which implies treatment by physical underlying problem of hypermobility is consistent with
means, does not provide a context or an identity for the characteristics of degenerative disc disease process.17,18
expertise in an anatomical or physiological system of the Similarly, the osteoarthritic process is attributed to small
body10 as with other health professions. To provide such imprecise motions that cause osteophytes that eventually
a context, in June 2013, the American Physical Therapy results in hypomobility. The examination is to assess as
Association adopted a guiding principle that states ‘the rigorously as possible the passive and active forces that
identity of physical therapy is the Movement System which are causing a deviation in the precision of joint motion.
is the core of physical therapy education, practice, and The examination requires attention to manual palpation
research.’11–13 about the joint segment of interest during passive and
active motion. For example, in the lumbar spine, a rec-
ommended palpation is on either side of the lumbar
MOVEMENT SYSTEM IMPAIRMENT spinous processes as the patient rocks backwards in the
SYNDROMES VERSUS MOVEMENT quadruped position. Often in the rotation syndrome, a
SYSTEM SYNDROMES small unilateral motion of flexion–rotation can be detected
as the patient rocks backwards. The proposed tissue
The preceding information was provided to clarify why adaptations contributing to the development of the
movement system impairment (MSI) syndromes of the accessory motion hypermobility are illustrated in the
lumbar spine are not intended to imply exclusive use of kinesiopathological model (Fig. 45-3).
the label movement system. All diagnoses made by physi-
cal therapists should be of the movement system (Fig.
45-2). This chapter contains just one approach. The THE KINESIOPATHOLOGICAL MODEL
theory of MSI14,15 is that multiple impairments combine
to alter the precise movement of a joint that eventually MSIs are believed to be induced by repeated movements
causes tissue irritation, pain and tissue damage. Another and prolonged alignments of daily activities because these
 45  Lumbar Spine 475

Tissue Adaptations Associated

with Repeated Movements
Muscular and Prolonged Alignment
Relative Flexibility
Flexibility refers to the intrinsic mobility of the motion
Skeletal Biomechanics Nervous segment. The term relative is used because the readiness
to move becomes more pronounced in a specific
direction(s) than in other directions as a result of the
repeated movements and prolonged postures of daily
Movement activities. For example, in younger individuals lumbar
flexion motion often occurs more readily than lumbar
extension motions, while in older individuals, movement
Metabolic Cardiovascular into extension occurs more readily than movement into
flexion.

Relative Stiffness
Pulmonary
Relative stiffness refers to the passive tension of muscle
and connective tissue that is present during elongation.
Stiffness is the resistance to deformation.20 Stiffness can
be defined as the change in tension per unit change in
length. In muscle, the connective tissue proteins such
FIGURE 45-2  ■  The human movement system. The musculoskel-
etal and nervous systems are the primary effectors of move- as titin and the extracellular matrix with its collagen,
ment. Impairments in any effector systems such as muscle are the tissues primarily responsible for stiffness.21
weakness, relative stiffness problems, altered activation pat- Hypertrophy of muscle has been shown to increase its
terns and pain will affect movement. The other systems are stiffness.22 Just as activities of daily living affect the flex-
support systems for the effectors, but are also affected by move-
ment and the lack of movement. The examination is designed
ibility of the motion segment, hypertrophy and stiffness
to detect impairments in the contributing systems and to make are also affected by these activities. The result is that
a movement system diagnosis. Treatment is based on move- one muscle group crossing the joint can be stiffer than
ment in all forms, from manipulation to mobilization to well- the antagonistic muscle crossing the same joint. As
designed exercise programmes and instruction in correct depicted in Figure 45-4, in the prone position when the
performance of functional and fitness activities. (From: Sah-
rmann SA. Movement System Impairment Syndromes of the knee is flexed, the pelvis anteriorly tilts and/or rotates
Extremities, Cervical and Thoracic Spines. Elsevier 2010.) causing lumbar extension and/or rotation. The mecha-
nisms for these motions are that (a) flexibility of the
lumbar spine into extension–rotation and (b) the stiffness
of tensor fascia lata and/or rectus femoris muscles is
behaviours induce changes in the effector systems that greater than the stiffness of the abdominal muscles
can be considered impairments. Impairment is defined as (which should help to maintain a constant position of
an abnormality in an anatomical, physiological or psy- the pelvis). The evidence for this readiness of the spine
chological system.19 An impairment can be a non-optimal to move during knee flexion will be discussed in the
but also a non-pathological change in the structure and/ research section of this chapter. Thus movements of the
or function of components of the movement system. The lumbopelvic region are not caused by muscle shortness,
theory is that a pattern of impairments develops that but because of the increased spinal flexibility (readiness
result in a principal impairment that does eventually to move) primarily and relative muscle stiffness second-
induce pathological changes in tissues. The multiple arily. Therefore stretching the stiff muscles will not stop
impairments comprise the syndrome and in combination the spinal motion.23 Direct efforts have to be made to
contribute to the principal impairment, the diagnosis. stop spinal motion and increase the stiffness of the muscle
The kinesiopathological model depicts these relation- groups that lengthened too readily. In the example given
ships (see Fig. 45-3). The primary mechanism underlying above, the patient needs to stop the spinal motion by
the changes is that the ‘body takes the path of least resis- contracting the abdominal muscles as part of a pro-
tance for movement’. Thus the changes in tissues associ- gramme to hypertrophy those muscles and increase their
ated with the repeated movements and prolonged stiffness. The MSI syndromes are named for the move-
alignments shape the path. Daily activities tend to be ment direction or alignment that most consistently
repetitious with some tissues stretched more than others causes symptoms and is impaired (non-optimal move-
and some muscles about the joint more active than others. ment), and when corrected the symptoms decrease or
As a consequence a pattern develops because of these are eliminated. The overall strategy for treatment is to
tissue adaptations. These adaptations are considered as prevent the motion and to ensure that the patient is
impairments and are indicative of a loss of optimal balance moving in the joints where the movement should be
of tissues about a joint or sometimes even the anterior taking place and not moving in joints that should remain
and posterior musculature of the trunk. relatively still.
476 PART IV  Overview of Contemporary Issues in Practice

Base Modulator Support

Muscular Cardio/pulmon
Nervous
Skeletal Metabolic

Biomechanics: Static/dynamics

Age, anthopometrics, sex

Repeated movements Personal general tissue mobility, genetics,
Inducers Modifiers
Sustained alignments characteristics activity level (excessive/insufficient)

Hypertrophy, atrophy,
Tissue adaptations long, short, stiff, stabilize,
Muscular, Neuro, Skeletal recruit, derecruit, co-contract
Motor performance coordination, boney/joint shape
Movement
Imprecise (arthro/osteokinematic)
Joint/Segment/Total body

Path of least resistance Relative flexibility/stiffness

Joint segment: hypermobility, hypomobility Tissue micro
directional predisposition trauma
Motor
learning
Movement system syndromes
Force production deficit/motor pattern incoordination Tissue
macro-
trauma/
pathology
Tissue pathology—Functional limitations

FIGURE 45-3  ■  The kinesiopathologic model. The model is intended to emphasize the general scheme for the development of move-
ment system impairment syndromes. Biomechanics act as an interface between the effector systems and play an important role in
the adaptations induced by repeated movements and sustained alignments of daily activities. Personal characteristics are also
important modifiers of the types of adaptations that are induced by activity. At the early stage repeated movements can be consid-
ered to be characteristic of motor performance but over time and with repetition, the more permanent form of motor learning takes
place. The tissue adaptations induce impairments in the movement, which is believed to be in the accessory motion of a joint. This
impairment is the result of changes in the relative flexibility of the joint and the relative stiffness of the muscular and connective
tissues about the joint. The impaired movement causes tissue microtrauma that becomes macrotrauma. The movement system
impairment syndrome is the result of this series of events. In some ways the syndromes can be generally subclassified as to whether
the primary deficit is in force production or in motor pattern coordination. Force production deficits require strengthening exercises
in addition to ensuring optimal activation patterns while motor pattern coordination deficits require primarily training of activation
patterns. (From: Sahrmann SA. Movement System Impairment Syndromes of the Extremities, Cervical and Thoracic Spines. Elsevier, 2010.)

Neuromuscular Activation Patterns (b) is not performed correctly; and (c) when the perfor-
mance is corrected the symptoms are eliminated or
Over time and with repeated use, muscles adapt in decrease. The examination consists of tests in standing,
response to (a) load; (b) the intensity and frequency of supine, side-lying, prone, quadruped and sitting. The
activation; and (c) the duration and magnitude of imposed tests involve movements of the spine and of the extremi-
length changes. The neuromuscular pattern of activation ties as well as performance of basic functional activities.
also leads to adaptation that reflects the characteristics of For the active tests in these positions the patient performs
use. This is the basis of the progression from motor per- the movement in the preferred or natural way while the
formance that is temporary, to motor learning that is therapist observes the pattern of motion. Spinal motion
permanent.24 The pattern of neuromuscular activation is also observed during basic functional activities. The
needs to be assessed, identified and corrected to optimize majority of functional activities involve greater degrees
the treatment programme. of movement at joints such as the hips and minimal or
no movement of the lumbar spine.
MOVEMENT SYSTEM IMPAIRMENT General Pattern and Distribution
SYNDROMES OF THE LUMBAR SPINE of Syndromes
The MSI syndromes are lumbar flexion, extension,25 Lumbar flexion syndromes are more common in younger
rotation, flexion–rotation26 and extension–rotation.27 The individuals. The characteristic flexibility of muscles and
diagnosis of the syndrome is based on the results of an connective tissue predispose the spine to flexion. Spinal
examination that identifies the movement direction and/ rotation also occurs more readily in the flexed as com-
or alignment that (a) most consistently causes symptoms; pared to the extended alignment. Most often those over
 Position A Position D

135° 135°

Position B Position E

90°
i

Position C

ii

135°
ii

90°
iii
FIGURE 45-4  ■  (A) Optimal balance of muscle stiffness and joint stability. The rectus femoris muscle is stretched without compensa-
tory lumbopelvic motion. Therefore the stiffness of the anterior supporting structures of the spine and the passive stiffness of the
abdominal muscles are greater than or equal to the stiffness of the rectus femoris muscle. (B) Shortness of rectus femoris muscle
with counterbalancing stiffness of spinal structures and abdominal muscles. Because the knee flexes to only 90°, the rectus femoris
muscle is short and the muscle excursion does not reach the expected standard. However, lumbopelvic compensatory motion is
not evident even though the rectus femoris muscle is short. It is not stiffer than the anterior supporting structures of the lumbar
spine and the passive extensibility of the abdominal muscles. (C) Shortness of rectus femoris muscle with compensatory lumbopelvic
motion (position Ci). With knee flexion, compensatory anterior pelvic tilt and lumbar extension occurs, even before the muscle
reaches the limit of its excursion. The pelvic tilt increases as the knee flexion range increases (position Cii). When the pelvis is
stabilized, which prevents anterior pelvic tilt, the knee flexion is limited to 90° (position Ciii). In contrast to the situation in position
B, the shortness of the rectus femoris muscle is associated with compensatory anterior pelvic tilt. Thus not only is the rectus femoris
shortened, but its stiffness is also greater than the stiffness of the anterior supporting structures of the lumbar spine and the
abdominal muscles. An important implication is that when the rectus femoris muscle is stretched to improve its overall length, the
through-the-range stiffness remains. Therefore knee flexion elicits anterior pelvic tilt as long as the rectus femoris muscle is relatively
stiffer than the structures preventing the anterior pelvic tilt or the lumbar extension. This phenomenon occurs even though the
rectus femoris muscle is able to fully elongate. Correcting the faulty, compensatory pattern requires increasing the stiffness of the
abdominal muscles and anterior supporting structures of the spine, in addition to stretching the rectus femoris muscle. It is possible
that the compensatory motion occurs only when the rectus femoris muscle reaches the end of its excursion. At this point the resis-
tance is particularly high and thus causes the compensatory motion of the pelvis. In this condition, increasing the length of the
rectus femoris muscle eliminates the motion of the pelvis. This condition is not common. (D) Compensatory motion without muscle
shortness. The knee flexes to 135° (position D), but early in the range there is an associated anterior pelvic tilt and lumbar extension.
When the pelvis is stabilized, the knee still flexes to 135°. Clearly the compensatory motion is not associated with a short muscle.
The most reasonable explanation is that the anterior supporting structures of the spine and the abdominal muscles are not as stiff
as the rectus femoris muscle that has normal length. The relative degree of through-the-range stiffness of the rectus femoris versus
the anterior trunk muscles and the anterior supporting structures of the spine is the key factor in determining the movement pattern
and in creating the compensatory motion. The compensatory motion occurred long before the muscle reached the end of its range.
Correction requires increasing the stiffness of the anterior trunk muscles. (E) Compensatory motion with passive flexion controlled
by active muscle contraction. When the knee is passively flexed, the stiffness of the rectus femoris muscle is greater than the stiff-
ness of the anterior supporting structures of the spine and the abdominal muscles, which causes compensatory anterior pelvic tilt
and lumbar extension (position Ei). When the hamstring muscles actively contract to flex the knee, the compensatory motion is
eliminated (position Eii). Possible explanations are that the posterior pelvic tilt elicited by hamstring contraction is sufficient to
counteract the stiffness of the rectus femoris. Another explanation is that the abdominal muscles contract enough to counterbalance
the anterior pelvic tilt and lumbar extension. (From Sahrmann, S. Diagnosis and Treatment of Movement Impairment Syndromes. Mosby,
2002.)
478 PART IV  Overview of Contemporary Issues in Practice

50 years of age will develop extension or extension- most frequently is designated as the syndrome or the
rotation problems. This is consistent with the anatomical diagnosis. The examination also provides information
changes in the spine of disc degeneration, spondylosis or about specific muscle performance, such as length,
spondylolysis, spondylolisthesis and spinal stenosis. Rota- strength, stiffness and activation patterns. Thus the ther-
tion motions include those of a specific motion about a apist has useful guidelines for developing the exercise
vertical axis of the trunk, side-bending and those imposed programme addressing neuromuscular function.
by lumbopelvic rotation often associated with hip
motions. Rotation can cover a wider spectrum of condi-
tions than pure flexion or extension problems and is the
Treatment
most common syndrome component. In summary, the In many ways, when a patient fails a test, that test becomes
syndromes have a relationship to spinal patho-anatomical one of the exercises. Identification of the offending move-
changes. These generalizations are intended as a guide ment direction also provides guidelines for correction of
and are not meant to imply that these general patterns functional activities. As part of the examination, the
have 100% application. patient is also learning what movements cause pain and
Though the labels of flexion, flexion–rotation, exten- how to correct the movement. Correcting functional
sion, extension–rotation or rotation are used, that does activities, which is also a form of therapeutic exercise, is
not infer that the contributing factors are the same for a essential. Functional activities include everything from
given syndrome. There are wide variations in factors that how to roll, sleeping position, how to go from supine to
contribute to a given syndrome. The variation in contrib- sitting, from sit-to-stand and reverse, how to walk, and
uting factors is greater for extension, extension–rotation how to go up and down stairs. Sitting position and types
and rotation syndromes than for flexion syndromes. of chairs need to be assessed as well as any fitness pro-
Therefore these labels are not meant to imply that the grammes or sports in which the patient participates.
treatment programme is the same for all individuals with
a given label, but the commonality is that the pain-
provoking motion is to be avoided. Thus the purposes of RESEARCH
the examination are not only to make a diagnosis, but to
also identify the contributing factors so that the treat- Clinical and laboratory-based studies of people with
ment programme is patient-specific. chronic LBP who were not in an acute flare-up were used
to assess the validity of the classifications and examine
Movement System Impairment elements of the kinesiopathologic model. The steps for
these studies were (a) defining a clinical examination;28
Examination (b) assessing the reliability of examiners to perform the
The examination is designed to provide the diagnosis, the test items;28–30 (c) determining the examiners’ reliability
principal impairment and the contributing factors. An to classify participants;29,31,32 and (d) assessing the validity
important aspect is that the patient first performs the test of the classifications.33 Motion-capture instrumentation
motion in the natural or preferred manner (primary test) was used to quantify select aspects of clinical tests, to
while the therapist observes the precision of motion and examine the relationship of those tests for different
notes the effect on symptoms. Then the therapist instructs patient classifications and to examine features of the kine-
the patient in correcting the movement (the secondary siopathologic model.
test) and notes the effect on symptoms. A major emphasis Therapists were reliable in determining the effect on
of the examination is to identify the motions of the spine symptoms of specific movement tests and in identifying
and extremities that cause pain and teach the patient how impaired movement. The classification accuracy was
to move to eliminate or minimize the symptoms. This about 70–80%.31,32,34 The premise that symptoms are
modification is necessary not only during specific exer- related to lumbar spine movement during both direct
cises, but also during all basic functional activities. The spinal motion and movement of the extremities was sup-
belief is that tissues are healing if there are no symptoms. ported by the finding that correction and prevention of
One of the values of the exam is that the patient is also spinal motion imposed by extremity movements during
learning what movements cause pain and how to decrease examination tests decreased or eliminated symptoms.35–37
or eliminate the symptoms. Another advantage is that the Examples of imposed spinal movement are lumbar
test items that the patient fails to perform correctly flexion–rotation during knee extension in sitting and
become the exercise. Though the exercises are consid- lumbopelvic rotation during hip rotation in prone
ered useful, the prevailing belief is that correcting the position.35–37 Based on the findings of examination tests
performance of functional activities is essential to correc- associated with direction-specific lumbar motions, valid-
tion of the problem. The basics of the examination are ity was demonstrated for extension, extension–rotation
given in Table 45-4. Each test is designed to assess the and rotation.33 The underlying premise, that a few
effect on symptoms associated with a given movement degrees of spinal motion that occurs too readily is present
direction and if the movement is impaired. Thus if symp- in patients with LBP, was supported by motion-capture
toms increase with forward bending and the lumbar studies. Among the tests used to assess spinal readiness
flexion range of motion is excessive, the test is positive to move were knee flexion and hip rotation in prone posi-
for flexion. If the forward bending is corrected and the tion. For both tests participants with LBP demonstrated
symptoms decrease that supports the diagnosis of lumbar earlier and more lumbopelvic rotation than back-healthy
flexion. The movement direction(s) eliciting symptoms participants.38 The onset of motion in participants with
 45  Lumbar Spine 479

TABLE 45-4  Movement System Impairment Examination for Low Back Pain
Name_________________ M F Hgt_____ Weight ____ Age _____ Date ____
Occupation ________________ Fitness Activity ______________________
Structural characteristics ___________________________________________
Pain Location: ___________________________________________ Severity _____

Position Test Segment Impairment Ext Rot Flex

Standing Spine Pain
Alignment Thoracic Kyphosis E
Flat F
Swayback E
Asymmetry R L R
Lumbar Lordosis E
Flat/flex F
Asymmetry R L R
Pelvis Anterior tilt E
Posterior tilt F
Lateral tilt R
Forward bend (Fb) Spine Pain F
Corrected Fb Pain Y N < F
Return Fb Pain E
Lumbar ext E
Corrected return Pain Y N < <E
Side-bending Pain R
Asymmetry R
Rotation Pain R
Asymmetry R
Single-leg stand Spine rotation X
Hip drop X

Total
Comments:
Position Test Segment Impairment Ext Rot Flex
Supine Hip flexor length compensation Lumbopelvic Anterior tilt E
TFL short/stiff R
Flex short/stiff E
R L asymmetrical R
Position LE extended Pain < = > >E <F
LE flexed Pain < = > <E >F
Support Pain < = > >E <F
L-spine
Hip–knee flexion Lumbopelvic pain E R
Pelvic rotation R
Hip abductor/lateral rot Lumbopelvic Pain R
Pelvic rotation R
Abdominal muscles Pelvis <2/5 E
>2/5

Side-lying Position L-spine Pain R

  Support at waist L-spine Pain < = > R
Hip lateral rotation Lumbopelvic Pain R
Pelvic rotation R
Hip abductor MMT Lumbopelvic Pain R
Weak/long
Hip abductor/adductor active Lumbopelvic Lateral pelvic tilt R

Total
Comments:
Position Test Segment Impairment Ext Rot Flex
Prone Position Lumbopelvic Pain E
  Support under abdomen Pain < = > <E >F
Knee flexion Lumbopelvic Pain E
Hip lateral rotation Lumbopelvic Pain R
Pelvic rotation R
Hip medial rotation Lumbopelvic Pain R
Pelvic rotation R

Continued on following page

480 PART IV  Overview of Contemporary Issues in Practice

TABLE 45-4 Movement System Impairment Examination for Low Back Pain (Continued)
Position Test Segment Impairment Ext Rot Flex
Quadruped Position Lumbopelvic Pain
Alignment Lumbar flexion F
Lumbar rotation R
Thoracic flexion E
Thoracic rotation R
Rocking backwards Lumbar Pain F
Flexion F
Rotation R
Extension E
Shoulder flexion Lumbar Pain R
Rotation R

Sitting Flexed Lumbar Pain F

Flat Pain F
Extended Pain E
Knee extension Lumbopelvic Pain F
Flexion-rotation R F

Standing Resting L-spine on wall Lumbopelvic Pain < = > <E >F
Shoulder flexion Pain < = > >E

Gait gait Lumbopelvic Pain R

Pelvic rotation R
Hip drop R
L-spine extension E

Total
Comments:

Movement System Impairment Diagnosis:

Flexion; extension; rotation; rotation-extension; rotation-flexion

Contributing Factors:

Functional Activities Needing Modification

Walking
Standing
Sitting
Recumbent
Position
Rolling
Work arrangement
Recreational/fitness activities

Symptom Modification Activities

Contract abdominals
Back against wall
Sitting
Quadruped
Recumbent: supine prone

Key Exercises

LBP was only a few seconds earlier and less than 5 degrees and left lower extremities in the rotation syndrome, but
more than onset of motion in back-healthy participants, the onset varied with hip lateral rotation of the right
supporting the concept that such readiness for lumbar versus the left lower extremity in the extension–rotation
motion is problematic.38 The lumbopelvic rotation during syndrome. This finding supports a key concept of relative
hip rotation in prone position was also found to elicit flexibility, which is that the lumbar spine moves too
symptoms in 60% of the men with LBP but only about readily in a specific direction, and that this behaviour
30% of the women.39–43 Lumbopelvic rotation also varies according to the classification. The finding of sym-
occurred earlier, and the early motion was a greater per- metrical onset of lumbopelvic rotation in the rotation
centage of total lumbopelvic motion in men than in syndrome and asymmetrical onset in the extension–
women.39–42 rotation syndrome was also the same in the test of trunk
Findings from the hip lateral rotation test also dem- lateral bending.45–47 Motion-capture quantification of the
onstrated differences between two of the LBP classifica- early lumbar motion demonstrated symmetrical motion
tions.44 The onset of lumboplevic rotation was elicited by to the right and left in the rotation syndrome and asym-
the same degree of hip lateral rotation of both the right metrical motion in the extension-rotation syndrome. We
 45  Lumbar Spine 481

believe that our research studies are consistent with the 7. Delitto A, Erhard R, Bowling R. A treatment-based classification
belief that early and frequent repetition of small degrees approach to low back syndrome: identifying and staging patients
for conservative treatment. Phys Ther 1995;75:470–89.
of lumbar motion in specific directions is a contributing 8. Fritz J, Cleland J, Childs J. Subgrouping patients with low back
factor to tissue microtrauma that becomes macrotrauma. pain: evolution of a classification approach to physical therapy.
Our studies also support the premise that findings from J Orthop Sports Phys Ther 2007;37:290–302.
a clinical examination can reliably and validly classify 9. Kamper SJ, Maher CG, Hancock MJ, et al. Treatment-based sub-
groups of low back pain. A guide to appraisal of research studies
patients with LBP according to the symptom-producing and a summary of current evidence. Best Pract Res Clin Rheumatol
motions, and on the readiness of the spine to move in a 2010;24:181–91.
specific direction. Furthermore, because our research has 10. Jull G, Moore A. Physiotherapy’s identity. Man Ther 2013;18:
demonstrated that correcting or stopping the spinal 447–8.
motion can decrease or eliminate the symptoms, the most 11. American Physical Therapy Association. Vision Statement. HOD
RC 14-13.
important treatment strategy is that of preventing the 12. American Physical Therapy Association. Guidelines for Vision
offending motion and lumbar stabilization should be Statement. HOD RC 15-13.
emphasized during functional activities and exercises. 13. Sahrmann SA. The human movement system – our professional
One study indicated that patients with LBP had more identity. Phys Ther 2014;94(7):1034–42. [Pub online 3/13/2014].
14. Sahrmann SA, editor. Diagnosis and Treatment of Movement
difficulty preventing the lumbopelvic rotation during hip Impairment Syndromes. St Louis: Mosby; 2002.
lateral rotation compared to back-healthy participants.48–50 15. Sahrmann SA, editor. Movement System Impairment Syndromes
This finding suggests that specific instruction and train- of the Extremities, Cervical and Thoracic Spines. St Louis: Else-
ing is necessary to achieve optimal results from a stabili- vier; 2010.
zation programme. 16. Neumann DA, editor. Kinesiology of the Musculoskeletal System.
Foundations of Physical Rehabilitation. St Louis: Mosby; 2002.
17. Onur TS, Wu R, Chu S, et al. Joint instability and cartilage com-
pression in a mouse model of posttraumatic osteoarthritis. J Orthop
CONCLUSIONS Res 2014;32:318–23.
18. Wright T. Biomechanical factors in osteoarthritis: the effects of
joint instability. HSS J 2012;8:15–17.
The MSI syndrome approach was derived from system- 19. World Health Organization Definition. <www.who.int/topics/
atic examination and treatment of patients with LBP. Use disabilities/en/>.
of a standard examination indicated that movements of 20. The American Heritage® Dictionary of the English Language,
the spine in specific directions consistently elicited symp- Fourth Edition copyright ©2000 by Houghton Mifflin Company.
toms. Correction of the movement or prevention of New York: Houghton Mifflin Company; Updated in 2009.
21. Wang K, McCarters R, Wright J, et al. Regulation of skeletal
spinal motion during extremity motions either decreased muscle stiffness and elasticity by titin isoforms: a test of the seg-
or eliminated symptoms. A derived kinesiopathologic mental extension model of resting tension. Proc Natl Acad Sci U
model proposes that the impaired, painful movements are S A 1991;88:7101–5.
present before the development of symptoms, thus there 22. Chleboun G, Howell JN, Conatser RR, et al. The relationship
between elbow flexor volume and angular stiffness at the elbow.
are signs before symptoms, and that the impairments Clin Biomech 1997;12:383.
(specifically altered activation patterns) are induced by 23. Moreside JM, McGill SM. Improvements in hip flexibility do not
adaptations of the musculoskeletal and nervous system. transfer to mobility in functional movement patterns. J Strength
Key features of the model are that the intrinsic relative Cond Res 2013;27:2635–43.
(directional) flexibility of the joint and relative stiffness 24. Schmidt R, editor. Motor Control and Learning: A Behavioral
Emphasis. 4th ed. Champaign, IL: Human Kinetics; 2005.
of muscular and connective tissues contribute to a readi- 25. Harris-Hayes M, Van Dillen LR, Sahrmann SA. Classification,
ness to move. This becomes problematic because the treatment and outcomes of a patient with lumbar extension syn-
body takes the path of least resistance for movement. The drome. Physiother Theory Pract 2005;21:181–96.
readiness to move in a specific direction is the basis of 26. Van Dillen LR, Sahrmann SA, Wagner JM. Classification, interven-
tion, and outcomes for a person with lumbar rotation with flexion
syndrome classification. Clinical and laboratory studies syndrome. Phys Ther 2005;85:336–51.
have assessed the examination, the validity of the classi- 27. Maluf KS, Sahrmann SA, Van Dillen LR. Use of a classification
fications and elements of the model. Future research is system to guide nonsurgical management of a patient with chronic
assessing the effectiveness of classification-specific treat- low back pain. Phys Ther 2000;80:1097–111.
ment, the factors inducing the readiness to move and the 28. Van Dillen LR, Sahrmann SA, Norton BJ, et al. Reliability of
physical examination items used for classification of patients with
underlying pathological tissue changes. low back pain. Phys Ther 1998;78(9):979–88.
29. Harris-Hayes M, Van Dillen LR. The inter-tester reliability of
physical therapists classifying low back pain problems based on
REFERENCES the movement system impairment classification system. PM R
1. Ford JJ, Hahne AJ. Pathoanatomy and classification of low back 2009;1:117–26.
disorders. Man Ther 2013;18:165–8. 30. Luomajoki H, Kool J, de Bruin E, et al. Reliability of movement
2. Foster NE, Hill JC, Hay EM. Subgrouping patients with low back control tests in the lumbar spine. BMC Musculoskelet Disord
pain in primary care. are we getting any better at it? Man Ther 2007;8:90–101.
2011;16:3–8. 31. Henry SM, Van Dillen LR, Trombley AR, et al. Reliability of
3. McKenzie R. The Lumbar Spine: Mechanical Diagnosis and novice raters in using the movement system impairment approach
Therapy. Waikanae: Spinal Publication; 1981. to classify people with low back pain. Man Ther 2013;18:35–40.
4. O’Sullivan P. Diagnosis and classification of chronic low back pain 32. Norton BJ, Sahrmann SA, Van Dillen FL. Differences in measure-
disorders: maladaptive movement and motor control impairments ments of lumbar curvature related to gender and low back pain.
as underlying mechanism. Man Ther 2005;10:242–55. J Orthop Sports Phys Ther 2004;34(9):524–34.
5. Van Dillen L, Sahrmann S, Norton B, et al. Movement system 33. Van Dillen LR, Sahrmann SA, Norton BJ, et al. Movement system
impairment-based categories for low back pain: stage 1 validation. impairment-based categories for low back pain: stage 1 validation.
J Orthop Sports Phys Ther 2003;33:126–42. J Orthop Sports Phys Ther 2003;33:126–42.
6. Weiner B. Spine update: the biopsychosocial model and spine care. 34. Trudelle-Jackson E, Sarvaiya-Shah SA, Wang SS. Interrater reli-
Spine 2008b;33:219–23. ability of a movement impairment-based classification system for
482 PART IV  Overview of Contemporary Issues in Practice

lumbar spine syndromes in patients with chronic low back pain. 43. Hoffman SL, Johnson MB, Zou D, et al. Gender differences in
J Orthop Sports Phys Ther 2008;38:371–6. modifying lumbopelvic motion during hip medial rotation in
35. Van Dillen LR, Sahrmann SA, Norton BJ, et al. Effect of active people with low back pain. Rehabil Res Pract 2012;2012:635312.
limb movements on symptoms in patients with low back pain. 44. Van Dillen LR, Gombatto SP, Collins DR, et al. Symmetry of
J Orthop Sports Phys Ther 2001;31(8):402–13. timing of hip and lumbopelvic rotation motion in 2 different sub-
36. Van Dillen LR, Sahrmann SA, Norton BJ, et al. The effect of groups of people with low back pain. Arch Phys Med Rehabil
modifying patient-preferred spinal movement and alignment 2007;88:351–60.
during symptom testing in patients with low back pain: a prelimi- 45. Gombatto SP, Klaesner JW, Norton BJ, et al. Validity and reli-
nary report. Arch Phys Med Rehabil 2003;84(3):313–22. ability of a system to measure passive tissue characteristics of the
37. Van Dillen LR, Maluf KS, Sahrmann SA. Further examination of lumbar region during trunk lateral bending in people with and
modifying patient-preferred movement and alignment strategies in people without low back pain. J Rehabil Res Dev 2008;45:
patients with low back pain during symptomatic tests. Man Ther 1415–29.
2009;14(1):52–60. 46. Gombatto SP, Norton BJ, Scholtes SA, et al. Differences in sym-
38. Scholtes SA, Gombatto SP, Van Dillen LR. Differences in lumbo- metry of lumbar region passive tissue characteristics between
pelvic motion between people with and people without low back people with and people without low back pain. Clin Biomech
pain during two lower limb movement tests. Clin Biomech 2008;23:986–95.
2009;24:7–12. 47. Gombatto SP, Norton BJ, Sahrmann SA, et al. Factors contributing
39. Gombatto SP, Collins DR, Sahrmann SA, et al. Gender differences to lumbar region passive tissue characteristics in people with and
in pattern of hip and lumbopelvic rotation in people with low back people without low back pain. Clin Biomech 2013;28:255–61.
pain. Clin Biomech 2006;21:263–71. 48. Scholtes SA, Norton BJ, Lang CE, et al. The effect of within-
40. Hoffman SL, Johnson MB, Zou D, et  al. Sex differences in lum- session instruction on lumbopelvic motion during a lower limb
bopelvic movement patterns during hip medial rotation in people movement in people with and people without low back pain. Man
with chronic low back pain. Arch Phys Med Rehabil 2011;92: Ther 2010;15:496–501.
1053–9. 49. Scholtes SA, Norton BJ, Gombatto SP, et al. Variables associated
41. Scholtes SA, Van Dillen LR. Gender-related differences in preva- with performance of an active limb movement following within-
lence of lumbopelvic region movement impairments in people with session instruction in people with and people without low back
low back pain. J Orthop Sports Phys Ther 2007;37:744–53. pain. Biomed Res Int 2013;2013:867–983.
42. Hoffman SL, Johnson MB, Zou D, et  al. Sex differences in lum- 50. Scholtes SA, Norton BJ, Gombatto SP, et al. Variables associated
bopelvic movement patterns during hip medial rotation in people with performance of an active limb movement following within-
with chronic low back pain. Arch Phys Med Rehabil 2011;92: session instruction in people with and people without low back
1053–9. pain. Biomed Res Int 2013;2013:867–983.

CHAPTER 45.5  ■  THE ROLE OF MOTOR CONTROL

TRAINING
Paul Hodges

INTRODUCTION individual uses their body (whether it is related to

muscle activity, posture/alignment or movement
Rehabilitative and preventative exercise that targets fea- and too much [e.g. excessive protection] or too
tures of sensorimotor control has been applied in the little [e.g. poor control of intersegmental motion]
clinical management of low back and pelvic pain for many control).
years. It appears in the clinical literature under many • Through careful assessment of the way the person
names (e.g. segmental stabilization training,1 movement moves and uses their body, the therapist identifies
impairment syndromes,2 motor control impairments,3 sub-optimal features related to this abnormal
motor control training4), and is included as a component loading.
in many other multimodal approaches.5 Although exer- • The therapist identifies a clinical solution to achieve
cise approaches that consider sensorimotor changes vary a change in the target feature of sensorimotor
in terms of the features that are prioritized in training, control, and this change in muscle activation,
the methods to achieve this and aspects of the underlying posture/alignment and/or movement modifies
philosophy, there are major areas of convergence. loading in a manner that affects the patient’s
Notably, each approach considers that pain, disability symptoms.
and/or recurrence associated with low back pain can be • From a central perspective, modification of move-
improved by modifying the way in which a person uses ment may also have other positive effects (e.g. expe-
their body, and motor learning principles are used to rience with healthy movement; recovery of body
varying degrees to achieve change.4 Common to these representation). This may impact on pain experi-
approaches is the proposal that: ence, even in the absence of a contribution of
• The manner in which a person moves, maintains peripheral nociceptive input.
posture/alignment and/or activates muscle is rele- Each element of this proposal requires further consider-
vant (in some way) to the presentation of the patient ation to judge the biological plausibility, clinical viability
in pain and this may involve peripheral and central and efficacy of this approach. It is through the systematic
elements. investigation of each element that evidence is building,
• From the perspective of peripheral nociceptive but it is unlikely that this (or any other) approach will be
input, it is assumed that loading on the tissues is optimal for everyone who presents with low back and
relevant and related to the manner in which the pelvic pain. A challenge facing clinical research is to
 45  Lumbar Spine 483

identify the people in pain for whom this approach will should aim to optimize control with an emphasis on
be optimal. This chapter overviews the clinical approach finding the balance between movement and stiffness.
and the philosophy underpinning the application of Both movement and stiffness are necessary, and the
motor control and motor learning principles to low back balance between them depends on the function. Move-
and pelvic pain. ment is critical for shock absorption,10 load transfer, varia-
tion (load sharing), and for the contribution of the trunk
and trunk muscles to other functions (e.g. breathing,
CLINICAL FRAMEWORK FOR MOTOR bladder and bowel function and balance11). Stiffness is
necessary to support load and control excessive displace-
CONTROL TRAINING ment.12 All functions require a different balance across a
Basic Principles spectrum; some require greater stiffness, others greater
movement. The challenge is to train a patient to function
Motor control training is an approach that relies on clini- across the spectrum, using the right strategy for the right
cal reasoning to identify and then modify features of the situation.
way a patient uses their body that may be related to their Another key aspect is the necessity to consider motor
symptoms. This involves careful assessment of posture/ control in the context of the biopsychosocial model of
alignment, movement and muscle activation; the devel- low back pain. Psychosocial issues (e.g. beliefs and atti-
opment of a clinical hypothesis of the relationship tudes about pain, depression13,14) and other biological
between these features and presentation; and relevant issues (e.g. inflammatory response15,16) influence a
clinical techniques to change the target features of sen- patient’s response and interact with motor control (e.g.
sorimotor control (Fig. 45-5). The basic objective is to anticipation of pain has a similar effect on motor control
optimize motor control. Although early iterations of as the experience of pain17,18).
motor control training assumed that low back and pelvic Contemporary understanding of the adaptations in
pain were associated with ‘clinical instability’ and the sensorimotor control to pain and injury forms the
selected treatments aimed to increase control,6 more foundation of this approach (see Chapter 6).19 In brief,
recently it has been emphasized that control problems changes in sensorimotor control that modify the loading
may present across a spectrum of too little, too much, or on tissue of the spine and pelvis can be characterized
inaccurate control.4,7 The former assumption of ‘instabil- by changes in: muscle morphology and behaviour associ-
ity’ often led to training excessive protection of the spine, ated with enhanced (e.g. increased amplitude, delayed
which can itself become part of the problem secondary relaxation) or compromised (e.g. delayed/reduced acti-
to increased load, reduced movement, etc. Many clinical vation, reduced muscle size, decreased fatigue resistance,
approaches were developed that aimed to restrict move- muscle fibre changes) contribution to lumbopelvic
ment with an emphasis on static alignment of spine and control; movement (e.g. reduced movement, reduced
pelvis.8,9 The contemporary view is that motor control acceleration, reduced or increased range, modified

Breathing issues

Correction of motor control 'faults' Continence/other

Posture/Alignment pelvic floor issues
Movement
Muscle activation Beliefs and
attitudes

Optimization of motor control Optimization of motor control

Adjacent regions
Static progression Dynamic progression

Static control of lumbopelvic Dynamic control of lumbopelvic Sensory function

orientation/alignment orientation/alignment and
movement
Balance issues

Functional re-education Muscle strength

Specific to patient goals and endurance

Fitness

FIGURE 45-5  ■  Clinical framework for motor control training. The basic progression of exercise from identification and retraining of
features of sensorimotor control considered to be related to the patient’s symptoms, through integration of control of these features
in more demanding contexts via static and dynamic progressions and finally into functional training of the tasks the patient has
identified as important for them. To the right is an array of features that may present as barriers to recovery of optimal motor
control. These should be screened for and included in the intervention as necessary.
484 PART IV  Overview of Contemporary Issues in Practice

sharing of motion between segments [e.g. hip and identified. Secondly, formal tests of independent activa-
spine], increased intersegmental translation); posture (e.g. tion of the anterior and posterior deep muscles are
sustained position at end of range in any direction, conducted to evaluate quality of control of deeper
reduced movement in sustained postures, postures asso- muscles and evidence of overactivity of more superficial
ciated with increased or decreased muscle activation); muscles. Movement assessment involves comparison of
and sensory function. Although deep muscles of the trunk the movement strategy adopted during basic physiologi-
are commonly compromised, this may not be the criti- cal movements (e.g. trunk flexion), standardized func-
cal feature. tional tasks (e.g. sit-to-stand) and formal movement
A fundamental basis of motor control training is the tests (e.g. hip rotation in prone). The aim is to identify
necessity for the intervention to be individualized to the features that deviate from the expected ideal, and to
patient’s presentation. It cannot be applied in a uniform then evaluate the response to correction. The ideal
manner as exercise needs to be targeted to the individual’s response minimizes pain/discomfort, as well as reduces
unique set of features of muscle activation, posture/ effort and optimizes other features (e.g. breathing,
alignment and movement that are related to their low balance). Figure 45-6 shows some key aspects of
back and/or pelvic pain, their unique functional demands, assessment.
their psychosocial profile and individual differences in
learning style. Identifying clinical phenotypes (sub-
Correction of Motor Control Faults
groups) may facilitate the process of selection of priority
targets for treatment. The initial phase of training identifies a technique to
The contemporary approach to motor control training assist patients to modify target features identified in
does not come from a single source, but involves an assessment. Motor learning principles are applied (e.g.
eclectic mix of assessments and treatments. The underly- segmentation, simplification, feedback, dosage, transfer
ing philosophy has been to combine the most informative of training) to modify motor control strategies. Tech-
(and validated) assessments for muscle activation, posture/ niques may include cognitive correction with manual
alignment and movement, and to draw on a range of guidance, manual cues, instruction and feedback. In the
approaches to identify optimal methods to achieve a initial phase of skill learning it may be appropriate to
change in motor control and progress the patient to func- target a single aspect of motor control. Ideally, this
tion. A comprehensive review and description of this feature should be one that achieves the greatest change
convergent approach to motor control training has most quickly, either based on relevance for symptoms,
recently been published as the culmination of collabora- potential for correction or patient preference.
tion between key individuals representing different
approaches.4
Progression of Exercise
Clinical Application of Motor Once optimal strategies for correction of each target
feature of motor control have been identified and
Control Training mastered, the next phase progresses exercise through
The approach begins with clinical problem solving to static and dynamic strategies. Static progression involves
identify whether modification of motor control is rele- training a patient to optimize control of muscle activa-
vant for the patient, and if so, to optimize posture, move- tion and posture/alignment, and to maintain alignment
ment and muscle activation by addressing the individual as load is applied either through movement of limbs
patient’s presenting features postulated to underpin or trunk. Although important, the static phase is rea-
ongoing symptoms or potential for recurrence. This sonably straightforward (there is a single goal – to
phase requires careful individual assessment and a test– maintain alignment), yet it is critical that patients are
retest approach to find the optimized behaviour for the also trained to move. Dynamic progression involves train-
individual. Recent developments in subgrouping can ing a patient to control the spine during movement.
facilitate decision making. Subgrouping aids pattern rec- This can involve unstable surfaces (relying on the
ognition (a feature of practice by skilled clinicians20), principle that balance cannot be maintained if the spine
which provides insight into the likely priority targets (in is stiff), control of alignment and muscle activation as
terms of postures, movements and muscle activation to the spine is moved, and control of the spine as a part
encourage and/or avoid) for training. of whole body function. The final phase involves pro-
gression into function. In the functional re-education
phase the patient is progressed to maintain control of
Assessment
their unique features of posture/alignment, movement
Formal assessment compares strategies for muscle acti- and muscle activation that were related to their symp-
vation, posture and movement with a supposed ideal. toms in their priority functions. Exercises from a range
Assessment of posture involves comparison of align- of different approaches (e.g. pilates, ball exercises, limb-
ment in sitting and/or standing against the ‘blueprint’ loading tasks, proprioceptive neuromuscular facilitation,
ideal spinal and limb alignment, deviations are cor- Klein-Vogelbach) can be used, sometimes with modi-
rected (e.g. excessive posterior pelvic tilt) and response fication and sometimes according to existing principles.
is evaluated. Muscle activation is analysed in several Diversity challenges the individual, maintains motiva-
steps. Firstly, during postural and movement assessment tion and identifies the perfect match for the patient’s
evidence of over/underactivity, atrophy/hypertrophy is preferences.
 45  Lumbar Spine 485

B Slump Flat Neutral Sway Active extension

Movement analysis
Property
• Timing
• Amplitude
• Sequence
• Quality
Segment
• Thoracolumbar control
– Excessive flexion/
extension
• Anterior pelvic sway
• Lumbar spine
– Increased or decreased
extension/lordosis
• Pelvic rotation
– Anterior/posterior
• Relationship between hip
and lumbar motion
C
FIGURE 45-6  ■  Components of the detailed assessment of motor control. Examples are shown of features that can be assessed to
build a clinical picture of causes of sub-optimal loading of the spine for an individual patient. (A) Muscle activation assessment
includes assessment of a patient’s ability to activate the deep anterior (left) and posterior (right) trunk muscles to identify deficits
in activation and evidence of pattern of over activity. (B) Assessment of posture/alignment includes identification of features of
posture that deviate from an ‘ideal’ and then evaluation of the relevance of any identified variation. (C) Movement assessment
includes analysis of features of movement strategy during basic physiological movements, specific functional tasks, patient-specific
functions and formal movement tests. Several key properties of movement are evaluated with specific attention to features of
movement that are commonly related to sub-optimal loading.
486 PART IV  Overview of Contemporary Issues in Practice

Potential Barriers to Recovery direction or duration or involve sub-optimal muscle

activation.
It is necessary to consider other features that may Secondly, pain may be centrally maintained by neural
present as barriers to recovery for an individual and processes associated with sensitization. This increased
their relevance for each patient. Such features include excitability can occur anywhere in the nervous system and
aspects of biopsychosocial presentation (e.g. fear/ is modulated by many factors including cognitive/
catastrophization, unhealthy pain cognitions) and other emotional aspects of pain, and a multitude of synaptic and
physical features that can impact on restoration of other neural mechanisms. Optimized motor control
optimal motor control. Although not relevant for all could be beneficial: if peripheral nociceptive input main-
patients, individuals may require intervention that targets tains some contribution to the pain state;21 to prevent/
features such as the contribution of the trunk muscles manage the development of pain in other body segments
to continence and breathing disorders (e.g. stress urinary secondary to modified motor control; or when experience
incontinence and chronic airways disease), dysfunction with healthy movement is beneficial to contribute to
of adjacent joints (e.g. poor foot control, restricted hip resolution of psychosocial and sensitizing mechanisms
mobility), sensory function, balance, strength and endur- (e.g. individuals who are fearful of movement/pain/
ance, and general physical fitness. Figure 45-5 can be injury).
considered a menu from which the necessary interven- Thirdly, neuropathic pain is related to nervous system
tions can be selected as appropriate for the individual injury. There is often a mechanical aspect, which may be
patient. modified by moving more optimally.
Motor control training could have an effect across the
spectrum of patients in pain. However, for individual
Common Misconceptions cases, better outcomes would be expected if treatments
There are several common misconceptions about motor are combined or if treatment is directed at the primary
control training. Firstly, the approach is not focused on mechanisms which may not be best targeted with motor
a single muscle/muscle group, posture or movement. control training (e.g. fear conditioning).
Several features of motor control may relate to a patient’s
symptoms and the specific combination to be addressed
can only be identified through careful assessment. Sec-
ondly, the approach must be tailored to the individual.
Is Motor Control Training Effective?
Subgrouping may aid identification of target features to Several systematic reviews confirm the efficacy of motor
address, but ultimately each patient needs to be consid- control training to reduce pain and disability,22,23 but the
ered as an individual to identify the relevant features of results of individual trials vary. Although early trials of
their presentation to influence symptoms. Thirdly, exer- individualized intervention targeted to specific subgroups
cise must be progressed to function. Fourthly, the identified large clinical effect sizes,24–26 the effect has been
approach is not appropriate for all patients with low back smaller in recent trials of standardized treatments in
and pelvic pain. Recent work is beginning to identify the patients with non-specific back pain.27,28 One interpreta-
patients who will achieve the greatest change with this tion of this outcome is that treatment is likely to be most
treatment (see below). Fifthly, the approach does not aim effective if directed in an individualized manner to spe-
to encourage stiffness. Optimal control involves training cific patients. This requires investigation.
a balance between movement and stiffness, and the
balance must be trained to match a spectrum of func-
tional demands. Is it Possible to Identify Patients Likely
to Respond?
Several recent trials have identified features that appear
EVIDENCE FOR MOTOR related to good outcome from this approach. Poor
CONTROL TRAINING activation of the deep trunk muscles is related to
outcome. Patients with poor activation of transversus
How Can Motor Control Training Relieve abdominis at baseline, achieve better improvement in
and Prevent Pain and Disability? pain.29,30 Most recently a study has confirmed that
patients who score high on a questionnaire of ‘lumbar
An individual may have ongoing or recurrent pain for instability’ do better with motor control training than
several reasons, and motor control training may have graded activity using the principles of cognitive behav-
different mechanisms. Firstly, pain may involve ongoing ioural therapy.31 On face value, this could suggest
nociceptive input from the periphery related to sub- patients with instability do better, but the lumbar
optimal tissue loading and the area may be sensitized. instability test has never been shown to relate to
Modification of the loading on the tissues (by changing instability and many elements of the questionnaire
posture/alignment, movement, or muscle activity) could could just be indicative of features of nociceptive
be expected to reduce symptoms. Tissue loading may be pain. The questionnaire may simply reflect those who
sub-optimal for many reasons. For instance, muscle acti- retain a nociceptive component related to sub-optimal
vation may be too much or too little, movement may tissue loading which may be amenable to motor control
be too much or too little, or a posture may load in a training.
 45  Lumbar Spine 487

Can Motor Control be Changed 15. Wang H, Schiltenwolf M, Buchner M. The role of TNF-alpha in
patients with chronic low back pain-a prospective comparative lon-
with Training? gitudinal study. Clin J Pain 2008;24:273–8.
16. Hodges PW, James G, Blomster L, et al. Can pro-inflammatory
Muscle activation,32 posture33 and movement34 can all be cytokine gene expression explain multifidus muscle fiber changes
changed with application of motor learning principles. after an intervertebral disc lesion? Spine 2014;39(13):1010–17.
These improvements transfer to function,32 can be main- 17. Moseley GL, Nicholas MK, Hodges PW. Does anticipation of back
pain predispose to back trouble? Brain 2004;127:2339–47.
tained35 and are related to clinical improvement.29 18. Tucker K, Larsson AK, Oknelid S, et al. Similar alteration of motor
Although the evidence is not universal36 (often because unit recruitment strategies during the anticipation and experience
of inadequate methods to assess motor adaptation37), of pain. Pain 2012;153:636–43.
there is growing evidence to support the approach. 19. Hodges PW, Falla D. Interaction between pain and sensorimotor
control. In: Jull GA, Moore A, Falla A, et al., editors. Grieve’s
Modern Musculoskeletal Physiotherapy. 4th ed. UK: Elsevier;
2015; in press.
CONCLUSION 20. Jones M, Rivett D. Clinical Reasoning for Manual Therapists.
Edinburgh: Butterworth Heinemann; 2004.
Motor control training is an individualized approach 21. Gracely RH, Lynch SA, Bennett GJ. Painful neuropathy: altered
central processing maintained dynamically by peripheral input.
aimed to target features of muscle activation, posture/ Pain 1992;51:175–94.
alignment and movement that contribute to a patient’s 22. Ferreira PH, Ferreira ML, Maher CG, et al. Specific stabilisation
symptoms. The approach involves an eclectic mix of exercise for spinal and pelvic pain: a systematic review. Aust J Phys-
techniques to restore optimal control via application of iother 2006;52:79–88.
motor learning theory. Outcomes are good, but perhaps 23. Macedo LG, Maher CG, Latimer J, et al. Motor control exercise
for persistent, nonspecific low back pain: a systematic review. Phys
best when the right patient is targeted with the right Ther 2009;89:9–25.
treatment. Current research priorities are to address 24. O’Sullivan PB, Twomey LT, Allison GT. Evaluation of specific
these issues as well as better understand the mechanisms stabilizing exercise in the treatment of chronic low back pain with
of the approach, with the aim to optimize its application radiologic diagnosis of spondylolysis or spondylolisthesis. Spine
1997;22:2959–67.
in clinical practice. 25. Hides JA, Jull GA, Richardson CA. Long term effects of specific
stabilizing exercises for first episode low back pain. Spine 2001;26:
243–8.
26. Stuge B, Laerum E, Kirkesola G, et al. The efficacy of a treatment
REFERENCES program focusing on specific stabilizing exercises for pelvic girdle
1. Richardson CA, Hodges PW, Hides JA. Therapeutic Exercise for pain after pregnancy: a randomized controlled trial. Spine 2004;
Lumbopelvic Stabilisation: A Motor Control Approach for the 29:351–9.
Treatment and Prevention of Low Back Pain. Edinburgh: Churchill 27. Goldby LJ, Moore AP, Doust J, et al. A randomized controlled trial
Livingstone; 2004. investigating the efficiency of musculoskeletal physiotherapy on
2. Sahrmann S. Diagnosis and Treatment of Movement Impairment chronic low back disorder. Spine 2006;31:1083–93.
Syndromes. St Louis: Mosby Inc; 2002. 28. Ferreira ML, Ferreira PH, Latimer J, et al. Comparison of general
3. O’Sullivan P. Diagnosis and classification of chronic low back pain exercise, motor control exercise and spinal manipulative therapy for
disorders: maladaptive movement and motor control impairments chronic low back pain: a randomized trial. Pain 2007;131:31–7.
as underlying mechanism. Man Ther 2005;10:242–55. 29. Ferreira PH, Ferreira ML, Maher CG, et al. Changes in recruit-
4. Hodges PW, van Dillen L, McGill S, et al. Integrated clinical ment of transversus abdominis correlate with disability in people
approach to motor control interventions in low back and pelvic with chronic low back pain. Br J Sports Med 2010;44:1166–72.
pain. In: Hodges PW, Cholewicki J, van Dieeneditors J, editors. 30. Unsgaard-Tondel M, Lund Nilsen TI, Magnussen J, et al. Is activa-
Spinal Control: The Rehabilitation of Back Pain. Edinburgh: Else- tion of transversus abdominis and obliquus internus abdominis
vier; 2013. p. 243–310. associated with long-term changes in chronic low back pain? A
5. Fritz JM, Erhard RE, Hagen BF. Segmental instability of the prospective study with 1-year follow-up. Br J Sports Med 2012;
lumbar spine. Phys Ther 1998;78:889–96. 46:729–34.
6. Panjabi MM. The stabilising system of the spine. Part II. 31. Macedo LG, Maher CG, Hancock MJ, et al. Predicting response
Neutral zone and instability hypothesis. J Spinal Disord 1992;5: to motor control exercises and graded activity for patients with low
390–7. back pain: preplanned secondary analysis of a randomized con-
7. Hodges P, Cholewicki J. Functional control of the spine. In: Vleem- trolled trial. Phys Ther 2014;94(11):1543–54.
ing A, Mooney V, Stoeckart R, editors. Movement, Stability and 32. Tsao H, Hodges PW. Immediate changes in feedforward postural
Lumbopelvic Pain. Edinburgh: Elsevier; 2007. adjustments following voluntary motor training. Exp Brain Res
8. Chek P. How to Eat, Move and Be Healthy! C.H.E.K Institute; 2007;181:537–45.
2004. 33. Falla D, Jull G, Russell T, et al. Effect of neck exercise on sitting
9. McGill SM, Karpowicz A. Exercises for spine stabilization: motion/ posture in patients with chronic neck pain. Phys Ther 2007;87:
motor patterns, stability progressions, and clinical technique. Arch 408–17.
Phys Med Rehabil 2009;90:118–26. 34. Hoffman SL, Johnson MB, Zou D, et al. Effect of classification-
10. Mok NW, Brauer SG, Hodges PW. Failure to use movement in specific treatment on lumbopelvic motion during hip rotation in
postural strategies leads to increased spinal displacement in low people with low back pain. Man Ther 2011;16:344–50.
back pain. Spine 2007;32:E537–43. 35. Tsao H, Hodges PW. Persistence of changes in postural control
11. Hodges P, Gurfinkel VS, Brumagne S, et al. Coexistence of stability following training of isolated voluntary contractions in people with
and mobility in postural control: evidence from postural compensa- recurrent low back pain. J Electromyogr Kinesiol 2008;18:
tion for respiration. Exp Brain Res 2002;144:293–302. 559–67.
12. Cholewicki J, Panjabi MM, Khachatryan A. Stabilizing function of 36. Wong AY, Parent EC, Funabashi M, et al. Do changes in trans-
trunk flexor-extensor muscles around a neutral spine posture. Spine versus abdominis and lumbar multifidus during conservative treat-
1997;22:2207–12. ment explain changes in clinical outcomes related to nonspecific
13. Leeuw M, Goossens ME, Linton SJ, et al. The fear-avoidance low back pain? A Systematic Review. J Pain 2014;15:e371–7.
model of musculoskeletal pain: current state of scientific evidence. 37. Mannion AF, Caporaso F, Pulkovski N, et al. Spine stabilisation
J Behav Med 2007;30:77–94. exercises in the treatment of chronic low back pain: a good clinical
14. Moseley GL. Reconceptualising pain according to its underlying outcome is not associated with improved abdominal muscle func-
biology. Phys Ther Rev 2007;12:169–78. tion. Eur Spine J 2012;21:1301–10.
 C H A P T E R 4 6 

The Sacroiliac Joint (Pelvic Pain):

MODELS OF ASSESSMENT AND MANAGEMENT

CHAPTER OUTLINE

Editor’s Introduction Ch 46.3  A Critical Viewpoint on Models, Testing

and Treatment of Patients with Lumbopelvic
Ch 46.1  A Person-Centred Biopsychosocial Pain  500
Approach to Assessment and Management of
Pelvic Girdle Pain  488 Annelies Pool-Goudzwaard
Darren Beales  •  Peter O’Sullivan
Ch 46.2  The Pelvic Girdle: A Look at How Time,
Experience and Evidence Change Paradigms  495
Diane Lee

EDITOR’S INTRODUCTION

Pelvic pain and the joints of the pelvis have about the extent of its capacity for movement.
fascinated clinicians and researchers from several There have been few randomized controlled
health disciplines over many decades. The trials evaluating the conservative treatment
region, not unexpectedly, has attracted interest approaches for pelvic joint dysfunction. Thus
for women during pregnancy but several studies clinical theory and reasoning still play a
using anaesthetic blocks have proven that it is a considerable role in decisions about the aetiology,
source of pain in the low back region in the assessment and management of painful pelvic
general population. Research in the field has joint dysfunction. In this chapter, three
increased and knowledge has grown approaches are presented from internationally
substantially, but it is still a region where there renowned clinicians and researchers. They
is considerable uncertainly from conservative illustrate the synergies and differences that are
musculoskeletal perspectives. There is definitive still present in theory and practice. They were
evidence that the pelvic joints can be a source chosen to inform readers of the breadth of
of pain, yet debate continues, for example, current thought and practice.

CHAPTER 46.1  ■  A PERSON-CENTRED

BIOPSYCHOSOCIAL APPROACH TO
ASSESSMENT AND MANAGEMENT
OF PELVIC GIRDLE PAIN
Darren Beales • Peter O’Sullivan

CHALLENGING HEALTH-CARE mystique within the field of manual therapy. Numerous,

complex and often confusing theories, assessment proce-
PRACTITIONER BELIEFS REGARDING dures and treatment approaches are associated with the
THE PELVIS pelvis.1–5 These approaches lack validity and may have
a detrimental effect on clinicians’ confidence6 in their
The pelvis and SIJ (sacroiliac joints), perhaps more than manual therapy skills because of a self-perceived inability
any other joint complex in the body, are shrouded by to ‘feel intra-pelvic motion’, observe ‘displacements’ and
488
 46  The Sacroiliac Joint (Pelvic Pain) 489

BOX 46-1  The Facts Regarding the Pelvis acknowledging the multifactorial nature of PGP and the
and Sacroiliac Joints (SIJs) importance of identifying both peripheral and/or central
mechanism(s) underlying pain and disability in the major-
• The pelvis and SIJs are designed primarily for load trans- ity (see Figs 46-1 and 46-2).33–35 This model is dynamic,
fer, are inherently stable7–9 and can safely transfer enor- flexible and considers both modifiable and non-modifiable
mous loads under normal conditions7 factors in order to better target person-centred care (Fig.
• The SIJ has very little movement in non-weight-bearing 46-1).
(average 2.5° rotation),10–14 and even less in weight-
bearing (average 0.2° rotation)15
• Movement of the SIJs cannot be validly or reliably assessed
by manual palpation, particularly in weight-bearing15–20 Neurophysiological Factors
• There is strong evidence that intra-articular displace-
ments within the SIJs do not occur21 and pelvic manipula- A number of potential factors need to be considered that
tion does not alter the position of the pelvic joints21 can result in/modulate both peripheral and central sensi-
• Asymmetry of the pelvis observed clinically is likely to tization of pelvic girdle structures (Fig. 46-1). Recent
occur due to changes in the spine and hips secondary to experimental pain research has demonstrated that saline
altered pelvic and trunk muscle activity, resulting in direc- injected into the posterior SIJ ligaments reproduced pain,
tional strain across pain-sensitive structures and not posi- positive SIJ provocation and active straight leg raise
tional changes within the SIJs themselves21 (ASLR) tests similar to the clinical presentation of
• The claim by some health-care practitioners to treat ‘non- PGP.26,36 These findings highlight that sensitization of
painful SIJ dysfunction(s)/displacements’ for pain in other
pelvic ligaments can mimic common clinical presenta-
body locations is not evidence-based
• No study has documented a relationship between liga- tions in the absence of tissue injury, ‘instability’ or ‘dys-
ment laxity of the SIJ and pelvic girdle pain, and relaxin function’. These findings are mirrored by a parallel study
levels are not related to pain or disability during in women with pregnancy-related PGP who demon-
pregnancy22,23 strated lower pain pressure thresholds both locally and
• A positive active straight leg raise reflects impaired motor peripherally, associated with positive clinical tests.27
activity of the hip/pelvic region24,25 associated with sensi- Observed relationships between PGP and central sen-
tized pelvic structures,26,27 and does not reflect an unstable sitizing factors such as sleep disturbance, depressed mood
pelvis and anxiety support the concept of top-down sensitizing
• A clinical diagnosis of SIJ pain can be made by: (a) the factors linked to these disorders.37 These findings suggest
finding of pain primarily located to the inferior sulcus of
that PGP is related to both local and central sensitization
the SIJ, and (b) positive pain provocation stress tests for
the SIJ28 affecting the pelvic structures. There is also evidence that
• The symphysis pubis may be a source of pain, and can be factors such as altered body perception are linked to PGP
identified through physical examination, though this disorders highlighting the potential role of the central
process has not been validated in the same way as the SIJs. nervous system in mediating common patient reports of
As with the SIJs, there is not a direct relationship between altered pelvic alignment.37 Clinical markers of peripheral
the amount of symphysis movement and pain29 sensitization are mechanical pain characteristics, local
• Pelvic girdle pain disorders may be associated with ‘exces- hyperalgesia, positive SIJ provocation tests and ASLR
sive’ as well as ‘insufficient’ motor activation of the lum- tests, whereas clinical markers of central sensitization are
bopelvic and surrounding musculature25,30–32 more commonly demonstrated by non-mechanical pain
• The strongest predictor of pelvic girdle pain not becom-
characteristics, widespread pressure and cold sensitiza-
ing chronic after pregnancy is the belief that it will not17
tion and allodynia.38,39 Body perception is also important
and can be measured with body scanning assessments and
the use of body perception questionnaires.40

diagnose complex disorders. Because of this it is impor-

tant to be clear of the ‘facts’ regarding the pelvis in the
Psychosocial Factors
context of current knowledge for both the health-care The vast majority of research investigating psychological
practitioners (HCPs) and the patient (Box 46-1). Fur- features of PGP has been completed in pregnancy-related
thermore, transmitting these beliefs to patients can be PGP subjects. However, these factors are also rel-
harmful, contributing to fear, avoidance, hypervigilance evant for non-pregnancy-related cases. Cognitive factors
and dependency on passive interventions with poor (thoughts and perceptions) such as fear and negative
efficacy. expectations of recovery impact on pain and disability in
PGP patients.37,41,42 Beliefs such as those related to per-
ceived lumbopelvic weakness are also a potential factor
in PGP.43 It is well known that HCPs’ beliefs and com-
EMBRACING THE BIOPSYCHOSOCIAL munication have an impact on patients’ beliefs and man-
MODEL OF PELVIC GIRDLE PAIN agement,44 highlighting the need for HCPs and patients
to adopt an evidence-based understanding of the disor-
Assessment of pelvic girdle pain (PGP) needs to be con- der. Affective factors (altered mood and emotion) such as
sidered from a biopsychosocial perspective; screening for depression, stress/emotional distress and catastrophizing
Red Flags and specific pathology in the minority, while have all been shown to be risk factors for ongoing PGP
490 PART IV  Overview of Contemporary Issues in Practice

Psychological factors Social factors Central

• Negative beliefs • Relationships neurophysiological
• Negative expectations • Family factors
• Stress • Work issues • Central sensitization
• Anxiety • Medical advice and • HPA-axis dysfunction
• Depression treatment • Glial cell activation
• Fear • Culture • Altered body schema
• Catastrophizing • Socioeconomics
• Hypervigilance • Support
• Maladaptive coping • Life stress events
strategies

TOP-DOWN
Comorbidities
• Continence
dysfunction
• Sexual dysfunction
• Pelvic disorders,
e.g., vulvodynia,
EPIGENETICS

endometriosis
GENETICS

Tissue Sensitivity • Abdominal disorders,

Disability e.g., irritable bowel
Pain Behaviour syndrome
• Poor health-related
quality of life

Individual Factors
BOTTOM-UP

• Onset menarche
• Parity

Lifestyle Factors Physical Factors Peripheral

• Sleep disturbance • Maladaptive: Neurophysiological
• Activity levels • Motor patterns Factors
• Sedentary behaviours • Movements • Peripheral sensitization FIGURE 46-1  ■  Biopsychosocial model of
• Smoking • Loading patterns • Pro-inflammatory hormones pelvic girdle pain. The interaction of con-
• Deconditioning • Sympathetic nervous tributing factors for an individual result in
• ASLR score system activity pain and pain behaviours, which in turn
• Ergonomic issues feedback into the system contributing to
a vicious pain cycle.

and associated disability.45–47 Social risk factors such as prior to pregnancy are associated with lower risk of chro-
socioeconomic status and work dissatisfaction have nicity.56 Smoking48,55 may also contribute to chronicity in
been identified as predictors for PGP in numerous PGP. Questioning of lifestyle factors is an important part
studies,43,48–50 highlighting the potential role of life-stress- of the interview process.
related factors in PGP. Clinical screening tools such as
the Orebro51 and STarT Back Screening Tool52 can be
used to identify those people with negative beliefs and
Physical Factors – Motor Control Factors
high levels of psychological distress, followed up with a Aberrant motor control strategies have been identified in
careful clinical interview. PGP subjects.24,25,30,57–59 A significant body of research has
investigated motor control patterns related to the ASLR
test as high levels of difficulty with an ASLR are predic-
Lifestyle Factors tive of greater levels of disability in PGP.47,60,61 Evidence
Reduced sleep is associated with chronic PGP.37 This has suggests increased co-contraction (bracing) of muscles in
previously been shown to influence factors such as pain the presence of persistent PGP.62–64 We have documented
thresholds and circulating cytokines.53 Strenuous and a co-contraction strategy in the abdominal wall of chronic
more physically demanding employment has also been PGP subjects24,25 linked to bracing of the diaphragm,
associated with greater risk of developing PGP,54,55 high- altered patterns of respiration and generation of increased
lighting the potential role of peripheral sensitizing intra-abdominal pressure, not observed in pain-free
factors. Lower general exercise levels have been associ- subjects.65 This finding is supported elsewhere.58 Other
ated with chronic PGP,54 while higher exercise levels research has documented increased activation of the
 46  The Sacroiliac Joint (Pelvic Pain) 491

Framework for assessment and targeted management of PGP

Underpinned by a strong therapeutic alliance which emphasizes person-centred care, active

management planning and consideration of the patient's health comorbidities, ‘life’ context, goals
and health literacy

PGP with pathology (1–2%)

• Malignancies
• Fractures
Undertake the • Infections
triage process • Inflammatory disorders

Refer for imaging/medical

investigation and management

Non-specific PGP (95%)

No clear patho-anatomical diagnosis

Consider risk profile, peripheral and

central sensitizing factors, movement
behaviours and lifestyle factors for
targeted management

Assessment of risk profile

Based on level of pain, disability and psychological distress
(Assisted by the use of validated screening questionnaires and clinical examination)

Low risk Medium risk High risk

(low levels of pain, disability (moderate levels of pain, (high levels of pain, disability
and psychological distress) disability and psychological and psychological distress)
• Explain biopsychosocial distress) • Targeted cognitive functional
nature of PGP • Targeted cognitive functional approach with emphasis on:
• Functionally targeted approach with an emphasis explaining biopsychosocial
exercise advise on explaining biopsychosocial nature of PGP, reducing
• Lifestyle advice nature of PGP, targeted levels of distress, vigilance
• Minimal intervention functional restoration, fear and fear avoidance through
required reduction and lifestyle change education, pain control,
relaxation, targeted
functional restoration, active
coping, discouraging pain
behaviours and facilitating
lifestyle change
• More time resources are
required for these patients
• May require integration with
‘multidisciplinary
management’

FIGURE 46-2  ■  A clinical framework for pelvic girdle pain (PGP) including triage, stratification by risk51,52 and targeted management
of contributing factors.

pelvic floor muscles in PGP patients,30 consistent with normalize movement behaviours in this context may be
bracing. These ‘bracing’ motor patterns are commonly provocative, with the need for the HCP to consider and
observed during the functional analysis of pain provoca- direct treatment at underlying pain-sensitizing mecha-
tive postural and movement tasks, challenging the popular nisms prior to or in conjunction with movement training.
belief that PGP is related to a loss of ‘core stability’. In many circumstances a positive ASLR appears to rep-
While these patterns have been described based on group resent a maladaptive (provocative) response of the motor
averages, importantly significant individual variations in system to PGP, by exerting excessive and abnormal
motor control strategies occur.24,25,65 load/strain on pain-sensitive structures. Attempts to
Significant debate exists to the basis of these findings. normalize movement behaviours within a cognitive–
We propose that in some situations a positive ASLR functional framework in these cases should result in pain
may represent an adaptive (protective) response to pain control and increased functional capacity. Identification
across highly sensitized pelvic structures. Attempts to of individual lumbopelvic motor control strategies during
492 PART IV  Overview of Contemporary Issues in Practice

pain-provocative postures and activities is a critical part explanation (verbal and written) regarding the interaction
of the clinical examination in order to determine targets of the contributing biopsychosocial factors that underpin
for functional restoration. the individual’s experience of pain sensitization and
Deconditioning of the trunk and lower limbs is disability.
common in PGP66–68 and is likely to be linked to avoid-
ance of movement and activity. This can be assessed with
functional movement tests such as squatting, lunging and
lifting.
Risk Profiling
Growing evidence supports risk profiling of patients with
musculoskeletal pain in clinical practice51,52 to assist with
Co-morbidities targeting management and resource allocation to those
Disorders of continence may be comorbid in as many as at risk of chronicity This approach can logically be
50% of women with PGP.30 Motor dysfunction of the adapted to PGP (Fig. 46-2).
pelvic floor/abdominal cylinder and excessive intra-
abdominal pressure generation provides a plausible
mechanistic link between these conditions.30,31,69,70 Various Cognitive–Functional Approach
pain disorders both local and peripheral to the pelvis are
comorbid with PGP, highlighting the potential role of
to Management
widespread pain sensitivity linked to abnormal central Consistent with the biopsychosocial nature of ‘non-
sensitization.71 specific’ PGP (Fig. 46-1), we propose that management
strategies that target modifiable maladaptive cognitive,
functional and lifestyle factors that drive pain sensitivity
Genetic and Individual Factors and disability in a person-centred manner should form
A familial relationship is known for PGP, with women the basis for care. The importance of a strong therapeutic
with PGP more likely to have a mother or sister who also alliance with empowering communication and language
has PGP.54,72 This may implicate a genetic link,73 although has been emphasized as an over-arching consideration in
social and behavioural influences may also mediate this patient–HCP interactions (Table 46-1). Other specific
effect. Earlier menarche has been associated with greater strategies for cognitive aspects of an individual’s presen-
risk for developing pregnancy-related PGP,74 though the tation include:
exact mechanism for this is unclear. The role of sex and • Education regarding patient’s contributing factors
stress hormones on peripheral and central pain mecha- and vicious cycle of pain from a biopsychosocial
nisms is well known,75 although to date there are no perspective.
definitive studies linking hormones levels to PGP. Addi- • Addressing faulty beliefs regarding causes, mecha-
tionally increased parity is a risk factor for PGP, although nisms and necessary treatment.
the exact mechanism for this is unknown.48,54,72,76 Further • Address fear, specifically related to the aggravating
research is ongoing in this area. factors and/or future course.
• Use personally meaningful strategies to reduce
stress and anxiety.
• Address pacing issues/avoidance behaviours.
KEY CONSIDERATIONS IN THE • Address coping strategies (avoidant and endurance).
BIOPSYCHOSOCIAL MANAGEMENT • Address lifestyle factors such as general physical
OF PELVIC GIRDLE PAIN activity levels, sedentary behaviours, work-related
stress and sleep hygiene.
An expansive, flexible clinical reasoning framework and • Utilize realistic, collaborative goal setting.
management system for PGP has been proposed that • Consider patient expectations.
acknowledges the complex interaction of contributing Cognitive considerations support a staged approach to
biopsychosocial factors, while identifying both the medi- physical restoration aimed at developing pain control and
ators as well as the moderators of the disorder in order enhancing functional capacity through; body relaxation,
to target care.33–35 This cognitive–functional approach normalization of body perception, correcting maladap-
has not been fully tested in PGP subjects, but encourag- tive postures and movement patterns, building confi-
ing results have been reported in persistent low back pain dence, conditioning, discouraging pain behaviours and
subjects.31,77 Figure 46-2 provides a framework for this encourage healthy lifestyle changes. Specific functionally
approach. based strategies include:
1. Body relaxation techniques – diaphragmatic breath-
ing, body scanning and visual imagery techniques
Communication and Language to focus relaxation.
HCP beliefs have a powerful effect on patient beliefs. 2. Body awareness – isolated lumbopelvic–hip control
Communication and language is an intermediary path- without excessive co-contraction and breath holding
way. Table 46-1 provides examples of HCP messages that using visual feedback (mirrors and video).
have been reported by patients as harmful versus those 3. Facilitation of normal relaxed postures – lumbopel-
that have the potential to empower patients to better vic control with relaxed thorax and diaphragmatic
manage their PGP. Critical to this process is a clear breathing.
 46  The Sacroiliac Joint (Pelvic Pain) 493

TABLE 46-1  Language and Communication is Powerful – It has the Capacity to Harm and Empower
Messages that Harm Messages that Heal
Promoting Structural Damage/Dysfunction Promote a Biopsychosocial Approach to Pelvic Pain
‘You have an unstable pelvis’ ‘Pelvic pain means that your pelvic structures are sensitized. Altered
‘Your pelvis is out of alignment’ postures, muscle tension, lack of sleep, inactivity, stress and worry can
‘Your pelvis goes out of place’ sensitize them’
‘Your pelvic pain is because you have a weak ‘The brain acts as an amplifier – the more you worry about your pain and
core’ focus on it the worse it gets’
‘Your pelvic ligaments are lax’ ‘Because you get pain relief with manipulation does not mean that your
‘You should use a pelvic belt when you exercise pelvis was out of place. The treatment gives short term pain relief and
to protect the pelvis’ helps relax the muscles’
‘Because you get pain relief wearing a pelvic belt does not mean the joints
Promote a Negative Future Outlook are unstable – it is like putting a brace on a sore knee for support’
‘Your pelvis will always be unstable’ ‘When you feel like your pelvis is out of alignment it is usually reflects
‘You will always have a weakness now so be muscle tension that gives the perception that you are lop-sided’
careful’
‘You will have to be careful when you get Promote Trust in the Body
pregnant’ ‘Your pelvic structures are the strongest structures in the body and can be
‘You won’t be able to have a natural birth’ trusted’
‘Having children has wrecked your pelvis – there ‘Pelvis’s don’t go out of place – they are too strong to do this’
is nothing you can do now’ ‘I don’t want you to rely on belts and braces, let’s teach you ways to be
confident in your pelvic structures again’
Hurt Equals Harm ‘The majority of pelvic girdle pain disorders get better – especially if you
‘Stop if you feel any pain’ have confidence in your body’
‘Let pain guide you’
Encourage Healthy Behaviours
‘Thinking positively, sleeping well, relaxation and regular exercise will help
your pelvic pain’
‘Protecting your pelvis and avoiding movement can make your pain
worse – relaxed confident movement helps’

Encourage Self-Management
‘Let’s find a way to give you control over the pain rather than giving short
fixes’

These messages are examples given to patients with pelvic girdle pain that resulted in fear and avoidance, and also messages use to
empower them to change

4. Retraining normal functional movement patterns • Facilitates empowerment of the individual for
(based on patient reports) without breath holding. self-management.
5. Discourage pain behaviours such as grimacing, • Increased self-confidence and self-efficacy.
moaning, holding painful body part, limping, avoid- • Pain control and reduced disability.
ance and the persistent use of aids such as braces.
6. Graded integration of movement into previously
reported painful, feared and/or avoided tasks, with CONCLUSION
pain control.
7. Targeted conditioning – lower limbs, trunk and We believe that clinicians need to abandon simplistic
upper limbs as indicated. biomechanical approaches to PGP and adopt an evidence-
8. Lifestyle change – regular physical activity guided based approach based on a biopsychosocial understand-
by pain levels and patient preference, pacing, sleep ing of PGP. The challenges of integrating biopsychosocial
hygiene, other general healthy lifestyle consider- thinking into health-care education, practice and research
ations (e.g. diet, smoking). are known.78,79 The model presented here provides a
Passive treatments such as manual therapy, massage and framework for meeting these challenges as well as future
acupuncture may be used as an adjunct to a cognitive– research.
functional approach in order to create opportunities
for behaviour change. Avoid sole reliance on passive REFERENCES
treatments as this may reinforce passive coping strate-
1. Cibulka MT. Understanding sacroiliac joint movement as a guide
gies. Furthermore it is important that communication to the management of a patient with unilateral low back pain. Man
related to passive treatment is evidence-based (Box 46-1) Ther 2002;7:215–21.
and does not contribute to harmful patient beliefs 2. DonTigny RL. Anterior dysfunction of the sacroiliac joint as a
(Table 46-1). major factor in the etiology of idiopathic low back pain syndrome.
Likely benefits of a cognitive–functional approach Phys Ther 1990;70:250–65, discussion 62–5.
3. Kuchera ML. Treatment of gravitational strain pathophysiology.
include: In: Vleeming A, Mooney V, Dorman T, et al., editors. Movement,
• Provides a biopsychosocial understanding of the Stability and Low Back Pain: The Essential Role of the Pelvis.
disorder (Fig. 46-1). Edinburgh: Churchill Livingstone; 1997. p. 477–99.
494 PART IV  Overview of Contemporary Issues in Practice

4. Oldreive WL. A classification of, and a critical review of the litera- 29. Bjorklund K, Nordstrom ML, Bergstrom S. Sonographic assess-
ture on, syndromes of the sacroiliac joint. J Man Manipulative Ther ment of symphyseal joint distention during pregnancy and post
1998;6:24–30. partum with special reference to pelvic pain. Acta Obstet Gynecol
5. Sandler SE. The management of low back pain in pregnancy. Man Scand 1999;78:125–30.
Ther 1996;1:178–85. 30. Pool-Goudzwaard AL, Slieker Ten Hove MC, Vierhout ME, et al.
6. Nolan D. Column. J Nat Back Exch 2013;25:16–18. Relations between pregnancy-related low back pain, pelvic floor
7. Snijders CJ, Vleeming A, Stoeckart R. Transfer of lumbosacral load activity and pelvic floor dysfunction. Int Urogynecol J Pelvic Floor
to iliac bones and legs. Part 1: biomechanics of self-bracing of the Dysfunct 2005;16:468–74.
sacroiliac joints and its significance for treatment and exercise. Clin 31. O’Sullivan PB, Beales DJ. Changes in pelvic floor and diaphragm
Biomech 1993;8:285–94. kinematics and respiratory patterns in subjects with sacroiliac joint
8. Vleeming A, Stoeckart R, Volkers AC, et al. Relation between form pain following a motor learning intervention: a case series. Man
and function in the sacroiliac joint. Part I: clinical anatomical Ther 2007;12:209–18.
aspects. Spine 1990;15:130–2. 32. Hungerford BA, Gilleard W, Hodges P. Evidence of altered lum-
9. Vleeming A, Volkers AC, Snijders CJ, et al. Relation between form bopelvic muscle recruitment in the presence of sacroiliac joint pain.
and function in the sacroiliac joint. Part II: biomechanical aspects. Spine 2003;28:1593–600.
Spine 1990;15:133–6. 33. O’Sullivan PB, Beales DJ. Diagnosis and classification of pelvic
10. Brunner C, Kissling R, Jacob HA. The effects of morphology and girdle pain disorders, Part 1: a mechanism based approach within
histopathologic findings on the mobility of the sacroiliac joint. a biopsychosocial framework. Man Ther 2007;12:86–97.
Spine 1991;16:1111–17. 34. O’Sullivan PB, Beales DJ. Diagnosis and classification of pelvic
11. Jacob HA, Kissling RO. The mobility of the sacroiliac joints in girdle pain disorders, Part 2: illustration of the utility of a classifica-
healthy volunteers between 20 and 50 years of age. Clin Biomech tion system via case studies. Man Ther 2007;12:e1–12.
1995;10:352–61. 35. Beales D, O’Sullivan P. A biopsychosocial model for pelvic girdle
12. Sturesson B, Selvik G, Uden A. Movements of the sacroiliac joints. pain: a contemporary evidence based perspective. physioscience
A roentgen stereophotogrammetric analysis. Spine 1989;14: 2011;7:63–71.
162–5. 36. Palsson TS, Hirata RP, Graven-Nielsen T. Experimental pelvic
13. Vleeming A, Buyruk HM, Stoeckart R, et al. An integrated therapy pain impairs the performance during the active straight leg raise
for peripartum pelvic instability: a study of the biomechanical test and causes excessive muscle stabilization. Clin J Pain 2015;In
effects of pelvic belts. Am J Obstet Gynecol 1992;166:1243–7. Press. doi:10.1097/AJP.0000000000000139.
14. Vleeming A, Van Wingerden JP, Dijkstra PF, et al. Mobility in the 37. Beales DJ, Lutz A, Thompson J, et al. Sleep, kinesiophobia and
sacroiliac joints in the elderly: a kinematic and radiological study. disturbed body schema are related to disability in chronic
Clin Biomech 1992;7:170–6. pregnancy-related lumbopelvic pain. Australian Physiotherapy
15. Sturesson B, Uden A, Vleeming A. A radiostereometric analysis of Association Conference Week 2013. Melbourne, Australia 2013 31
movements of the sacroiliac joints during the standing hip flexion October-2 November.
test. Spine 2000;25:364–8. 38. O’Sullivan P, Waller R, Wright A, et al. Sensory characteristics of
16. Freburger JK, Riddle DL. Using published evidence to guide the chronic non-specific low back pain: a subgroup investigation. Man
examination of the sacroiliac joint region. Phys Ther 2001; Ther 2014;19:311–18.
81:1135–43. 39. Smart KM, Blake C, Staines A, et al. The Discriminative validity
17. Holmgren U, Waling K. Inter-examiner reliability of four static of “nociceptive,” “peripheral neuropathic,” and “central sensitiza-
palpation tests used for assessing pelvic dysfunction. Man Ther tion” as mechanisms-based classifications of musculoskeletal pain.
2008;13(1):50–6. Clin J Pain 2011;27:655–63.
18. Robinson HS, Brox JI, Robinson R, et al. The reliability of selected 40. Wand BM, James M, Abbaszadeh S, et al. Assessing self-perception
motion- and pain provocation tests for the sacroiliac joint. Man in patients with chronic low back pain: development of a back-
Ther 2007;12:72–9. specific body-perception questionnaire. J Back Musculoskelet
19. van der Wurff P, Hagmeijer RH, Meyne W. Clinical tests of the Rehabil 2014;27:463–73.
sacroiliac joint. A systemic methodological review. Part 1: reliabil- 41. Vollestad NK, Stuge B. Prognostic factors for recovery from post-
ity. Man Ther 2000;5:30–6. partum pelvic girdle pain. Eur Spine J 2009;18:718–26.
20. van der Wurff P, Meyne W, Hagmeijer RH. Clinical tests of the 42. Gutke A, Lundberg M, Ostgaard HC, et al. Impact of postpartum
sacroiliac joint. A systematic methodological review. Part 2: validity. lumbopelvic pain on disability, pain intensity, health-related quality
Man Ther 2000;5:89–96. of life, activity level, kinesiophobia, and depressive symptoms. Eur
21. Tullberg T, Blomberg S, Branth B, et al. Manipulation does not Spine J 2011;20:440–8.
alter the position of the sacroiliac joint. A roentgen stereophoto- 43. Ostgaard HC, Andersson GB, Karlsson K. Prevalence of back pain
grammetric analysis. Spine 1998;23:1124–8, discussion 9. in pregnancy. Spine 1991;16:549–52.
22. Aldabe D, Ribeiro DC, Milosavljevic S, et  al. Pregnancy-related 44. Darlow B, Fullen BM, Dean S, et al. The association between
pelvic girdle pain and its relationship with relaxin levels health care professional attitudes and beliefs and the attitudes and
during pregnancy: a systematic review. Eur Spine J 2012;21: beliefs, clinical management, and outcomes of patients with low
1769–76. back pain: a systematic review. Eur J Pain 2012;16:3–17.
23. Vollestad NK, Torjesen PA, Robinson HS. Association between the 45. Bjelland EK, Stuge B, Engdahl B, et al. The effect of emotional
serum levels of relaxin and responses to the active straight leg raise distress on persistent pelvic girdle pain after delivery: a longitudinal
test in pregnancy. Man Ther 2012;17:225–30. population study. BJOG 2013;120:32–40.
24. Beales DJ, O’Sullivan PB, Briffa NK. Motor control patterns 46. Gutke A, Josefsson A, Oberg B. Pelvic girdle pain and lumbar pain in
during an active straight leg raise in chronic pelvic girdle pain relation to postpartum depressive symptoms. Spine 2007;32:1430–6.
subjects. Spine 2009;34:861–70. 47. Olsson CB, Grooten WJ, Nilsson-Wikmar L, et al. Catastroph-
25. O’Sullivan PB, Beales DJ, Beetham JA, et al. Altered motor control izing during and after pregnancy: associations with lumbo-
strategies in subjects with sacroiliac joint pain during the active pelvic pain and postpartum physical ability. Phys Ther 2012;92:
straight-leg-raise test. Spine 2002;27:E1–8. 49–57.
26. Palsson TS, Graven-Nielsen T. Experimental pelvic pain facilitates 48. Albert HB, Godskesen M, Korsholm L, et al. Risk factors in devel-
pain provocation tests and causes regional hyperalgesia. Pain oping pregnancy-related pelvic girdle pain. Acta Obstet Gynecol
2012;153:2233–40. Scand 2006;85:539–44.
27. Palsson TS, Beales D, Slater H, et al. Pregnancy is characterised 49. Berg G, Hammar M, Moller-Nielsen J, et al. Low back pain during
by widespread deep-tissue hypersensitivity independent of lumbo- pregnancy. Obstet Gynecol 1988;71:71–5.
pelvic pain intensity, a facilitated response to manual orthopedic 50. Albert HB, Godskesen M, Westergaard J. Prognosis in four syn-
tests and poorer self-reported health. J Pain 2015;In Press. dromes of pregnancy-related pelvic pain. Acta Obstet Gynecol
doi:10.1016/j.jpain.2014.12.002. Scand 2001;80:505–10.
28. Laslett M, Aprill CN, McDonald B, et al. Diagnosis of sacroiliac 51. Linton SJ, Hallden K. Can we screen for problematic back pain?
joint pain: validity of individual provocation tests and composites A screening questionnaire for predicting outcome in acute and
of tests. Man Ther 2005;10:207–18. subacute back pain. Clinical Journal of Pain 1998;14:209–15.
 46  The Sacroiliac Joint (Pelvic Pain) 495

52. Hill JC, Dunn KM, Lewis M, et al. A primary care back pain 66. Sjodahl J, Gutke A, Oberg B. Predictors for long-term disability in
screening tool: identifying patient subgroups for initial treatment. women with persistent postpartum pelvic girdle pain. Eur Spine J
Arthritis Rheum 2008;59:632–41. 2013;22:1665–73.
53. Menefee LA, Cohen MJ, Anderson WR, et al. Sleep disturbance 67. Gutke A, Ostgaard HC, Oberg B. Association between muscle
and nonmalignant chronic pain: a comprehensive review of the function and low back pain in relation to pregnancy. J Rehabil Med
literature. Pain Med 2000;1:156–72. 2008;40:304–11.
54. Larsen EC, Wilken-Jensen C, Hansen A, et al. Symptom-giving 68. Mens JM, Vleeming A, Snijders CJ, et al. Reliability and validity of
pelvic girdle relaxation in pregnancy. I: prevalence and risk factors. hip adduction strength to measure disease severity in posterior
Acta Obstet Gynecol Scand 1999;78:105–10. pelvic pain since pregnancy. Spine 2002;27:1674–9.
55. Wu WH, Meijer OG, Uegaki K, et al. Pregnancy-related pelvic 69. Beales DJ, O’Sullivan PB, Briffa NK. Motor control patterns
girdle pain (PPP), I: terminology, clinical presentation, and preva- during an active straight leg raise in chronic pelvic girdle pain
lence. Eur Spine J 2004;13:575–89. subjects. Spine 2009;34:861–70.
56. Mogren IM. Previous physical activity decreases the risk of low 70. O’Sullivan PB, Beales DJ, Beetham JA, et al. Altered motor control
back pain and pelvic pain during pregnancy. Scand J Public Health strategies in subjects with sacroiliac joint pain during the active
2005;33:300–6. straight-leg-raise test. Spine 2002;27:E1–8.
57. Beales DJ, O’Sullivan PB, Briffa NK. The effects of manual pelvic 71. Woolf CJ. Central sensitization: implications for the diagnosis and
compression on trunk motor control during an active straight leg treatment of pain. Pain 2011;152:S2–15.
raise in chronic pelvic girdle pain subjects. Man Ther 2010; 72. Mogren IM, Pohjanen AI. Low back pain and pelvic pain
15:190–9. during pregnancy: prevalence and risk factors. Spine 2005;30:
58. de Groot M, Pool-Goudzwaard AL, Spoor CW, et al. The active 983–91.
straight leg raising test (ASLR) in pregnant women: differences in 73. Fillingim RB, Wallace MR, Herbstman DM, et al. Genetic con­
muscle activity and force between patients and healthy subjects. tributions to pain: a review of findings in humans. Oral Dis
Man Ther 2008;13:68–74. 2008;14:673–82.
59. Hu H, Meijer OG, van Dieen JH, et al. Muscle activity during 74. Bjelland EK, Eberhard-Gran M, Nielsen CS, et al. Age at men-
the active straight leg raise (ASLR), and the effects of a pelvic belt arche and pelvic girdle syndrome in pregnancy: a population study
on the ASLR and on treadmill walking. J Biomech 2010;43: of 74 973 women. BJOG 2011;118:1646–52.
532–9. 75. Fillingim RB, Ness TJ. Sex-related hormonal influences on pain
60. Mens JM, Vleeming A, Snijders CJ, et al. Validity of the active and analgesic responses. Neurosci Biobehav Rev 2000;24:
straight leg raise test for measuring disease severity in patients with 485–501.
posterior pelvic pain after pregnancy. Spine 2002;27:196–200. 76. Bjelland EK, Eskild A, Johansen R, et al. Pelvic girdle pain in
61. Mukkannavar P, Desai BR, Mohanty U, et al. Pelvic girdle pain in pregnancy: the impact of parity. Am J Obstet Gynecol 2010;
Indian postpartum women: a cross-sectional study. Physiother 203(146):e1–6.
Theory Pract 2014;30:123–30. 77. Vibe Fersum K, O’Sullivan P, Skouen JS, et al. Efficacy of
62. Cote JN, Bement MK. Update on the relation between pain and classification-based cognitive functional therapy in patients with
movement: consequences for clinical practice. Clin J Pain 2010; non-specific chronic low back pain: a randomized controlled trial.
26:754–62. Eur J Pain 2012;17:916–28.
63. Dankaerts W, O’Sullivan P, Burnett A, et al. Altered patterns of 78. Foster NE, Delitto A. Embedding psychosocial perspectives
superficial trunk muscle activation during sitting in nonspecific within clinical management of low back pain: integration of psy-
chronic low back pain patients: importance of subclassification. chosocially informed management principles into physical thera-
Spine 2006;31:2017–23. pist practice–challenges and opportunities. Phys Ther 2011;91:
64. Schinkel-Ivy A, Nairn BC, Drake JD. Investigation of trunk muscle 790–803.
co-contraction and its association with low back pain development 79. Pincus T, Kent P, Bronfort G, et al. Twenty-five years with the
during prolonged sitting. J Electromyogr Kinesiol 2013;23: biopsychosocial model of low back pain-is it time to celebrate? A
778–86. report from the twelfth international forum for primary care
65. Beales DJ, O’Sullivan PB, Briffa NK. Motor control patterns research on low back pain. Spine 2013;38:2118–23.
during an active straight leg raise in pain-free subjects. Spine
2009;34:E1–8.

CHAPTER 46.2  ■  THE PELVIC GIRDLE: A LOOK AT

HOW TIME, EXPERIENCE AND
EVIDENCE CHANGE PARADIGMS
Diane Lee

Scientific research suggests that optimal function of the whether the SIJ should move, it has not been estab-
pelvis is essential for all tasks,1 and yet agreement is lished on how to reliably assess it.
lacking for: 3. Best ways to restore optimal function of the pelvis.
1. What optimal function of the pelvis requires. When When, and how, should the SIJ be mobilized or
should the sacroiliac joint (SIJ) move and when stabilized?
should it not? The biomechanics of the SIJ and In clinical practice, it is common to see complex
pubic symphysis are poorly understood for many patients with a combination of PGP, urinary inconti-
tasks that aggravate people with pelvic girdle pain nence, pelvic organ prolapse and/or diastasis rectus
(PGP). abdominis.2,3 A thorough evaluation often reveals many
2. Best ways to evaluate the functional status of the past injuries, thoughts/beliefs and emotional states that
pelvis. Even if agreement could be reached on have collectively led to changes in strategies for posture,
496 PART IV  Overview of Contemporary Issues in Practice

movement, continence and pelvic organ support. Does interpret joint motion, or lack thereof, during analysis of
the presence of pain, incontinence or prolapse mean the multiple screening tasks.
pelvis requires treatment? If not, how should a clinician
determine where to intervene to effect the greatest
improvement in function and reduction in symptoms?
The One Leg Standing (OLS) Test
There is little scientific evidence to guide clinicians for Standing on one leg and flexing the contralateral hip is a
these complex, yet common, patients.4 Clinical reasoning task often used to evaluate both mobility and control of
remains the recommended approach for determining the the pelvis. Jacob and Kissling determined that 0.4–4.3°
best treatment for the individual patient.5 of rotation is possible in the non-weight-bearing SIJ in
healthy, non-painful subjects.7 Sturesson and colleagues
found no statistical differences in the available range of
SIJ motion in subjects with PGP and impairment during
THE INTEGRATED SYSTEMS MODEL OLS.8–10 These findings suggest that although mobility
FOR DISABILITY AND PAIN may vary between subjects, PGP is not predictive of more
or less motion at the SIJ.
The Integrated Systems Model for Disability and Pain (ISM)6 Hungerford et al. (2004) found that the amplitude of
is a framework to help clinicians organize knowledge and SIJ motion was symmetric in healthy/pain-free subjects
develop clinical reasoning to facilitate wise decisions for and asymmetric in those with PGP.11 However, Dreyfuss
treatment. A key feature of this approach is finding the and colleagues found that 20% of healthy/pain-free sub-
primary driver. In short, this involves understanding jects had movement asymmetries of the SIJ and, again,
the relationships between, and within, multiple regions there appears to be no correlation between PGP and
of the body and how impairments in one region can asymmetric SIJ motion.12 So the question remains as
impact the other. Specific tests are used to determine sites to when noted movement asymmetries of the SIJ are
of non-optimal alignment, biomechanics and control relevant to the clinical picture.
(defined as failed load transfer [FLT]) during analysis of a Asymmetric motion of the SIJs during left and right
task. Subsequently, the timing of FLT, as well as the OLS is a sign of FLT (non-optimal alignment and bio-
impact of correcting one site on another, is noted. Clini- mechanics) and a key feature of the ISM approach and
cal reasoning of the various results determines the site of requires that clinicians can reliably perceive these differ-
the primary driver, or the primary region of the body, ences. Unfortunately, inter-tester reliability is lacking for
that if corrected will have a significant impact on the SIJ mobility analysis during this test (Table 46-2). Fol-
function of the whole body/person. lowing a systematic review of commonly used mobility
Further tests of specific systems (e.g. articular, neural, tests for the SIJ, Van der Wurff and colleagues,13,14
myofascial, visceral) then determine the underlying concluded:
impairment causing the non-optimal alignment, biome-
chanics and/or control of the primary driver for the spe- ‘Therefore, at this time, it is questionable whether any
cific task being assessed. Once the impaired system has SIJ tests are of any value for clinical practice14 [and that]
been determined, specific techniques and training for … There are no indications that ‘upgrading’ of the
release, alignment, control and integration into move- methodological quality would have improved the final
ment, strength and conditioning can be implemented to conclusion13’.
improve the function of the primary driver and thus
impact the function of the whole body/person. When the methods of these studies are considered,
The ISM approach requires that a clinician is able to several questions arise. How did the testers perceive the
reliably perceive (visually and/or kinaesthetically) and information – visually (look at the posterior superior iliac

TABLE 46-2  The Inter-Tester Reliability of Commonly Used Tests for Mobility of the Sacroiliac Joint
Study Palpation Points Tactile vs Visual Finding
Potter and Rothstein S2 and inferior PSIS No comment on tactile Unreliable
(1985)15 versus visual
Carmichael (1987)16 Several palpation Both visual and tactile Unreliable
points
Herzog et al. (1989)17 S2 and inferior PSIS No comment on tactile Reliable
versus visual
Dreyfuss et al. S2 and inferior PSIS No comment on tactile vs. Unreliable
(1994)12 visual
Meijne et al. (1999)18 Several palpation Both visual and tactile Unreliable
points
Van der Wurff et al Systematic review of all mobility and pain
(2000)13,14 provocation tests of the SIJ and confirm lack
of reliability and validity of all mobility tests
 46  The Sacroiliac Joint (Pelvic Pain) 497

spine (PSIS) move relative to the sacrum), kinaestheti-

cally (feel the PSIS move relative to the sacrum), or visu-
ally and kinaesthetically and does this matter? Some
clinicians appear to have better visual accuracy than kin-
aesthetic, others have better kinaesthetic sense and a few
are good at both. When the clinician is instructed to rely
on their predetermined best sense (visual or kinaesthetic),
their inter-tester reliability appears to improve, when
tested informally during course instruction. Multiple
mechanisms may drive this difference; however, those
who are less reliable when using vision often have unilat-
eral mobility restrictions of their upper neck. Were the
testers in the reliability studies (Table 46-2) screened for
asymmetric mobility of their upper neck?
Hungerford et al.11 also investigated control of SIJ
motion on the weight-bearing side during OLS. In the
pain-free subjects the innominate remained posteriorly
rotated relative to the sacrum, whereas in the PGP popu-
lation the innominate rotated anteriorly; a movement
clinicians can reliably palpate.19 This research suggests
that when assessing control of the SIJ, the key thing to
note is any anterior rotation of the innominate relative
to the sacrum, a sign of FLT when the pelvis is loaded.
Standing on one leg is a whole body task and a key
component of many more complex functional tasks.
While the pelvis plays an essential role for standing on
one leg, the task requires more than optimal function of
the pelvis. When the pelvis fails to transfer load optimally
(loses control or fails to move when it should) it is impor-
tant to consider the impact of the rest of the body on the FIGURE 46-3  ■  Active mobility of the right sacroiliac joint during
the one leg standing task in this subject reveals only extrinsic
pelvis and not just assume that the primary problem is motion of the pelvis on the left hip joint (hip joint abduction).
within the pelvis. No intra-pelvic motion was palpable at the right sacroiliac joint.
Multiple studies on subjects with low back and pelvic (Reproduced with permission from Diane G. Lee Physiotherapist
pain show that motor control changes in the trunk are Corporation©.)
variable, individual and task-specific. Some muscles are
compromised (timing of activation is delayed or absent)
while others are augmented (early and increased activa- ring,20 rotation should not occur during this task and was,
tion). The common link between tasks and individuals is therefore, non-optimal (FLT). Increased tone in a spe-
that the strategy chosen is non-optimal and there are cific fascicle of the right iliocostalis lumborum pars tho-
often multiple sites of FLT. racis (ILPT) extending from the iliac crest to the right
The following brief case report highlights the ISM seventh rib (Figs. 46-6) was present.
approach and how clinical experience, and the research During right OLS, her right SIJ lost control (the right
evidence, has changed paradigms for understanding what innominate anteriorly rotated relative to the sacrum)
a ‘non-moving PSIS relative to the sacrum’ during OLS (Fig. 46-7). This motion was intrinsic to, or within, the
may mean and one possible clinical relevance of a noted pelvis. Her seventh thoracic ring continued to translate
movement asymmetry of the SIJ in a subject with mul- to the left/rotate to the right and persistent increased
tiple sites of FLT and chronic PGP. tone was noted again in the right ILPT.
There were two sites of FLT for both of these tasks,
the seventh thoracic ring and the right SIJ. To determine
CASE REPORT the primary driver (best region to begin to treat), the
timing of FLT was noted during both tasks. The seventh
Jill was a triathlete with a primary complaint of chronic thoracic ring was translated laterally to the left/rotated
right PGP aggravated by running, her meaningful task. to the right prior to initiation of weight transfer and this
The OLS task is a useful screening test in that it pertains translation/rotation increased before the right SIJ failed
to her meaningful task. During left OLS (Fig. 46-3) her to move during left OLS and before the right SIJ lost
pelvis laterally tilted (abducted) at the left hip (extrinsic control during right OLS. This suggested that the
pelvic motion) and minimal motion of the right SIJ seventh thoracic ring was the primary driver. Confirma-
occurred compared to the left SIJ during right OLS (Fig. tion of this hypothesis required consideration of the
46-4) (i.e. asymmetric intrinsic pelvic motion was impact of a correction of the pelvis on the seventh tho-
present). In addition, her seventh thoracic ring translated racic ring alignment, biomechanics and control and then
to the left and rotated to the right (Fig. 46-5). While the impact of a pelvic ring correction on the seventh
these are optimal biomechanics for rotation of a thoracic thoracic ring alignment, biomechanics and control during
498 PART IV  Overview of Contemporary Issues in Practice

FIGURE 46-4  ■  Active mobility of the left sacroiliac joint in the

same subject as Figure 46-3 reveals palpable intra-pelvic motion
(i.e. motion between the innominate and the sacrum at the left
sacroiliac joint). (Reproduced with permission from Diane G. Lee
Physiotherapist Corporation©.) FIGURE 46-6  ■  When a fascicle of the right iliocostalis lumborum
pars thoracis (ILPT) extending from the iliac crest to the seventh
rib fails to eccentrically lengthen during left one leg standing,
posterior rotation of the right innominate can be restricted and
posterior rotation of the right seventh rib (inducing a left lateral
translation/right rotation of the entire thoracic ring) is facilitated.
Inset: Note the specific point of insertion on the iliac crest of the
fascicle of the ILPT according to MacIntosh and Bogduk (1991).22
(Reproduced with permission from Diane G. Lee Physiotherapist
Corporation©. This figure is reproduced with permission from the
authors and the Spine journal.)

both tasks. Correcting the seventh thoracic ring align-

A ment and control23 restored the mobility of the right SIJ
during left OLS and control of the right SIJ during right
OLS, correcting (alignment and control) the pelvis had
no impact on the seventh thoracic ring, therefore the
seventh thoracic ring was considered to be the driver.
Specific system tests (articular, neural, myofascial and
visceral) pertaining to the seventh thoracic ring con-
firmed that the specific hypertonic fascicle noted in the
right ILPT was, in part, responsible for the non-optimal
alignment and biomechanics of both the seventh thoracic
ring and the pelvic ring. This muscle was one of several
trunk muscle dys-synergies, the discussion of which is
outside the scope of this chapter. Since much of the
B neural drive for the abdominal wall and lumbopelvic
musculature comes from the lower thorax, it is plausible
FIGURE 46-5  ■  A thoracic ring has been defined21 as two adjacent that low thoracic ring impairments can lead to some
thoracic vertebrae, the left and right ribs that articulate with
these vertebrae, the sternum/manubrium and all the associated muscles being compromised and others augmented, as
joints connecting these bones. (B) The biomechanics of right the evidence has clearly shown. However, what is not
rotation of a typical thoracic ring.20 Left lateral translation occurs known from these studies is the best way to restore
in conjunction with right rotation of the thoracic ring. The right synergy and optimal recruitment strategies. According to
rib posteriorly rotates, the left rib anteriorly rotates and at the
end of the available range the thoracic spinal segment rotates the ISM approach,24 treatment was directed to restoring
and side flexes to the right. (Reproduced with permission from optimal function of the primary driver, the seventh tho-
Diane G. Lee Physiotherapist Corporation©.) racic ring, following which symmetric SIJ mobility and
 46  The Sacroiliac Joint (Pelvic Pain) 499

kinaesthetic senses are foundational tools for assessing

the human form in function. Understanding our indi-
vidual strengths, weaknesses, accuracies and mispercep-
tions enhances our reliability and skills necessary to find
a finding. While clinical reasoning can be taught through
texts and online media, there will always be a need for
hands-on practical courses; this is the art and skill of
physiotherapy that is so difficult to measure with science.
The Integrated Systems Model for Disability and Pain
is a clinical reasoning approach and ‘the advantages of a
clinical reasoning approach is that it is responsive to new
knowledge and evidence, is flexible and allows for change
and growth’.5 The four editions of The Pelvic Girdle25–28
have evolved over 32 years of clinical practice and clearly
reflect how time, experience and evidence challenge para-
digms for assessment and treatment of the SIJ. Clinical
expertise, a component of evidence-based practice, means
having the skill to determine whether or not the SIJ is
moving and the clinical reasoning ability to interpret the
relevance of the finding for wise treatment decisions. As
our clinical expertise for evaluating mobility and control
of the SIJ improves, perhaps our ability to demonstrate
this scientifically will be confirmed in time for the fifth
edition of this text.

REFERENCES
FIGURE 46-7  ■  Two sites of failed load transfer were noted during 1. Vleeming A, Schuenke MD, Masi AT, et al. The sacroiliac joint: an
right one leg standing in this subject, the right SIJ (horizontal overview of its anatomy, function and potential clinical implica-
arrow on the pelvis) and the seventh thoracic ring (horizontal tions. J Anat 2012;221(6):537–67.
arrow on the seventh thoracic ring). Inset: Note the specific 2. Smith MD, Russell A, Hodges PW. Is there a relationship between
point of insertion on the iliac crest of the fascicle of the ILPT parity, pregnancy, back pain and incontinence? Int Urogynecol J
according to MacIntosh and Bogduk (1991).22 (This figure is repro- 2008;19(2):205–11.
duced with permission from the authors and the Spine Journal.) 3. Spitznagle TM, Leong FC, Van Dillen LR. Prevalence of diastasis
recti abdominis in a urogynecological patient population. Int Uro-
gynecol J Pelvic Floor Dysfunct 2007;18(3):321–8.
4. Vleeming A, Albert HB, Ostgaard HC, et al. European guidelines
for the diagnosis and treatment of pelvic girdle pain. Eur Spine J
2008;17:794–819.
control was restored without direct intervention to her 5. Jull G. Management of cervical spine disorders: where to now?
pelvis. IFOMPT Quebec City, Canada. 30 September–5 October; 2012.
In this case, the asymmetric mobility of the SIJs was 6. Lee L-J, Lee D. Clinical Practice – The Reality for Clinicians. In:
primarily secondary to a hypertonic iliocostalis lumbo- Chapter 7 In The Pelvic Girdle. 4th ed. Edinburgh: Elsevier; 2011.
rum pars thoracis (ILPT) and not directly related to a 7. Jacob HAC, Kissling RO. The mobility of the sacroiliac joints in
healthy volunteers between 20 and 50 years of age. Clinical Biome-
stiff or ‘stuck’ right SIJ therefore no manual therapy chanics 1995;10(7):352–61.
intervention was indicated for her right SIJ. The right 8. Sturesson B. Load and movement of the sacroiliac joint. PhD
SIJ was noted to be not moving when it should (left OLS) thesis. Lund University, Sweden 1999.
and moving when it should not (right OLS); however, the 9. Sturesson B, Selvik G, Uden A. Movements of the sacroiliac joints:
a Roentgen stereophotogrammetric analysis. Spine 1989;14(2):
reason was extrinsic to the pelvis. In clinical practice 162–5.
there are many different drivers for pelvic girdle pain; Jill 10. Sturesson B, Uden A, Vleeming A. A radiosteriometric analysis of
was a thorax-driven PGP case. movements of the sacroiliac joints during the standing hip flexion
test. Spine 2000;25(3):364.
11. Hungerford B, Gilleard W, Lee D. Alteration of pelvic bone
motion determined in subjects with posterior pelvic pain using skin
CONCLUSION markers. Clinical Biomechanics 2004;19:456.
12. Dreyfuss P, Dryer S, Griffin J, et al. Positive sacroiliac screening
Clearly, the pelvis can no longer be considered as an tests in asymptomatic adults. Spine 1994;19(10):1138–43.
individual entity in either assessment or treatment. It is 13. Van der Wurff P, Hagmeijer R, Meyne W. Clinical tests of the
sacroiliac joint. A systematic methodological review: part 1: reli-
part of a functional whole and tests are required that ability. Man Ther 2000;5(1):30–6.
reflect the essential role it plays in the function, or lack 14. Van der Wurff P, Meyne W, Hagneijer RHM. Clinical tests of the
thereof, of multiple systems (posture/equilibrium, mus- sacroiliac joint. A systematic methodological review. Part 2: validity.
culoskeletal, urogynaecological, respiratory, digestive) Man Ther 2000;5(2):89–96.
and its relationship to multiple regions of the body. 15. Potter NA, Rothstein J. Intertester reliability for selected clinical
tests of the sacroiliac joint. Phys Ther 1985;65(11):1671–5.
When to treat the pelvis and when to look elsewhere for 16. Carmichael JP. Inter- and intra-examiner reliability of palpation
the primary driver requires the skill to not only interpret for sacroiliac joint dysfunction. J Manipulative Phys Ther 1987;
a finding but to find it reliably. For clinicians, visual and 10(4):164–71.
500 PART IV  Overview of Contemporary Issues in Practice

17. Herzog W, Read L, Conway PJW, et al. Reliability of motion 24. Lee D, Lee L-J. Clinical Reasoning, Treatment Planning and Case
palpation procedures to detect sacroiliac joint fixations. J Manipula- Reports. In: Chapter 9 in: Lee D 2011, The Pelvic Girdle. 4th ed.
tive Phys Ther 1989;12(2):86–92. Edinburgh: Elsevier; 2011.
18. Meijne W, van Neerbos K, Aufdemkampe G, et al. Intraexaminer 25. Lee D. The Pelvic Girdle. In: An approach to the Examination and
and interexaminer reliability of the Gillet test. J Manipulative Treatment of the Lumbo-pelvic-hip Region. Edinburgh: Churchill
Physiol Ther 1999;22(1):4–9. Livingstone; 1989.
19. Hungerford B, Gilleard W, Moran M, et al. Evaluation of the reli- 26. Lee D. The Pelvic Girdle. In: An Approach to the Examina-
ability of therapists to palpate intra-pelvic motion using the stork tion and Treatment of the Lumbo-pelvic-hip Region. 2nd ed.
test on the support side. J Phys Therapy 2007;87(7):879. Edinburgh: Churchill Livingstone; 1999.
20. Lee D. Biomechanics of the thorax: a clinical model of in vivo 27. Lee D. The Pelvic Girdle. In: An Approach to the Examina-
function. J Man Manipulative Ther 1993;1:13. tion and Treatment of the Lumbo-pelvic-hip Region. 3rd ed.
21. Lee D. Manual Therapy for the Thorax. www.dianelee.ca; 1994. Edinburgh: Churchill Livingstone; 2004.
22. MacIntosh JE, Bogduk N. The attachments of the lumbar erector 28. Lee D. The Pelvic Girdle. In: An Integration of Clinical Ex-
spinae. Spine 1991;16(7):783–92. pertise and Research. Edinburgh: Churchill Livingstone, Elsevier;
23. Lee L-J. Thoracic stabilization & the functional upper limb: restor- 2011.
ing stability with mobility, Course Notes. Vancouver, BC. 2003.

CHAPTER 46.3  ■  A CRITICAL VIEWPOINT ON

MODELS, TESTING AND
TREATMENT OF PATIENTS WITH
LUMBOPELVIC PAIN
Annelies Pool-Goudzwaard

INTRODUCTION study proved the contrary, mimicking solely TrA.19

Often the form–force closure model is considered
The lumbopelvic region is a fascinating area considering scientifically substantiated. However, evidence is
its evolutionary adaptation to bipedalism and its develop- lacking that optimal form and force closure is jeop-
ment through life.1 Several models have been developed ardized in all patients with LPP. Likewise, evidence
to support clinicians’ clinical reasoning in patients with for the model of myofascial slings, compressing the
lumbopelvic pain (LPP). This chapter will critically ap- SIJs via tension in the thoracolumbar fascia is also
praise two theoretical models and discuss the abilities and lacking.13,20 The model, based on in vitro studies,1,12,20
flaws of the diagnostic process. In addition an adapted is not validated and is questioned for its stiffening
classification system from O’Sullivan and Beales2 will effect on the SIJ.21 Therefore we cannot confirm
be proposed focusing on different motor-strategy pat- that non-optimal muscle recruitment of trunk/
terns of LPP patients,3–7 describing per group how to pelvis/hip muscles will lead to loss of force closure,
intervene. despite plausible force-transfer via all connected
myofascial structures throughout the body.22
B. The model of muscular spinal control has devel-
THEORETICAL MODELS oped from static into also including dynamic mus-
cular control.6,7 Considering the primary model of
Models are introduced to simplify and clarify. Two global and local muscles,14 recent research points
important models are leading in the diagnosis and inter- out that the demonstrated separation and simplifi-
vention of LPP: the model of form and force closure1,8–13 cation of local muscle functioning prior16,23–25 and
and the debated model of local and global muscles in separately from global muscles seems too simple
spinal control.3,6,7,14 to encompass real life.5,7,26 Anticipatory postural
A. The model of form and force closure is based on adjustments and preparatory trunk movements are
the contribution of the sacroiliac joint (SIJ) form reported in both local and global muscles during
and additional compressive forces to create stiff- activities, for example in walking.27–31 Recent studies
ness, ensuring integrity of the pelvic ring during have demonstrated that the most important key
loading.1,8–11,13 Additional muscle slings or ‘cross- factor in spinal control is the ability to respond to
bracing structures’ are described for optimal force challenges either statically or dynamically with
closure.1,10,13 All muscles with work-lines perpen- variability.32–34 Healthy subjects tend to use differ-
dicular to the SIJs, like transversus abdominus ent patterns of contraction of local and global
(TrA) and pelvic floor (PF) muscles will be able to muscles when carrying out the same task.28,35–37 To
increase compressive forces,8,15 as confirmed by in enable this, feedback control is plausible.35 With
vitro and in vivo studies,16–18 although one in vitro this knowledge in mind it seems not logical to train
 46  The Sacroiliac Joint (Pelvic Pain) 501

all patients in TrA-activation prior to global muscles Stork which transcends the 0.2°, may be influenced by
during all activities. This will introduce ‘learned the presence of deformation within the innominates.42
motor control behaviour’ and diminish the ability We can conclude that a level of diagnostic confusion
of variability to choose different motor control is present which increases the likelihood of inappropriate
strategies during activities. Some patients contract treatment.46 Still, clinicians tell patients that their pelvic
their TrA continuously since they understand that joints are blocked, twisted, not optimally aligned or
otherwise their lumbar spine and/or pelvis will not unstable. In addition they indicate that pain can be
be (optimally) stabilized. derived from these diagnosed patterns, although tests
lack sufficient reliability and validity. By explaining these
models as truths to patients we alter their belief system
THE DIAGNOSTIC PROCESS (either positively or negatively). So, how can we diagnose
and treat LPP patients if we skip the non-reliable and
As clinicians we can diagnose SIJ pain according valid tests?
to evidence-based standards (reliability and validity),
by using the multi-test regimen of pain provocation
tests.36–40 But do we have the ability to feel differences in CLASSIFICATION OF LOW BACK
the neutral zone, joint play or end-feel or how the SIJs PAIN PATIENTS
are positioned? Consider one’s palpation ability and
interpretation in light of the following facts: (a) anatomi- Within the algorithm of diagnosing LPP, clinical reason-
cal intra- and inter-individual differences in the SIJ’s form ing should not focus on the possible underlying con-
and position are large;1,41–43 (b) degrees of motion reported structs of pain. By restraining from drawing conclusions
in vivo are very small (mean of 1.2° and maximum 2°);44 if not in accordance with evidence-based standards, the
and (c) deformation is present within the innominates focus can shift to what we can alter to optimize a patient’s
during movement.44 If we are honest we cannot diagnose functioning. This is possible by focusing on motor strate-
SIJ mobility and position. Mobility tests do not reach gies visible in LPP patients during functional tasks.
sufficient reliability or validity,45,46 e.g. palpation of pelvic O’Sullivan and Beales (2007) introduced a classification
torque by posterior superior iliac spine and anterior supe- system describing altered adaptive or maladaptive motor
rior iliac spine only reaches a moderate kappa on inter- strategies as excessive force closure and reduced force
tester reliability (κ = 0.55).46 The same holds for closure, and elicited the importance of central pain pro-
intra-tester reliability (κ = 0.46) during the standing cesses.2 Since information is lacking on quantifying
flexion test.47 The inter-tester reliability is worse (κ = differences in force closure, this author suggests an adap-
0.052)47 and a multi-test regimen does not reach suffi- tation of the classification model (see Fig. 46-8) by intro-
cient reliability.44 The Standing Stork test, scoring mod- ducing the term ‘activity’ and adding the motor control
erate to good on inter- and intra-tester reliability lacks loop.3–7
validity.47,48 The suspected reduction of movement in the Visible differences in patients’ motor control can be
SIJ on the standing side does not occur. In contrast, a adaptive and/or compensatory to very different drivers.
displacement of 0.2° occurs in both SIJs.48 Actually, the As clinicians we will never be able to identify what the
movement we palpate of the PSIS during the Standing main driver is. Different sensoric input (Fig. 46-8A) by

Personal drivers D. Social drivers Excessive activity

Mix

C. Brain–CNS E. Motoric output Reduced activity

B. Transmission
A. Sensoric input
of data

FIGURE 46-8  ■  The adapted classification scheme from O’Sullivan & Beales,2 incorporating the optimal motor control loop.
502 PART IV  Overview of Contemporary Issues in Practice

altered proprioceptive feedback from joints, ligamentous

tissues, tendons and muscle spindles34,49–51 as well as loss
of speed and quality of information transmission can
interfere with motor control in LPP patients52–55 (Fig.
46-8B). The brain (Fig. 46-8C) adapts. Changes are
visible within the senso-motoric cortex of the brain.56–59
Also personal drivers are present (Fig. 46-8C). The
intensity of the pain can be influenced by negative emo-
tions,60,61 fear of pain or damage, directly altering motor
control.62–64 Even more, by observing another’s painful
action one’s own motor control immediately alters during
execution of the same action (Pool-Goudzwaard et al.,
unpublished data). Also, multiple other personal, biologi-
cal, social and cultural factors (as food involvement)65
interfere with someone’s pain intensity, feelings, behav-
iour and motor control67–70 (Fig. 46-8D). The extensive
input to and processes within the brain influence the
output to the motor system differently in all LPP patients
(Fig. 46-8E). We will still see differences in strategies and
classify them accordingly.
The proposed classification scheme consists of three
groups:
The first group are patients with excessive muscle activ-
ity during tasks. Signs of this pattern are increased activ-
ity in muscles surrounding the abdominal cavity, including
the PF, abdominal muscles and the diaphragm (holding FIGURE 46-9  ■  An example of a patient with excessive activity in
breath), leading to an increase of intra-abdominal pres- muscles. She is not able to relax and sit in a slump position and
sure and stiffening of the spine.2,18,68–72 Other signs of is continuously contracting her abdominal wall as well as her
excessive activity are a decrease of variability, an increase paraspinal muscles.
in rigidity, loss of precision in motoric tasks and an inabil-
ity to relax after muscle activity (Fig. 46-9).51,52,73 This
muscle usage can have negative side effects since higher
activity levels within the PF muscles are associated with
PF dysfunction such as stress urinary incontinence (OR
4.2) and dyspareunia (OR 42).18
The second group within the classification scheme
demonstrate reduced muscle activity during tasks. A lack
of muscle activity can be visible in abdominal and PF
muscles.2 Often the abdomen and the pelvic floor are
pushed outwards (Fig. 46-10). This strategy might also
increase intra-abdominal pressure when patients hold
their breath and provide stretch to the facial sheets sur-
rounding the abdominal cavity, stiffening the spine.72
These patients may also report PF dysfunctions, for
example stress urinary incontinence.67
From clinical experience a group of patients demon-
strate a mixed behaviour with some muscles being very
active and others showing reduced activity, for example
contracting all abdominal muscles meanwhile pushing
the PF downwards.
Differences in strategies can be observed during all
kind of activities while focusing on static and dynamic
response to increasing difficult tasks,3,6,74,75 As a start the FIGURE 46-10  ■  A lumbopelvic pain patient keeping the same
active straight leg raise (ASLR) test can be used as a suit- rigid lumbar spine in four point kneeling as during sitting and
able low-load task to distinguish between the groups. standing – An example of bracing leading to stiffness.
The ASLR is advocated as a test for load transfer over
the pelvis and can be used to diagnose pelvic pain.67,76–78
Mens et al. (2012) demonstrated high sensitivity and controlling the effect of hip-flexors with contralateral
specificity for diagnosing LPP.78 Some patients score hamstring activity.80,81 In LPP patients the innominate is
negative on the ASLR,79 although simultaneous increase pulled forwards on the lifting side, visible during X-ray.76
of PF activity is demonstrated.79 During ASLR healthy LPP patients can demonstrate the different strategies
subjects are able to move the complete pelvis as one, described above68,80–82
 46  The Sacroiliac Joint (Pelvic Pain) 503

For all LPP patients it is crucial to encourage patients to

INTERVENTIONS adopt variability in static and dynamic motor control and
make them aware of these strategies in daily life.
Interventions can focus on the restoration of function,
with a different emphasis depending on classification- REFERENCES
subgroup. As a clinician you can have an impact on the 1. Vleeming A, Schuenke MD, Masi AT, et al. The sacroiliac joint: an
motor loop at several points (Fig. 46-8): overview of its anatomy, function and potential clinical implica-
a. Input to the system can be altered by passively tions. J Anat 2012;221:537–67.
moving the lumbopelvic–hip complex,83 to enlarge 2. O’Sullivan PB, Beales DJ. Diagnosis and classification of pelvic
girdle pain disorders–part 1: a mechanism based approach within a
input from mechano-sensors. For this propriocep- biopsychosocial framework. Man Ther 2007;12:86–97.
tive firing, a large range of motion is necessary to 3. Reeves NP, Narendra KS, Cholewicki J. Spine stability: lessons
stimulate as many sensors as possible in the pelvic from balancing a stick. Clin Biomech 2011;26:325–30.
region. This indicates that we do not mobilize 4. Reeves NP, Narendra KS, Cholewicki J. Spine stability: the six
painful SIJs at the end of range, but only increase blind men and the elephant. Clin Biomech 2007;22:266–74.
5. Hodges PW, Coppieters MW, MacDonald D, et al. New insight
firing from the mechano-sensors at this end-range. into motor adaptation to pain revealed by a combination of model-
Instead, we want to move the complete lumbopelvic– ling and empirical approaches. Eur J Pain 2013;17:1138–46.
hip complex in a large range of motion, including 6. Reeves NP, Cholewicki J. Spine system science; a primer on the
either nutation or counter-nutation of the SIJ. The systems approach. In: Hodges PW, Cholewicky J, van Dieen J,
editors. Spinal Control: The Rehabilitation of Back Pain.
emphasis during these passive movements can be to Edinburgh: Elsevier; 2013.
the non-painful side regarding the importance of 7. Hodges PW, McGill S, Hides JA. Motor control of the spine and
pain inhibition on motor control.84 changes in pain: Debate about extrapolation from research observa-
b. Although it is not possible to train proprioception tions of motor control strategies to effective treatments for back
located in one single joint or to differentiate pain. In: Hodges PW, Cholewicki J, van Dieen J, editors. Spinal
Control: The Rehabilitation of Back Pain. Edinburgh: Elsevier;
between velocity and movement, you can train the 2013.
patient by drawing attention to positioning. Video 8. Snijders CJ, Vleeming A, Stoeckart R. Transfer of lumbosacral load
recording a patient trying to feel where to stop or to iliac bones and legs: part 1: biomechanics of self-bracing of the
move allows instant play back, to make patients sacroiliac joints and its significance for treatment and exercise. Clin
Biomech 1993;8:285–94. [Accessed 12/24/2013 9:44:53 AM].
aware of what they are doing. 9. Vleeming A, Stoeckart R, Volkers AC, et al. Relation between form
c. It is important to train the brain. Studies have dem- and function in the sacroiliac joint. part I: clinical anatomical
onstrated that by attention to tasks the changes in aspects. Spine 1990;15:130–2.
the senso-motoric cortex can be normalized.57,85 10. Vleeming A, Volkers AC, Snijders CJ, et al. Relation between form
Furthermore clinicians have a large influence on and function in the sacroiliac joint. part II: biomechanical aspects.
Spine 1990;15:133–6.
a patient’s personal belief system since it is driven 11. Pool-Goudzwaard AL, Vleeming A, Stoeckart R, et al. Insuffi-
by what they experience,86 anticipate,62,64,86,87 see65 cient lumbopelvic stability: a clinical, anatomical and biomechani-
and hear.88 cal approach to ‘a-specific’ low back pain. Man Ther 1998;3:
d. Patients should be aware of the influence of the 12–20.
12. Vleeming A, Pool-Goudzwaard AL, Stoeckart R, et al. The poste-
social environment on their pain and behaviour. We rior layer of the thoracolumbar fascia. its function in load transfer
as clinicians are part of this social environment and from spine to legs. Spine (Phila Pa 1976) 1995;20:753–8.
have a direct influence on the patient. In case of 13. Lee D. The Pelvic Girdle: An Integration of Clinical Expertise and
fear, giving information that no damage can be Reserach. Edinburgh: Elsevier; 2011.
done and that movement is necessary to give input 14. Bergmark A. Stability of the lumbar spine: a study in mechanical
engineering. Acta Orthop 1989;60:1–54.
to the human body is crucial. Extensive literature is 15. Pel JJ, Spoor CW, Goossens RH, et al. Biomechanical model study
available on the effect of behavioural techniques.66 of pelvic belt influence on muscle and ligament forces. J Biomech
e. One can alter the output to the motoric system; 2008;41:1878–84. [Accessed 12/27/2013 5:11:07 AM].
depending into what subgroup you classify the 16. Richardson CA, Hides JA, Wilson S, et al. Lumbo-pelvic joint
protection against antigravity forces: motor control and segmental
patient. In the subgroup ‘excessive activity’ the stiffness assessed with magnetic resonance imaging. J Gravit Physiol
emphasis can be placed on relaxation, breathing 2004;11:119–22.
freely, decrease in muscle tension and awareness of 17. Richardson CA, Snijders CJ, Hides JA, et al. The relation between
high muscle activity during tasks. No emphasis the transversus abdominis muscles, sacroiliac joint mechanics, and
needs to be placed on a single muscle group as the low back pain. Spine (Phila Pa 1976) 2002;27:399–405.
18. Pool-Goudzwaard A, van Dijke GH, van Gurp M, et al. Contribu-
TrA.7 Perhaps the most important effect of training tion of pelvic floor muscles to stiffness of the pelvic ring. Clin
TrA and multifidus lies in optimal reengagement of Biomech (Bristol, Avon) 2004;19:564–71.
the senso-motoric cortex instead of a ‘stabilizing’ 19. Gnat R, Spoor K, Pool-Goudzwaard A. Simulated transversus
effect.84 When PF dysfunctions are present do not abdominis muscle force does not increase stiffness of the pubic
symphysis and innominate bone: an in vitro study. Clin Biomech
start with TrA training, since TrA and PF muscles 2013;28:262–7.
co-contract. This might be counterproductive.89,90 20. Willard FH, Vleeming A, Schuenke MD, et al. The thoracolumbar
In the subgroup ‘reduced activity’, the emphasis can fascia: anatomy, function and clinical considerations. J Anat
be placed on increasing muscle tone and awareness 2012;221:507–36.
of how muscles can be used during activities. In the 21. Bogduk N. Clinical Anatomy of the Lumbar Spine and Sacrum.
3rd ed. Philadelphia, Pa: Churchill Livingstone.; 1997. p. 128
mixed group you can train awareness of over- and 22. Brown SH, McGill SM. Transmission of muscularly generated
under-active muscles during activities combining force and stiffness between layers of the rat abdominal wall. Spine
relaxation with training. 2009;34:E70–5.
504 PART IV  Overview of Contemporary Issues in Practice

23. Hodges P, Cresswell A, Thorstensson A. Preparatory trunk motion 49. Brumagne S, Cordo P, Lysens R, et al. The role of paraspinal
accompanies rapid upper limb movement. Exp Brain Res muscle spindles in lumbosacral position sense in individuals with
1999;124:69–79. and without low back pain. Spine 2000;25:989–94.
24. Hodges P, Richardson C, Jull G. Evaluation of the relationship 50. Brumagne S, Cordo P, Verschueren S. Proprioceptive weighting
between laboratory and clinical tests of transversus abdominis func- changes in persons with low back pain and elderly persons during
tion. Physiother Res Int 1996;1:30–40. upright standing. Neurosci Lett 2004;366:63–6.
25. Hodges PW, Richardson CA. Altered trunk muscle recruitment in 51. Brumagne S, Janssens L, Janssens E, et al. Altered postural control
people with low back pain with upper limb movement at different in anticipation of postural instability in persons with recurrent low
speeds. Arch Phys Med Rehabil 1999;80:1005–12. back pain. Gait Posture 2008;28:657–62.
26. Allison GT, Morris SL. Transversus abdominis and core stability: 52. Claeys K, Brumagne S, Dankaerts W, et al. Decreased variability
has the pendulum swung? Br J Sports Med 2008;42:930–1. in postural control strategies in young people with non-specific low
27. Morris SL, Lay B, Allison GT. Corset hypothesis rebutted– back pain is associated with altered proprioceptive reweighting. Eur
transversus abdominis does not co-contract in unison prior to J Appl Physiol 2011;111:115–23.
rapid arm movements. Clin Biomech 2012;27:249–54. 53. Radebold A, Cholewicki J, Panjabi MM, et al. Muscle response
28. Morris SL, Lay B, Allison GT. Transversus abdominis is part of a pattern to sudden trunk loading in healthy individuals and in
global not local muscle synergy during arm movement. Hum Mov patients with chronic low back pain. Spine (Phila Pa 1976)
Sci 2013;32:1176–85. 2000;25:947–54.
29. Lee L, Coppieters MW, Hodges PW. Anticipatory postural adjust- 54. Radebold A, Cholewicki J, Polzhofer GK, et al. Impaired postural
ments to arm movement reveal complex control of paraspinal control of the lumbar spine is associated with delayed muscle
muscles in the thorax. J Electromyogr Kinesiol 2009;19:46–54. response times in patients with chronic idiopathic low back pain.
30. Lee L, Coppieters MW, Hodges PW. Differential activation of the Spine 2001;26:724–30.
thoracic multifidus and longissimus thoracis during trunk rotation. 55. Cholewicki J, Silfies SP, Shah RA, et al. Delayed trunk muscle
Spine 2005;30:870–6. reflex responses increase the risk of low back injuries. Spine
31. Saunders SW, Schache A, Rath D, et al. Changes in three dimen- 2005;30:2614–20.
sional lumbo-pelvic kinematics and trunk muscle activity with 56. Tsao H, Galea M, Hodges P. Reorganization of the motor cortex
speed and mode of locomotion. Clin Biomech 2005;20:784–93. is associated with postural control deficits in recurrent low back
32. Dupeyron A, Rispens SM, Demattei C, et al. Precision of estimates pain. Brain 2008;131:2161–71.
of local stability of repetitive trunk movements. Eur Spine J 57. Tsao H, Tucker K, Hodges P. Changes in excitability of corticomo-
2013;22:2678–85. tor inputs to the trunk muscles during experimentally-induced
33. Willigenburg NW, Kingma I, van Dieen JH. Center of pressure acute low back pain. Neuroscience 2011;181:127–33.
trajectories, trunk kinematics and trunk muscle activation 58. Tsao H, Danneels LA, Hodges PW. ISSLS prize winner: smudging
during unstable sitting in low back pain patients. Gait Posture the motor brain in young adults with recurrent low back pain. Spine
2013;38:625–30. 2011;36:1721–7.
34. Willigenburg NW, Kingma I, Hoozemans MJ, et al. Precision 59. Tsao H, Druitt TR, Schollum TM, et al. Motor training of the
control of trunk movement in low back pain patients. Hum Mov lumbar paraspinal muscles induces immediate changes in motor
Sci 2013;32:228–39. coordination in patients with recurrent low back pain. J Pain
35. Goodworth AD, Peterka RJ. Contribution of sensorimotor 2010;11:1120–8.
integration to spinal stabilization in humans. J Neurophysiol 60. Bruehl S, Liu X, Burns JW, et al. Associations between daily
2009;102:496–512. chronic pain intensity, daily anger expression, and trait anger
36. Laslett M. Evidence-based diagnosis and treatment of the painful expressiveness: an ecological momentary assessment study. Pain
sacroiliac joint. J Man Manipulative Ther 2008;16:142. 2012;153:2352–8.
37. Van der Wurff P, Hagmeijer R, Meyne W. Clinical tests of the 61. Burns JW. Arousal of negative emotions and symptom-specific reac-
sacroiliac joint: a systematic methodological review. part 1: tivity in chronic low back pain patients. Emotion 2006;6:309–19.
reliability. Man Ther 2000;5:30–6. 62. Moseley GL, Nicholas MK, Hodges PW. Does anticipation of back
38. van der Wurff P, Meyne W, Hagmeijer RH. Clinical tests of pain predispose to back trouble? Brain 2004;127:2339–46.
the sacroiliac joint: a systematic methodological review. part 2: 63. Moseley GL, Hodges PW. Are the changes in postural control
validity. Man Ther 2000;5:89–96. associated with low back pain caused by pain interference? Clin J
39. van der Wurff P. Clinical diagnostic tests for the sacroiliac joint: Pain 2005;21:323–9.
motion and palpation tests. Aust J Physiother 2006;52:308. 64. Tucker K, Larsson AK, Oknelid S, et al. Similar alteration of motor
40. Szadek KM, van der Wurff P, van Tulder MW, et al. Diagnostic unit recruitment strategies during the anticipation and experience
validity of criteria for sacroiliac joint pain: a systematic review. of pain. Pain 2012;153:636–43.
J Pain 2009;10:354–68. 65. Bell R, Marshall DW. The construct of food involvement in behav-
41. Bakland O, Hansen JH. The “axial sacroiliac joint”. Anat Clin ioral research: scale development and validation. Appetite
1984;6:29–36. 2003;40:235–44.
42. Pool-Goudzwaard A, Gnat R, Spoor K. Deformation of the innom- 66. Sarafino EP. Health Psychology: Biopsychosocial Interactions.
inate bone and mobility of the pubic symphysis during asymmetric John Wiley & Sons Inc; 1998.
moment application to the pelvis. Man Ther 2012;17:66–70. 67. O’Sullivan PB, Beales DJ. Changes in pelvic floor and diaphragm
43. Vleeming A, Van Wingerden J, Dijkstra P, et al. Mobility in kinematics and respiratory patterns in subjects with sacroiliac joint
the sacroiliac joints in the elderly: a kinematic and radiological pain following a motor learning intervention: a case series. Man
study. Clin Biomech 1992;7:170–6. Ther 2007;12:209–18.
44. Sturesson B, Uden A, Vleeming A. A radiostereometric analysis of 68. Beales DJ, O’Sullivan PB, Briffa NK. Motor control patterns
the movements of the sacroiliac joints in the reciprocal straddle during an active straight leg raise in chronic pelvic girdle pain
position. Spine 2000;25:214–17. subjects. Spine 2009;34:861–70.
45. van Kessel-Cobelens AM, Verhagen AP, Mens JM, et al. Pregnancy- 69. Beales DJ, O’Sullivan PB, Briffa NK. The effects of manual pelvic
related pelvic girdle pain: intertester reliability of 3 tests to deter- compression on trunk motor control during an active straight leg
mine asymmetric mobility of the sacroiliac joints. J Manipulative raise in chronic pelvic girdle pain subjects. Man Ther 2010;
Physiol Ther 2008;31:130–6. 15:190–9.
46. Albert H, Godskesen M, Westergaard J. Evaluation of clinical tests 70. Healey EL, Fowler NE, Burden AM, et al. The influence of dif-
used in classification procedures in pregnancy-related pelvic joint ferent unloading positions upon stature recovery and paraspinal
pain. Eur Spine J 2000;9:161–6. muscle activity. Clin Biomech 2005;20:365–71.
47. Sturesson B, Uden A, Vleeming A. A radiostereometric analysis of 71. Mens J, Hoek van Dijke G, Pool-Goudzwaard A, et al. Possible
movements of the sacroiliac joints during the standing hip flexion harmful effects of high intra-abdominal pressure on the pelvic
test. Spine 2000;25:364–8. girdle. J Biomech 2006;39:627–35.
48. Hungerford BA, Gilleard W, Moran M, et al. Evaluation of the 72. Hodges PW, Gandevia SC. Changes in intra-abdominal pressure
ability of physical therapists to palpate intrapelvic motion with the during postural and respiratory activation of the human diaphragm.
stork test on the support side. Phys Ther 2007;87:879–87. J Appl Physiol 2000;89:967–76.
 46  The Sacroiliac Joint (Pelvic Pain) 505

73. Brumagne S, Janssens L, Knapen S, et al. Persons with recurrent in muscle activity and force between patients and healthy sub-
low back pain exhibit a rigid postural control strategy. Eur Spine J jects. Man Ther 2008;13:68–74.
2008;17:1177–84. 83. Schleip R, Muller DG. Training principles for fascial connective
74. Lee AS, Cholewicki J, Reeves NP, et al. Comparison of trunk pro- tissues: scientific foundation and suggested practical applications.
prioception between patients with low back pain and healthy con- J Bodyw Mov Ther 2013;17:103–15.
trols. Arch Phys Med Rehabil 2010;91:1327–31. 84. Nijs J, Daenen L, Cras P, et al. Nociception affects motor output:
75. Xu Y, Choi J, Reeves NP, et al. Optimal control of the spine system. a review on sensory-motor interaction with focus on clinical impli-
J Biomech Eng 2010;132:051004. cations. Clin J Pain 2012;28:175–81.
76. Mens J, Vleeming A, Snijders CJ, et al. The active straight 85. Tsao H, Danneels L, Hodges PW. Individual fascicles of the para-
leg raising test and mobility of the pelvic joints. Eur Spine J spinal muscles are activated by discrete cortical networks in humans.
1999;8:468–73. Clin Neurophysiol 2011;122:1580–7.
77. Mens JM, Damen L, Snijders CJ, et al. The mechanical effect of a 86. Moseley GL, Nicholas M, Hodges PW. Pain differs from non-
pelvic belt in patients with pregnancy-related pelvic pain. Clin painful attention-demanding or stressful tasks in its effect on pos-
Biomech 2006;21:122–7. tural control patterns of trunk muscles. Exp Brain Res 2004;
78. Mens JM, Huis In ‘t Veld YH, Pool-Goudzwaard A. The active 156:64–71.
straight leg raise test in lumbopelvic pain during pregnancy. Man 87. Moseley GL, Brhyn L, Ilowiecki M, et al. The threat of predictable
Ther 2012;17:364–8. and unpredictable pain: differential effects on central nervous
79. Pool-Goudzwaard AL, Slieker TH, Vierhout ME, et al. Relations system processing? Aust J Physiother 2003;49:263–7.
between pregnancy-related low back pain, pelvic floor activity and 88. Crombez G, Viane I, Eccleston C, et al. Attention to pain and
pelvic floor dysfunction. Int Urogynecol J Pelvic Floor Dysfunct fear of pain in patients with chronic pain. J Behav Med
2005. 2013;36:371–8.
80. Hu H, Meijer OG, van Dieen JH, et al. Muscle activity during 89. Sapsford RR, Hodges PW, Richardson CA, et al. Co-activation of
the active straight leg raise (ASLR), and the effects of a pelvic belt the abdominal and pelvic floor muscles during voluntary exercises.
on the ASLR and on treadmill walking. J Biomech 2010;43: Neurourol Urodyn 2001;20:31–42.
532–9. 90. Bo K, Sherburn M, Allen T. Transabdominal ultrasound measure-
81. Hu H, Meijer OG, Hodges PW, et al. Understanding the active ment of pelvic floor muscle activity when activated directly or via
straight leg raise (ASLR): an electromyographic study in healthy a transversus abdominis muscle contraction. Neurourol Urodyn
subjects. Man Ther 2012;17:531–7. 2003;22:582–8.
82. de Groot M, Pool-Goudzwaard AL, Spoor CW, et al. The active
straight leg raising test (ASLR) in pregnant women: differences
 CHAPTER 47 

Hip-Related Pain
Kay Crossley • Alison Grimaldi • Joanne Kemp

labral tissue blend into this ligament. During weight

ARTICULAR AND MUSCLE bearing, the head of the femur relocates in the acetabu-
CONTROL OF THE HIP lum, widening the acetabular notch and placing the trans-
verse acetabular ligament under a tensile load.8
Articular and neuromuscular control of the hip is pro- The ligamentum teres is an intra-articular ligament
vided by three components working synergistically: (a) arising from the fovea of the head of the femur, becoming
bony morphology; (b) passive joint structures such as the triangular in shape and inserting into the anterior and
acetabular labrum, hip joint capsule and hip ligaments; posterior aspect of the transverse acetabular ligament.9 It
and (c) hip musculature. also communicates with the synovium within the hip.10
The ligamentum teres has a rich supply of mechano­
Bony Morphology receptors and due to its attachment to the transverse
acetabular ligament, becomes taut in weight bearing.
The hip joint (femoroacetabular joint) is a synovial joint This suggests a proprioceptive role, especially in weight-
formed by the head of femur inferiorly and the acetabu- bearing activities.10
lum superiorly. The acetabulum sits within the bony The iliofemoral ligament and pubofemoral liga-
pelvis and faces inferiorly, laterally and is normally ante- ment reinforce the anterior capsule and limit extremes
verted (forward facing) by approximately 23°.1 The of extension and abduction. The ischiofemoral liga-
femoral head faces superiorly, medially and is anteverted ment has fibres that run in a spiral pattern and
between 10–15° in adults. The anteversion of the acetab- limit hyperextension.
ulum and head of femur reduces the bony stability in the
anterior hip joint. This morphological structure enables
the three degrees of movement (i.e. flexion and extension,
adduction and abduction, and external and internal
Hip Musculature
rotation). Dynamic stability is thought to be provided by a syner-
gistic interplay between various hip muscles. Hip muscles
may be considered to be stabilizers, prime movers or play
Passive Joint Structures a dual role. The stabilization role of each muscle is based
Acetabular Labrum on its line of action in relation to the joint axis, its primary
action and the ratio between its physiological cross-
The acetabular labrum extends around the rim of the sectional area (PCSA) relative to muscle fibre length
acetabulum, from the posterior to the anterior aspect of (MFL).11–13 Muscles with a smaller PCSA to MFL ratio
the transverse acetabular ligament.2 It is considered vital (PCSA cm2 : MFL cm <1.0) are considered to be ‘prime
to maintain joint fluid pressure, limiting extravasation of movers’ of a joint, whereas those muscles with a larger
articular cartilage fluid and distributing force to maintain PCSA relative to muscle fibre length (PCSA cm2 : MFL
healthy chondral surfaces.3 The labrum deepens the ace- cm >1.0) are considered to be ‘joint stabilizers’. Muscles
tabulum by 21%4 and absorbs up to 28% of hip joint with an equal PCSA and MFL (PCSA cm2 : MFL cm =
forces.4 The acetabular labrum is thinnest and most vul- 1.0) are considered to have the capacity to generate large
nerable in its anterior aspect. The blood supply enters forces over a variety of muscle lengths, acting as both
though the adjacent joint capsule with only the outer stabilizers and prime movers. Primary hip stabilizers are
third of the labrum vascularized, whereas the inner two- thought to locate the head of femur within the acetabu-
thirds are avascular.5 Nociceptive free nerve endings are lum via posterior, medial or inferior forces exerted on the
distributed throughout the labrum6 while the damaged femoral head. This may minimize stress on potentially
labral tissue contains cytokines,7 suggesting a nociceptive- vulnerable structures, such as the anterosuperior acetabu-
producing capacity. lar labrum and acetabular rim, while maximizing the neu-
romotor control of the hip. The primary hip stabilizers,
Ligaments of the Hip with both a PCSA : MFL ratio ≥1.0 and a posterior–
medial–inferior line of action, include iliopsoas, gluteus
The transverse acetabular ligament traverses the acetabu- medius, gluteus maximus, quadratus femoris, obturator
lar notch, connecting the anterior and posterior labral internus, inferior and superior gemelli, and adductor
edges. The collagen fibres forming the deepest layer of brevis and pectineus.
506
 47  Hip-Related Pain 507

JOINT-RELATED HIP PAIN

Background
Hip pain is common in active young to middle-aged men
and women. It accounts for approximately 12% of soccer-
related injuries,14 and is the third most common injury in
the Australian Football League.15 In general populations,
estimates of prevalence range from 7% in adolescents16
to 14% in older adults.17 Joint-related hip pain refers to
a number of intra-articular pathologies, including femo-
roacetabular impingement (FAI), labral pathology and
early degenerative change such as chondropathy.18,19 It
has been suggested that hip pain and associated hip mor-
phology and pathology may form part of a continuum
where pain and pathology in young to middle-aged
people progresses into hip osteoarthritis (OA).20
The following section outlines the hip pathologies
commonly seen in clinical practice, assessment of
patients with hip pain and rationale for the treatment
of hip pain.

Femoroacetabular Impingement
FAI refers to variations in hip joint morphology, where FIGURE 47-1  ■  Cam impingement. The arrow indicates reduced
the normal sphericity of the head of femur or acetabu- femoral head neck offset.
lum are altered.21 Diagnosis of these morphological
variants can be made from radiographs,21,22 computer-
ized tomography23 or magnetic resonance imaging
(MRI).23,24 Femoroacetabular impingement is considered FAI, resulting in smaller, less-severe chondral lesions.21
to be a normal variation in hip morphology,25–27 with This observation is consistent with a recent report that,
the prevalence of cam FAI ranging from 4% in healthy in contrast to cam lesions, pincer impingement may
women28 to 24% in healthy men.24 Moreover, elite protect the hip from OA development.38 The third type
young male basketball players are ten times more likely of FAI seen is the mixed presentation where both cam
to have a cam lesion than their aged-matched controls.29 and pincer lesions are seen, which has been reported in
However, 23% of people with radiographic FAI com- 88% of people with FAI.30
plain of hip pain,30 most likely resulting from overload
of the adjacent acetabular labrum and intra-articular Acetabular Labral Pathology
chondral surfaces.25,31–33
There are three types of FAI typically described. Acetabular labral tears can compromise the labral func-
The most prevalent is a cam lesion, seen in 78% of tion and therefore directly impact joint health. The prev-
people with FAI,30 which describes the reduction in alence of labral tears is greatest anteriorly,2,6,39,40 which
femoral head neck offset resulting from additional bony may be related to the relatively thinner labrum in this
tissue at the anterior, superior or anterosuperior aspect region2,41 or to the presence of cam lesions on the antero-
of the head neck junction21,30 (Fig. 47-1). This lesion superior aspect of the femoral head–neck junction.32
may increase the shearing forces acting on the anterior Tears of the acetabular labrum are seen commonly at
labrum and chondral surfaces.21 Recently, pre-existing arthroscopy, with up to 93% of patients undergoing hip
cam-type FAI has been identified as a risk factor for arthroscopy having a concomitant labral tear.40,42 The
hip OA and total hip arthroplasty.20,34–36 It is unknown presence of FAI is associated with labral tears, most likely
whether other factors may explain why certain indi- due to impingement of the labrum between then bony
viduals with cam lesions progress to hip OA whereas components of the hip.43–45
others do not.
Pincer impingement is a morphologic variation in the Chondropathy of the Hip
acetabulum observed in approximately 42% of people
with FAI.30 This either manifests as a deep acetabulum, Articular cartilage is a complex structure consisting of
most commonly anteriorly,21,37 or as a retroverted acetab- chondrocytes and a surrounding extracellular matrix46
ulum, which leads to an apparent deeper anterior acetab- that comprises hydrophilic proteoglycans, including
ular wall. Pincer-type FAI may directly compress the aggrecan, which enable cartilage to withstand very high
acetabular labrum between a deep acetabulum and compressive loads.46 Articular cartilage is avascular and
normal, spherical femoral head,21 leading to labral lesions aneural, relying on the normal distribution of synovial
and subsequent chondral damage. However, pincer fluid within the joint for nutrition and ongoing optimal
impingement appears to be more benign than cam-type health.47 Factors such as labral tears that impact on the
508 PART IV  Overview of Contemporary Issues in Practice

normal function of the synovium and synovial fluid and available in clinical practice and arthroscopy remains the
the distribution of loads imparted to the chondral sur- gold standard for diagnosis.
faces have important implications for chondral health. Importantly, while imaging may assist with the diag-
Consequently, chondral lesions of the hip are often nosis, abnormalities seen on radiographs, computed
seen in conjunction with other hip pathology at hip tomography or MRI provide only part of the picture and
arthroscopy, especially at the anterior or superior aspect should be considered alongside clinical test results.
of the acetabular rim and at the chondrolabral junc-
tion.31,42,48 In the knee, meniscal pathology at knee Red Flags
arthroscopy increases the relative risk of knee OA by
3–14 times.49,50 As such it is possible that factors such A number of ‘Red Flags’ should be considered with any
as labral pathology33,51–53 may be associated with an patient presenting with hip pain. These may include
increased the risk of hip chondropathy, and ultimately rheumatoid and multijoint arthropathies, avascular
OA development.34–36,51,54,55 necrosis of the head of the femur, slipped upper femoral
epiphysis, Perthes disease, tumours, synovial chondrama-
tosis, fractured neck of femur and lumbar nerve root
Assessment compression. If symptoms are not improving as antici-
pated, a timely referral to the appropriate medical prac-
A comprehensive assessment of the hip joint should titioner should be undertaken.
include a thorough subjective examination, physical
examination and appropriate use of investigations. No
single test provides a definitive diagnosis of joint-related
hip pain. The most accurate diagnosis of the source of
Treatment
hip pain can only be made when findings from all aspects First-line treatment of hip joint pain usually comprises
of assessment are considered. conservative management. Medical and surgical manage-
ment may be included in order to obtain resolution of
symptoms if conservative treatment has not succeeded.
Key Clinical Diagnostic Features
of Joint-Related Hip Pain
Conservative Management
While Table 47-1 below describes each pathology as a
separate entity, these almost always coexist in clinical While there is little evidence to guide therapists regard-
practice. The increasing severity of symptoms seen is ing the most appropriate components of rehabilitation
associated with the progression of degenerative hip programmes for hip-related pain, commonly reported
disease from FAI to hip OA. principles of rehabilitation are hip muscle strengthening,
restoration of neuromotor control, addressing remote
factors that may alter the kinetic chain function, and
The Role of Imaging: When to
unloading the damaged or vulnerable structures.2,86–90
and When Not to Image?
Conservative therapy generally consists of three compo-
Imaging plays an important role in diagnosing the source nents to address these principles: (a) advice; (b) exercise;
of hip pain, planning appropriate treatment and estab- and (c) manual therapy.
lishing a likely prognosis. It should be considered in all
patients who have failed to respond to conservative treat- Advice.  Advice generally relates to strategies designed to
ment after 6 weeks and prior to undertaking further protect and unload vulnerable structures of the hip, based
medical or surgical treatment. on our understanding of the functional anatomy and bio-
Cam lesions can be assessed with confidence utilizing mechanics of the hip. In people with hip pain related to
X-ray. Plain radiographs correlate well with computed FAI, avoidance of impingement (flexion, internal rotation
tomography and MRI findings and are more accessible and adduction or any combination of these activities) as
for patients and clinicians.83 An alpha angle >60–65° is much as possible is advised. Once symptoms have
considered to indicate a cam lesion.64,65 The presence of resolved, positions of impingement can be reintroduced
a cam lesion is associated with an increased risk of labral in a graduated fashion as long as they remain pain-free.
pathology and chondropathy84 in people with hip pain, This may involve activity modification on a day-to day
and hence its presence may increase clinical suspicion of basis, such as prolonged sitting in low chairs, as well as
coexisting lesions. The gold standard imaging for labral during athletic pursuits. For example, footballers may be
pathology is MRI arthrography, which has enhanced advised to spend less time changing direction and getting
accuracy over standard MRI.67,85 However, whereas stan- down low to the ball. Gait retraining may also minimize
dard MRI produces false-positive results (underestima- excessive hip extension at the end of stance phase of gait,
tion of labral pathology) with poorer accuracy,67 newer to decrease the loads on anterior hip joint structures.91
sequences, including those available with a 3 tesla magnet Since greater body mass index is a feature of those with
show promise for the evaluation of labral tears. Similarly, advancing hip pathology, and will increase hip joint loads,
chondropathy can now be assessed using high-resolution advice regarding weight management is appropriate in
MRI, which reveals changes in the chondral matrix.69 this group of patients. General advice relating to the
However, these imaging techniques are not yet readily management of hip OA should also be given in those
 47  Hip-Related Pain 509

Table 47-1  Key Clinical Diagnostic Features of Joint-Related Hip Pain

Clinical Diagnostic Features Commonly Seen in All Hip Pathologies
Subjective Examination
Area and nature of pain Groin, lateral hip, anterior hip, buttock or thigh pain
Aggravating factors Aggravated by running, kicking, twisting actions, getting in and out of car
Deep flexion, prolonged sitting, up and down stairs
Clinical examination Increased tone and tenderness gluteus medius, piriformis, TFL, iliopsoas, adductor magnus and
longus, biceps femoris

Clinical Diagnostic Features Specific to FAI

Subjective Examination
Loading history Onset of symptoms often after episode of increased loading during sport/activity
Clinical examination Reduced +/− painful ROM hip flexion,56 IR@9056–59 Abduction60
Pain on FADIR,56 FABER
Reduced strength adduction, ER, flexion, abduction61
Altered gait in all planes of motion,62,63 reduced step length
Investigations X-ray – AP pelvis and lateral Dunn view –
Cam lesion: alpha angle >60;64 >6565
Pincer lesion: lateral centre edge angle >4038
CT scan66

Clinical Diagnostic Features Specific to Labral Pathology

Subjective Examination
Area and nature of pain Sometimes ache at rest and night
Aggravating factors Mechanical symptoms, locking, catching, giving way2,67
Loading history Onset of symptoms possibly after episode of increased loading during sport/activity, but often
no cause known
Clinical examination Reduced ± painful ROM hip flexion, IR@90
Pain on FADIR,68 FABER
Reduced strength68
Altered gait – reduced step length, reduced hip extension, possibly limp
Investigations CT scan66
MRI69

Clinical Diagnostic Features Specific to Chondropathy

Subjective Examination
Area and nature of pain Usually ache at rest and night
Aggravating factors Mechanical symptoms, locking, catching, giving way
Pain on uneven surfaces
Loading history Sometimes onset following episode of increased load, but often no change in loading pattern
reported
Clinical examination Reduced strength70
Reduced ROM ±− painful flexion, IR@9070
?Increased BMI71
Painful FADIR, FABER
Reduced balance in dynamic tasks72
Investigations dGEMRIC (gadolinium-enhanced) MRI55,69

Clinical Diagnostic Features Specific to Hip OA

Subjective Examination
Area and nature of pain Always ache at rest and night
Aggravating factors Stiffness, difficulty putting on shoes, getting in and out of car, sitting, sit to stand, prolonged
standing, walking, up and down stairs, uneven surfaces
Loading history Past or current history of high-load occupations and high-intensity sporting activities.73 Usually
no change of load prior to onset
Clinical examination Reduced ± painful ROM hip flexion ≤115, IR@90 ≤1574–77
Pain on FADIR, FABER
Reduced strength78,79
Altered gait – reduced step length, reduced hip extension, limp
Increased BMI75,80
Stiffness at end-range ROM tests
Investigations X-ray – may have joint space narrowing, osteophytes, hypertrophy of subchondral bone,
subchondral cysts81,82

AP, anteroposterior; BMI, Body mass index; CT, Computerized tomography; dGEMRIC, Delayed gadolinium-enhanced magnetic
resonance imaging of cartilage; ER, External rotation; FABER, Flexion/abduction/external rotation; FADIR Flexion/adduction/internal
rotation; FAI, Femoroacetabular impingement; IR, Internal rotation; MRI, Magnetic resonance imaging; ROM, Range of motion; TFL,
Tensor fascia lata.
510 PART IV  Overview of Contemporary Issues in Practice

with chondropathy and hip OA, and may include general with hip OA (Fig. 47-4).99,100 There is minimal evidence
fitness, lower limb strengthening exercises, chronic to date supporting the use of manual therapy in the man-
disease management, pain management, weight manage- agement of FAI, labral or chondral pathology, and care
ment and coping strategies. should be taken with manual techniques that place a
person with painful FAI at end-range impingement.
Exercise.  Exercise therapies should be individualized for However, contemporary clinical practice suggests that
the patient, based on age, gender, personal preference soft tissue and dry-needling techniques aimed at nor­
(group-based versus individual exercise programmes, malizing tone in overactive hip musculature may be
aquatic versus land-based programmes, home versus beneficial.
gym-based programs), desired activity or sporting
requirements. While there is no evidence of neuromotor Effectiveness of Conservative Therapies
dysfunction in people with hip-related pain, anatomical
studies support a theoretical role for their importance in The effectiveness of strengthening interventions in
promoting joint stability. Contrasting the lack of evi- improving physical function outcomes101,102 and global
dence for neuromotor control, a number of studies have lower limb strength101 in people with advanced hip OA
identified lower muscle strength in people with a variety has been previously demonstrated. These interventions
of hip problems, including FAI,61 labral tears,68 post hip may improve physical function by altering hip joint
arthroscopy70 and hip OA78 (see Table 47-1). These loads.103 However, the efficacy of hip strengthening exer-
impairments are generally observed in all directions, but cises on pain in people with other hip-related pain is
will be patient-specific. uncertain. Two studies reported a reduction in pain in
Conservative management generally includes activity groups with strength exercise intervention,101,104 whereas
modification and physical therapy including exercise other studies did not see a difference between exercise
programmes.92 An exercise programme will usually and education versus education alone.102,105
include specific exercises to strengthen the hip-stabilizing
muscle groups, general lower limb strength exercises Medical and Surgical Management
targeting the gluteal, quadriceps and calf muscles, core
and trunk strengthening and adjunctive stretching exer- With the exception of hip OA, the evidence for the phar-
cises that do not place the hip into a position of impinge- macological management of hip pain is scarce. Recom-
ment. Strengthening exercises should be progressed from mendations for those with hip OA include paracetamol,
non-weightbearing to weight bearing, to resistance oral and topical NSAIDs and intra-articular corticoste-
to functional and sports-specific exercises (Figs 47-2 roid injections.106,107 The use of glucosamine and
and 47-3). chondroitin-sulphate is not recommended due to lack of
In recent times a number of studies have suggested supporting evidence in people with hip OA.106 Intra-
optimal exercises to activate the hip abductors93,94 and hip articular cortisone injections are sometimes used in con-
extensors94,95 and rotators96 (see Figs 47-2 and 47-3). temporary clinical practice in those with FAI, labral
Exercises with high activation of these muscles included pathology and chondropathy prior to surgical manage-
double leg95,96 and single leg bridging,96 side plank with ment with varied effect. The evidence supporting this
abduction,94 front plank with extension,94 single leg practice is minimal, with small case series only indicating
squats94 and resisted band walking.93 While these studies a positive effect for up to 12 months.108 Generally a posi-
have been conducted in healthy people without hip pain, tive temporary effect is thought to indicate the presence
they provide a basis for optimal exercises to strengthen of intra-articular pathology in the hip.
hip muscles in people with hip pain. Hip arthroscopy is an orthopaedic surgical procedure
In addition, exercises to increase fitness and facilitate that is increasing in popularity, which has contributed
weight loss should be encouraged in a fashion that to an increased understanding of hip pain and pathol-
does not adversely increase intra-articular loads within ogy. The primary aims of hip arthroscopy are to reduce
the hip joint. Examples of such exercise programmes pain associated with intra-articular pathology, increase
may include cycling, swimming, walking and modified daily and sporting function and possibly reduce the risk
running programmes tailored to the needs of the indi- of secondary hip OA.42,109 Hip arthroscopy is considered
vidual patient. advantageous over open techniques due to the reduction
in risks such as infection and poor wound healing, and
Manual Therapy.  Manual therapy is commonly used by a rapid recovery.42 Outcomes for hip arthroscopy appear
physiotherapists in the management of hip OA97 and may positive;51,110–112 however, to date no studies have com-
include joint mobilizations and soft tissue techniques. pared the efficacy of hip arthroscopy surgery to con-
Manual therapy aims to increase hip range of motion and servative management in people with hip pain. Moreover,
reduce stiffness and pain. Hip flexion range is modifiable there is little known of the factors that may be associ-
by physiotherapists and rehabilitation programmes ated with outcomes in individuals undergoing hip
should be targeted to improve this range in patients with arthroscopic surgery. Recent studies have reported
hip pain. This may be achieved through the use of manual reduced hip muscle strength and hip joint range of
soft tissue techniques,98 stretching techniques98 and hip motion70 exist in people following hip arthroscopy, and
extension strengthening exercises.79 Recent studies have altered gait biomechanics pre- and post-operatively.62,63
shown that manual therapy with patient education results It would seem reasonable to include these components
in better outcomes than education alone in people in a targeted post-operative rehabilitation programme;


Isometric
contractions
To improve
deep abductor
muscle
recruitment
and assist with
pain relief
Slow, ramped isometric abduction Slow, ramped isometric abduction
Bilateral or unilateral focus ‘Preparation to lift’ top leg Slow, ramped isometric abduction Supported single leg stance
Bilateral or unilateral focus Painfree. Minimize adduction

Frontal plane
abductor
loading
Weight-bearing
abductor
strengthening

Spring-resisted sliding platform Spring-resisted sliding platform Side-stepping for Home version of resisted abduction.
Bilateral abduction in upright posture Bilateral abduction in trunk deconditioned/older patients Single leg abduction slide with band
forward/minisquat posture Focus on controlled abduction resistance. Primary weight-bearing side
push from trail leg maintains a minisquat position. Maintain
deep external rotator activation with
rotational control of femur and pelvis in
functional tasks
Hip external
rotator
strength
progression
from non-
weight-bearing
to functional
exercise
Low load high repetitions focus on Introduce control of rotation of
building endurance in stabilizing muscle pelvis and femur in partial
groups weight-bearing
47  Hip-Related Pain

FIGURE 47-2  ■  Examples of abductor and external rotator exercises.

511
 512

Bridging
Focus on early and
sustained gluteal
activation

Bilateral bridging Offset bridging Weight shift – heel off-leg lift while Single leg bridge
Gluteals on ‘close side’ foot carry maintain stable pelvis Hip flexion/extension through one leg
most of the weight

Functional
strengthening
Trunk inclines
forward for
gluteal bias.
Minimize hip
adduction for
optimal abductor
control

Double leg squat Offset squat Single leg squat Step ups
PART IV  Overview of Contemporary Issues in Practice

Flat foot side carries most of the Use upper limb support as required
body weight

High-level and
sports-specific
training
Focus on
endurance, and
gluteal function
in sports-specific
activities

Stand on affected leg, stabilizing Standing on uneven surface Maintaining gluteal activation Spinning discs create rotational
hip and pelvis while kicking maintaining gluteal activation during large hip range with high challenge while maintaining gluteal
repetitions for endurance function, pelvic and hip stability

FIGURE 47-3  ■  Examples of extensor exercises.



Hip joint
mobilizations to
be used with
care, usually in
patients with
more advanced
degenerative
joint disease

Lateral distraction mobilization with Inferior glide mobilization with seatbelt Caudal glide mobilization Rotation mobilization to increase hip
seatbelt rotation range

FIGURE 47-4  ■  Examples of hip joint mobilization techniques.

47  Hip-Related Pain
513
514 PART IV  Overview of Contemporary Issues in Practice

however, no studies have tested appropriate rehabilita- While many general health124–126 and drug-related
tion programmes. factors127,128 may impact on tendon pain and loadbearing
status, mechanical loading has a powerful influence. The
Controversies, Uncertainties homoeostasis within a tendon may be disturbed by a
change in type, intensity or frequency of loading stimu-
and Future Directions lus.129 Load may be applied longitudinally along the
The concept of FAI as a cause of hip pathology and tendon fibres (tensile load), or perpendicular to the col-
end-stage hip disease is relatively new, and many uncer- lagen fibres (compression). Rapid increases in intensity
tainties remain regarding these relationships. Studies or frequency of tensile loading may result in overload and
have recently indicated a relationship between cam FAI a net catabolic effect. Similarly, tensile loading of inad-
and end-stage hip disease in men35 and women.35,36 Cam equate intensity or frequency (stress deprivation) results
FAI is more prevalent in men than women in the general in structural degradation and a reduction in the loadbear-
population,24,113 yet the prevalence of end-stage hip ing capacity of the tendon.130 Compressive load, com-
disease is roughly equal in men and women.114 We have monly encountered at tendon–bone interfaces such as
a limited understanding of gender-specific risk factors tendon insertion sites, engenders adaptation that increases
for hip joint-related pain and end-stage hip disease. resistance to compression but weakens the tendon against
Factors causing the development of cam FAI are also tensile loading.131–133 The combination of compression
unclear. The prevalence of cam FAI is greater in young and tensile overload may represent the most noxious
elite male athletes than age-matched controls,29 and also environment for a tendon.134 Using these principles,
in people with a family history of FAI.115 It appears imposing such forces during assessment and minimizing
that both genetics and load-related factors play a part them during rehabilitation may improve the effectiveness
in the development of FAI. Moreover, no studies have of both.
determined the factors that lead to the development of
symptoms in people with FAI. Recently, surgical removal
of the cam lesion has become more commonplace with
Assessment
positive reduction of hip symptoms post-operatively.51 Apart from the cardinal signs of pain experienced directly
However, it is unclear whether such surgery changes over the tendon and tenderness on direct palpation,
the natural history of the disease in people with cam functional and specific tendon-loading tests are key
FAI. Finally, the clinical differential diagnosis of FAI, components for the differential diagnosis of tendon-
labral pathology and chondral pathology is difficult, related pain. As confidence in a clinical diagnosis
particularly as arthroscopy remains the gold standard increases with the number of key diagnostic features
for the clinical diagnosis of chondral pathology. However, that are consistent with a particular pathology, consider-
as the likelihood of these conditions coexisting is high,71 ing information gathered from the subjective examina-
appropriate conservative management for each of these tion together with results of a battery of clinical tests
does not usually vary a great deal. Future studies focus- is recommended.
ing on each of these issues will greatly increase our
understanding of the aetiology and risk factors associ- Key Clinical Diagnostic Features of
ated with development of these conditions. This will Tendinopathy-Related Hip Pain
enable the provision of more appropriate strategies to
reduce the likelihood of progression of hip pathology Key diagnostic features and clinical tests described to
in susceptible individuals. date in the literature for gluteal135–141 and proximal ham-
string tendinopathy120,121,135,142 have been outlined in
Table 47-2. Note that the diagnostic accuracy of the
clinical orthopaedic tests for these tendon pathologies are
TENDINOPATHY-RELATED HIP PAIN not well established143,144 and a comprehensive physical
Background examination of other potential pain sources such as the
lumbar spine, peripheral nerves, hip joint and other sur-
Gluteal and proximal hamstring tendinopathies are rounding soft tissues is also required.
increasingly recognized sources of pain around the hip
and pelvis. Gluteal tendinopathy affects up to 23.5% of The Role of Imaging: When
women and 8.5% of men between 50–79 years,116 whereas to and When Not to Image?
proximal hamstring tendinopathy may occur or coexist
with gluteal tendinopathy in older individuals. However, Imaging may be required as an adjunct to clinical testing,
the prevalence of these conditions is not restricted to older where there is a history of trauma or marked loss of func-
or sedentary populations. Athletes, particularly middle- tion (to assess tendon avulsion), or where the clinical
and long-distance runners, also experience considerable diagnosis is unclear and/or there has been a failure to
disability and reduced performance secondary to painful progress with a tendon-focused management plan. Ultra-
gluteal117–119 or proximal hamstring tendinopathy.120–123 sound or MRI are both useful to assess the tendons
Despite advances in radiological assessment of pelvic ten- and associated bursae at the greater trochanter and
dinopathies, gold standards in clinical diagnosis and man- ischium.146–149 MRI has the advantage of providing a
agement are yet to be elucidated. wider field of view and may detect other local
 47  Hip-Related Pain 515

Table 47-2  Key Clinical Diagnostic Features of Gluteal and Proximal Hamstring Tendinopathy
Clinical Diagnostic Features Specific to Gluteal Tendinopathy
Subjective Examination
Area of pain Lateral hip (*GT), extending down the lateral thigh
Aggravating factors Side lying – pain over GT
Walking especially at speed or uphill
Stair climbing
Stiffness/pain over GT on rising to stand after sitting
Loading history Onset after change in activity, slip or fall, or may present insidiously
A positive test reproduces pain over the greater GT ± the lateral thigh
Physical Examination
Functional loading tasks Sustained single leg stance138
Single leg squat, step up, hop135
Specific tendon-loading tasks Passive hip external rotation in 45° hip F137
Resisted external derotation test (resisted IR from EOR ER at 90° F, and prone)138
FABER136,141
Modified Ober’s Test141
Palpation Marked tenderness of the GT139,140

Clinical Diagnostic Features Specific to Proximal Hamstring Tendinopathy

Subjective Examination
Area of pain Ischial pain, extends down the posterior thigh as pain or a feeling of tightness limiting full
stride length in running
Aggravating factors Sitting, particularly on hard surfaces
Walking/running particularly with long strides or uphill
Forward leaning/forward bending with straight knee
Deep lunge or high step up
Loading history Onset after a change in activity, a slip or fall resulting in a large tensile load (e.g. water
skiing or front splits) or a direct compressive blow to the ischium, or may present
insidiously
A positive test reproduces pain over IT ± the posterior thigh
Physical Examination
Functional loading tasks Single leg bent knee bridge – Low load
Single leg straight-leg bridge (plank) – Moderate load142
Single leg deadlift – High load121,135,142
Specific tendon-loading tasks Bent Knee Stretch & Modified Bent Knee Stretch Test
(Isometric knee F in supine, EOR hip F and knee E)144,145
Puranen Oravo Test (standing hamstring stretch on bench)145
Shoe Off Test; Heel Drag Test (isometric load against other foot/floor)142
Palpation Marked tenderness on palpation of the ischial tuberosity, particularly laterally at the
semimembranosis origin

E, Extension; EOR, End of range; ER, External rotation; F, Flexion; FABER, Flexion/abduction/external rotation; GMed, Gluteus medius;
GMin, Gluteus minimus; GT, Greater trochanter; *GT, the patient should indicate the greater trochanter as the maximal area of pain, or
the region from which the pain emanates; IT, Ischial tuberosity.

pathologies. Lumbar spine imaging is also often employed may be required to help establish and maintain appropri-
for non-responders, to assist in explicating involvement ate muscle length and tone, particularly as stretching
of the spine. Caution is required, however, with the inter- the affected musculotendinous unit is usually unhelpful
pretation of imaging abnormalities. Pathology in the due to the accompanying compression–tension load
lumbar spine, as well as the gluteal and hamstring tendons, combination.132
is evident in asymptomatic individuals.146,148,150 Imaging
findings must always be considered only alongside clini- Gluteal Tendinopathy
cal test results.
For the gluteus medius and minimus tendons the combi-
nation of compressive and tensile loads is highest in
adduction, when the abductor muscles are working hard
Treatment at length. For an athlete, a provocative load may be
Gluteal and proximal hamstring tendinopathy interven- running at speed or hopping, whereas for an older or
tion centres on load management. Advice and education deconditioned individual, stair climbing or standing on
regarding minimizing provocative loads is an early prior- one leg to dress may represent relative overload. Abduc-
ity. A graduated exercise protocol aims to stimulate posi- tor muscle weakness, or a shift in muscle balance or
tive biological changes within the tendon and address length tension relationship,151 may result in increased hip
any associated aberrant motor patterns. Manual therapy adduction.152 Once symptomatic, compression alone (e.g.
516 PART IV  Overview of Contemporary Issues in Practice

lying on the affected side) or compression with passive Effectiveness of Conservative Therapies
adduction will aggravate the condition, particularly if sus-
tained or end-range – sitting with the knees crossed, The evidence to date suggests there is no ‘magic bullet’
standing ‘hanging on one hip’ in adduction, lying on the solution to tendinopathy, and an exercise-based approach
unaffected side with the affected hip flexed and adducted, is considered most likely to provide greatest medium- to
hip flexion/adduction stretches. Patients should be edu- longer-term results. The challenge for health profession-
cated regarding what constitutes a provocative load and als is to provide improved short- and long-term results.
how to avoid or minimize these loads in everyday activi- Information on early success of exercise intervention for
ties and sport.153 gluteal tendinopathy is limited to one study reporting a
The exercise programme aims to reduce pain and 7% success rate at 1 month,157 and for proximal ham-
improve the efficiency of the hip abductor musculature string tendinopathy another study reporting a 10%
to minimize the excessive pelvic tilt or shift that increases success rate at 3 months.120 Both studies included a sub-
hip adduction.154 Early prescription of slowly ramped stantial stretching component, the gluteal tendinopathy
isometric hip abductor exercises often assists pain relief study included no hip abductor muscle strengthening,
(see Fig. 47-2), possibly due to the activation of segmen- and the hamstring study included provocative high
tal and/or extrasegmental descending pain inhibition compression–high active tension exercises. Patient edu-
mechanisms.155,156 Weight-bearing functional retraining cation and exercise modifications to avoid provocative
that aims to minimize hip adduction, progresses from tendon loads and promote positive adaptation hold great
double leg, to offset and then single leg tasks with upper potential for improving outcomes in tendinopathy about
limb support, and ultimately with no support and for the hip.
athletes more dynamic landing control tasks (see Fig.
47-3). Targeted concentric–eccentric abductor strength-
ening is often well tolerated quite early if applied without Controversies, Uncertainties
compression. An ideal medium is a sliding platform with
spring resistance. Standing on such a platform and
and Future Directions
actively abducting the hips against resistance allows At this time, one of the greatest controversies with
graduated increases in tensile loading without compres- respect to management of tendinopathies is the role of
sion as the hips move from neutral to inner range abduc- injection therapy – the most common being cortico-
tion (see Fig. 47-2). steroid injections (CSI) and blood-derived products
(autologous blood injections and platelet-rich plasma).
Although widely used in clinical practice, there is poor
Proximal Hamstring Tendinopathy
evidence regarding their usefulness and unknown effects
For the proximal hamstring tendons the combination of on local tissue health in the longer term. Despite the
high compressive and tensile loads occurs in hip flexion, short-term pain reduction imparted by CSI in tendi-
when the tendons wrap around the ischium and the ham- nopathic conditions, even a single injection has been
strings are active in this lengthened position.135,153 The shown to delay and reduce outcomes over the medium
semimembranosis tendon sits deepest and is exposed to to longer term.158,159
greatest compression, which may explain the higher inci- Limited studies have evaluated CSI for gluteal or
dence of semimembranosis pathology.122 Activities and proximal hamstring tendinopathies. Reduction of lateral
positions utilizing the combination of high compression hip pain has been reported for 72–75% of patients after
and active tension should be minimized, for example sus- 1 month,157,160 and 41–55% at 3–4 months157,161,162 follow-
tained or loaded trunk forward inclination, walking or ing CSI. After 12 months Brinks et al.161 showed no dif-
running up inclines or high steps, straight-leg deadlifts ference in outcome between groups provided with CSI
or similar actions on one leg (‘cranes’, ‘aeroplanes’) in the and ‘usual care’ (analgesics as required). One retrospec-
gym. Symptomatic tendons are provoked by compression tive study assessed the effects of CSI on proximal ham-
alone, such as sitting on the ischia, particularly on a hard string tendinopathy, describing a 50% success rate at 1
surface. month; however only 24% sustained a positive benefit for
The exercise programme provides pain-reducing iso- more than 6 months.163
metric contractions, and targeted strengthening of the Injections of biologically active blood products are
hamstrings and gluteus maximus within the framework purported to ‘kick start’ the healing process by ini-
of lower quadrant conditioning.153 Isometric hamstring tiating the production of new collagen and stimulating
strengthening is best performed early, in low or no hip revascularization.164 No studies to date evaluate the
flexion to minimize compression (Fig. 47-5). Loading can efficacy of autologous blood injections or platelet-rich
progress to higher load isometrics and heavy slow loading plasma injections for gluteal or proximal hamstring
in the form of hamstring curls, hamstring biased bridge tendinopathy. From the wider literature a recent
variations and Nordic curls126 (Fig. 47-5). Achieving good review reported inadequate evidence to support platelet-
gluteus maximus recruitment is essential during rich plasma injections in tendinopathy management
hip extension tasks to avoid relative overload of the ham- and suggested that ‘the use of autologous whole
string complex. Functional weight-bearing strengthening blood should not be recommended’.165 Much further
such as bridging and squatting should be included to research is required to clearly establish the efficacy
re-establish optimal recruitment patterns, commencing and safety of these and other emerging injectable
at low flexion angles (Fig. 47-3, rows 1 and 2). therapies.


Isometric
contractions
To improve
hamstring
muscle
recruitment
and assist with
pain relief
Leg load only – ankle weight – band Isometric hip ext and/or knee flex Higher load. Progress to weight
shift, then single leg lifts
Isometric hip ext and/or knee flex

Heavy slow
loading
Hamstring
strengthening

126
Slow resisted hamstring curls Hamstring biased bridging progressions Concentric eccentric roller exercise
Knees more extended. Start these once Roller alone – roller with band Nordic curls later in rehabilitation126
good gluteal function is achieved

FIGURE 47-5  ■  Examples of hamstring exercises.

47  Hip-Related Pain
517
518 PART IV  Overview of Contemporary Issues in Practice

24. Reichenbach S, Jüni P, Werlen S, et al. Prevalence of cam-type

REFERENCES deformity on hip magnetic resonance imaging in young males: a
1. Stem E, O’Connor M, Kransdorf M, et al. Computed tomography cross-sectional study. Arthritis Care Res (Hoboken) 2010;62(9):
analysis of acetabular anteversion and abduction. Skeletal Radiol 1319–27. PubMed PMID: 20853471.
2006;35(6):385–9. 25. Bardakos NV, Vasconcelos JC, Villar RN. Early outcome of hip
2. Lewis CL, Sahrmann SA. Acetabular labral tears. Phys Ther arthroscopy for femoroacetabular impingement: the role of
2006;86(1):110–21. femoral osteoplasty in symptomatic improvement. J Bone Joint
3. Haemer JM, Carter DR, Giori NJ. The low permeability of Surg Br 2008;90(12):1570–5.
healthy meniscus and labrum limit articular cartilage consolida- 26. Byrd JWT, Jones KS. Arthroscopic Femoroplasty in the manage-
tion and maintain fluid load support in the knee and hip. J Biomech ment of cam-type Femoroacetabular impingement. Clin Orthop
2012;45(8):1450–6. Relat Res 2009;467(3):739–46.
4. Tan V, Seldes RM, Katz MA, et al. Contribution of acetabular 27. Pollard TCB, Villar RN, Norton MR, et al. Femoroacetabular
labrum to articulating surface area and femoral head coverage in impingement and classification of the cam deformity: the refer-
adult hip joints: an anatomic study in cadavera. Am J Orthop (Belle ence interval in normal hips. Acta Orthop 2010;81(1):134–41.
Mead NJ) 2001;30(11):809–12. [Epub 2002/01/05. eng]; PubMed 28. Gosvig KK, Jacobsen S, Sonne-Holm S, et al. The prevalence of
PMID: 11757858. cam-type deformity of the hip joint: a survey of 4151 subjects of
5. Petersen W, Petersen F, Tillmann B. Structure and vasculariza- the Copenhagen Osteoarthritis Study. Acta Radiol 2008;49(4):436–
tion of the acetabular labrum with regard to the pathogenesis and 41. PubMed PMID: 18415788.
healing of labral lesions. Arch Orthop Trauma Surg 2003;123(6): 29. Siebenrock K, Ferner F, Noble P, et  al. The cam-type defor-
283–8. mity of the proximal femur arises in childhood in response
6. Narvani AA, Tsiridis E, Tai CC, et al. Acetabular labrum and its to vigorous sporting activity. Clin Orthop Relat Res 2011;469:
tears. Br J Sports Med 2003;37(3):207–11. PubMed PMID: 3229–40.
12782544. 30. Allen D, Beaulé PE, Ramadan O, et al. Prevalence of associated
7. Dhollander AAM, Lambrecht S, Verdonk PCM, et al. First deformities and hip pain in patients with cam-type femoroacetab-
insights into human acetabular labrum cell metabolism. Osteoar- ular impingement. J Bone Joint Surg Br 2009;91(5):589–94.
thritis Cartilage 2012;20(7):670–7. 31. Singh PJ, O’Donnell JM. The outcome of hip arthroscopy in
8. Konrath GA, Hamel AJ, Olson SA, et  al. The role of the acetabu- Australian football league players: a review of 27 hips. Arthros-
lar labrum and the transverse acetabular ligament in load trans- copy: The Journal of Arthroscopic & Related Surgery. 2010;26(6):
mission in the hip. J Bone Joint Surg Am 1998;80(12): 743–9.
1781–8. 32. Philippon MJ, Weiss DR, Kuppersmith DA, et al. Arthroscopic
9. Rao J, Zhou YX, Villar RN. Injury to the ligamentum teres. labral repair and treatment of femoroacetabular impingement in
Mechanism, findings, and results of treatment. Clin Sports Med professional hockey players. Am J Sports Med 2010;38(1):
2001;20(4):791–9, vii. PubMed PMID: MEDLINE:11675887. 99–104.
10. Bardakos NV, Villar RN. The ligamentum teres of the adult hip. 33. Byrd JWT, Jones KS. Hip Arthroscopy in athletes: 10-year
J Bone Joint Surg Br 2009;91-B(1):8–15. follow-up. Am J Sports Med 2009;37(11):2140–3.
11. Retchford T, Crossley KM, Grimaldi A, et al. Can local muscles 34. Agricola R, Heijboer M, Bierma-Zeinstra S, et al. Cam-type
augment stability in the hip? A narrative literature review. J Mus- deformities strongly predict total hip replacement within 5 years
culoskelet Neuronal Interact 2013;13(1):1–12. in those with early symptomatic OA: a prospective cohort study
12. Neumann DA. Kinesiology of the hip: a focus on muscular actions. (check). Osteoarthritis Cartilage 2012;20(Suppl. 1):S203.
J Orthop Sports Phys Ther 2010;40(2):82–94. 35. Agricola R, Heijboer MP, Bierma-Zeinstra SMA, et  al. Cam
13. Ward SR, Winters TM, Blemker SS. The architectural design of impingement causes osteoarthritis of the hip: a nationwide
the gluteal muscle group: implicati ons for movement and reha- prospective cohort study (CHECK). Ann Rheum Dis 2012.
bilitation. J Orthop Sports Phys Ther 2010;40(2):95–102. 36. Nicholls AS, Kiran A, Pollard TCB, et al. The association between
14. Walden M, Hagglund M, Ekstrand J. UEFA Champions League hip morphology parameters and nineteen-year risk of end-stage
study: a prospective study of injuries in professional football osteoarthritis of the hip a nested case-control study. Arthritis
during the 2001–2002 season. Br J Sports Med 2005;39: Rheum 2011;63(11):3392–400.
542–6. 37. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-
15. Orchard J, Seward H. AFL Injury Report: 2009. Available from: acetabular impingement due to acetabular retroversion. Treat-
<http://www.afl.com.au/injury%20report/tabid/13706/ ment with periacetabular osteotomy. J Bone Joint Surg Am
default.aspx>; 2008. 2003;85(2):278–86.
16. Spahn G, Schiell R, Langlotz A, et al. Hip pain in adolescents: 38. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does
results of a cross-sectional study in German pupils and a review not lead to osteoarthritis of the hip whereas acetabular dysplasia
of the literature. Acta Paediatr 2005;94:568–73. does: acetabular coverage and development of osteoarthritis in a
17. Christmas C, Crespo CJ, Franckowiak SC, et al. How common is nationwide prospective cohort study (CHECK). Osteoarthritis
hip pain among older adults? Results from the Third National Cartilage 2013;21(10):1514–21.
Health and Nutrition Examination Survey. J Fam Pract 39. Farjo LA, Glick JM, Sampson TG. Hip arthroscopy for acetabular
2002;51(4):345–8. [Epub 2002/04/30. eng]; PubMed PMID: labral tears. Arthroscopy 1999;15(2):132–7.
11978258. 40. McCarthy JC, Noble PC, Schuck MR, et al. The role of labral
18. Byrd JWT, Jones KS. Prospective analysis of hip arthroscopy with lesions to development of early degenerative hip disease. Clin
10-year followup. Clin Orthop Relat Res 2010;468(3):741–6. Orthop Relat Res 2001;393:25–37.
19. Clohisy JC, Knaus ER, Hunt DM, et al. Clinical presentation of 41. Seldes RM, Tan V, Hunt J, et al. Anatomy, histologic features,
patients with symptomatic anterior hip impingement. Clin Orthop and vascularity of the adult acetabular labrum. Clin Orthop Relat
Relat Res 2009;467(3):638–44, [English]. Res 2001;382:232–40.
20. Clohisy JC, Dobson MA, Robison JF, et al. Radiographic struc- 42. Clohisy JC, Baca G, Beaulé PE, et al. Descriptive epidemiology
tural abnormalities associated with premature, natural hip-joint of femoroacetabular impingement: a North American cohort of
failure. J Bone Joint Surg Am 2011;93:3–9. patients undergoing surgery. Am J Sports Med 2013.
21. Ganz R, Parvizi J, Beck M, et al. Femoroacetabular impingement: 43. Ito K, Minka MA II, Leunig M, et al. Femoroacetabular impinge-
a cause for osteoarthritis of the hip. Clin Orthop Relat Res ment and the cam-effect. A MRI-based quantitative anatomical
2003;417:112–20. study of the femoral head-neck offset. J Bone Joint Surg Br
22. Tannast M, Kubiak-Langer M, Langlotz F, et al. Noninvasive 2001;83(2):171–6.
three-dimensional assessment of femoroacetabular impingement. 44. Peelle MW, Della Rocca GJ, Maloney WJ, et al. Acetabular and
J Orthop Res 2007;25(1):122–31. PubMed PMID: MEDLINE: Femoral Radiographic Abnormalities Associated with Labral
17054112. Tears. Clin Orthop Relat Res 2005;441:327–33.
23. Banerjee P, McLean CR. Femoroacetabular impingement: a 45. Tanzer M, Noiseux N. Osseous abnormalities and early osteoar-
review of diagnosis and management. Curr Rev Musculoskelet thritis: the role of hip impingement. Clin Orthop Relat Res
Med 2011;4(1):23–32. PubMed PMID: MEDLINE:21475562. 2004;429:170–7. PubMed PMID: MEDLINE:15577483.
 47  Hip-Related Pain 519

46. Muir H. The chondrocyte, architect of cartilage. Biomechanics, 69. Gold SL, Burge AJ, Potter HG. MRI of hip cartilage. Clin Orthop
structure, function and molecular biology of cartilage matrix mac- Relat Res 2012;470:3321–31.
romolecules. Bioessays 1995;17(12):1039–47. 70. Kemp JL, Schache AG, Makdissi M, et al. People with chondropa-
47. O’Hara BP, Urban JPG, Maroudas A. Influence of cyclic loading thy have greater physical impairments than those without follow-
on the nutrition of articular cartilage. Ann Rheum Dis 1990; ing hip arthroscopy. Osteoarthritis Cartilage 2013;21(Suppl.):
49:536–9. S274.
48. McCarthy JC, Lee JA. Hip arthroscopy: indications, outcomes, 71. Kemp JL, Makdissi M, Schache AG, et al. Hip chondropathy is
and complications. J Bone Joint Surg Am 2005;87(5):1138–45. prevalent at arthroscopy and is associated with co-existing pathol-
49. Roos H, Laurén M, Adalberth T, et al. Knee osteoarthritis after ogy, but not patient reported outcomes. Osteoarthritis Cartilage
meniscectomy: prevalence of radiographic changes after twenty- 2013;21(Suppl.):S138.
one years, compared with matched controls. Arthritis Rheum 72. Hatton AL, Kemp JL, Brauer SG, et al. Dynamic single-leg
1998;41(4):687–93. balance performance is impaired in individuals with hip chon-
50. Englund M, Lohmander LS. Risk factors for symptomatic knee dropathy. Arthritis Care Res (Hoboken) 2013;66(5):709–16.
osteoarthritis fifteen to twenty-two years after meniscectomy. 73. Bierma-Zeinstra S, Koes B. Risk factors and pronostic factors of
Arthritis Rheum 2004;50(9):2811–19. hip and knee osteoarthritis. Nat Clin Pract Rheumatol 2007;3(2):
51. Kemp JL, Collins NJ, Makdissi M, et al. Hip arthroscopy for 78–85.
intra-articular pathology: a systematic review of outcomes with 74. Holla JF, van der Leeden M, Roorda LD, et al. Diagnostic accu-
and without femoral osteoplasty. Br J Sports Med 2012;46(9): racy of range of motion measurements in early symptomatic hip
632–43. and/or knee osteoarthritis. Arthritis Care Res (Hoboken)
52. Byrd JWT, Jones KS. Hip arthroscopy for labral pathology: pro- 2012;64(1):59–65. [Epub 2011/09/29. eng]; PubMed PMID:
spective analysis with 10-year follow-up. Arthroscopy 2009;25(4): 21954179.
365–8. 75. Holla JFM, Steultjens MPM, van der Leeden M, et  al. Deter-
53. Tamura S, Nishii T, Takao M, et al. Associations of hip dysplasia minants of range of joint motion in patients with early symp-
and FAI on modes of acetabular labral tears – 3 dimensional analy- tomatic osteoarthritis of the hip and/or knee: an exploratory
sis by high-resolution CT arthrography. Osteoarthritis Cartilage study in the CHECK cohort. Osteoarthritis Cartilage 2011;19:
2012;20(Suppl. 1):S214–15. 411–19.
54. Pollard TCB, Batra RN, Judge A, et al. Genetic predisposition to 76. Arokoski MH, Haara M, Helminen HJ, et al. Physical function in
the presence and 5-year clinical progression of hip osteoarthritis. men with and without hip osteoarthritis. Arch Phys Med Rehabil
Osteoarthritis Cartilage 2012;20(5):368–75. 2004;85(4):574–81. PubMed PMID: 15083432.
55. Pollard TCB, McNally EG, Wilson DC, et al. Localized cartilage 77. Altman R, Alarcon G, Appelrouth D, et al. The American College
assessment with three-dimensional dGEMRIC in asymptomatic of Rheumatology criteria for the classification and reporting of
hips with normal morphology and cam deformity. J Bone Joint osteoarthritis of the hip. Arthritis Rheum 1991;34(5):505–14.
Surg Am 2010;92(15):2557–69. 78. Arokoski MH, et al. Hip muscle strength and cross sectional area
56. Ratzlaff C, Simatovic J, Wong H, et al. Reliability of hip examina- in men with and without hip osteoarthritis. J Rheumatol 2002;
tion tests for femoroacetabular impingement (FAI). Arthritis Care 29(10):2185–95.
Res (Hoboken) 2013;65(10):1690–6. 79. Pua YH, Wrigley TV, Cowan SM, et al. Hip flexion range of
57. Audenaert EA, Peeters I, Vigneron L, et al. Hip morphological motion and physical function in hip osteoarthritis: mediating
characteristics and range of internal rotation in femoroacetabular effects of hip extensor strength and pain. Arthritis Care Res 2009;
impingement. Am J Sports Med 2012;40(6):1329–36. 61(5):633–40.
58. Kapron AL, Anderson AE, Peters CL, et al. Hip internal rotation 80. Lievense AM, Bierma-Zeinstra SMA, Verhagen AP, et al. Influ-
is correlated to radiographic findings of cam femoroacetabular ence of obesity on the development of osteoarthritis of the hip: a
impingement in collegiate football players. Arthroscopy 2012; systematic review. Rheumatology 2002;41(10):1155–62.
28(11):1661–70. 81. Altman RD, Gold GE. Atlas of individual radiographic features in
59. Yuan BJ, Bartelt RB, Levy BA, et al. Decreased range of motion osteoarthritis, revised. Osteoarthritis Cartilage 2007;15(Suppl. 1):
is associated with structural hip deformity in asymptomatic ado- A1–56.
lescent athletes. Am J Sports Med 2013;41(7):1519–25. 82. Xu L, Hayashi D, Guermazi A, et al. The diagnostic performance
60. Nussbaumer S, Leunig M, Glatthorn J, et al. Validity and test- of radiography for detection of osteoarthritis-associated features
retest reliability of manual goniometers for measuring passive hip compared with MRI in hip joints with chronic pain. Skeletal
range of motion in femoroacetabular impingement patients. BMC Radiol 2013;42(10):1421–8, [English].
Musculoskelet Disord 2010;11:194–204. 83. Nepple JJ, Kim YJ, Clohisy J. Do plain radiographs correlate with
61. Casartelli NC, Maffiuletti NA, Item-Glatthorn JF, et al. Hip CT for imaging of cam-type femoroacetabular impingement?
muscle weakness in patients with symptomatic femoroacetabular Clin Orthop Relat Res 2012;470:3313–20.
impingement. Osteoarthritis Cartilage 2011;19(7):816–21. 84. Reichenbach S, Leunig M, Werlen S, et al. Association between
62. Brisson N, Lamontagne M, Kennedy MJ, et al. The effects of cam cam-type deformities and magnetic resonance imaging–detected
femoroacetabular impingement corrective surgery on lower- structural hip damage: a cross-sectional study in young men.
extremity gait biomechanics. Gait Posture 2012;37:258–63. Arthritis Rheum 2011;63(12):4023–30.
63. Hunt MA, Gunether JR, Gilbart MK. Kinematic and kinetic dif- 85. Zlatkin MB, Pevsner D, Sanders TG, et al. Acetabular labral tears
ferences during walking in patients with and without symptomatic and cartilage lesions of the hip: indirect MR arthrographic cor-
femoroacetabular impingement. Clin Biomech (Bristol, Avon) relation with arthroscopy–a preliminary study. AJR Am J Roent-
2013;5:519–23. genol 2010;194(3):709–14.
64. Agricola R, Waarsing JH, Thomas GE, et al. Cam impingement: 86. Tyler TF, Slattery AA. Rehabilitation of the hip following sports
defining the presence of a cam deformity by the alpha angle. Data injury. Clin Sports Med 2010;29(1):107–26.
from the CHECK cohort and Chingford cohort. Osteoarthritis 87. Shindle MK, Domb BG, Kelly BT. Hip and pelvic problems in
Cartilage 2014;22(2):218–25. athletes. Oper Tech Sports Med 2007;15(4):195–203.
65. Beaulé PE, Hynes K, Parker G, et al. Can the alpha angle assess- 88. Enseki KR, Martin R, Kelly BT. Rehabilitation after arthroscopic
ment of cam impingement predict acetabular cartilage delamina- decompression for femoroacetabular impingement. Clin Sports
tion? Clin Orthop Relat Res 2012;470:3361–7. Med 2010;29(2):247–55. PubMed PMID: 20226317.
66. Heyworth B, Dolan M, Nguyen J, et al. Preoperative three- 89. Philippon MJ, Christensen JC, Wahoff MS. Rehabilitation
dimensional CT predicts intraoperative findings in hip arthros- after arthroscopic repair of intra-articular disorders of the hip
copy. Clin Orthop Relat Res 2012;470(7):1950–7. in a professional football athlete. J Sport Rehabil 2009;18(1):
67. Groh MM, Herrera J. A comprehensive review of hip labral tears. 118–34.
Curr Rev Musculoskelet Med 2009;2(2):105–17. PubMed PMID: 90. Stalzer S, Wahoff M, Scanlan M. Rehabilitation following hip
MEDLINE:19468871. arthroscopy. Clin Sports Med 2006;25(2):337–57.
68. Yazbek PM, Ovanessian V, Martin RL, et al. Nonsurgical treat- 91. Lewis CL, Sahrmann SA, Moran DW. Effect of hip angle on
ment of acetabular labrum tears: a case series. J Orthop Sports anterior hip joint force during gait. Gait Posture 2010;32(4):
Phys Ther 2011;41(5):346–53. PubMed PMID: 21335929. 603–7.
520 PART IV  Overview of Contemporary Issues in Practice

92. Wall PDH, Fernandez M, Griffin DR, et al. Nonoperative treat- female population: a cross-sectional study. Osteoarthritis Carti-
ment for femoroacetabular impingement: a systematic review of lage 2013;21(4):544–50.
the literature. PM R 2013;5(5):418–26. 114. Dagenais S, Garbedian S, Wai E. Systematic review of the preva-
93. Cambridge EDJ, Sidorkewicz N, Ikeda DM, et al. Progressive hip lence of radiographic hip osteoarthritis. Clin Orthop Relat Res
rehabilitation: the effects of resistance band placement on gluteal 2009;467:623–37.
activation during two common exercises. Clin Biomech (Bristol, 115. Pollard TCB, Villar RN, Norton MR, et al. Genetic influences in
Avon) 2012;27(7):719–24. the aetiology of femoroacetabular impingement: a sibling study.
94. Boren K, Conrey C, Le Coguic J, et al. Electromyographic analy- J Bone Joint Surg Br 2010;92-B(2):209–16.
sis of gluteus medius and gluteus maximus during rehabilitation 116. Segal NA, Felson DT, Torner JC, et al. Greater trochanteric pain
exercises. Int J Sports Phys Ther 2011;6(3):206–23. syndrome: epidemiology and associated factors. Arch Phys Med
95. Fisher BE, Lee Y, Pitsch EA, et al. Method for assessing brain Rehabil 2007;88(8):988–92. PubMed PMID: 17678660. Pubmed
changes associated with gluteus maximus activation. J Orthop Central PMCID: 2907104.
Sports Phys Ther 2013;43(4):214–21. 117. Del Buono A, Papalia R, Khanduja V, et al. Management of the
96. Giphart E, Stull J, LaPrade R, et al. Recruitment and activity of greater trochanteric pain syndrome: a systematic review. Br Med
the pectineus and piriformis muscles during hip rehabilitation Bull 2012;102:115–31. PubMed PMID: 21893483.
exercises. Am J Sports Med 2012;40(7):1654–63. 118. Grumet RC, Frank RM, Slabaugh MA, et al. Lateral hip pain in
97. Cowan SM, Blackburn MS, McMahon K, et al. Current Austra- an athletic population: differential diagnosis and treatment
lian physiotherapy management of hip osteoarthritis. Physiother- options. Sports Health 2010;2(3):191–6. PubMed PMID:
apy 2010;96(4):289–95. PubMed PMID: 21056163. 23015937. Pubmed Central PMCID: 3445102.
98. Godges JJ, Macrae H, Longdon C, et al. The effects of two 119. Spiker AM, Dixit S, Cosgarea AJ. Triathlon: running injuries.
stretching procedures on hip range of motion and gait economy. Sports Med Arthrosc 2012;20(4):206–13. PubMed PMID:
J Orthop Sports Phys Ther 1989;10(9):350–7. [Epub 1989/01/01. 23147090.
eng]; PubMed PMID: 18791317. 120. Cacchio A, Rompe JD, Furia JP, et al. Shockwave therapy for the
99. Bennell K. Physiotherapy management of hip osteoarthritis. treatment of chronic proximal hamstring tendinopathy in profes-
J Physiother 2013;59(3):145–57. sional athletes. Am J Sports Med 2011;39(1):146–53. PubMed
100. Poulsen E, Hartvigsen J, Christensen HW, et al. Patient educa- PMID: 20855554.
tion with or without manual therapy compared to a control group 121. Fredericson M, Moore W, Guillet M, et al. High hamstring ten-
in patients with osteoarthritis of the hip. A proof-of-principle dinopathy in runners: meeting the challenges of diagnosis, treat-
three-arm parallel group randomized clinical trial. Osteoarthritis ment, and rehabilitation. Phys Sportsmed 2005;33(5):32–43.
Cartilage 2013;21(10):1494–503. PubMed PMID: 20086362.
101. Rooks DS, Huang J, Bierbaum BE, et al. Effect of preoperative 122. Lempainen L, Sarimo J, Mattila K, et al. Proximal hamstring
exercise on measures of functional status in men and women tendinopathy: results of surgical management and histopathologic
undergoing total hip and knee arthroplasty. Arthritis Care Res findings. Am J Sports Med 2009;37(4):727–34. PubMed PMID:
(Hoboken) 2006;55(5):700–8. 19218559.
102. Fernandes L, Storheim K, Sandvik L, et al. Efficacy of patient 123. White KE. High hamstring tendinopathy in 3 female long dis-
education and supervised exercise vs patient education alone in tance runners. J Chiropr Med 2011;10(2):93–9. PubMed PMID:
patients with hip osteoarthritis: a single blind randomized clinical 22014863. Pubmed Central PMCID: 3110412.
trial. Osteoarthritis Cartilage 2010;18(10):1237–43. 124. Del Buono A, Battery L, Denaro V, et al. Tendinopathy and
103. Lewis CL, Sahrmann SA, Moran DW. Anterior hip joint force inflammation: some truths. Int J Immunopathol Pharmacol
increases with hip extension, decreased gluteal force, or decreased 2011;24(1 Suppl. 2):45–50. PubMed PMID: 21669137.
iliopsoas force. J Biomech 2007;40(16):3725–31. 125. Gaida JE, Ashe MC, Bass SL, et al. Is adiposity an under-
104. French HP, Brennan A, White B, et al. Manual therapy for osteo- recognized risk factor for tendinopathy? A systematic review.
arthritis of the hip or knee – A systematic review. Man Ther Arthritis Rheum 2009;61(6):840–9. PubMed PMID: 19479698.
2011;16(2):109–17. 126. Petersen J, Thorborg K, Nielsen MB, et al. Preventive effect of
105. Abbott JH, Robertson MC, Chapple C, et al. Manual therapy, eccentric training on acute hamstring injuries in men’s soccer: a
exercise therapy, or both, in addition to usual care, for osteoar- cluster-randomized controlled trial. Am J Sports Med 2011;
thritis of the hip or knee: a randomized controlled trial. 1: clinical 39(11):2296–303. PubMed PMID: 21825112.
effectiveness. Osteoarthritis Cartilage 2013;21(4):525–34. 127. de Oliveira LP, Vieira CP, Da Re Guerra F, et al. Statins induce
106. Hochberg MC, Altman RD, April KT, et al. American College of biochemical changes in the Achilles tendon after chronic treat-
Rheumatology 2012 recommendations for the use of nonpharma- ment. Toxicology 2013;311(3):162–8. PubMed PMID: 23831763.
cologic and pharmacologic therapies in osteoarthritis of the hand, 128. Wise BL, Peloquin C, Choi H, et al. Impact of age, sex, obesity,
hip, and knee. Arthritis Care Res (Hoboken) 2012;64(4):465–74. and steroid use on quinolone-associated tendon disorders. Am J
107. Zhang W, Doherty M, Arden N, et al. Eular evidence based Med 2012;125(12):1228.e23–8. PubMed PMID: 23026288.
recommendations for the management of hip osteoarthritis: repot Pubmed Central PMCID: 3502655.
of a task force of the EULAR Standing Committee for Interna- 129. Magnusson SP, Langberg H, Kjaer M. The pathogenesis of ten-
tional Clincal Studies Including Therapeutics (ESCISIT). Ann dinopathy: balancing the response to loading. Nat Rev Rheumatol
Rheum Dis 2005;64:669–81. 2010;6(5):262–8. PubMed PMID: 20308995.
108. Hauser RA, Orlofsky A. Regenerative Injection Therapy (Prolo- 130. Thornton GM, Shao X, Chung M, et al. Changes in mechanical
therapy) for hip labrum lesions: rationale and retrospective study. loading lead to tendonspecific alterations in MMP and TIMP
Open Rehabi J 2013;6:59–68. expression: influence of stress deprivation and intermittent cyclic
109. Ellis HB, Briggs KK, Philippon MJ. Innovation in hip arthros- hydrostatic compression on rat supraspinatus and Achilles tendons.
copy: is hip arthritis preventable in the athlete? Br J Sports Med Br J Sports Med 2010;44(10):698–703. PubMed PMID: 18801769.
2011;45(4):253–8. [Epub 2011 Feb]; PubMed PMID: MEDLINE: 131. Almekinders LC, Weinhold PS, Maffulli N. Compression etiology
21304160. in tendinopathy. Clin Sports Med 2003;22(4):703–10. PubMed
110. Clohisy JC, Beaulé PE, O’Malley A, et al. Hip disease in the PMID: 14560542.
young adult: current concepts of etiology and surgical treatment. 132. Cook JL, Purdam C. Is compressive load a factor in the develop-
J Bone Joint Surg Am 2008;90(10):2267–81. ment of tendinopathy? Br J Sports Med 2012;46(3):163–8.
111. Robertson WJ, Kadrmas WR, Kelly BT. Arthroscopic manage- PubMed PMID: 22113234.
ment of labral tears in the hip: a systematic review. Clin Orthop 133. Vogel KG, Ordog A, Pogany G, et al. Proteoglycans in the com-
Relat Res 2007;455:88–92. pressed region of human tibialis posterior tendon and in liga-
112. Ng VY, Arora N, Best TM, et al. Efficacy of surgery for femoro- ments. J Orthop Res 1993;11(1):68–77. PubMed PMID: 8423522.
acetabular impingement: a systematic review. Am J Sports Med 134. Soslowsky LJ, Thomopoulos S, Esmail A, et  al. Rotator cuff
2010;38(11):2337–45. tendinosis in an animal model: role of extrinsic and overuse
113. Leunig M, Jüni P, Werlen S, et al. Prevalence of cam and pincer- factors. Ann Biomed Eng 2002;30(8):1057–63. PubMed PMID:
type deformities on hip MRI in an asymptomatic young Swiss 12449766.
 47  Hip-Related Pain 521

135. Cook JL, Purdam CR. The challenge of managing tendinopathy 151. Grimaldi A. Assessing lateral stability of the hip and pelvis. Man
in competing athletes. Br J Sports Med 2014;48(7):506–9. PubMed Ther 2011;16(1):26–32. PubMed PMID: 20888285.
PMID: 23666020. 152. Birnbaum K, Siebert CH, Pandorf T, et al. Anatomical and bio-
136. Fearon AM, Scarvell JM, Neeman T, et al. Greater trochanteric mechanical investigations of the iliotibial tract. Surg Radiol Anat
pain syndrome: defining the clinical syndrome. Br J Sports Med 2004;26(6):433–46. PubMed PMID: 15378277.
2013;47(10):649–53. 153. Grimaldi A. Lateral Hip Pain with Dr Alison Grimaldi. Phys-
137. Bird PA, Oakley SP, Shnier R, et al. Prospective evaluation of ioedge Podcasts 2012.
magnetic resonance imaging and physical examination findings in 154. Grimaldi A, Mellor R, Bennell K, et al. Gluteal tendinopathy: a
patients with greater trochanteric pain syndrome. Arthritis Rheum proposed pathoaetiological mechanism-based management
2001;44(9):2138–45. approach. Submitted. 2014.
138. Lequesne M, Mathieu P, Vuillemin-Bodaghi V, et al. Gluteal 155. Kosek E, Ekholm J. Modulation of pressure pain thresholds
tendinopathy in refractory greater trochanter pain syndrome: during and following isometric contraction. Pain 1995;61(3):481–
diagnostic value of two clinical tests. Arthritis Rheum 2008;59(2): 6. PubMed PMID: 7478692.
241–6. 156. Kosek E, Lundberg L. Segmental and plurisegmental modulation
139. Tortolani P, Carbone JJ, Quartararo LG. Greater trochanteric of pressure pain thresholds during static muscle contractions in
pain syndrome in patients referred to orthopedic spine specialists. healthy individuals. Eur J Pain 2003;7(3):251–8. PubMed PMID:
Spine J 2002;2(4):251–4. 12725848.
140. Williams BS, Cohen SP. Greater trochanteric pain syndrome: a 157. Rompe JD, Segal NA, Cacchio A, et al. Home training, local
review of anatomy, diagnosis and treatment. Anesthesia and anal- corticosteroid injection, or radial shock wave therapy for greater
gesia. Anesth Analg 2009;108(5):1662–70. trochanter pain syndrome. Am J Sports Med 2009;37(10):1981–
141. Woodley SJ, Nicholson HD, Livingstone V, et al. Lateral hip 90. PubMed PMID: 19439758.
pain: findings from magnetic resonance imaging and clinical 158. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corti-
examination. J Orthop Sports Phys Ther 2008;38(6):313–28. costeroid injections and other injections for management of ten-
142. Bowman KFJ, Cohen SB, Bradley JP. Operative management of dinopathy: a systematic review of randomised controlled trials.
partial-thickness tears of the proximal hamstring muscles in ath- Lancet 2010;376(9754):1751–67. PubMed PMID: 20970844.
letes. Am J Sports Med 2013;41(6):1363–71. 159. Scott A, Khan KM. Corticosteroids: short-term gain for long-
143. Reiman MP, Goode AP, Hegedus EJ, et al. Diagnostic accuracy term pain? Lancet 2010;376(9754):1714–15. PubMed PMID:
of clinical tests of the hip: a systematic review with meta-analysis. 20970846.
Br J Sports Med 2013;47(14):893–902. PubMed PMID: 22773321. 160. Labrosse JM, Cardinal E, Leduc BE, et al. Effectiveness of
144. Reiman MP, Loudon JK, Goode AP. Diagnostic accuracy of clini- ultrasound-guided corticosteroid injection for the treatment of
cal tests for assessment of hamstring injury: a systematic review. J gluteus medius tendinopathy. AJR Am J Roentgenol 2010;194(1):
Orthop Sports Phys Ther 2013;43(4):223–31. PubMed PMID: 202–6. PubMed PMID: 20028924.
23321899. 161. Brinks A, van Rijn RM, Willemsen SP, et al. Corticosteroid injec-
145. Cacchio A, Borra F, Severini G, et al. Reliability and validity of tions for greater trochanteric pain syndrome: a randomized con-
three pain provocation tests used for the diagnosis of chronic trolled trial in primary care. Ann Fam Med 2011;9(3):226–34.
proximal hamstring tendinopathy. Br J Sports Med 2012;46(12): PubMed PMID: 21555750. Pubmed Central PMCID: 3090431.
883–7. PubMed PMID: 22219215. 162. Cohen SP, Strassels SA, Foster L, et al. Comparison of fluoro-
146. Blankenbaker DG, Ullrick SR, Davis KW, et al. Correlation of scopically guided and blind corticosteroid injections for greater
MRI findings with clinical findings of trochanteric pain syndrome. trochanteric pain syndrome: multicentre randomised controlled
Skeletal Radiol 2008;37(10):903–9. PubMed PMID: 18566811. trial. BMJ 2009;338:b1088. PubMed PMID: 19366755. Pubmed
147. Connell DA, Bass C, Sykes CA, et al. Sonographic evaluation of Central PMCID: 2669115.
gluteus medius and minimus tendinopathy. Eur Radiol 2003;13(6): 163. Zissen MH, Wallace G, Stevens KJ, et al. High hamstring tendi-
1339–47. PubMed PMID: 12764651. nopathy: MRI and ultrasound imaging and therapeutic efficacy of
148. De Smet AA, Blankenbaker DG, Alsheik NH, et al. MRI appear- percutaneous corticosteroid injection. AJR Am J Roentgenol
ance of the proximal hamstring tendons in patients with and 2010;195(4):993–8. PubMed PMID: 20858830.
without symptomatic proximal hamstring tendinopathy. AJR Am 164. Marx RE. Platelet-rich plasma (PRP): what is PRP and what is
J Roentgenol 2012;198(2):418–22. PubMed PMID: 22268187. not PRP? Implant Dent 2001;10(4):225–8. PubMed PMID:
149. Petchprapa CN, Bencardino JT. Tendon injuries of the hip. Magn 11813662.
Reson Imaging Clin N Am 2013;21(1):75–96. PubMed PMID: 165. de Vos RJ, van Veldhoven PL, Moen MH, et al. Autologous
23168184. growth factor injections in chronic tendinopathy: a systematic
150. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic review. Br Med Bull 2010;95:63–77. PubMed PMID: 20197290.
resonance imaging of the lumbar spine in people without back
pain. N Engl J Med 1994;331(2):69–73. PubMed PMID: 8208267.
 C H A P T E R 4 8 

The Knee: Introduction

CHAPTER OUTLINE

Ch 48.1  Acute Knee Injuries  522 Ch 48.3  Knee Osteoarthritis  536

Lee Herrington Kim Bennell • Rana Hinman • Melanie Holden •
Ch 48.2  Patellofemoral Pain  528 George Peat
Kay Crossley • Sallie Cowan • Bill Vicenzino

CHAPTER 48.1  ■  ACUTE KNEE INJURIES

Lee Herrington

INTRODUCTION of the loads involved in dynamic overload is important in

preventing deceleration injuries, because when rehabili-
If external or internal forces directed at the knee are of tating an individual post injury (or surgical repair of that
sufficient magnitude and duration, they will result in injury), the goal is to restore pain-free function and
structural disruption of one or more of the anatomical prevent the injury reoccurring. This is essentially the
structures in and around the joint. Tissue failure will same as attempting to prevent the injury happening in
result if stress is applied too quickly, exceeds the tissue’s the first instance, and the person involved requires reha-
tolerance limits or if it is applied repetitively without bilitation in a manner that has the end goal of developing
sufficient time for recovery. This type of failure has been the intrinsic ability (strength and neuromuscular control)
termed dynamic overload. Dynamic overload of the tissue to match the loads involved, thereby preventing tissue
may be a result of an acceleration or deceleration injury. stress and injury from occurring.
An acceleration injury occurs when the body or body
parts are stationary or moving slower than the applied
force. The injury producing force accelerates the body or COMMON ACUTE KNEE INJURIES
body part beyond the tissue’s ability to withstand or resist
that force, such as when a footballer is being tackled and Injury to the anterior cruciate ligament (ACL) would
the force of contact by the opposing player’s foot against appear to be by far the most debilitating acute knee
the lateral aspect of the leg exceeds the ability of the injury, followed by injury to the menisci, collateral liga-
medial collateral ligament to resist the force, potentially ments then posterior cruciate ligament. Definitive statis-
resulting in damage. In the case of deceleration injury, tics are unavailable. However, acute knee injury may
the body or body parts are rapidly decelerated. Examples account for 14–40% of all acute musculoskeletal inju-
include landing from a jump or attempting to stop and ries.1,2 Meniscal injury may be responsible for 9% of all
quickly change direction (cutting). If the body is not able acute musculoskeletal trauma, with collateral ligaments
to oppose these forces the resulting movement would 7% and anterior cruciate ligament 4%.3 Meniscal injuries
apply a substantial valgus force on the knee, which is the have been reported to occur at a rate of 0.3–0.6 per 1000
classic mechanism for anterior cruciate ligament injury. (training) hours,4 rising to 3–13 per 1000 (training) hours
Acceleration injuries are typically related to contact in a military population.5 ACL injury rates are around
injuries, whereas deceleration injuries usually involve no 0.1–0.4 per 1000 (training) hours;4 however, injury rate
contact with external loads or forces (i.e. other players) may be as high as 1 in 20 females who play soccer and
as the forces are generated internally. While prevention basketball at a competitive level.6
of contact injuries may be difficult, if not impossible, it
would appear that if dynamic overload of the tissues
could be prevented during the deceleration phase, then NATURE OF LOADS
the risk of injury is reduced and potentially removed. In
order to achieve this, the loads involved in sporting and Non-contact deceleration injuries typically involve a
functional activities need to be understood. Appreciation failure to control multidirectional forces. One of the
522
 48  The Knee: Introduction 523

most common movement patterns associated with knee 0.5–1 Nm/kg during single leg landing from a 30–40  cm
injury is that of dynamic valgus collapse (Fig. 48-1), box. These forces increase considerably once the sce-
which has been associated with injury to the ACL, medial nario is ‘more real’, for example dribbling a basketball
collateral ligament, medial and lateral meniscus and artic- or holding a lacrosse stick and cutting increases the
ular joint surfaces.7 Dynamic valgus collapse involves the load by greater than 0.3 Nm/kg.12,13 The levels of loads
sudden deceleration of the knee, with the limb if uncon- described here are substantial for those working towards
trolled, moving into a position of hip adduction and full rehabilitation of the knee following injury and pre-
internal rotation, knee abduction and tibial external rota- venting injury (or re-injury) as they represent the
tion and with the knee often slightly flexed during either minimum level of force the body is required to gener-
landing or cutting. All of these factors contribute to gen- ate to control these potentially deleterious forces. The
erating substantial knee external abduction and flexor ability to absorb these forces during dynamic tasks may
moments, along with a rapid increase in vertical ground alter the internal or external forces acting on the joint
reaction force (compressive loading to the joint). and potentially decrease the loading placed on the passive
Increased knee abduction and flexor moments have joint structures.10 The hip abductor external rotator
been associated with ACL injury6 and patellofemoral muscle group has to be able to generate a minimum
joint pain.8 Elevated vertical ground reaction forces force equivalent to 60% of body weight for multiple
(VGRF) have been associated with joint irritation and repetitions in order to counter the forces pushing the
degeneration,7 increased meniscal loading and damage,9 knee into valgus (external knee abduction moment)
increased tibiofemoral joint anterior shear loads10 and during a variety of functional tasks, as described above.
raised patellofemoral joint reaction force.11 Typical Likewise, to counter the VGRF, the combined closed
VGRF values associated with common tasks would be chain lower limb extensor muscle strength must be
1.5–2.5 times body weight when running, 2.5–3 times equal to or greater than twice body weight, to match
body weight (when landing from a forward hop) and the typical loads applied to the body.
rapidly changing direction (cutting) and 1.5–3 times The key components in dealing with these forces in
body weight landing from a 30  cm box. Knee abduc- order to prevent injury or re-injury will be the develop-
tion moments typically range from 0.6 Newton metre ment of sufficient strength to counteract the loads applied
per kilogram body weight (Nm/kg) during running, to and appropriate neuromuscular control strategies to
0.4–0.9 Nm/kg during cutting (depending on angle) and apply the strength in an appropriate manner.

A B

FIGURE 48-1  ■  (A) Good alignment, hip, knee and ankle all flexing in sagittal plane only, pelvis in neutral position, trunk aligned over
pelvis. (B) Poor movement showing valgus collapse, involves foot pronation, knee abduction, hip adduction and internal rotation,
tilting of the pelvis and leaning of the trunk.
524 PART IV  Overview of Contemporary Issues in Practice

exercises and closed chain exercises to optimize strength

STRENGTHENING recovery. Alongside sufficient strength, the ability to gen-
erate force rapidly (power) will substantially impact on
The immediate post-injury (or post-surgery) period is functional performance, especially the performance of
often characterized by significant reduction in function sport-specific speed- and agility-based tasks.31 Both
due to pain, joint effusion and decreased muscle activation. Angelozzi et al.32 and Myer et al.33 reported significant
If these issues are not addressed they are likely to substan- deficits in the rate of force development in patients post
tially impact on long-term functional performance.6 ACL reconstruction surgery despite successfully return-
ing to sport, this may predispose the athlete to increased
risk of secondary injury.34,35
Muscle Inhibition Decreased gluteal muscle activity has been associated
Quadriceps muscle weakness is a common consequence with increased knee valgus angles and abduction moments
of knee injury. The decrement in quadriceps function has during a variety of functional tasks,9 with improvements
been termed arthrogenic muscle inhibition (AMI).14 AMI in hip abduction-lateral rotation strength and activation
is a neurological decline in muscle activation resulting leading to superior neuromuscular control and alignment
from both pain and joint effusion.15 AMI hinders reha- of the lower limb.8,36 Hollman et al.37 reported that
bilitation by preventing strength gains in the quadriceps. strength and recruitment of gluteal muscles were signifi-
AMI becomes problematic if it is not reversed and muscle cant factors in maintaining limb alignment upon landing.
function restored, as this can lead to decreased functional Consequently, training should target both isolated
ability and biomechanical deficits,16 re-injury and the strength and coordinated activation within patterns of
development of osteoarthritis.17 The management of movement. Homan et al.38 demonstrated that individuals
AMI requires a multifacet approach involving the use of with poor gluteal strength used a greater proportion of
a number of treatment modalities, directed at sensory their maximal isometric voluntary contraction during
control and aimed at altering the motor drive, increasing landing tasks, so work capacity (endurance) will also be a
the stimulus to the muscle.17 factor to consider when training these individuals. The
One approach to preventing AMI is to incorporate single-leg squat was the best exercise for recruitment of
means to block or modify the sensory signals that are the gluteus medius and maximus activation in combina-
generating the inhibitory stimulus. Fundamentally this tion, so might provide the most appropriate interven-
will involve reducing pain and knee effusion. The use of tion39 (Fig. 48-2).
cryotherapy appears to be beneficial in reducing AMI
developed in the presence of knee effusion,18,19 as does
transcutaneous electrical stimulation (TENS).18 Both
these modalities block sensory pain signalling. There DEVELOPMENT OF
appears to be little evidence other than anecdotal for the NEUROMUSCULAR CONTROL
use of either compression or elevation to control effusion,
though they may be considered.16 To improve motor When landing or cutting the impact with the ground
stimulus, muscle stimulation appears beneficial in reduc- creates forces and moments of force that not only accel-
ing AMI20 either when used in conjunction with an exer- erate flexion of the hip, knee and ankle dorsiflexion, but
cise programme21,22 or to provide a superimposed twitch in resolving the forces involved, create multdirectional
(involuntary muscle contraction) alongside a volitional loads on the knee joint. It has been proposed10 that the
isometric quadriceps contraction.23 High-load resistance greater the energy absorption by muscle during these
training may also prove useful.24 Electromyographic bio- tasks, the greater the potential decrease in the amount of
feedback may be beneficial in overcoming AMI, although energy transferred to the capsule-ligamentous and articu-
this is supported by a single case study.25 lar tissues of the knee. In order to undertake this role
successfully, the muscular system must not only acquire
Strength, Power and Work sufficient strength to match the forces involved, but also
must be suitably trained to coordinate the application of
Capacity Development this muscular force. This coordination involves appropri-
Once normal activation patterns for quadriceps have ate timing of muscle force, as well as the appropriate
been established, progressive strengthening is then degree and direction of force. Essentially, the sole aim of
required. Quadriceps strength deficits following ACL neuromuscular training is to educate the neuromuscular
reconstruction have been related to restricted knee system to react in an appropriate and timely manner
motion during gait26 and poorer self-reported function.27 to reduce the loads on the passive joint structures of
This quadriceps weakness is associated with decreased the knee.
knee flexion on landing26,28 with consequential increase Neuromuscular rehabilitation requires the regaining
in joint loading29 and the potential for secondary joint of symmetrical motion and appropriate movement strate-
injury. When considering the mode of training, Risberg gies in order to limit deleterious loads and motion, to
et al.30 reported that closed chain activities (e.g. squatting reduce risk of re-injury and improve function.14 Simple
and step ups) in isolation were associated with a 20% verbal and visual feedback given in isolation can posi-
deficit in quadriceps strength compared with training tively influence both landing and running biomechanics.
involving a combination of open (knee extension) and Feedback is a fundamental tool to enhance learning and
closed kinetic chain exercises. This indicates the need to performance of motor skills and may be the quickest
incorporate both joint isolation (open kinetic chain) and simplest form of training available. Feedback has
 48  The Knee: Introduction 525

A B C

FIGURE 48-2  ■  (A) Basic exercise to load hip abductor and external rotators during squatting task, they squat pushing out against
band. (B) Progression onto single-leg squat which increased load on hip abductor external rotator muscles. (C) Progression of load
onto hip abductor external rotator muscles, then squat while pushing out against band.

been shown to be a vital part of motor skill learning programme evolves progressively through an initial phase
associated with optimizing lower limb movements, involving discrete closed movements in a block practice
decreasing VGRF, knee valgus angles and moments.40,41 format, an intermediate phase, which incorporates a
Neuromuscular training therefore needs to incorporate combination of some closed and some controlled open
appropriate verbal and visual feedback to optimize (re-) skill elements, and finally, practice elements that involve
learning the skill. open movements in a random practice format.44
Neuromuscular rehabilitation often relies on closed Limb loading is performed using a closed kinetic
skill activities carried out in a set order,42 which typically chain. Initially, activities are introduced to improve
involves repeated practices of the closed skill (identical movement skills and control during limb loading tasks
movement tasks in stable predictable environments most prior to undertaking load acceptance (landing) tasks.32
often carried out at a pace defined by the participant). To This is followed by introducing loads and reducing stabil-
more appropriately reflect the motor skill requirements ity, as demonstrated in a single-leg squat (Fig. 48-2). A
of sports and dynamic functional movements in everyday qualitative assessment scoring system during both unilat-
life, the programmes require progressively increasing the eral limb load and load acceptance activities has been
complexity where more open skill (non-planned skills/ described and discussed elsewhere.32,45 Structured verbal
tasks) elements become incorporated in a more random plus video input significantly reduces both VRGF and
fashion, once the closed skill tasks have been mastered.43 knee valgus angles on landing34 and should be incorpo-
This involves activities that are initially controlled and rated in the rehabilitation programme.
self-paced, allowing the participant to understand and Progression within the closed skill training element
master the specifics of the appropriate movement pat- and the open skill element are described within Figures
terns in environments that are predictable and static and 48-3 and 48-4, respectively. Jump landing training sig-
allow the individual to plan their movements in advance nificantly reduces knee abduction moments and angles
(closed skill practice).44 The activities then progress to and VGRF46 improve performance47 and reduce the risk
incorporate more random elements, where the environ- of ACL injury.6
ment is unpredictable and changing and the participant
needs to adapt their movements in response (open skill
practice).44
A progressive structured neuromuscular training pro- CONCLUSION
gramme that develops the participant’s movement and
landing skills through progressively more challenging Rehabilitation of a deceleration dynamic overload injury
tasks is depicted in Figures 48-3 and 48-4. The to the knee requires an appreciation of the nature of the
526 PART IV  Overview of Contemporary Issues in Practice

Closed chain limb loaded activities

Examples: Single-leg squats, Progression: Increase load

step up-down-sideways, lunges and challenge stability

Load acceptance (landing) activities (bilateral or unilateral)

Progression: In place → forward Progression (within direction):

→ sideways → rotation → combination Challenge stability → over barriers
→ off boxes

Plyometric activities (bilateral or unilateral)

Progression: In place → forward Progression (within direction):

→ sideways → rotation → combination Challenge stability → over barriers
→ off boxes

Key: → = indication of progression from one to the next

FIGURE 48-3  ■  Progression of unilateral loading and load acceptance tasks during closed skill practice.

Closed skill load acceptance task Open skill (random)

Sagittal
In place (forward)
landings
Stability Over Variable surface
challenge barriers
Box-hurdle heights
Shadowing partners

Plyometric Off boxes Perturbation

(repetitive) (from Sport-specific
landings height)
Transerve Frontal
(turning) (sideways)
landings landings

FIGURE 48-4  ■  Progression of unilateral load acceptance tasks during open skill practice.

forces involved in both the injury itself and during REFERENCES

the tasks set that are specific to the injured individual and 1. Button K, Iqbal A, Letchford R, et al. Clinical effectiveness of knee
the overall demands of the sport. Once understood, con- rehabilitation techniques and implications for a self-care model.
trolling these forces becomes the paramount goal of Physiotherapy 2012;98:288–300.
rehabilitation to prevent further overload of the tissues. 2. Van Middelkoop M, van Linschoten C, Berger M, et al. Knee
Control of these forces initially requires sufficient complaints seen in general practice: active sport participants versus
non-sport participants. BMC Musculoskelet Disord 2008;19:
strength within the muscular system and then, appropri- 9–36.
ate neuromuscular control strategies to coordinate the 3. Schappert S, Burt C. Ambulatory care visits to physician
application of the muscular force at the appropriate time offices, hospital outpatient departments and emergency depart-
and with the appropriate degree and direction of force. ments: United states, 2001–2002. Vital Health Stat 2006;13:
1–66.
In order to attain the first goal, appropriate progressive 4. Wasserstein D, Khoshbin A, Dwyer T, et al. Risk factors for recur-
resistance training principles must be applied to regain rent anterior cruciate ligament reconstruction: a population study
the proper levels of strength and force development. To in Ontario, Canada. Am J Sports Med 2013;41:2099–107.
successfully achieve the second rehabilitation goal, a 5. Jones J, Burks R, Owens B, et al. Incidence and risk factors associ-
motor skill learning programme needs be undertaken ated with meniscal injuries among active service US military service
members. J Athl Train 2012;47:67–73.
where the patient is able to apply appropriate movement 6. Hewett T, Di Stasi S, Myer G. Current concepts for injury preven-
strategies, to minimize injury risk, in an open randomly tion in athletes after anterior cruciate ligament reconstruction. Am
changing environment. J Sports Med 2013;41:216–24.
 48  The Knee: Introduction 527

7. Logerstedt D, Snyder-Mackler L, Ritter R, et al. Knee pain and 28. Morrissey M, Hooper D, Drechsler W, et al. Relationship of leg
mobility impairments: meniscal and articular cartilage lesions. muscle strength and knee function in the early period after anterior
J Orthop Sports Phys Ther 2010;40:A1–35. cruciate ligament reconstruction. Scand J Med Sci Sports 2004;14:
8. Khayambashi K, Mohammadkhani Z, Ghaznavi K, et al. The 360–6.
effects of isolated hip abductor and external rotator muscle 29. Becker R, Berth A, Nehring M, et al. Neuromuscular quadriceps
strengthening on pain, health status, and hip strength in females dysfunction prior to osteoarthritis of the knee. J Orthop Res
with patellofemoral pain: a randomized controlled trial. J Orthop 2004;22:768–73.
Sports Phys Ther 2012;42:22–9. 30. Risberg M, Holm I, Myklebust G, et al. Neuromuscular training
9. Zazulak B, Hewett T, Reeves N, et al. Deficits in neuromuscular versus strength training during the first 6 months after anterior
control of the trunk predict knee injury risk: a prospective cruciate ligament reconstruction: a randomised clinical trial. Phys
biomechanical-epidemiological study. Am J Sports Med 2007;35: Ther 2007;87:1–14.
1123–30. 31. Herrington L, Myer G, Horsley I. Task based rehabilitation pro-
10. Norcross M, Blackburn T, Goerger B, et al. The association tocol for elite athletes following anterior cruciate ligament recon-
between lower extremity energy absorption and biomechanical struction: a clinical commentary. Phys Ther Sport 2013;14:
factors related to anterior cruciate ligament injury. Clin Biomech 188–98.
2010;25:1031–6. 32. Angelozzi M, Madaama M, Corsica C, et al. Rate of force develop-
11. Grabiner M, Feuerbach J, Lundin T, et al. Visual guidance to force ment as an adjunctive outcome measure for return to sport deci-
plates does not influence ground reaction variability. J Biomech sions after anterior cruciate ligament reconstruction. J Orthop
1999;28:1115–17. Sports Phys Ther 2012;42:772–80.
12. Chaudhari A, Andriacchi T. The mechanical consequences of 33. Myer G, Martin L, Ford K, et al. No association from time from
dynamic frontal plane limb alignment for non-contact ACL injury. surgery with functional deficits in athletes after anterior cruciate
J Biomech 2006;39:330–8. ligament reconstruction. Am J Sports Med 2012;40:2256–63.
13. Fedie R, Caristedt K, Willson J, et al. Effect of attending to a ball 34. Di Stasi S, Myer G, Hewett T. Neuromuscular training to target
during a side cut maneuver on lower extremity biomechanics in deficits associated with second anterior cruciate ligament injury.
male and female athletes. Sports Biomech 2010;9:165–77. J Orthop Sports Phys Ther 2013;43:777–92.
14. Hurley M. The effects of joint damage on muscle function, pro- 35. Comfort P, Allen M, Graham-Smith P. Comparison of peak ground
prioception and rehabilitation. Man Ther 1997;2:11–17. reaction force and rate of force development during variations of
15. Palmieri-Smith R, Villwock M, Downie B, et al. Pain and effusion the power clean. J Strength Cond Res 2011;25:1235–9.
and quadriceps activation and strength. J Athl Train 2013;48: 36. Philippon M, Decker M, Giphart J, et al. Rehabilitation exercise
186–91. progression for the gluteus medius muscle with consideration for
16. Palmieri-Smith R, Thomas A, Woitys E. Maximising quadriceps iliopsoas tendinitis: an in-vivo electromyography study. Am J Sports
strength after ACL reconstruction. Clin Sports Med Med 2011;39:1777–85.
2009;27:405–24. 37. Hollman J, Hohl J, Kraft J, et al. Modulation of frontal plane
17. Hart J, Ingersoll C. Quadriceps EMG frequency content following kinematics by hip extensor strength and gluteus maximus recruit-
isometric lumbar extension. J Electromyogr Kinesiol 2010;20: ment during a jump landing task in healthy women. J Sport Rehabil
840–4. 2013;22:184–90.
18. Hopkins J, Ingersoll C, Edwards J, et al. Cryotherapy and transcu- 38. Homan K, Norcross M, Goerger B, et al. The influence of gluteal
taneous electric neuromuscular stimulation decrease arthrogenic activity and lower extremity kinematics. J Electromyogr Kinesiol
muscle inhibition of vastus medialis after knee joint effusion. J Athl 2013;23:411–15.
Train 2002;37:25–31. 39. Distefano L, Clark M, Padua D. Evidence supporting balance
19. Rice D, McNair P, Dalbeth N. Effects of cryotherapy on arthro- training in healthy individuals: a systematic review. J Strength Cond
genic muscle inhibition using an experimental model of knee swell- Res 2009;23:18–31.
ing. Arthritis Rheum 2009;61:78–83. 40. Cowling E, Steele J, McNair P. Effect of verbal instructions on
20. Jubeau M, Gondin J, Martin A, et al. Differences in twitch poten- muscle activity and risk of injury to the anterior cruciate ligament
tiation between voluntary and stimulated quadriceps contractions during landing. Br J Sports Med 2003;37:126–30.
of equal intensity Scand. Sand J Med Sci Sports 2009;30:1–7. 41. Milner C, Fairbrother J, Srivatsan A, et al. Simple verbal instruc-
21. Fitzgerald G, Piva S, Irrgang J. A modified neuromuscular electri- tion improves knee biomechanics during landing in female athletes.
cal stimulation protocol for quadriceps strength training following Knee 2012;19:399–403.
anterior cruciate ligament reconstruction. J Orthop Sports Phys 42. McCormick B. Task complexity and jump landings in injury
Ther 2003;33:492–501. prevention for basketball players. J Strength Cond Res 2012;34:
22. Hasegawa S, Kobayashi M, Arai T, et al. Effect of early implemen- 89–92.
tation of electrical muscle stimulation to prevent muscle atrophy 43. Verstegen M, Falsone S, Orr R, et al. Suggestions from the field
and weakness in patients after anterior cruciate ligament recon- for return to sports participation following anterior cruciate liga-
struction. J Electromyogr Kinesiol 2011;21:622–30. ment reconstruction: American football. J Orthop Sports Phys
23. Ediz L, Ceylan M, Turktas U, et al. A randomised controlled trial Ther 2012;42:337–44.
of electrostimulation effects on effusion, swelling and pain recovery 44. Herrington L, Comfort P. Training for prevention ACL injury:
after anterior cruciate reconstruction: a pilot study. Clin Rehabil incorporation of progressive landing skill challenges into a program.
2011;26:413–22. J Strength Cond Res 2013;35:59–65.
24. Aagaard P, Simonsen E, Andersen J, et al. Neural inhibition during 45. Whatman C, Hing W, Hulme P. Physiotherapist agreement when
maximal eccentric and concentric quadriceps contractions: effect of visually rating movement quality during lower extremity functional
resistance. J Appl Physiol 2000;89:2249–57. screening tests. Phys Ther Sport 2012;13:87–96.
25. Maitland M, Ajemain S, Suter E. Quadriceps femoris and ham- 46. Munro A, Herrington L. The effect of videotape augmented feed-
string muscle function in a person with an unstable knee. Phys Ther back on drop jump landing strategy: implications for anterior cruci-
1999;79:66–75. ate ligament and patellofemoral joint injury prevention. Knee
26. Lewek M, Rudolph K, Axe M, et al. The effect of insufficient 2014;21(5):891–5.
quadriceps strength on gait after anterior cruciate ligament recon- 47. Herrington L. The effects of 4 weeks of jump training on landing
struction. Clin Biomech 2002;17:56–63. knee valgus and crossover hop performance in female basketball
27. Schmitt L, Paterno M, Hewett T. The impact of quadriceps femoris players. J Strength Cond Res 2010;24:3427–32.
strength asymmetry on functional performance at return to sport
following anterior cruciate ligament reconstruction. J Orthop
Sports Phys Ther 2012;42:750–9.
528 PART IV  Overview of Contemporary Issues in Practice

CHAPTER 48.2  ■  PATELLOFEMORAL PAIN

Kay Crossley • Sallie Cowan • Bill Vicenzino

support this synergistic relationship between the vasti,

ARTICULAR AND MUSCLE CONTROL OF with studies demonstrating a relatively balanced relation-
THE PATELLOFEMORAL JOINT ship in terms of magnitude and timing of activation
during a wide variety of tasks.8,24–36
Anatomy and Motor Control of
the Patellofemoral Joint and Anatomy of Remote Structures and
Adjacent Structures Impact on the Patellofemoral Joint
The patellofemoral joint (PFJ) is the articulation between There are a number of other factors that may impact on
the patella and the femoral trochlea. The patella is a sesa- the PFJ – these include structures both proximal and
moid bone located within the patellar ligament, with five distal to the joint. Proximally, these factors include
facets that articulate with the femur. The geometry of femoral internal rotation,37–40 altered hip motor
these facets varies between individuals and may affect control,41,42 increased apparent knee valgus38,43,44 and
patellar tracking.1–3 In healthy individuals, aspects of the inadequate flexibility of hamstrings, ITB and tensor
femoral trochlea including its depth, as well as the shape fascia latae.40,45 Distally, factors include increased tibial
and height of the lateral trochlea, can affect patellar rotation, pronated foot type39 and inadequate flexibility
tracking.4–8 From 20–30° of knee flexion, the patella is of gastrocnemius.40
confined within the trochlea and hence, the bony joint
components provide inherent stability. However, outside
of this range there is little intrinsic bony support for the
patella and stability must be provided by other soft tissue
PATELLOFEMORAL PAIN
structures, both passively and actively. Background
Lateral passive support is provided by the fibrous
superficial and deep lateral retinacula. Fibrous expansions Patellofemoral pain (PFP) is the term for PFJ disorders
from vastus lateralis9 and the iliotibial band (ITB) con- that is preferred over synonyms such as anterior knee
tribute to these retinacula, with additional lateral support pain, patellofemoral pain syndrome and chondromalacia
provided by two distal components of the ITB.10,11 Since patellae.46 The prevalence of PFP is high in active popu-
most of the lateral retinaculum arises from the ITB, exces- lations39,45,47–51 and PFP frequently accounts for presenta-
sive lateral tracking may occur if the ITB is tight. Medi- tions to general medical52,53 and sports medicine49,54
ally, the retinaculum is thinner and is thought to be less practitioners. PFP generally refers to pain in the anterior
significant in influencing patellar tracking. Three liga- aspect of the knee (sometimes retro-patellar and occa-
ments described as joint capsule thickenings, the patello- sionally referring symptoms to the posterior aspects of
femoral, patellomeniscal and patellotibial ligaments, lie the knee). It is often referred to as a ‘diagnosis of exclu-
beneath the retinaculum.7 Of these, the medial patello- sion’, i.e. made when other potential sources of pain (e.g.
femoral ligament is the primary restraint to lateral patellar meniscal, patellar tendon) are ruled out. Nociception
translation, with the others thought to be less important.12–14 from any or all of the PFJ structures such as synovium,
Thus, the PFJ is inherently unstable and relies heavily subchondral bone55,56 or the infrapatellar fat pad57–59 may
on active stabilization via the muscular system. The most result in the individual experiencing pain.
important muscular support is provided by the quadri- Patellofemoral pain is mostly associated with activities
ceps, in particular vastus medialis and lateralis (VL). The that load the PFJ, such as stair ambulation, squatting,
vastus medialis is generally divided into two components rising from sitting and running. Both extrinsic and intrin-
– the vastus medialis obliquus (VMO) and the vastus sic factors can modulate PFJ load. Extrinsic factors are
medialis longus. While there is some conjecture as to those that affect the external forces exerted on the body
whether these are separate entities, most authors agree during weight-bearing activities (e.g. body mass, speed of
that the two components have differing functions due to gait, surfaces, footwear, frequency of loading). Factors
their fibre orientation, attachments and thus angle of related to the individual (intrinsic factors) can also influ-
force on the patella.15–20 The oblique alignment of VMO ence PFJ alignment and hence, the distribution of the
provides a mechanical advantage for stabilizing the PFJ loads (e.g. the geometry of the femoral trochlea,
patella, which counterbalances the larger cross-sectional increased foot pronation, increased femoral and tibial
area and thus force-producing capacity of VL. Indeed, rotation and increased tightness of the ITB, as described
studies indicate that while VMO is unable to extend the above).
knee on its own, it is active throughout knee extension
aiding in centralizing the patella within the trochlea and Evidence for Impairments in Local
enhancing the efficiency of VL.16,21,22 In addition, a recent
in vivo study demonstrated that improving VMO func-
Motor Control in Patellofemoral Pain
tion also reduces the load imposed on the lateral cartilage In people with PFP it is proposed that the normal
of the patellofemoral joint.23 Electromyographic studies balanced activation of VMO and VL is disrupted.
 48  The Knee: Introduction 529

Inadequate motor control of VMO may result in a lateral Perthes or other hip conditions, tumours, stress fractures,
shift of the patellar60 or an increase in lateral patellofemo- apophysitis, tendinopathies).
ral pressure.61 Indeed, individuals with PFP produce less
quadriceps torque than those without pain,62,63 but there The Role of Imaging
is controversy in the literature regarding an imbalance in
the magnitude of vasti activation in PFP.31–33,64–70 Dis- Imaging is rarely needed in the assessment of PFP. Radio-
rupted vasti motor control may also take the form of graphs and computerized tomography provide informa-
delayed activation of VMO relative to VL, and a number tion on the morphology of the joint and presence of
of studies have supported this line of thought and dem- osteoarthritis, in addition to screening for serious pathol-
onstrated a delay in both reflex onset time and electro- ogy if suspected. Magnetic resonance imaging provides
myographic activation of VMO relative to VL.31,70–76 greater information on the soft tissue structures and some
However, there is also some conflict with a number of of the newer sequences (T2 relaxation times and T1ρ)
authors describing no differences in electromyographic hold promise to evaluate the early stages of cartilage
onsets.32,33,67,70,77,78 These inconsistencies may in part be damage.94,95 Interpretation of imaging abnormalities must
accounted for by a wide variation in electromyographic always be considered alongside clinical test results.
methodology79 and the inherent heterogeneity in the
PFP population. Treatment
Evidence for Impairments in Remote Conservative treatments are the cornerstone of PFP
management. Effective treatments usually integrate tech-
Contributors to Patellofemoral Pain niques that target the local PFJ factors, in addition to the
Clinically, poor hip and pelvic muscle control are com- more remote (distal and proximal) factors. There are
monly addressed in the treatment of PFP, and evidence many different approaches that can be used to address
to support this association is increasing. Greater femoral these factors, including exercise, manual therapy, taping,
internal rotation has been associated with PFP80 and bracing and foot orthoses. In practice, many or all of
may contribute to its development.39 There is also evi- these approaches are used, in isolation or in combination,
dence for decreased hip abductor and rotator strength depending on the patient’s presentation, clinician’s exper-
in PFP,81–86 alteration in gluteus medius motor control,87– tise and the preferences of both patient and clinician.
89
decreased sagittal plane balance stability90 and
decreased trunk side flexion strength.88 However, not Exercise
all studies have described dysfunction in hip abductor
and external rotator strength or motor control in indi- Exercise forms a major part of PFP management and
viduals with PFP.88,91 Distally, excessive subtalar joint generally includes: (a) vasti retraining; (b) hip muscle
pronation92 has been linked with greater tibial segment93 retraining; (c) strengthening/endurance building for
and hip joint internal rotation. In addition, restricted lower limb and trunk muscles; (d) coordination and
ankle dorsiflexion is associated with decreased knee balance training; and (e) retraining of functional activities
flexion angles during squatting,93 which may be a risk (including sports- or work-related).
factor for PFP.39 However, it appears that the evidence 1. Vasti retraining is recommended to restore the
supporting distal impairments in people with PFP is motor control of the medial and lateral vasti.
less than for proximal.80 Retraining focuses on increasing the patient’s ability
to activate their VMO, ideally with little VL activ-
ity or lateral hamstring co-contraction. We can use
Assessment the principals of motor retraining, applied within
A comprehensive assessment of the PFJ should include a three phases: (a) formal motor skill training; (b)
thorough interview (history, symptom mapping and integration of skill into low-load tasks; and (c) pro-
description), physical examination and appropriate use of gression to higher load tasks.
investigations. No single test provides a definitive diag- Participants are taught to activate their VMO in
nosis of PFP and the findings from all aspects of assess- different positions (e.g. sitting, lying, standing) or
ment are considered. different degrees of knee flexion, hip abduction or
knee rotation. Many patients need a variety of strat-
egies to assist VMO activation, including imagery
Key Clinical Diagnostic Features
or visual cues, facilitation techniques (e.g. palpa-
of Patellofemoral Pain
tion, taping, dry needles/acupuncture, feedback
Key diagnostic features and clinical tests are described in [e.g. surface EMG, real-time ultrasound, tactile or
Table 48-1. Note that the diagnostic accuracy of the clini- visual]), or inhibitory techniques to reduce over-
cal tests for PFP are not well established and a compre- activity in the VL or lateral hamstrings (e.g. inhibi-
hensive physical examination of other potential pain tory taping, feedback).
sources such as other knee structures, hip joint, lumbar After mastering the ability to achieve and maintain
spine and other surrounding soft tissues is also required. a VMO contraction, the patient is progressed
In addition, all patients presenting with anterior knee through tasks, based on their ability to maintain
pain should be assessed for other conditions (e.g. osteo- control and the absence of significant pain. The
chondritis dissecans, slipped capital femoral epiphysis, absence of significant pain can be measured with
530 PART IV  Overview of Contemporary Issues in Practice

TABLE 48-1  Key Clinical Diagnostic Features of Patellofemoral Pain

Clinical Diagnostic Features Specific to Patellofemoral Pain
Interview
Area of pain Usually anterior, but might be medial, lateral or infrapatellar. Pain is frequently vague or not
specific to a palpable structure
Aggravating factors Activities that load the PFJ – such as stair climbing, prolonged sitting with knee flexion or rising
from sitting, squatting, lunging, running (especially downhill)
Noises/other May have clicks, clunks or crepitus
symptoms May report giving way. Possibly due to subluxation or quadriceps muscle inhibition
Loading history Often insidious, may occur after change in loading/activity or following acute knee injury
Physical Examination
Observation – standing VMO wasting may be obvious, might observe alterations in motor control; generalized
quadriceps wasting or weakness might be present
Altered static alignment/postures may be evident (e.g. femoral internal rotation, knee valgus, foot
pronated with lowered medial longitudinal arch)
Observation-functional Global deficits might be evident during simple tasks (e.g. walking), or only be evident in higher
tasks loaded tasks (e.g. running, hopping or single-leg squat). Frequent deficits include:
• Loss of knee flexion control during weight acceptance phase
• Poor control of trunk and pelvis
• Poor control of femoral internal rotation (observed as apparent knee valgus)
• Poor control of foot alignment (e.g. excessively pronated)
Functional loading Activities that load the PFJ (e.g. single-leg squat, hop or stairs) will aggravate pain
tasks PFJ taping often decreases pain
Palpation Tenderness on medial or lateral facets of patella, might be tender in infrapatellar (including fat
pad) region or may have no tenderness
ITB lateral retinaculum might be tender/tight on palpation
Might have effusion, usually small supra- or infrapatellar soft tissue swelling
Knee range of motion Most commonly normal, occasionally restricted when severe
PFJ movement Might be malaligned (e.g. laterally tilted and positioned)
Movements are often restricted – could be in any direction but commonly on medial glide
Flexibility May have loss of flexibility – hamstrings and quadriceps, but also ITB, iliopsoas and triceps surae
Strength Specific loss of control might be evident (e.g. VMO/quadriceps, hip external rotators), but must
assess for more global loss of strength (including trunk and hip musles, triceps surae)

ITB, Iliotibial band; PFJ, Patellofemoral joint; VMO, vastus medialis obliquus.

the pain monitoring system96 (where pain is 3. Lower limb muscle strengthening/endurance build-
recorded on a 10-cm visual analogue scale) and pain ing is likely to be necessary for all patients. Ade-
levels of 0–2 are considered safe. Pain levels up to quate strength and endurance are needed, especially
5 momentarily during exercise or immediately fol- in the quadriceps, hip muscles, trunk muscles and
lowing exercise are acceptable, but not extending to triceps surae. Strengthening programmes may be
the following morning. Examples of low-load tasks commenced early (see above for maintaining
include lunges, squats and step ups (Fig. 48-5A–D). control and monitoring pain) and progressed
For these tasks, further progressions can be made according to patient response and American College
from minimal weight bearing (using hand rails or of Sports Medicine guidelines.97 For many patients,
other supports) to full weight bearing (and eventu- a generalized strengthening programme alone can
ally added loading) and through various knee flexion result in reduced pain and improved function.
ranges (Fig. 48-5E–H). However, patients with poor vasti or gluteal coor-
2. Hip muscle retraining may be required to improve dination may be unable to progress through a
motor control of the hip abductors, external rota- strengthening programme without first addressing
tors and extensors. The principles are the same as their motor control deficits.
for vasti retraining, and the two programmes are 4. Coordination and balance training is essential to
easily integrated, such that the gluteal muscles are restore lower limb function. This retraining is gen-
activated in a coordinated manner with the VMO erally combined with other exercise prescription
during tasks such as lunge, squat and step (Fig. and will involve a variety of tasks.
48-5C–H). The hip abductors and external rotators 5. Retraining of functional activities is usually the final
work to maintain a level pelvis and hence, simple stage of the exercise-based interventions. People
instructions may be used during exercises includ- with PFP may need to return to high loaded activi-
ing: ‘keep the pelvis level/horizontal’ (to control hip ties, which involve knee flexion during full weight
adduction) and ‘keep the knee centre over the foot bearing (e.g. stair descent, deep squats), or higher
centre’ (to control femoral internal rotation). intensity activities such as running. In order to
 48  The Knee: Introduction 531

A B C D

E F G H

FIGURE 48-5  ■  Vasti retraining. Activation of vastus medialis obliquus in different positions, including low and higher loading activi-
ties. (A) Retraining focuses on increasing the patient’s ability to activate their vastus medialis obliquus, ideally with little vastus
lateralis activity or lateral hamstring co-contraction. (B) Progressing to low-load activity (e.g. partial weight-bearing lunge), maintain-
ing feedback on activation, as well as position of knee and hip, relative to foot. (C) Double-leg squat. (D) Step up. (E) Single-leg step
down. (F) Step up with additional loads. (G) Single-leg squat/balance. (H) Combine gluteal and vasti control with balance and
proprioception.

progress to these high PFJ loaded activities, patients cutaneous/proprioceptive input. Regardless of the mech-
need additional training. They need to train their anism, patellar tape provides temporary pain relief that
motor control, strength and endurance in the quad- can be used to improve compliance and performance with
riceps and global muscles (e.g. triceps surae, hip and an exercise programme and enable pain-free activities of
trunk muscles), balance and coordination in these daily living (e.g. stairs), work or sports. The commonly
higher loading tasks. The choice of exercise and used taping techniques (Fig. 48-6A) to reduce pain
decisions to progress are based on the patient’s include: (a) medial glide; (b) medial tilt; (c) fat pad unload-
needs, their ability to maintain control and the ing; (d) superior tilt; or (e) rotation. Adverse skin reac-
absence of significant pain. tions are frequently encountered and are best avoided
with the use of adhesive gauze (e.g. Fixomull,™ Smith &
Taping Nephew), skin preparation (protective barrier or plastic
skin) and advice not to remove the tape too quickly.
Patellar taping has been used to manage PFP since it was An alternative taping technique is to tape the tibia into
first described by Jenny McConnell in 1986.98 While a relative internal rotation on the femur (or relative exter-
researchers and clinicians agree that patellar tape can nal rotation of the femur on the tibia)101 (Fig. 48-6B).
effectively reduce a patient’s pain, the mechanisms under- This particular technique is based on the premise that
pinning these taping effects still remain unclear. It is internal rotation of the knee will reduce the Q-angle and
likely that positive benefits are imparted partly due to lower stresses in the PFJ. As for the patellar taping tech-
subtle changes in patellar position and PFJ contact area99 niques, test–re-test of a symptom provocative physical
and partly due to changes in motor control,100 or task (e.g. stair climbing, squatting) with and without the
532 PART IV  Overview of Contemporary Issues in Practice

A B C

FIGURE 48-6  ■  Taping and manual therapy. (A) Patellofemoral taping: medial glide. (B) Mulligan tibiofemoral taping. Taping the tibia
into relative internal rotation on the femur. (C) Self patellofemoral mobilizations. Tilting the medial border of the patella posteriorly
(i.e. medial tilt).

tape in situ can be used by clinicians to evaluate the

appropriateness of using this technique in any specific
individual patient.

Manual Therapy
Manual therapy for PFP involves joint and soft tissue
mobilization, manipulation and massage. Joint mobiliza-
tions might include manual gliding techniques of the
patellofemoral or tibiofemoral joints, whereas soft tissue
therapies could involve friction massage of tight lateral
retinacula structures and deep tissue massage or myofas-
cial release massage applied to the fascia/muscles of the
thigh (predominantly anterolateral). The emphasis is on
sustained loading of the soft tissues,102 usually in a posi-
tion that lengthens the treated soft tissues (e.g. for lateral
retinacula structures: medial tilt of patella, tibiofemoral
joint in approximately 30–90° flexion (Fig. 48-6C). FIGURE 48-7  ■  Anti-pronation foot taping. Symptom modification
test–re–test approach of assessing the potential benefit of foot
Applied passively by either the patient or clinician, these orthoses, in this case using some reverse 6 anti-pronation tape.
techniques are designed to optimize movement and
facilitate the exercise programme. Studies evaluating
efficacy of such techniques applied in isolation show a difference in mid foot width between weight bearing and
lack of benefit,103 which supports the common clinical non-weight bearing.106 Currently this evidence is difficult
practice that manual therapy is seldom or never done in for the clinician to directly apply to an individual patient.
isolation. To decide if a patient is likely to benefit from a foot
orthosis, the clinician might consider using a test–re–test
approach of observing a symptom-provocative physical
Foot Orthoses
task (e.g. stair climbing, jogging) without and with an
In-shoe foot orthoses have been recommended as a treat- anti-pronation foot taping technique (Fig. 48-7) or a
ment option for PFP. This is based on the premise that temporary orthosis.107 A substantial improvement in the
these devices reduce the amount of foot pronation and patient’s ability to perform the symptom-provocative task
hence, tibial rotation.104 In so doing, these devices reverse could indicate a potential benefit of foot orthoses. Pre-
part of the abnormal biomechanics often associated with liminary evidence also suggests that immediate improve-
PFP. Their application in isolation is clinically not ments with foot orthoses predict beneficial effects 12
uncommon, but evidence indicates that their effect is weeks later.108
optimized if delivered as part of a multimodal manage-
ment care plan.103 Effectiveness of Treatments
There is preliminary, low-level evidence indicating
that a favourable response to foot orthoses occurs in There is considerable evidence for the efficacy of differ-
those with greater peak rear foot eversion105 or greater ent treatment approaches for PFP. Systematic reviews
 48  The Knee: Introduction 533

and meta-analyses provide level I evidence for the use of more likely (odds ratio 2.31, 95% confidence interval
multimodal interventions (combination of retraining, 1.37–3.88) to report having had patellofemoral pain as an
strengthening, balance/coordination, functional retrain- adolescent than those patients undergoing an arthro-
ing, taping and manual therapy)103 and also for individual plasty for isolated tibiofemoral osteoarthritis. Clearly,
treatments in isolation.100,103,109 Recent reviews conclude more research is required to confirm the link between
that tailored patellar taping immediately reduces pain PFP and patellofemoral osteoarthritis, but recent reports
with a large effect, while other techniques have only small using newer imaging sequences report adverse changes
(untailored medial patellar taping) or negligible (Kinesio (T1ρ relaxation times) in the patellar cartilage of patients
Tape® Tex) effects on pain in the immediate term.100 with patellofemoral pain that correlate strongly with the
There is limited evidence for better short-term outcomes severity of patellar tilt.94 Also, Farrokhi et al.124 identified
with foot orthoses versus flat inserts,103,109 versus wait and elevated patellofemoral stress in people with PFP as a
see110 and beneficial effects for exercise (versus control), potential mechanism underpinning a link between PFP
closed chain exercises (versus open chain exercises) and and structural joint disease. Until studies identify whether
acupuncture (versus control).108 While there is no level I PFP and patellofemoral osteoarthritis exist along a con-
evidence for the use of hip strengthening for PFP, recent tinuum of disease, clinicians who treat patients with per-
randomized controlled trials (level II evidence) support sistent PFP should consider the possibility of early
the use of hip-strengthening programmes to reduce pain degenerative joint changes.
and improve function.111,112 However, there is moderate
evidence for no additive effectiveness of knee braces to
exercise therapy on pain and conflicting evidence on CONTROVERSIES, UNCERTAINTIES
function.113 AND FUTURE DIRECTIONS
The evidence suggests that, in implementing evidence-
based practice for the conservative management of PFP, Patellofemoral chondral/cartilage lesions are problematic
clinicians can employ a multimodal treatment, or indi- and fairly common among young adults with PFP. While
vidual components (except bracing), based on patient a number of surgical treatment options are available,
preferences and presentations and clinician preferences including microfracture, autologous or juvenile chondro-
and expertise. cyte implantation, osteochondral autograft transfer and
osteochondral allograft implantation, there is a paucity of
evidence for their effectiveness. Additionally, non-surgical
EMERGING ISSUES AND approaches are increasingly being used. These include
NEW ADVANCES injections of hyaluronic acid, platelet-rich plasma or
other cytokines concentrated from autologous blood125
Hip muscle dysfunction has long been identified as a and stem cells.
feature of PFP41,42 and there are an increasing number of Basic science, pre-clinical and clinical studies suggest
studies evaluating the effects of hip-strengthening proto- a promising role for platelet-rich plasma injections for
cols for the treatment of PFP. However, due to the cartilage injuries and joint pain. However, the specifics
imprecise relationship between hip strength and biome- of platelet-rich plasma treatment, including the volume
chanics, and evidence that hip biomechanics are better of plasma, number of injections and intervening interval,
predictors of PFP than hip strength,114,115 one emerging have not yet been optimized. Clinical acceptance of
area of research centres on the retraining of movement platelet-rich plasma therapies has occurred quickly,
patterns. This emerging area of clinically relevant probably because of both the safety profile and the
research consists of employing strategies that change relative ease of preparation. However, there is no high-
lower limb biomechanics, such as using a variety of feed- quality evidence that supports its extensive clinical use.125
back methods from real-time gait analysis systems116 to Similarly, the clinical evidence for other injection treat-
mirrors,117 changing stride frequency118 and running ments is currently lacking.
barefoot.119 While such techniques show promise for There are many new directions in the management of
patients with aberrant lower limb biomechanics, further PFP. Perhaps the most relevant area will be the move to
research is required to test the efficacy of these pro- develop interventions that are more targeted to the
grammes. Also, as advances are made in low-cost tech- patient.
nologies (e.g. Nintendo Wii,® Microsoft Kinect,® ViMove
by DorsaVi®) it may be possible to use such devices to REFERENCES
provide real-time feedback to retrain movement in the 1. Ahmed AM, Burke DL, Hyder A. Force analysis of the patellar
clinic or home. mechanism. J Orthop Res 1987;5:69–85.
Another significant paradigm shift in the field of PFP, 2. van Kampen A, Huiskes R. Three dimensional tracking pattern of
the human patella. J Orthop Res 1990;8:372–82.
has been the awareness that the natural history of PFP is 3. Heegaard J, Leyvrax PF, van Kampen A, et al. Contribution of
not one of spontaneous recovery in a proportion of those joint geometry and soft tissue structures on patellar stability. Trans
with PFP.120,121 Most notably, there is increasing specula- Orthop Res 1994;40:667.
tion that PFP may be a prelude to patellofemoral osteo- 4. Farahmand F, Tahmasbi MN, Amis AA. Lateral force-displacement
arthritis.120,122 While no current studies have prospectively behavious of the human patella and its variation with knee
flexion – a biomechanical study in vitro. J Biomech 1998;31:
studied people with PFP to verify this relationship, a 1147–52.
case-control study123 observed that individuals undergo- 5. Grelsamer RP, Klein JR. The biomechanics of the patellofemoral
ing an arthroplasty for patellofemoral osteoarthritis were joint. J Orhop Sports Phys Ther 1998;28(5):286–97.
534 PART IV  Overview of Contemporary Issues in Practice

6. Senavongse W, Tantisatirapong T. Patellofemoral joint instability: 32. Morrish GM, Woledge RC. A comparison of the activation of
a biomechanical study. Int J Appl Biomed Eng 2008;1(1): muscles moving the patella in normal subjects and in patients with
61–4. chronic patellofemoral problems. Scand J Rehabil Med 1997;29(1):
7. Fulkerson JP, Shea KP. Current concepts review: disorder of patel- 43–8.
lofemoral alignment. J Bone Joint Surg Am 1990;72A:1424–9. 33. Powers CM, Landel RF, Perry J. Timing and intensity of vastus
8. Reynolds L, Levin T, Medeiros J, et al. EMG activity of vastus muscle activity during functional activities in subjects with and
medialis obliquus and vastus lateralis and there role in patella without patellofemoral pain. Phys Ther 1996;76:946–55.
alignment. Am J Phys Med 1983;62:61. 34. Signorile JF, Kacsik D, Perry A, et al. The effect of knee and foot
9. Reider B, Marshall JL, Koslin D, et al. The anterior aspect of the position on the electromyographical activity of the superficial
knee joint. J Bone Joint Surg Am 1981;63A:351–6. quadriceps. J Orthop Sports Phys Ther 1995;22(1):2–9.
10. Terry GC, Hughston JC, Norwood LA. The anatomy of the ilio- 35. Smith GP, Howe TE, Oldham JA, et al. Assessing quadriceps
patellar band and iliotibial tract. Am J Sports Med 1986;14:39–45. muscles recruitment order using rectified averaged surface EMG
11. Williams PL, Warwick R. Grays Anatomy. 36th ed. Edinburgh: in young normals and ‘weak’ and healthy elderly subjects. Clin
Churchill Livingstone; 1980. Rehabil 1995;9(1):40–6.
12. Conlan T, Garth WP, Lemons JE. Evaluation of the medial soft- 36. Wild JJ, Franklin TD, Woods GW. Patellar pain and quadriceps
tissue restraints of the extensor mechanism of the knee. J Bone rehabilitation: an EMG study. Am J Sports Med 1982;10:12–15.
Joint Surg Am 1993;75A:682–93. 37. Noehren B, Pohl MB, Sanchez Z, et al. Proximal and distal kine-
13. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral matics in female runners with patellofemoral pain. Clin Biomech
patellar translation in the human knee. Am J Sports Med 2012;27(4):366–71. PubMed PMID: 22071426.
1998;26(1):59–65. 38. Barton CJ, Levinger P, Webster KE, et al. Walking kinematics in
14. Hautamaa PV, Fithian DC, Kaufman KR, et al. Medial soft tissue individuals with patellofemoral pain syndrome: a case control
restraints in lateral patellar instability and repair. Clin Orthop study. Gait Posture 2011;33(2):386–91.
Relat Res 1998;349:174–82. 39. Boling M, Padua D, Marshall S, et al. A prospective investigation
15. Bose K, Kanagasuntherum R, Osman M. Vastus medialis oblique: of biomechanical risk factors for patellofemoral pain syndrome.
an anatomical and physiological study. Orthopaedics 1980;3: Am J Sports Med 2009;37(11):2108–16.
880–90. 40. Grayson TH. Disorders of the Patellofemoral Joint. 2nd ed. Bal-
16. Lieb FJ, Perry J. Quadriceps function. J Bone Joint Surg Am timore: Williams and Wilkins; 1990.
1968;50-A:1535–48. 41. Powers CM. The influence of altered lower-extremity kinematics
17. Raimondo RA, Ahmad CS, Blankevoort L, et al. Patellar stabiliza- on patellofemoral joint dysfunction: a theoretical perspective.
tion – a quantitative evaluation of the vastus medialis obliquus J Orthop Sports Phys Ther 2003;33(11):639–46. PubMed PMID:
muscle. Orthopedics 1998;21(7):791–5. WOS:000186785000002.
18. Scharf W, Weinstable R, Othrner E. Anatomical separation and 42. Prins MR, van der Wurff P. Females with patellofemoral pain
clinical importance of two different parts of the vastus medialis syndrome have weak hip muscles: a systematic review. Aust J
muscle. Acta Anat 1985;123:108–11. Physiother 2009;55:9–15.
19. Thiranagama R. Nerve supply of the human vastus medialis 43. Messier S, Davis S, Curl W, et al. Etiological factors associated
muscle. J Anat 1990;170:193–8. with patellofemoral pain in runners. Med Sci Sports Exerc
20. Amis AA, Senavongse W, Bull AM. Patellofemoral kinematics 1991;23(9):1008–15.
during knee flexion–extension: an in vitro study. J Orthop Res 44. Callaghan MJ. What does proprioception testing tell us about
2006;24:2201–11. patellofemoral pain? Man Ther 2011;16(1):46–7. [Epub
21. Bull AMJ, Senavongse WW, Taylor AR, et al., editors. The Effect 2010/08/13. eng]; PubMed PMID: 20702131.
of the Oblique Portions of the Vastus Medialis and Lateralis on 45. Witvrouw E, Lysens R, Bellemans J, et al. Intrinsic risk factors for
Patellar Tracking. 11th Conference of the ESB; 1998; Toulouse, the development of anterior knee pain in an athletic population.
France. A two-year prospective study. Am J Sports Med 2000;28(4):480–9.
22. Goh JCH, Lee PYC, Bose K. A cadaver study of the function of PubMed PMID: 10921638.
the oblique part of vastus medialis. J Bone Joint Surg Am 1995;2: 46. Davis IS, Powers CM. Patellofemoral pain syndrome: proximal,
225–31. distal, and local factors, an international retreat, April 30-May 2,
23. Elias JJ, Kilambi S, Goerke DR, et al. Improving vastus medialis 2009, Fells Point, Baltimore, MD. J Orthop Sports Phys Ther
obliquus function reduces pressure applied to lateral patellofemo- 2010;40(3):A1–16.
ral cartilage. J Orthop Res 2009;27:578–83. 47. Rathleff MS, Roos EM, Olesen JL, et al. Lower mechanical pres-
24. Spairani L, Barbero M, Cescon C, et al. An electromyographic sure pain thresholds in female adolescents with patellofemoral
study of the vastii muscles during open and closed kinetic chain pain syndrome. J Orthop Sports Phys Ther 2013;43(6):414–21.
submaximal isometric exercises. Int J Sports Phys Ther 2012; [Epub 2013/03/20. eng]; PubMed PMID: 23508216.
7(6):617–26. 48. Barber Foss KD, Myer GD, Chen SS, et al. Expected prevalence
25. Duffell LD, Dharni H, Strutton PH, et al. Electromyographic from the differential diagnosis of anterior knee pain in adolescent
activity of the quadriceps components during the final degrees of female athletes during preparticipation screening. J Athl Train
knee extension. J Back Musculoskeletal Rehabil 2011;24(4): 2012;47(5):519–24. [Epub 2012/10/17. eng]; PubMed PMID:
215–23. 23068589. Pubmed Central PMCID: 3465032.
26. Brownstein BA, Lamb RL, Mangine RE. Quadriceps torque and 49. Taunton JE, Ryan MB, Clement DB, et al. A retrospective case-
integrated eletromyography. J Orthop Sports Phys Ther control analysis of 2002 running injuries. Br J Sports Med
1985;6:309–14. 2002;36:95–101.
27. Gryzlo SM, Patek RM, Pink M, et al. Electromyographic analysis 50. Van Tiggelen D, Cowan S, Coorevits P, et al. Delayed vastus
of knee rehabilitation exercises. J Orthop Sports Phys Ther medialis obliquus to vastus lateralis onset timing contributes to
1994;20:36–43. the development of patellofemoral pain in previously healthy men.
28. Isear JA, Erickson JC, Worrell TW. EMG analysis of lower Am J Sports Med 2009;37(6):1099–105.
extremity muscle recruitment patterns during an unloaded squat. 51. Duvigneaud N, Bernard E, Stevens V, et al. Isokinetic assessment
Med Sci Sports Exerc 1997;29(4):532–9. of patellofemoral pain syndrome: a prospective study in female
29. Karst GM, Willett GM. Reflex response times of vastus medialis recruits. Isokinet Exerc Sci 2008;16(4):213–19. PubMed PMID:
oblique and vastus lateralis in normal subjects and in subjects with ISI:000262452000002. [English].
patellofemoral pain – letter of response. J Orthop Sports Phys 52. van Middelkoop M, van Linschoten R, Berger MY, et al. Knee
Ther 1997;26(2):108–9. complaints seen in general practice: active sport participants
30. Lange GW, Hintermeister RA, Schlegel T, et al. Electromyo- versus non-sport participants. BMC Musculoskelet Disord
graphic and kinematic analysis of graded treadmill walking and 2008;9:36. PubMed PMID: ISI:000254554000001.
the implications for knee rehabilitation. J Orthop Sports Phys 53. Wood L, Muller S, Peat G. The epidemiology of patellofemoral
Ther 1996;23(5):294–301. disorders in adulthood: a review of routine general practice
31. Mariano P, Caruso I. An electromyographic investigation of sub- morbidity recording. Prim Health Care Res Dev 2011;12(2):
luxation of the patella. J Bone Joint Surg Am 1979;61:169–71. 157–64.
 48  The Knee: Introduction 535

54. Baquie P, Brukner P. Injuries presenting to an Australian sports postural task. Arch Phys Med Rehabil 2002;83(7):989–95. PubMed
medicine centre: a 12 month study. Clin J Sport Med 1997;7: PMID: ISI:000176600700017.
28–31. 77. Grabiner MD, Koh MA, Von Haefen I. Effect of concomitant hip
55. Insall J, Falvo KA, Wise DW. Chondromalacia Patellae. A pro- joint adduction and knee joint extension forces on quadriceps
spective study. J Bone Joint Surg Am 1976;58(1):1–8. activation. Eur J Exp Musculoskeletal Res 1992;1:155–60.
56. Fulkerson JP. Diagnosis and treatment of patients with patello- 78. Karst GM, Willett GM. Onset timing of electromyographic activ-
femoral pain. Am J Sports Med 2002;30(3):447–56. ity in the vastus medialis oblique and vastus lateralis muscles in
57. Tsirbas A, Paterson RS, Keene GCR. Fat pad impingement: a subjects with and without patellofemoral pain syndrome. Phys
missed cause of patello femoral pain? Aust J Sci Med Sport Ther 1995;75(9):813–23.
1990;December:24–6. 79. Chester R, Smith T, Sweeting D, et al. The relative timing of
58. Fulkerson JP. Disorders of the Patellofemoral Joint. 3rd ed. Bal- VMO and VL in the aetiology of anterior knee pain: a systematic
timore: Williams & Wilkins; 1997. review and meta-analysis. BMC Musculoskelet Disord 2008;9:64.
59. Matthews LS, Sonstegard DA, Henke JA. Load bearing charac- 80. Barton CJ, Levinger P, Menz HB, et al. Kinematic gait character-
teristics of the patello-femoral joint. Acta Orthop 1977;48(5): istics associated with patellofemoral pain syndrome: a systematic
511–16. review. Gait Posture 2009;30(4):405–16. PubMed PMID: WOS:
60. Sakai N, Lou Z-P, Rand JA, et al. The influence of weakness in 000273040200002.
the vastus medialis oblique muscle on the patellofemoral joint: an 81. Magalhaes E, Abdalla R, Fukuda T, et al. A comparison of hip
in vitro biomechanical study. Clin Biomech 2000;15:335–9. strength between sedentary females with and without patello-
61. Neptune RR, Wright IC, van den Bogert AJ. The influence of femoral pain syndrome. J Orthop Sports Phys Ther 2010;
orthotic devices and vastus medialis strength and timing on patel- 40:641–7.
lofemoral loads during running. Clin Biomech 2000;15(8):611–18. 82. Nakagawa T, Moriya E, Maciel C, et al. Trunk, pelvis, hip, and
[Epub 2000/08/11. eng]; PubMed PMID: 10936434. knee kinematics, hip strength, and gluteal muscle activation
62. Powers CM, Perry J, Hsu A, et al. Are patellofemoral pain and during a single-leg squat in males and females with and without
quadriceps femoris muscle torque associated with locomotor func- patellofemoral pain syndrome. J Orthop Sports Phys Ther
tion? Phys Ther 1997;77(10):1063–75. 2012;42:491–501.
63. Thomee R, Renstrom P, Karlsson J, et al. Patellofemoral pain 83. Ireland ML, Willson JD, Ballantyne BT, et al. Hip strength in
syndrome in young women. II. Muscle function in patients and females with and without patellofemoral pain. J Orthop Sports
healthy controls. Scand J Med Sci Sports 1995;5:245–51. Phys Ther 2003;33(11):671–6. [Epub 2003/12/13. eng]; PubMed
64. Boucher J, King M, Lefebre R, et al. Qudriceps femoris muscle PMID: 14669962.
activity in patellofemoral pain syndrome. Am J Sports Med 1992; 84. Cichanowski HR, Schmitt JS, Johnson RJ, et al. Hip strength
20(5):527–32. in collegiate female athletes with patellofemoral pain. Med
65. Petschnig R, Baron R, Engel A, et al. Objectivation of the effects Sci Sports Exerc 2007;39(8):1227–32. PubMed PMID: ISI:
of knee problems on vastus medialis and vastus lateralis with EMG 000248581500004.
and dynamometry. Phys Med Rehabil 1991;2:50–4. 85. Robinson R, Nee RJ. Analysis of hip strength in females seeking
66. Miller JP. Vastus medialis obliquus and vastus lateralis activity in physical therapy treatment for unilateral patellofemoral pain syn-
patients with and without patellofemoral pain syndrome. J Sport drome. J Orthop Sports Phys Ther 2007;37(5):232–8.
Rehabil 1997;6:1–10. 86. Bolgla LA, Malone TM, Umberger BR, et al. Hip strength and
67. Sheehy P, Burdett RC, Irrgang JJ, et al. An electromyographic hip and knee kinematics during stair descent in females with and
study of vastus medialis oblique and vastus lateralis activity while without patellofemoral pain syndrome. J Orthop Sports Phys
ascending and descending steps. J Orthop Sports Phys Ther Ther 2008;38(1):12–18.
1998;27:423–9. 87. Aminaka N, Pietrosimone BG, Armstrong CW, et al. Patellofemo-
68. Coqueiro K, Bevilaqua-Grossi D, Berzin F, et al. Analysis on the ral pain syndrome alters neuromuscular control and kinetics during
activation of the VMO and VLL muscles during semisquat exercises stair ambulation. J Electromyogr Kinesiol 2011;21:645–51.
with and without hip adduction in individuals with patellofemoral 88. Cowan SM, Crossley KM, Bennell KL. Altered hip and trunk
pain syndrome. J Electromyogr Kinesiol 2005;15:596–603. muscle function in individuals with patellofemoral pain. Br J
69. Souza DR, Gross M. Comparison of vastus medialis obliquus: Sports Med 2009;43(8):584–8. [Epub 2008/10/08. eng]; PubMed
vastus lateralis muscle integrated electromyographic ratios PMID: 18838402.
between healthy subjects and patients with patellofemoral pain. 89. Brindle TJ, Mattacola C, McCrory J. Electromyographic changes
Phys Ther 1991;71(4):310–20. in the gluteus medius during stair ascent and descent in subjects
70. Cavazzuti L, Merlo A, Orlandi F, et al. Delayed onset of electro- with anterior knee pain. Knee Surg Sports Traumatol Arthrosc
myographic activity of vastus medialis obliquus relative to vastus 2003;11(4):244–51. [Epub 2003/04/16. eng]; PubMed PMID:
lateralis in subjects with patellofemoral pain syndrome. Gait 12695878.
Posture 2010;32:290–5. 90. Negahban H, Etemadi M, Naghibi S, et al. The effects of muscle
71. Cesarelli M, Bifulco P, Bracale M. Study of the control strategy fatigue on dynamic standing balance in people with and without
of the quadriceps in anterior knee pain. IEEE Trans Rehabil Eng patellofemoral pain syndrome. Gait Posture 2013;37(3):336–9.
2000;8:330–41. 91. Hollman JH, Galardi CM, Lin I-H, et al. Frontal and transverse
72. Cowan SM, Bennell KL, Hodges PW, et al. Delayed onset of plane hip kinematics and gluteus maximus recruitment correlate
electromyographic activity of vastus medialis obliquus relative to with frontal plane knee kinematics during single-leg squat tests in
vastus lateralis in subjects with patellofemoral pain syndrome. women. Clin Biomech 2014;29:468–74.
Arch Phys Med Rehabil 2001;82(2):183–9. [Epub 2001/03/10. 92. Tiberio D. The effect of excessive subtalar joint pronation on
eng]; PubMed PMID: 11239308. patellofemoral mechanics: a theoretical model. J Orthop Sports
73. Perez PL, Gossman MR, Lechner D, et al., editors. Electromyo- Phys Ther 1987;9(4):160–5. [Epub 1987/01/01. eng]; PubMed
graphic Temporal Characteristics of the Vastus Medialis Oblique PMID: 18797010.
and the Vastus Lateralis in Women with and without Patellofemo- 93. Macrum E, Bell DR, Boling M, et al. Effect of limiting ankle-
ral Pain. 12th International Congress of the World Confederation dorsiflexion range of motion on lower extremity kinematics and
for Physical Therapy; 1995; Washington, DC, U.S.A. muscle-activation patterns during a squat. J Sport Rehabil
74. Witvrouw E, Delvaux K, Lysens R, et al. Reflex response times of 2012;21(2):144–50.
vastus medialis oblique and vastus lateralis in normal subjects and 94. Thuillier DU, Souza RB, Wu S, et al. T1r imaging demonstrates
in subjects with patellofemoral pain – response. J Orthop Sports early changes in the lateral patella in patients with patellofemoral
Phys Ther 1997;26(2):109–10. pain and maltracking. Am J Sports Med 2013;41(8):1813–18.
75. Voight M, Weider D. Comparative reflex response times of the 95. Li X, Benjamin C, Link TM, et al. In vivo T1r and T2 mapping
vastus medialis and the vastus lateralis in normal subjects and of articular cartilage in osteoarthritis of the knee using 3T MRI.
subjects with extensor mechanism dysfunction. Am J Sports Med Osteoarthritis Cartilage 2007;15:789–97.
1991;10:131–7. 96. Thomee R. A comprehensive treatment approach for patellofemo-
76. Cowan SM, Hodges PW, Bennell KL, et al. Altered vastii recruit- ral pain syndrome in young women. Phys Ther 1997;77(12):
ment when people with patellofemoral pain syndrome complete a 1690–703.
536 PART IV  Overview of Contemporary Issues in Practice

97. Garber CE, Blissmer B, Deschenes MR, et al. Quantity and patellofemoral pain syndrome: a randomized controlled clinical
quality of exercise for developing and maintaining cardiorespira- trial with 1-year follow-up. J Orthop Sports Phys Ther
tory, musculoskeletal, and neuromotor fitness in apparently 2012;42(10):823–30.
healthy adults: guidance for prescribing exercise. Med Sci Sports 112. Khayambashi K, Mohammadkhani Z, Ghaznavi K, et al. The
Exerc 2011;43(7):1334–59. effects of isolated hip abductor and external rotator muscle
98. McConnell J. The management of chondromalacia patellae: a strengthening on pain, health status, and hip strength in females
long term solution. Aust J Physiother 1986;32(4):215–23. with patellofemoral pain: a randomized controlled trial. J Orthop
99. Crossley KM, Cowan SM, Bennell KL, et al. Patellar taping: is Sports Phys Ther 2012;42(1):22–9.
clinical success supported by scientific evidence? Man Ther 113. Swart NM, Van Linschoten R, Bierma-Zeinstra SMA, et al. The
2000;5(3):142–50. additional effect of orthotic devices on exercise therapy for patients
100. Barton C, Balachandar V, Lack S, et al. Patellar taping for patel- with patellofemoral pain syndrome: a systematic review. Br J
lofemoral pain: a systematic review and meta-analysis to evaluate Sports Med 2012;46(8):570–7.
clinical outcomes and biomechanical mechanisms. Br J Sports 114. Rathleff MS, Rathleff CR, Crossley KM, et al. Hip strength and
Med 2013;48(6):417–24. patellofemoral pain – a systematic review. Br J Sports Med
101. Mulligan B, editor. ‘NAGS’, ‘SNAGS’, ‘MWMS’. 6th ed. Wel- 2014;48(14):1088.
lington, New Zealand: Hutcheson Bowman and Stewart Ltd; 115. Noehren B, Hamill J, Davis I. Prospective evidence for a hip etiol-
2010. ogy in patellofemoral pain. Med Sci Sports Exerc 2013;45(6):
102. McConnell J. Management of patellofemoral problems. Man 1120–4.
Ther 1996;1:60–6. 116. Noehren B, Scholz J, Davis I. The effect of real-time gait retrain-
103. Collins NJ, Bisset LM, Crossley KM, et al. Efficacy of nonsurgical ing on hip kinematics, pain and function in subjects with patel-
interventions for anterior knee pain: systematic review and meta- lofemoral pain syndrome. Br J Sports Med 2011;45(9):691–6.
analysis of randomized trials. Sports Med 2012;42(1):31–48. 117. Willy RW, Scholz JP, Davis IS. Mirror gait retraining for the
[Epub 2011/12/14. eng]; PubMed PMID: 22149696. treatment of patellofemoral pain in female runners. Clin Biomech
104. Mills K, Blanch P, Chapman AR, et al. Foot orthoses and gait: a 2012;27(10):1045–51.
systematic review and meta-analysis of literature pertaining to 118. Lenhart RL, Thelen DG, Wille CM, et al. Increasing running
potential mechanisms. Br J Sports Med 2010;44(14):1035–46. step rate reduces patellofemoral joint forces. Med Sci Sports Exerc
105. Barton CJ, Menz HB, Levinger P, et al. Greater peak rear foot 2014;46(3):557–64.
eversion predicts foot orthoses efficacy in individuals with patel- 119. Bonacci J, Vicenzino B, Spratford W, et al. Take your shoes off to
lofemoral pain syndrome. Br J Sports Med 2011;45:697–701. reduce patellofemoral joint stress during running. Br J Sports Med
106. Vicenzino B, Collins N, Cleland J, et al. A clinical prediction rule 2014;48(6):425–8.
for identifying patients with patellofemoral pain who are likely to 120. Thomas MJ, Wood L, Selfe J, et al. Anterior knee pain in younger
benefit from foot orthoses: a preliminary determination. Br J adults as a precurser to subsequent patellofemoral osteoarthritis:
Sports Med 2008;44(12):doi: 10.1136/bjsm.2008.052613. a systematic review. BMC Musculoskelet Disord 2010;11:201.
107. Vicenzino B. Foot orthotics in the treatment of lower limb condi- 121. Collins NJ, Bierma-Zeinstra SMA, Crossley KM, et al. Prognostic
tions: a musculoskeletal physiotherapy perspective. Man Ther factors for patellofemoral pain: a multicentre observational analy-
2004;9(4):185–96. sis. Br J Sports Med 2013;47:227–33.
108. Barton CJ, Menz HB, Crossley KM. Clinical predictors of foot 122. Crossley KM, Hinman RS. The patellofemoral joint: the forgot-
orthoses efficacy in individuals with patellofemoral pain. Med ten joint in knee osteoarthritis. Osteoarthritis Cartilage 2011;
Sci Sports Exerc 2011;43(9):1603–10. PubMed PMID: WOS: 19(7):765–7. PubMed PMID: WOS:000293323000001.
000293951800001. 123. Utting MR, Davies G, Newman JH. Is anterior knee pain a pre-
109. Barton CJ, Munteanu SE, Menz HB, et al. The efficacy of foot disposing factor to patellofemoral osteoarthritis? Knee 2005;12:
orthoses in the treatment of individuals with patellofemoral pain 362–5.
syndrome: a systematic review. Sports Med 2010;40(5):377–95. 124. Farrokhi S, Keyak JH, Powers CM. Individuals with patellofemo-
[Epub 2010/05/04. eng]; PubMed PMID: 20433211. ral pain exhibit greater patellofemoral joint stress: a finite element
110. Mills K, Blanch P, Dev P, et al. A randomised control trial of short analysis study. Osteoarthritis Cartilage 2011;19(3):287–94.
term efficacy of in-shoe foot orthoses compared with a wait and 125. Andia I, Maffulli N. Platelet-rich plasma for managing pain and
see policy for anterior knee pain and the role of foot mobility. inflammation in osteoarthritis. Nat Rev Rheumatol 2013;9(12):
Br J Sports Med 2012;46(4):247–52. 721–30.
111. Fukuda TY, Melo WP, Zaffalon BM, et  al. Hip postero-
lateral musculature strengthening in sedentary women with

CHAPTER 48.3  ■  KNEE OSTEOARTHRITIS

Kim Bennell • Rana Hinman • Melanie Holden • George Peat

The reported prevalence of knee OA varies greatly,

IMPACT ON INDIVIDUALS AND SOCIETY from 6.3–70.8%, depending on the sample and whether
OA is defined by radiographs, symptoms or self-reported
Individuals with knee osteoarthritis (OA) frequently diagnosis.11 The prevalence will continue to rise as the
experience chronic pain, functional limitations, psycho- population ages12 and as levels of obesity, a risk factor,
logical problems and reduced quality of life.1–6 Rates of continue to grow.13 The cost implications of knee OA are
co-morbidity are high, with many people reporting addi- considerable, with costs related to lost productivity, com-
tional conditions, including cardiac diseases, type 2 dia- munity and social services for OA, and from a range of
betes, obesity and other joint pain.7 Several recent studies treatments, particularly knee joint replacement surgery.14
have reported higher all-cause mortality in individuals Given the considerable individual and societal burden of
with knee OA compared with the general population,8–10 knee OA, treatments that reduce symptoms and slow
possibly due to co-morbidities8 or presence of low-grade functional decline are needed15 while efforts to discover
chronic systemic inflammation.10 structural disease-modifying interventions continue.
 48  The Knee: Introduction 537

breakdown of cartilage that in turn increases synovial

CONCEPTS OF OSTEOARTHRITIS inflammation,23 and a vicious cycle is formed.
Although pathological changes go some way to
Osteoarthritis, often erroneously referred to as ‘wear- explaining the pain mechanisms involved in OA, MRI
and-tear’ or ‘degenerative joint disease’, has been tradi- features suggestive of OA (including cartilage damage,
tionally viewed as a disease primarily involving progressive osteophytes and bone marrow lesions) are also com-
destruction of articular cartilage that causes joint dys- monly found in individuals with no knee pain.18 Other
function and pain.16 However, inconsistent correlation factors must play a part:26 OA may be best concep-
between clinical symptoms and radiographic OA chal- tualized within a biopsychosocial framework in which
lenge the view that pain is simply a result of cartilage pain results from a complex interaction between struc-
damage. Plain radiographs offer a relatively limited, late tural changes, social and psychological factors.19,27,28
view of OA pathology and an increasing body of litera- Clear evidence now exists showing that psychological
ture is now based on magnetic resonance imaging (MRI). and social factors, including helplessness, anxiety, depres-
Studies using this more sensitive imaging modality have sion, self-efficacy and participation restriction, are asso-
also only found weak associations between knee pain and ciated with knee pain and OA.6,29,30 Variability in pain
cartilage volume and thickness.17 Thus articular cartilage, over time has been linked to fluctuations in psycho-
normally aneural and avascular, seems unlikely to be a logical factors;6 however, the causal direction of this
major direct contributor to symptoms.18,19 relationship is difficult to determine and questions
Pathologically, OA is now known to involve all joint remain about whether psychological factors influence
tissues, including cartilage, bone, synovium/capsule, liga- pain or vice versa.6,26
ments and muscle, and there is increased cell activity and
new tissue formation within all of the joint, including
remodelling of bone adjacent to synovial joints, and new RISK FACTORS FOR DEVELOPMENT
bone formation (osteophyte) at the joint margins.20 This AND PROGRESSION
paints a rather different picture from that of ‘wear-and-
tear’, to one of ‘wear-and-repair’ in which osteoarthritis The development of knee OA results from both local
is conceptualized as a repair process that is generally slow, joint-specific factors and systemic factors (Fig. 48-8).31
but efficient.20 Longitudinal studies with up to 14 years Women are not only more likely to have OA than men,
of follow-up show that the course of OA varies between but they also have more severe OA.32 Other systemic
individuals and is not always progressive.21,22 risk factors include race/ethnicity, genetics and diet.31,33
Inflammation, previously believed to be irrelevant to Obesity and being overweight are well-established local
knee OA,16 is now believed to be an important factor risk factors for knee OA,34 as are knee injury35 and occu-
directly linked to clinical symptoms and cartilage degra- pation, particularly jobs requiring both carrying and
dation.23,24 In both the early and late phases of OA, kneeling or squatting.36 There is mixed evidence on the
inflammation of the synovial membrane (synovitis) is effects of physical activity, exercise and sport on knee OA,
common.24,25 Why the synovium becomes inflamed in with some studies suggesting an increased risk of OA in
OA remains controversial. The most accepted hypothesis those who exercise more regularly or intensely,37 but
is that once degraded, cartilage fragments contact the others showing no association between recreational activ-
synovium, which reacts by producing excess inflamma- ity, running, or generally high activity levels and knee
tory mediators (enzymes) that are responsible for carti- OA.31,38 Other local risk factors for knee OA include joint
lage degeneration. These enzymes cause further biomechanics, knee alignment and joint laxity.33

Local factors
Occupation Obesity
Physical activity/sport Strength Pain intensity
Joint injury Alignment Pain duration
Limb-length inequality Bone characteristics Multisite pain
Joint shape Somatosensory Baseline disability
Age Obesity
dysfunction

Progression OA-related
Incident OA Advanced OA
disability

Systemic factors Physical

Strength
Age Genetics Medical/ activity
Sex Obesity psychosocial
Race/ethnicity Osteoporosis co-morbidity
Nutrition

FIGURE 48-8  ■  Risk factors for osteoarthritis (OA) and related disability. (Reprinted from PM & R. Suri P, Morgenroth DC, Hunter DJ.
Epidemiology of osteoarthritis and associated comorbidities, S10–19. © 2012, with permission from Elsevier.)
538 PART IV  Overview of Contemporary Issues in Practice

Comparatively few studies have examined risk factors way of the knee during weight-bearing activities.52 This
for structural progression of knee OA. For many poten- has been identified as a problem in a substantial propor-
tial risk factors there is still only limited or conflicting tion of individuals with knee OA affecting their ability to
evidence on their relationship to disease progression39 function.52,53 The causes of varus thrust and self-reported
and challenges in the design and interpretation of these instability are likely to be multifactorial, resulting from
studies may be a contributory factor.33,40 However, there factors such as passive joint laxity, structural damage,
is fairly consistent evidence linking older age, varus knee muscle weakness, pain and altered neuromuscular control.
alignment, presence of OA in multiple joints, radio- A better understanding of the underlying causes is needed
graphic severity at baseline, and higher body mass index to help design appropriate interventions to stabilize the
to higher risk of future progression of knee OA.39 A knee and reduce these phenomena.
number of studies have also evaluated the course of func- Neuromuscular function is important to balance
tional status over time in individuals with knee OA. external moments applied to the knee joint54,55 and
Increasing age, greater pain and functional limitations, improve the dynamic stability of the joint during walking.
obesity, poor general health and concurrent co-morbidities However, alterations in neuromuscular function may
are all predictors of poor functional outcome in knee OA. increase knee load.56 Muscle weakness is consistently
However, lower levels of mental health symptoms includ- found in people with knee OA.57 Recent interest in the
ing anxiety and depression, greater self-efficacy and social patterns of muscle activation associated with knee OA
support, and regular physical activity appear to protect suggests that some patients adopt a co-contraction strat-
against functional decline.31 egy involving activation of many muscles in a less specific
fashion.58–60 While these neuromuscular alterations most
likely represent coping strategies and thus may have
THE ROLE OF BIOMECHANICS AND short-term benefits, they may have long-term negative
NEUROMUSCULAR FACTORS consequences by altering the distribution and increasing
the magnitude of load and potentially speeding structural
Joint loading, acting within the context of systemic and disease progression. This has led to the recommendation
local joint-specific susceptibility, plays a role in the aetiol- that novel exercise approaches designed to reduce levels
ogy of knee OA.41 Since direct measurement of joint of co-contraction should be developed to address these
loads in vivo is generally not feasible in humans, three- neuromuscular changes.58,60 However, if co-contraction is
dimensional gait analysis is typically used to infer com- an adaptive response, then removing this strategy without
pressive joint loads during walking. For knee OA, the addressing more appropriate means to control joint sta-
most relevant and widely studied load parameter is the bility may be detrimental. The most effective form of
external knee adduction moment (KAM) in the frontal physical therapy to address these impairments is cur-
plane, generated because the ground reaction force vector rently not known.
passes medial to the joint centre. This moment forces the
knee into varus, compressing the medial joint compart-
ment and stretching lateral structures. As such, the KAM
has been used as an indicator of medial joint load.42,43 Of
DIAGNOSIS AND ASSESSMENT
importance, longitudinal studies have found that higher Diagnosis
KAM indices are associated with an increased risk of
structural progression in people with knee OA.44,45 Given In the absence of any agreed ‘gold standard’, the diag-
this, physical therapy interventions that reduce the KAM nosis of knee OA may be made on clinical grounds
may slow disease progression. without normally requiring imaging or laboratory inves-
Impairments in the local mechanical environment tigations.33 After excluding important differential diag-
and neuromotor control systems, such as malalignment, noses,61 a working diagnosis of OA may be applied to
varus thrust and altered muscle-activation patterns, exist patients aged 45 years and over, reporting persistent joint
and can influence knee load and thereby structural pain that is worse with use, and morning stiffness lasting
progression. Malalignment, particularly varus malalign- no more than half an hour.20 The presence of known
ment in those with medial compartment OA, often arises risk factors and classical symptoms and signs may help
or worsens as a consequence of the osteoarthritic process strengthen clinical suspicion (Box 48-1), serving mainly
due to cartilage loss, bony attrition and meniscal damage. to identify the more advanced cases.63–66 However, it
The presence of malalignment is a clinical marker of the should be noted that many clinical signs may not have
likelihood of both structural deterioration46 and decreases the level of reliability or diagnostic validity one might
in function.47 wish for clinical decision making.33,67–69
Failure to dynamically control frontal plane motion at Under a working diagnosis of OA, practitioners will
the knee joint can manifest as a visually observed varus confront a spectrum of clinical and pathological severity
thrust with dynamic worsening or abrupt onset of varus ranging from intermittent symptoms to constant aches
alignment in the early part of stance phase.48 Varus thrust with severe, acute exacerbations70–72 and from early struc-
is associated with higher knee load during walking,49,50 tural changes visible only on MRI3,73 to complete loss of
faster disease progression49 and greater pain during joint space.74 While many patients clearly value having a
weight-bearing activities.51 Another consequence of lack diagnosis,75 the benefits of this cannot be assumed76,77 and
of dynamic control may be symptomatic knee instability time and care must be taken over its explanation to
reported by the patient as buckling, slipping or giving patients. Emerging with a new or reinforced belief that
 48  The Knee: Introduction 539

BOX 48-1  Risk Factors, Symptoms and Signs pharmacological treatment strategies85 with surgery
that Should Be Associated with reserved for end-stage disease that is unresponsive to
Increased Clinical Suspicion of other interventions. Education, exercise and if appro-
Knee Osteoarthritis priate, weight loss, are the core recommended treat-
ments for knee OA.
Older age Given the chronicity of the disease, treatments
Higher body mass index that encourage patient self-management are particularly
Family history of osteoarthritis important. Furthermore, treatments need to address
History of previous ligament/cartilage injury to knee both the physical and psychosocial issues identified
History of repetitive, cumulative, or heavy loading (for on assessment and referral to other appropriate health
example, as part of occupation) professionals may be required. A more patient-focused
Persistent knee pain*
communication style that involves reassurance, encour-
Reduced function*
Limited duration knee stiffness (<30 minutes)* agement, support, empathy, asking questions and
Coarse crepitus* listening is associated with greater therapeutic alliance
Restricted knee flexion range of motion* between the clinician and patient and improves patient
Bony enlargement* outcomes.86,87 Adherence is greater when clinicians
Fixed flexion deformity are perceived as supportive rather than paternalistic,88
Modest effusion and clinicians need to ensure that their communica-
tion style promotes, rather than hinders, patient
*Key criteria from EULAR Task Force recommendations62 self-management.

‘it’s my age’, ‘it’s wear-and-tear, and therefore inevitably

progressive and activity/exercise are contra-indicated’, or
Education
‘nothing can be done’ should be taken as a strong indica- Patient education is an integral component of knee OA
tor of a failed consultation. treatment and should cover a range of topics including
pain management, exercise, diet, activity–rest cycling,
goal-setting and problem solving. Educational strategies
Beyond Diagnosis that improve the patient’s understanding of the neuro-
Assessment serves many purposes other than diagnosis. physiology and neurobiology of pain can have a positive
Careful evaluation of pain and functional limitation is effect on chronic musculoskeletal pain.2,89 Key messages
integral to many of these purposes, but cannot be ade- for patients with knee OA have been identified through
quately understood within a strict biomedical framework a consensus exercise involving over 50 international
(Fig. 48-8). Pain experience and function are influenced experts and patients.90
by a wider set of determinants, some potentially modifi-
able, whose identification requires a more holistic assess-
ment (e.g. Table 48-2).
Exercise
A myriad patient-reported outcome measures are Exercise is universally recommended by clinical guide-
available to the clinician and there are many excellent lines for the management of all patients with knee
published reviews of these instruments to guide selec- OA.91–93 Systematic reviews and meta-analyses consis-
tion.78 Further attempts to streamline and simplify the tently support the short-term benefit of exercise for
administration of patient-reported outcome measures for improving pain and physical function in people with knee
routine clinical practice are underway.79–81 Simple, easily OA,94–96 even those with severe disease awaiting total
interpretable measures already exist, such as a standard- joint replacement.97 For those who are overweight/obese,
ized 0–10 numerical rating scale for pain intensity. The the combination of exercise and dietary weight loss is
use of physical performance tests is recommended to more effective for symptoms than either treatment
complement the picture gained from patient-reported alone.98 Although the magnitude of benefits may be con-
outcome measures with an evaluation of what the patient sidered small-to-moderate, this is comparable to reported
can do82,83 (Table 48-3). estimates for simple analgesics and oral non-steroidal
anti-inflammatory drugs for OA pain.99 Importantly,
exercise is associated with relatively few side effects com-
TREATMENT STRATEGIES pared to drug treatments. In contrast to symptomatic
benefit from exercise, evidence from a limited number of
Management of knee OA has traditionally focused on studies to date does not show any effects of exercise in
treatment of pain and disability associated with estab- reducing knee load100–102 or in slowing structural disease
lished disease. However, there is interest in treatment progression in people with knee OA.103
that can also slow or prevent structural progression Clinical guidelines for managing OA92 strongly recom-
to advanced disease. Regardless of the management mend that people with knee OA participate in cardiovas-
goals, treatment for knee OA should be individualized cular and/or resistance land-based exercise, as well as
based on assessment findings and be patient-centred aquatic exercise. In particular, aquatic exercise may be
involving shared decision making between the patient useful for those who are overweight/obese or who have
and clinician. The optimal management of knee OA severe disease. Results of a recent systematic review
requires a combination of non-pharmacological and support a combination of strengthening, flexibility and
 540

TABLE 48-2  Holistic Assessment

Holistic Assessment
Assess the effect of osteoarthritis on the person’s function, quality of life, occupation, mood, relationships and leisure activities. Below are example topics
The patient’s The patient’s The patient’s mood Pain assessment Effect of osteoarthritis on: Other musculoskeletal Co-morbidities
existing support network • Screen for Assess: • Activities of daily living pain • If two or more
thoughts • Is the patient depression • Self-help strategies • Family duties • Is there evidence of morbidities, consider
• What concerns isolated or do • Are there any other the patient is using • Hobbies a chronic pain any interaction
do they have? they have a carer? stresses in their life? • Current drugs being • Lifestyle expectations syndrome? • Is the patient fit for
• What are their • How is the main The patient’s attitude used, including their • Quality of sleep • Are there other surgery?
expectations? support giver to exercise doses, frequency, • Energy levels treatable sources of • Assess the most
• What do they coping? timing and any • Their occupation, pain (for example, appropriate therapy
• Previous exercise
PART IV  Overview of Contemporary Issues in Practice

know about • What are their possible side effects including short- and peri-articular pain or • Is the patient prone
experience
osteoarthritis? ideas, concerns • Evidence of pain long-term ability to bursitis)? to falls?
• Beliefs about
and expectations? exercise catastrophizing perform their job (are
• Potential barriers • Self-efficacy around any adjustments to
and facilitators to pain managements home or workplace
exercise required?)

(Adapted from20)
 48  The Knee: Introduction 541

TABLE 48-3  Description of the Minimum Core Set of Physical Performance Measures for Hip
and Knee Osteoarthritis* as Recommended by the Osteoarthritis Research
Society International83
Test Equipment Needed Description
30-second chair • Timer/stop watch Maximum number of chair stand repetitions
stand test • Straight back chair with a 44 cm (17 inch) possible in 30 seconds
seat height, preferably without arms
40 m fast-paced • Timer/stop watch A fast-paced walking test that is timed over
walk test • 10 m marked walkway with space to 4 x 10 m for a total of 40 m performed in
safely turn around at each end comfortable footwear
• 2 cones placed approximately 2 m beyond
each end of the walkway
• Calculator to convert time to speed
Stair climb test • Timer/stop watch Time in seconds it takes to ascend and
• Set of stairs descend a flight of stairs. The number of
stairs will depend on individual availability

*There are currently no consensus recommendations for performance tests in younger patients at high risk of osteoarthritis, although
Kroman et al.84 provide a review of the evidence on these.

aerobic exercise for improving function.94 Neither the may assist decisions about exercise dosage, patients
type96 nor intensity104,105 of the strengthening exercise should be advised that it is normal to feel some discom-
appears to influence outcome. More recently, neuromus- fort or pain during exercise. Practical exercise prescrip-
cular exercise typically performed in functional weight- tion tips for physiotherapists are shown in Box 48-2.
bearing positions and emphasizing quality and efficiency
of movement, as well as alignment of the trunk and lower
limb joints, has been promoted for knee OA.106 In addition
Manual Therapy
to structured exercise, encouraging and supporting Manual therapy is often used in the management of knee
patients to increase overall physical activity levels is also OA,112 generally in combination with other interventions
important.107 Effect sizes for individual supervised exercise such as exercise. There are a limited number of clinical
treatments are greater than those for class-based pro- trials of manual therapy with relatively recent systematic
grammes and home exercise.95 Furthermore, 12 or more reviews reporting fair evidence for short-term benefits
directly supervised exercise sessions with a health profes- and limited evidence for long-term benefits of manual
sional significantly improve pain and function to a greater therapy, although the studies had a high risk of bias.113,114
extent when compared with less than 12 supervised exer- Another systematic review and meta-analysis suggested
cise sessions.95 While this may be the case, there is still that the addition of manual therapy to exercise may be
unwillingness in many healthcare settings to fund this more effective than exercise alone.115 However, none of
level of intervention as a core component of knee OA care. the studies included in this review directly compared the
While effective in the short term, the benefits of treatments as was done in a more recent randomized
exercise decline over the longer term due to lack of controlled trial involving 206 people with hip or knee
adherence.108 A dose–response relationship has been OA.116 In this high-quality study, manual physiotherapy
demonstrated between adherence rates and exercise provided significant benefits for pain and disability over
effects.109 A complex array of factors can influence adher- usual care that were sustained to 1 year. However, there
ence. These include attitude towards exercise, perceived was no added benefit from the combination of manual
severity of knee symptoms (those with more severe symp- physiotherapy and exercise and indeed the combination
toms are most likely to adhere), ideas about the cause of was generally less effective or at best no more effective
arthritis (those thinking arthritis is due to age or ‘wear- than either intervention alone. The authors reasoned
and-tear’ are less adherent) and the perceived effective- that, given a fixed clinic visit time, combining manual
ness of the intervention. Numerous strategies have been therapy and exercise therapy necessitates reducing the
suggested to help improve adherence to exercise in people dose of both, compared with a clinic visit focusing on one
with OA,110 including individualizing the exercise pro- or the other and that this may have explained the results.
gramme, educating about the disease process and benefits Nonetheless, the results show the benefits of manual
of exercise, regular monitoring from the therapist, inte- therapy for people with knee OA.
grating behavioural graded activity principles, use of
‘booster sessions’, self-monitoring, reinforcement by
other individuals, telephone and/or mail contact as well
Braces
as participating in exercise with a spouse or other family Neoprene or elastic sleeves are the simplest and cheapest
member.111 type of knee braces available. Although they offer little
An important common misperception is that pain joint support, they provide compression and warmth and
during exercise in patients with knee OA indicates joint have been shown to significantly improve quality of life
damage. Although experiences of pain when exercising and function.117 Unloader braces are semi-rigid knee
542 PART IV  Overview of Contemporary Issues in Practice

BOX 48-2  Practical Exercise Prescription for symptoms. In contrast, a recent parallel-group RCT
Patients with Knee Osteoarthritis showed that 6-week use of a patellofemoral brace (com-
pared to no brace) resulted in significant reductions in
• As similar reductions in pain and improvements in func- knee pain, and in the volume of bone marrow lesions
tion can be gained with various types of exercise, the (lesions seen in the subchondral bone on MRI and a
patient should chose the type of exercise they prefer marker of disease progression) in the PFJ.123 These
• An exercise programme to improve muscle strength, promising results are the first evidence that bracing
aerobic capacity and flexibility is recommended may be able to influence underlying joint structure in
• Strengthening exercises should target major lower limb knee OA.
muscles such as the quadriceps, hip abductors and exten-
sors, hamstrings and gastrocnemius
• Aerobic exercise such as walking can also assist in weight Footwear and Orthoses
loss/prevention of weight gain and in improving mood
and anxiety Given that knee OA is mechanically driven,124 and foot-
• Aquatic exercise may be beneficial for those who are wear and shoe insoles can influence the centre of pressure
overweight/obese or those with more severe disease at the foot (and thus knee load via the knee lever arm),125,126
• Tai chi may be a useful exercise option for some these strategies may assist in the management of patients
• Balance exercises should be included if assessment reveals with knee OA, and may, in fact, have the ability to slow
balance impairments or if the patient has a history disease progression.
of falls Most research has focused on lateral wedge insoles. A
• Increasing overall general physical activity levels during
recent systematic review, which evaluated the effect of
everyday life is important in addition to structured
exercise lateral wedges on the external KAM,127 demonstrated that
• Treatment benefits in terms of reduced pain and improved these insoles reduced the peak KAM. Unfortunately, the
function can be gained from individual, class-based and load-reducing effects of lateral wedges have not trans-
home-based programmes lated into clinically meaningful reductions in pain128 nor
• Although individual treatments show the greatest treat- slowing of structural disease progression (cartilage
ment benefits for pain and function, superiority of one volume on MRI) when compared to neutral insoles.129 In
delivery mode over the other remains unclear contrast, the limited literature available evaluating medial
• Group exercise and home exercise are similarly effective wedges for lateral tibiofemoral OA suggests that these
and patient preference should be considered in the insoles can reduce pain in women with bilateral valgus
decision-making process of preferred delivery mode
malalignment.130 Given the dearth of studies evaluating
• Home-based programmes can be supplemented with
supervised programmes (class or individual) to maximize the clinical effects of other shoe orthoses in knee OA such
the cost-effective benefits as shock-absorbing insoles131 and medial arch supports,
• Discomfort or pain during exercise is to be expected. the usefulness of these is not yet known.
However, severe or intense pain during exercise, pain that Clinical guidelines recommend every patient with
does not subside to usual levels within a few hours after knee OA receive advice concerning appropriate foot-
exercise, increased night pain following exercise, or swell- wear.85,91 Compared to barefoot walking regular off-the-
ing or increased swelling in the hours following exercise shelf shoes increase medial knee load by 7–14%,
or the next morning indicate that the type or dosage of depending on shoe type.127 Shoe types that are more
exercise need to be modified likely to increase medial knee load include high-heeled
shoes and shoes that promote foot stability rather than
mobility.132–138 Biomechanical evidence suggests light-
weight, flat and flexible footwear may be optimal for knee
OA. Recently, novel innovative footwear has been devel-
braces designed for people with predominant medial or oped specifically to reduce knee loads in people with knee
lateral tibiofemoral joint OA and varus or valgus malalign- OA. Shoes with ‘variable stiffness’ soles (where the lateral
ment. They apply an external three-point corrective sole is stiffer compared to medial) can reduce the KAM
force that improves symptoms118 and reduces biomechan- compared to shoes with a uniformly stiff sole,139,140 but do
ical load on the affected compartment119,120 as well as not appear to significantly reduce knee pain. ‘Mobility’
muscle activation and co-contraction levels.121 Thus, shoes incorporate a flexible grooved sole (and engineered
valgus bracing offers great potential for slowing disease to mimic barefoot walking) and can also reduce the peak
progression in medial knee OA if load reduction can be KAM by 8% compared to self-selected walking shoes;141
sustained. Long-term studies are now required to evalu- however, the efficacy of these shoes in treating symptoms
ate the effects of bracing on joint structure. of knee OA has not been evaluated. Unstable rocker-
For patients with patellofemoral joint (PFJ) OA or soled shoes (Masai Barefoot Technology®) have been
whose predominant symptoms arise from the PFJ, a proposed as an option for knee OA given their potential
patellofemoral brace may be useful. These aim to unload to improve gait stability and reduce joint load.142 These
the lateral compartment of the PFJ by applying a force shoes reduce peak KAM by up to 13% in overweight
to the patella in a medial direction.122 However, the males (who are at risk of developing knee OA);143 however,
symptomatic benefits are unclear. No significant effects a 12-week randomized controlled trial comparing unsta-
on pain were noted in a cross-over trial comparing patel- ble shoes to normal walking shoes showed no symptom-
lofemoral bracing to a control bracing condition in atic effects in a sample with symptomatic knee OA.142
people with lateral PFJ OA and anterior knee pain Thus, at present, it is not clear what role innovative shoe
 48  The Knee: Introduction 543

designs may play, if any, in managing symptoms associ- 2. Hurley MV. Muscle dysfunction and effective rehabilitation of
ated with knee OA. knee osteoarthritis: what we know and what we need to find out.
Arthritis Rheum 2003;49:444–52.
3. Hunter DJ, Zhang W, Conaghan PG, et al. Systematic review of
Gait Aids and Gait Retraining the concurrent and predictive validity of MRI biomarkers in OA.
Osteoarthritis Cartilage 2011;19:557–88.
Emerging research suggests that gait retraining can 4. Jordan KM, Arden NK, Doherty M, et al. EULAR Recommenda-
tions 2003: an evidence based approach to the management of
reduce the KAM during walking, and thus may have knee osteoarthritis: report of a Task Force of the Standing Com-
potential as a structure-modifying treatment strategy. A mittee for International Clinical Studies Including Therapeutic
systematic review of gait modification strategies identi- Trials (ESCISIT). Ann Rheum Dis 2003;62:1145–55.
fied 14 different strategies that have been evaluated for 5. Murphy SL, Lyden AK, Phillips K, et al. Subgroups of older
their effects on the KAM.144 adults with osteoarthritis based upon differing comorbid symptom
presentations and potential underlying pain mechanisms. Arthritis
Use of a walking cane is conditionally recommended Res Ther 2011;13:R135.
in clinical guidelines for knee OA.92 Biomechanical evi- 6. Wise BL, Niu J, Zhang Y, et al. Psychological factors and their
dence shows that using a cane in the contralateral hand relation to osteoarthritis pain. Osteoarthritis Cartilage 2010;18:
can reduce the KAM by 6–17%.145 Greatest offloading of 883–7.
7. de Rooij M, Steultjens MPM, Avezaat E, et al. Restrictions and
the knee occurs when greater amounts of body weight contraindications for exercise therapy in patients with hip and knee
are placed through the cane, when body weight is placed osteoarthritis and co-morbidity. Phys Ther Rev 2013;18:101–11.
through the cane earlier (rather than later) during stance 8. Betancourt MCC, Dehghan A, Campos N, et al. Osteoarthritis
phase of gait, and when the cane is placed at a greater and mortality: meta-analysis of two prospective cohorts. Osteoar-
lateral distance away from the affected limb. Thus, it is thritis Cartilage 2013;21:s151.
9. Hunter DJ. Osteoarthritis. Best Pract Res Clin Rheumatol 2011;
important that clinicians train patients with knee OA to 25:801–14.
use walking canes appropriately in order to ensure 10. Nuesch E, Dieppe P, Reichenbach S, et al. All cause and disease
maximum benefit. There has been one RCT evaluating specific mortality in patients with knee or hip osteoarthritis: popu-
the efficacy of walking canes in people with knee OA,146 lation based cohort study. BMJ 2011;342:d1165.
11. Pereira D, Peleteiro B, Araujo J, et al. The effect of osteoarthritis
reporting that 60 days of cane use significantly reduced definition on prevalence and incidence estimates: a systematic
pain, improved physical function and reduced analgesic review. Osteoarthritis Cartilage 2011;19:1270–85.
use. Further research is now required to determine 12. Wilmoth JR. Demography of longevity: past, present, and future
whether long-term use of a cane can have disease- trends. Exp Gerontol 2000;35:1111–29.
modifying effects. 13. James WP. The epidemiology of obesity: the size of the problem.
J Intern Med 2008;263:336–52.
14. OECD. 2011. Health at a Glance 2011: OECD Indicators, OECD
Acupuncture Publishing. <http://dx.doi.org/10.1787/health_glance-2011-en>.
15. Bennell K. Physiotherapy management of hip osteoarthritis.
Meta-analyses show that acupuncture is effective for the J Physiother 2013;59:145–57.
16. Jordan JM, Gracely RH. A special osteoarthritis and cartilage issue
treatment of chronic pain, including OA.147 One recent on pain in osteoarthritis. Osteoarthritis Cartilage 2013;21:
systematic review concluded that acupuncture can be 1143–4.
considered one of the more effective physical treatments 17. Hunter DJ, Arden N, Conaghan PG, et al. Definition of osteoar-
for alleviating knee OA pain in the short term.148 The thritis on MRI: results of a Delphi exercise. Osteoarthritis Carti-
addition of acupuncture to exercise delivered by physio- lage 2011;19:963–9.
18. Guermazi A, Niu J, Hayashi D, et al. Prevalence of abnormalities
therapists was also cost-effective.149 The benefits of acu- in knees detected by MRI in adults without knee osteoarthritis:
puncture may result from factors over and above the population based observational study (Framingham Osteoarthritis
specific effects of needling such as positive expectation of Study). BMJ 2012;345:e5339.
treatment benefit.147 19. Hunter DJ, Guermazi A, Roemer F, et al. Structural correlates of
pain in joints with osteoarthritis. Osteoarthritis Cartilage
2013;21:1170–8.
20. NICE. Osteoarthritis: National Clinical Guideline for Care and
CONCLUSION Management in Adults. Guideline. London: National Institute for
Health and Clinical Excellence, UK; 2008 Report No: CG59
Treatment of knee OA requires a biopsychosocial Contract No: CG59.
21. Leyland KM, Hart D, Javaid MK, et al. The natural history of
approach with an emphasis on assisting the patient to radiographic knee osteoarthritis: a fourteen year population-based
self-manage their condition. Education, exercise and, if cohort study. Arthritis Rheum 2012;64(7):2243–51. doi:10.1002/
appropriate, weight loss, are key treatments recom- art.34415.
mended by all clinical guidelines. Attention to adherence 22. Soni A, Kiran A, Hart DJ, et al. Prevalence of reported knee pain
over twelve years in a community-based cohort. Arthritis Rheum
strategies is important to ensure longer-term benefits. To 2012;64:1145–52.
date, there are no established structural disease-modifying 23. Berenbaum F. Osteoarthritis as an inflammatory disease (osteoar-
treatments. However, given the link between higher knee thritis is not osteoarthrosis! Osteoarthritis Cartilage 2013;21:
load and disease progression, treatments that reduce knee 16–21.
load such as braces, modified footwear, gait aids and gait 24. Sellam J, Berenbaum F. The role of synovitis in pathophysiology
and clinical symptoms of osteoarthritis. Nat Rev Rheumatol
retraining have potential. 2010;6:625–35.
25. Ayral X, Pickering EH, Woodworth TG, et al. Synovitis: a poten-
tial predictive factor of structural progression of medial tibiofemo-
ral knee osteoarthritis – results of a 1 year longitudinal arthroscopic
REFERENCES study in 422 patients. Osteoarthritis Cartilage 2005;13:361–7.
1. Neame R, Doherty M. Osteoarthritis update. Clin Med 26. Neogi T. The epidemiology and impact of pain in osteoarthritis.
2005;5:207–10. Osteoarthritis Cartilage 2013;21:1145–53.
544 PART IV  Overview of Contemporary Issues in Practice

27. Dieppe PA, Lohmander LS. Pathogenesis and management of 52. Felson DT, Niu J, McClennan C, et al. Knee buckling: preva-
pain in osteoarthritis. Lancet 2005;365:965–73. lence, risk factors, and associated limitations in function. Ann
28. Hunter DJ, McDougall JJ, Keefe FJ. The symptoms of osteoar- Intern Med 2007;147:534–40.
thritis and the genesis of pain. Rheum Dis Clin North Am 53. Fitzgerald GK, Piva SR, Irrgang JJ. Reports of joint instability in
2008;34:623–43. knee osteoarthritis: its prevalence and relationship to physical
29. Schneider S, Junghaenel DU, Keefe FJ, et al. Individual differ- function. Arthritis Rheum 2004;51:941–6.
ences in the day-to-day variability of pain, fatigue, and well-being 54. Shelburne KB, Torry MR, Pandy MG. Contributions of muscles,
in patients with rheumatic disease: associations with psychological ligaments, and the ground-reaction force to tibiofemoral joint
variables. Pain 2012;153:813–22. loading during normal gait. J Orthop Res 2006;24:1983–90.
30. Wilkie R, Peat G, Thomas E, et al. Factors associated with 55. Sritharan P, Lin YC, Pandy MG. Muscles that do not cross the knee
restricted mobility outside the home in community-dwelling contribute to the knee adduction moment and tibiofemoral com-
adults ages fifty years and older with knee pain: an example of use partment loading during gait. J Orthop Res 2012;30:1586–95.
of the International Classification of Functioning to investigate 56. Winby CR, Lloyd DG, Besier TF, et al. Muscle and external load
participation restriction. Arthritis Rheum 2007;57:1381–9. contribution to knee joint contact loads during normal gait.
31. Suri P, Morgenroth DC, Hunter DJ. Epidemiology of osteoarthri- J Biomech 2009;42:2294–300.
tis and associated comorbidities. PM R 2012;4:S10–19. 57. Bennell KL, Wrigley TV, Hunt MA, et al. Update on the role of
32. Srikanth VK, Fryer JL, Zhai G, et al. A meta-analysis of sex dif- muscle in the genesis and management of knee osteoarthritis.
ferences prevalence, incidence and severity of osteoarthritis. Rheum Dis Clin North Am 2013;39:145–76.
Osteoarthritis Cartilage 2005;13:769–81. 58. Childs JD, Sparto PJ, Fitzgerald GK, et al. Alterations in lower
33. Zhang Y, Jordan JM. Epidemiology of osteoarthritis. Clin Geriatr extremity movement and muscle activation patterns in individuals
Med 2010;26:355–69. with knee osteoarthritis. Clin Biomech 2004;19:44–9.
34. Felson D, Lawrence R, Dieppe P, et al. Osteoarthritis: new 59. Heiden TL, Lloyd DG, Ackland TR. Knee joint kinematics,
insights: part 1: the disease and its risk factors. Ann Intern Med kinetics and muscle co-contraction in knee osteoarthritis patient
2000;133:635–46. gait. Clin Biomech 2009;24:833–41.
35. Lohmander LS, Englund PM, Dahl LL, et al. The long-term 60. Hortobagyi T, Westerkamp L, Beam S, et al. Altered hamstring-
consequence of anterior cruciate ligament and meniscus injuries: quadriceps muscle balance in patients with knee osteoarthritis.
osteoarthritis. Am J Sports Med 2007;35:1756–69. Clin Biomech (Bristol, Avon) 2005;20:97–104.
36. Felson DT, Hannan MT, Naimark A, et al. Occupational physical 61. Porcheret M, Healey E, Dziedzic K, et al. Osteoarthritis: a
demands, knee bending, and knee osteoarthritis: results from the modern approach to diagnosis and management. Arthritis Res UK
Framingham Study. J Rheumatol 1991;18:1587–92. 2011;6:1–9.
37. Blagojevic M, Jinks C, Jeffery A, et al. Risk factors for onset of 62. Zhang W, Doherty M, Peat G, et al. EULAR evidence-based
osteoarthritis of the knee in older adults: a systematic review and recommendations for the diagnosis of knee osteoarthritis. Ann
meta-analysis. Osteoarthritis Cartilage 2010;18:24–33. Rheum Dis 2010;69:483–9.
38. Felson DT, Niu J, Clancy M, et al. Effect of recreational physical 63. Schouten JS, Valkenburg HA. Classification criteria: methodolog-
activities on the development of knee osteoarthritis in older adults ical considerations and results from a 12 year following study in
of different weights: the Framingham Study. Arthritis Rheum the general population. J Rheumatol Suppl 1995;43:44–5.
2007;57:6–12. 64. Peat G, Duncan RC, Wood LR, et al. Clinical features of symp-
39. Chapple CM, Nicholson H, Baxter GD, et  al. Patient character- tomatic patellofemoral joint osteoarthritis. Arthritis Res Ther
istics that predict progression of knee osteoarthritis: a systematic 2012;14:R63.
review of prognostic studies. Arthritis Care Res 2011;63: 65. Peat G, Thomas E, Duncan R, et al. Clinical classification criteria
1115–25. for knee osteoarthritis: performance in the general population and
40. Zhu Y. Bias introduced by conditioning on an intermediate vari- primary care. Ann Rheum Dis 2006;65:1363–7.
able: comment on the article by Zhang et al. Arthritis Care Res 66. Peat G, Thomas E, Duncan R, et al. Estimating the probability
2011;63:784. of radiographic osteoarthritis in the older patient with knee pain.
41. Brandt KD, Dieppe P, Radin E. Etiopathogenesis of osteoarthritis. Arthritis Rheum 2007;57:794–802.
Med Clin North Am 2009;93:1–24, xv. 67. Cibere J, Bellamy N, Thorne A, et al. Reliability of the knee
42. Zhao D, Banks SA, Mitchell KH, et al. Correlation between the examination in osteoarthritis: effect of standardization. Arthritis
knee adduction torque and medial contact force for a variety of Rheum 2004;50:458–68.
gait patterns. J Orthop Res 2007;25:789–97. 68. Wood L, Peat G, Wilkie R, et al. A study of the noninstrumented
43. Schipplein OD, Andriacchi TP. Interaction between active and physical examination of the knee found high observer variability.
passive knee stabilizers during level walking. J Orthop Res J Clin Epidemiol 2006;59:512–20.
1991;9:113–19. 69. Riddle DL. Validity of clinical measures of frontal plane knee
44. Miyazaki T, Wada M, Kawahara H, et al. Dynamic load at baseline alignment: data from the osteoarthritis initiative. Man Ther
can predict radiographic disease progression in medial compart- 2012;17:459–65.
ment knee osteoarthritis. Ann Rheum Dis 2002;61:617–22. 70. Gooberman-Hill R, Woolhead G, Mackichan F, et al. Assessing
45. Bennell KL, Bowles KA, Wang Y, et al. Higher dynamic medial chronic joint pain: lessons from a focus group study. Arthritis
knee load predicts greater cartilage loss over 12 months in medial Rheum 2007;57:666–71.
knee osteoarthritis. Ann Rheum Dis 2011;70:1770–4. 71. Hawker GA, Stewart L, French MR, et al. Understanding the pain
46. Sharma L, Song J, Dunlop D, et al. Varus and valgus alignment experience in hip and knee osteoarthritis – an OARSI/OMERACT
and incident and progressive knee osteoarthritis. Ann Rheum Dis initiative. Osteoarthritis Cartilage 2008;16:415–22.
2010;69:1940–5. 72. Marty M, Hilliquin P, Rozenberg S, et al. Validation of the
47. Sharma L, Song J, Felson DT, et al. The role of knee alignment KOFUS (Knee Osteoarthritis Flare-Ups Score). Joint Bone Spine
in disease progression and functional decline in knee osteoarthri- 2009;76:268–72.
tis. JAMA 2001;286:188–95. 73. Cibere J, Zhang H, Thorne A, et al. Association of clinical find-
48. Chang AH, Chmiel JS, Moisio KC, et al. Varus thrust and knee ings with pre-radiographic and radiographic knee osteoarthritis in
frontal plane dynamic motion in persons with knee osteoarthritis. a population-based study. Arthritis Care Res 2010;62:1691–8.
Osteoarthritis Cartilage 2013;21:1668–73. 74. Kellgren JH, Lawrence JS. Rheumatism in miners. II. X-ray study.
49. Chang A, Hayes K, Dunlop D, et al. Thrust during ambulation Br J Ind Med 1952;9:197–207.
and the progression of knee osteoarthritis. Arthritis Rheum 75. Arthritis and Musculoskeletal Alliance. Standards of Care for
2004;50:3897–903. People with Osteoarthritis. 2004.
50. Kuroyanagi Y, Nagura T, Kiriyama Y, et al. A quantitative assess- 76. Bedson J, McCarney R, Croft P. Labelling chronic illness in primary
ment of varus thrust in patients with medial knee osteoarthritis. care: a good or a bad thing? Br J Gen Pract 2004;54:932–8.
Knee 2012;19:130–4. 77. Moynihan R, Doust J, Henry D. Preventing overdiagnosis: how
51. Lo GH, Harvey WF, McAlindon TE. Associations of varus thrust to stop harming the healthy. BMJ 2012;344:e3502.
and alignment with pain in knee osteoarthritis. Arthritis Rheum 78. Collins NJ, Misra D, Felson DT, et al. Measures of knee function:
2012;64:2252–9. International Knee Documentation Committee (IKDC)
 48  The Knee: Introduction 545

Subjective Knee Evaluation Form, Knee Injury and Osteoarthritis tis: the IDEA randomized clinical trial. JAMA 2013;310:
Outcome Score (KOOS), Knee Injury and Osteoarthritis Outcome 1263–73.
Score Physical Function Short Form (KOOS-PS), Knee Outcome 99. Zhang W, Nuki G, Moskowitz RW, et al. OARSI recommenda-
Survey Activities of Daily Living Scale (KOS-ADL), Lysholm tions for the management of hip and knee osteoarthritis: part III:
Knee Scoring Scale, Oxford Knee Score (OKS), Western Ontario changes in evidence following systematic cumulative update of
and McMaster Universities Osteoarthritis Index (WOMAC), research published through 2009. Osteoarthritis Cartilage
Activity Rating Scale (ARS), and Tegner Activity Score (TAS). 2010;18:476–99.
Arthritis Care Res 2011;63:S208–28. 100. Bennell KL, Hunt MA, Wrigley TV, et al. Hip strengthening
79. Fries JF, Cella D, Rose M, et al. Progress in assessing physical reduces symptoms but not knee load in people with medial knee
function in arthritis: PROMIS short forms and computerized osteoarthritis and varus malalignment: a randomised controlled
adaptive testing. J Rheumatol 2009;36:2061–6. trial. Osteoarthritis Cartilage 2010;18:621–8.
80. Broderick JE, Schneider S, Junghaenel DU, et al. Validity and 101. Foroughi N, Smith RM, Lange AK, et al. Lower limb muscle
reliability of patient-reported outcomes measurement information strengthening does not change frontal plane moments in women
system instruments in osteoarthritis. Arthritis Care Res 2013;65: with knee osteoarthritis: a randomized controlled trial. Clin
1625–33. Biomech 2011;26:167–74.
81. Arthritis Res UK & Chartered Society of Physiotherapy. The 102. Lim BW, Hinman RS, Wrigley TV, et al. Does knee malalignment
Musculoskeletal Patient-Reported Outcome Measure (M-PROM). mediate the effects of quadriceps strengthening on knee adduction
2013. moment, pain, and function in medial knee osteoarthritis? A ran-
82. Stratford PW, Kennedy DM. Performance measures were neces- domized controlled trial. Arthritis Rheum 2008;59:943–51.
sary to obtain a complete picture of osteoarthritic patients. J Clin 103. Mikesky AE, Mazzuca SA, Brandt KD, et al. Effects of strength
Epidemiol 2006;59:160–7. training on the incidence and progression of knee osteoarthritis.
83. Dobson F, Hinman RS, Roos EM, et al. OARSI recommended Arthritis Rheum 2006;55:690–9.
performance-based tests to assess physical function in people diag- 104. Tanaka R, Ozawa J, Kito N, et al. Efficacy of strengthening or
nosed with hip or knee osteoarthritis. Osteoarthritis Cartilage aerobic exercise on pain relief in people with knee osteoarthritis:
2013;21:1042–52. a systematic review and meta-analysis of randomized controlled
84. Kroman SL, Roos EM, Bennell KL, et al. Measurement proper- trials. Clin Rehabil 2013;27:1059–71.
ties of performance-based outcome measures to assess physical 105. Jan M, Lin C, Lin Y, et al. Effects of weight-bearing versus
function in young and middle-aged people known to be at high nonweight-bearing exercise on function, walking speed, and posi-
risk of hip and/or knee osteoarthritis: a systematic review. Osteo- tion sense in participants with knee osteoarthritis: a randomized
arthritis Cartilage 2014;22(1):26–39. controlled trial. Arch Phys Med Rehabil 2009;90:897–904.
85. Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommenda- 106. Ageberg E, Link A, Roos EM. Feasibility of neuromuscular train-
tions for the management of hip and knee osteoarthritis, part II: ing in patients with severe hip or knee OA: the individualized
OARSI evidence-based, expert consensus guidelines. Osteoarthri- goal-based NEMEX-TJR training program. BMC Musculoskelet
tis Cartilage 2008;16:137–62. Disord 2010;11:126.
86. Pinto RZ, Ferreira ML, Oliveira VC, et al. Patient-centred com- 107. Dunlop DD, Song J, Semanik PA, et al. Objective physical activity
munication is associated with positive therapeutic alliance: a sys- measurement in the osteoarthritis initiative: are guidelines being
tematic review. J Physiother 2012;58:77–87. met? Arthritis Rheum 2011;63(11):3372–82.
87. Hall AM, Ferreira PH, Maher CG, et al. The influence of the 108. Pisters MF, Veenhof C, van Meeteren NL, et al. Long-term effec-
therapist-patient relationship on treatment outcome in physical tiveness of exercise therapy in patients with osteoarthritis of the hip
rehabilitation: a systematic review. Phys Ther 2010;90:1099–110. or knee: a systematic review. Arthritis Rheum 2007;57:1245–53.
88. Chan DK, Lonsdale C, Ho PY, et al. Patient motivation and 109. Ettinger WH Jr, Burns R, Messier SP, et al. A randomized trial
adherence to postsurgery rehabilitation exercise recommenda- comparing aerobic exercise and resistance exercise with a health
tions: the influence of physiotherapists’ autonomy-supportive education program in older adults with knee osteoarthritis. The
behaviors. Arch Phys Med Rehabil 2009;90:1977–82. Fitness Arthritis and Seniors Trial (FAST). JAMA 1997;277:25–31.
89. Louw A, Diener I, Butler DS, et al. The effect of neuroscience 110. Jordan JL, Holden MA, Mason EE, et al. Interventions to improve
education on pain, disability, anxiety, and stress in chronic mus- adherence to exercise for chronic musculoskeletal pain in adults.
culoskeletal pain. Arch Phys Med Rehabil 2011;92:2041–56. Cochrane Database Syst Rev 2010;(20):CD005956.
90. Nicholson P, French S, Hodges P, et al., editors. Key patient mes- 111. Marks R. Knee osteoarthritis and exercise adherence: a review.
sages. OARSI Scientific Congress; 2014; Paris: Osteoarthr Curr Aging Sci 2012;5:72–83.
Cartilage. 112. Walsh NE, Hurley MV. Evidence based guidelines and current
91. Fernandes L, Hagen KB, Bijlsma JW, et al. EULAR recommen- practice for physiotherapy management of knee osteoarthritis.
dations for the non-pharmacological core management of hip and Musculoskeletal Care 2009;7:45–56.
knee osteoarthritis. Ann Rheum Dis 2013;72:1125–35. 113. Brantingham JW, Bonnefin D, Perle SM, et al. Manipulative
92. Hochberg MC, Altman RD, Toupin April K, et al. American therapy for lower extremity conditions: update of a literature
College of Rheumatology 2012 recommendations for the use of review. J Manipulative Physiol Ther 2012;35:127–66.
nonpharmacologic and pharmacologic therapies in osteoarthritis 114. French HP, Brennan A, White B, et al. Manual therapy for osteo-
of the hand, hip, and knee. Arthritis Care Res 2012;64:465–74. arthritis of the hip or knee – a systematic review. Man Ther
93. Conaghan PG, Dickson J, Grant RL. Care and management of 2011;16:109–17.
osteoarthritis in adults: summary of NICE guidance. BMJ 115. Jansen MJ, Viechtbauer W, Lenssen AF, et al. Strength training
2008;336:502–3. alone, exercise therapy alone, and exercise therapy with passive
94. Uthman OA, van der Windt DA, Jordan JL, et  al. Exercise for manual mobilisation each reduce pain and disability in people with
lower limb osteoarthritis: systematic review incorporating trial knee osteoarthritis: a systematic review. J Physiother 2011;57
sequential analysis and network meta-analysis. BMJ 2013;347: :11–20.
f5555. 116. Abbott JH, Robertson MC, Chapple C, et al. Manual therapy,
95. Fransen M, McConnell S. Exercise for osteoarthritis of the knee. exercise therapy, or both, in addition to usual care, for osteoar-
Cochrane Database Syst Rev 2008;(4):CD004376. thritis of the hip or knee: a randomized controlled trial. 1: clinical
96. Pelland L, Brosseau L, Wells G, et al. Efficacy of strengthening effectiveness. Osteoarthritis Cartilage 2013;21(4):525–34.
exercises for osteoarthritis (part I): a meta-analysis. Phys Ther Rev 117. Kirkley A, Webster-Bogaert S, Litchfield R, et al. The effect of
2004;9:77–108. bracing on varus gonarthrosis. J Bone Joint Surg Am 1999;81:
97. Wallis JA, Taylor NF. Pre-operative interventions (non-surgical 539–48.
and non-pharmacological) for patients with hip or knee osteoar- 118. Brouwer R, Jakma T, Verhagen A, et al. Braces and orthoses for
thritis awaiting joint replacement surgery – a systematic review treating osteoarthritis of the knee. Cochrane Lib 2005;(1):
and meta-analysis. Osteoarthritis Cartilage 2011;19:1381–95. CD004020.
98. Messier SP, Mihalko SL, Legault C, et al. Effects of intensive diet 119. Lindenfeld TN, Hewett TE, Andriacchi TP. Joint loading with
and exercise on knee joint loads, inflammation, and clinical out- valgus bracing in patients with varus gonarthrosis. Clin Orthop
comes among overweight and obese adults with knee osteoarthri- Relat Res 1997;344:290–7.
546 PART IV  Overview of Contemporary Issues in Practice

120. Pollo FE, Otis JC, Backus SI, et al. Reduction of medial compart- 136. Shakoor N, Sengupta M, Foucher KC, et al. Effects of common
ment loads with valgus bracing of the osteoarthritic knee. Am J footwear on joint loading in osteoarthritis of the knee. Arthritis
Sports Med 2002;30:414–21. Care Res 2010;62:917–23.
121. Fantini Pagani CH, Willwacher S, Kleis B, et al. Influence of a 137. Sacco IC, Trombini-Souza F, Butugan MK, et al. Joint loading
valgus knee brace on muscle activation and co-contraction in decreased by inexpensive and minimalist footwear in elderly
patients with medial knee osteoarthritis. J Electromyogr Kinesiol women with knee osteoarthritis during stair descent. Arthritis
2013;23:490–500. Care Res 2012;64:368–74.
122. McWalter EJ, Hunter DJ, Harvey WF, et al. The effect of a patel- 138. Trombini-Souza F, Kimura A, Ribeiro AP, et al. Inexpensive foot-
lar brace on three-dimensional patellar kinematics in patients with wear decreases joint loading in elderly women with knee osteoar-
lateral patellofemoral osteoarthritis. Osteoarthritis Cartilage thritis. Gait Posture 2011;34:126–30.
2011;19:801–8. 139. Erhart JC, Dyrby CO, D’Lima DD, et al. Changes in in vivo knee
123. Felson D, Parkes M, Gait A, et al. A Randomised Trial Of A Brace loading with a variable-stiffness intervention shoe correlate with
For Patellofemoral Osteoarthritis Targeting Knee Pain and Bone changes in the knee adduction moment. J Orthop Res 2010;28:
Marrow Lesions. ACR Annual Meeting, San Diego, USA. 2013. 1548–53.
124. Andriacchi TP, Mundermann A. The role of ambulatory mechan- 140. Erhart JC, Mundermann A, Elspas B, et al. A variable-stiffness
ics in the initiation and progression of knee osteoarthritis. Curr shoe lowers the knee adduction moment in subjects with symp-
Opin Rheumatol 2006;18:514–18. toms of medial compartment knee osteoarthritis. J Biomech
125. Kean CO, Bennell KL, Wrigley TV, et al. Modified walking shoes 2008;41:2720–5.
for knee osteoarthritis: mechanisms for reductions in the knee 141. Shakoor N, Lidtke RH, Sengupta M, et al. Effects of specialized
adduction moment. J Biomech 2013;46:2060–6. footwear on joint loads in osteoarthritis of the knee. Arthritis
126. Hinman RS, Bowles KA, Metcalf BB, et al. Lateral wedge insoles Rheum 2008;59:1214–20.
for medial knee osteoarthritis: effects on lower limb frontal plane 142. Nigg B, Emery C, Hiemstra L. Unstable shoe construction and
biomechanics. Clin Biomech 2012;27:27–33. reduction of pain in osteoarthritis patients. Med Sci Sports Exerc
127. Radzimski AO, Mundermann A, Sole G. Effect of footwear on the 2006;38:1701–8.
external knee adduction moment – a systematic review. Knee 143. Buchecker M, Wagner H, Pfusterschmied J, et al. Lower extrem-
2012;19:163–75. ity joint loading during level walking with Masai barefoot technol-
128. Parkes MJ, Maricar N, Lunt M, et al. Lateral wedge insoles as a ogy shoes in overweight males. Scand J Med Sci Sports
conservative treatment for pain in patients with medial knee osteo- 2012;22:372–80.
arthritis: a meta-analysis. JAMA 2013;310:722–30. 144. Simic M, Hinman RS, Wrigley TV, et al. Gait modification strate-
129. Bennell K, Bowles K, Payne C, et al. Lateral wedge shoe insoles gies for altering medial knee joint load: a systematic review.
for medial knee osteoarthritis: 12 month randomised controlled Arthritis Care Res 2011;63(3):405–26.
trial. BMJ 2011;342:2912. 145. Simic M, Bennell KL, Hunt MA, et al. Contralateral cane use and
130. Rodrigues P, Ferreira A, Pereira R, et al. Effectiveness of medial- knee joint load in people with medial knee osteoarthritis: the effect
wedge insole treatment for valgus knee osteoarthritis. Arthritis of varying body weight support. Osteoarthritis Cartilage
Care Res 2008;59:603–8. 2011;19:1330–7.
131. Turpin KM, De Vincenzo A, Apps AM, et al. Biomechanical and 146. Jones A, Silva PG, Silva AC, et al. Impact of cane use on pain,
clinical outcomes with shock-absorbing insoles in patients with function, general health and energy expenditure during gait in
knee osteoarthritis: immediate effects and changes after 1 month patients with knee osteoarthritis: a randomised controlled trial.
of wear. Arch Phys Med Rehabil 2012;93:503–8. Ann Rheum Dis 2012;71:172–9.
132. Kerrigan D, Johansson J, Bryant M, et al. Moderate-heeled shoes 147. Vickers AJ, Cronin AM, Maschino AC, et al. Acupuncture for
and knee joint torques relevant to the development and progres- chronic pain: individual patient data meta-analysis. Arch Intern
sion of knee osteoarthritis. Arch Phys Med Rehabil 2005;86: Med 2012;172:1444–53.
871–5. 148. Corbett MS, Rice SJ, Madurasinghe V, et al. Acupuncture and
133. Kerrigan D, Karvosky M, Lelas J, et al. Men’s shoes and knee joint other physical treatments for the relief of pain due to osteoarthritis
torques relevant to the development and progression of knee of the knee: network meta-analysis. Osteoarthritis Cartilage
osteoarthritis. J Rheumatol 2003;30:529–33. 2013;21:1290–8.
134. Kerrigan D, Lelas J, Karvosky M. Women’s shoes and knee osteo- 149. Whitehurst DG, Bryan S, Hay EM, et al. Cost-effectiveness of
arthritis. Lancet 2001;357:1097–8. acupuncture care as an adjunct to exercise-based physical therapy
135. Kerrigan DC, Todd MK, Riley PO. Knee osteoarthritis and high- for osteoarthritis of the knee. Phys Ther 2011;91:630–41.
heeled shoes. Lancet 1998;351:1399–401.
 CHAPTER 49 

Ankle Injury
Claire Hiller  •  Kathryn Refshauge

Ankle injuries are among the most common injuries in syndesmosis injury using simple tests available in any
both sporting and non-sporting populations.1–5 The most setting.
common ankle injuries presenting to the clinic are ankle Chronic ankle instability (CAI) is the most commonly
sprains and ankle fractures. It is not the intent of this used term to describe ongoing problems following an
chapter to discuss detailed assessment and management ankle sprain.11 Reported problems include recurrent
of these conditions, but rather to highlight the recent sprain, the ankle feeling unstable or giving way, altered
issues and advances in the area of ankle sprain and the range of motion (either increased laxity or stiffness) and
related syndesmosis injury and chronic ankle instability, pain.12 These problems may exist in isolation or combina-
and fracture. tion.13 CAI can result in disability, decreased physical
activity or job participation,14–17 and the development of
ankle osteoarthritis.18
EPIDEMIOLOGY CAI appears to be highly prevalent. A systematic
review found that between 15% and 64% of people had
Acute ankle sprains are among the most common sporting not recovered 3 years after their ankle sprain.19 It has
injuries4 and are responsible for a high proportion been reported that 8% of people in the general popula-
of attendances at emergency centres.2 A recent meta- tion have ongoing problems after ankle sprain, and for
analysis found that the incidence of ankle sprains was the majority these problems had persisted for more than
higher in female athletes, the young, and athletes of 10 years.15 Despite research increasing exponentially in
indoor and court sports. However, the pooled prevalence the past few years, much remains unknown about CAI.
across subgroups was similar, being approximately 11%
of all injuries.3 The incidence of lateral sprains (0.93 per
1000 athlete exposures) was almost three times higher PROGNOSIS
than syndesmosis sprains (0.38) and nine times higher
than medial sprains (0.06).3 The majority of studies on The typical clinical course after a lateral ankle sprain is a
incidence of ankle injuries have focused primarily on marked decrease in pain and increase in function within
lateral ankle sprain; however, the incidence of syndesmo- 2 weeks.19 Whereas most people recover, up to 18% still
sis injury appears to be increasing. have problems years later.15 While it appears intuitive
Syndesmosis sprain, also known as a ‘high’ ankle sprain, that the severity of a lateral ankle sprain would be related
is a sprain of the soft tissues of the inferior tibiofibular to recovery time or likelihood of residual problems, evi-
joint. Originally, only the interosseous membrane was dence for this is lacking.20 Currently it is unknown who
considered to constitute the syndesmosis. Recent evi- will develop ongoing problems after an ankle sprain,
dence suggests that an injury of any of the following unless the injury involves the joint.
anatomic structures is considered a syndesmosis sprain: It has frequently been reported that recovery from an
the ankle interosseous membrane, the interosseous liga- ankle syndesmosis injury takes longer than recovery from
ment, the anterior tibiofibular ligament and the posterior a lateral ankle sprain.9,21–23 The reported delayed recovery
inferior tibiofibular ligament with its transverse liga- varies widely, ranging from 2 to 20 times that of lateral
ment.6 The inferior tibiofibular joint is a very stable joint ankle sprain. To increase precision, and overcome some
due to both bony congruence and ligamentous restraints.6 of the methodological flaws of previous studies, a recent
The inferior tibiofibular joint is so strong it is reported prospective study used magnetic resonance imaging
that the syndesmosis and ankle mortise only widen 1 mm (MRI) to determine recovery times for syndesmosis
during normal gait.7 An increase in this widening by as injury. This study found that it took four times longer to
little as 1 mm decreases the contact area of the tibiofibu- return to sport or activity after syndesmosis injury than
lar joint by 42%.8 after ankle sprain (62 versus 15 days mean recovery
The reported incidence of ankle syndesmosis injury time).24 The same study found that any person with a
varies between 1%9 and 25%10 of all ankle sprains. This lateral ankle sprain or syndesmosis injury who had not
wide range may be due to a real increase in incidence, or recovered within 2 weeks of injury, was likely to have
may be due to improved diagnosis of syndesmosis injury. prolonged recovery if the vertical jump height was
While ankle sprains are easily recognized, diagnosis of reduced or the score on the Fear Avoidance Beliefs Ques-
syndesmosis injuries has proved more elusive. However, tionnaire Sport subscale was high.24 In addition, a positive
recent evidence has improved diagnostic accuracy of squeeze test or an increased tenderness on palpation of
547
548 PART IV  Overview of Contemporary Issues in Practice

the anterior interosseous membrane has been found to but reliability and accuracy of diagnosis are strongly
be strongly related to time to return to sport.25–27 operator-dependent. Most research in the area of ultra-
There has been no investigation of prognosis for sound diagnosis has used expert radiographers rather
people who have developed CAI, except for an acknowl- than trained clinicians, and demonstrated that ultrasound
edgement that some injuries ultimately progress to post- has a high degree of accuracy for diagnosis of acute36 and
traumatic ankle osteoarthritis.18 chronic ATFL injury40,41 and anterior tibiofibular liga-
ment injury.42 One recent study compared bedside ultra-
sound in the emergency department, utilized by clinicians
RISK FACTORS with 6 hours of training, with MRI to identify ATFL
injury. The results of bedside ultrasound were compara-
Many risk factors for ankle injuries have been proposed ble to MRI indicating that the use of real-time ultrasound
with few definitive findings. The risk of an ankle injury in the clinic has promise for initial triaging and decisions
was found to be increased in people with greater postural for further investigations.43
sway, lower postural stability, decreased eccentric inver-
sion strength at slow speeds of isokinetic testing, and
higher concentric plantarflexion strength at high speeds
Fracture
of isokinetic testing.28 However, no risk factors have been One of the important differential diagnoses at initial pre-
substantiated for an initial ankle sprain. Systematic sentation is the possible presence of an ankle fracture. It
reviews of studies which investigated mixed groups of is not uncommon for a lateral sprain to be accompanied
participants (i.e. those with and those without a previous by an avulsion fracture, particularly in children. Ankle
history of sprain) have suggested that females of younger syndesmosis injuries are usually incomplete, but may be
age,3 with poor postural control,29,30 and limited dorsiflex- accompanied by an ankle fracture or less commonly by a
ion29 are at higher risk of future ankle sprain. fracture of the proximal fibula.44
There are no confirmed risk factors for syndesmosis The Ottawa Ankle Rules (OAR) should be utilized to
injury, and unlike other ankle sprains a previous ankle rule out fractures or the need for X-rays.45 X-rays should
sprain or high ankle sprain does not appear to increase only be ordered if there is pain in either malleolar zone
the likelihood of re-injury.31 One study noted that there and any of: bone tenderness at either malleolar tip, or
is a higher risk of syndesmosis injury among American along the distal 6 cm of the posterior edge of the tibia or
football players who play on artificial surfaces compared fibular, or inability to bear weight for four steps both
with natural grass.10 immediately after injury and in the clinician’s rooms. The
The only confirmed predictor for CAI is a history of likelihood of an acute injury being an ankle fracture when
previous ankle sprain.20 A recent systematic review of the OAR is negative is around 1.4%.46
prospective studies that followed people after their first A modification of the OAR has been developed for
sprain to identify those who developed CAI, found only paediatric use to further decrease exposure to X-rays.47
four studies. The score on the Cumberland Ankle Insta- On clinical examination, if the only findings are tender-
bility Tool (a questionnaire to measure ankle instability ness and swelling over the distal fibula or adjacent lateral
with excellent psychometric properties)32 and number of ligaments distal to the tibial anterior joint line, an X-ray
foot lifts in 30 seconds with the eyes closed33 did not is not required. These injuries have been deemed low-
predict re-sprain. One study found that severity of the risk ankle injuries that can be managed conservatively.
index sprain predicted re-sprain but methodological Such low-risk injuries include lateral ankle sprains, non-
issues suggest that the findings should be interpreted with displaced Salter–Harris types I and II fractures of the
caution.20 distal fibula and avulsion fractures of the distal fibula or
lateral talus.47 Although all investigations of the OAR
have been conducted in emergency departments, it is
DIAGNOSIS highly likely that the decision rules would generalize to
most clinicians in any setting.
It is now clear that early, accurate diagnosis of the spe-
cific ankle injury is critical to ensure effective treatment
that is specific to the injury. The diagnoses that are Ankle Sprain
most commonly missed are fracture, syndesmosis injury, Inversion Sprain
talar dome lesion or occasionally the less common inju-
ries and abnormalities such as subtalar sprain or tarsal The mechanism of injury for an inversion sprain has long
coalition.34 been believed to be inversion of the plantar flexed ankle.48
Imaging is often used to confirm differential diagnosis However, recent case reports using three-dimensional
of ankle injury. X-rays are mainly used for identifying biomechanical analysis of real-time ankle sprain inci-
bony injury (e.g. fractures or a tibiofibular diastasis asso- dents, report that inversion with internal rotation may be
ciated with a syndesmosis injury).35 The use of stress a more important mechanism.49
X-rays for lateral ligament36 or syndesmosis injury37 The primary clinical diagnostic tests for inversion
does not have high diagnostic accuracy. MRI has the best sprain are the anterior drawer and talar tilt tests. Despite
diagnostic accuracy for ligament and syndesmosis their common use there is little evidence of their diag-
injury36,38,39 but is relatively expensive to be considered nostic accuracy.50 It may be that the anterior drawer test
for routine use. Ultrasound imaging is cheap and quick carried out 4–5 days post injury, together with the
 49  Ankle Injury 549

presence of pain on palpation of the ligament, and evi- and fibular translation tests (intraclass correlation coef-
dence of bruising, may be more accurate diagnostic indi- ficient <0.46).54
cators of a ligament sprain.51 More recently, diagnostic accuracy of the clinical
There are a number of systems used to grade the examination for syndesmosis injury was determined by
severity of an ankle sprain injury52 with no system having comparing test findings with findings on MRI.55 Eight
evidence for high reliability or validity, and none is uni- symptoms and five physical signs were investigated.
versally accepted. For the clinician it is more important Symptoms included mechanism of injury (dorsiflexion
to ensure identification of severe pathologies and any and external rotation of the foot), inability to continue
associated injuries to ensure implementation of the most to play or walk, pain or dysfunction out of proportion
appropriate treatment and timely referral if required. to injury, pain in the shank or knee during injury,
swelling above the ankle, inability to hop, pain during
lunge with external rotation of the foot, and presence of
Syndesmosis Injury
a posterior impingement. Five diagnostic tests were
During the history, a high index of suspicion should be investigated: palpation of syndesmosis ligaments; palpa-
raised that the injury has disrupted the ankle syndesmosis tion of deltoid ligament; squeeze test; dorsiflexion
if the mechanism of injury involved external rotation of lunge with compression; and dorsiflexion with external
the foot. Other physical findings consistent with syndes- rotation stress test. The dorsiflexion with external rota-
motic injuries include palpatory tenderness over the syn- tion test was found to have the highest sensitivity (71%)
desmotic ligaments and swelling proximal to the ankle and the squeeze test the highest specificity (88%). A com-
joint line.53 bination of the two tests did not further improve sensitiv-
Many diagnostic clinical tests have been proposed but ity or specificity. Of all investigated symptoms, the only
until recently there has been little evidence to support one to reach the predetermined level of 70% sensitivity
their use. A recent systematic review of diagnostic tests was the inability to hop, and for specificity were pain out
for syndesmosis injury found only two studies that exam- of proportion to the injury (whether too much or too
ined the validity of some tests.54 Diagnostic validity of the little in relation to the mechanism) and pain in the shank
anterior drawer, cotton, dorsiflexion, external rotation or knee.
and fibula translation tests was poor. Results for validity Taken together, these findings suggest the key ques-
of the squeeze test were conflicting (LR −1.50 to +1.50), tions in the history include: mechanism of injury (dorsi-
and reliability of other diagnostic tests was variable. flexion or external rotation); inability to walk; or inability
Intra-rater reliability was high in terms of percentage to perform a single leg hop. If any of the syndesmosis
close agreement (PCA) for the squeeze, cotton, external ligaments are painful to palpation and the dorsiflexion
rotation and dorsiflexion tests (PCA >83%). Inter-rater and rotation test is positive, then the squeeze test should
reliability was good (intraclass correlation coefficient be performed to confirm the injury. If the squeeze test is
>0.70) for the external rotation stress test, and fair to positive then it is very likely to be a syndesmosis injury
poor for the squeeze, dorsiflexion, cotton, anterior drawer and MRI is recommended (Table 49-1).

TABLE 49-1  Summary of Recommended Syndesmosis Clinical Diagnostic Test Protocols

Protocol Positive Findings Rationale
Syndesmosis ligament palpation Palpation of Report of pain The classic feature of
anterior during palpation ankle syndesmosis
tibiofibular of the ligament/ injury is thought to
ligament/ membrane25,56,57 be palpatory
posterior inferior tenderness over the
tibiofibular anterior and posterior
ligament tibiofibular ligaments
–transverse and between the tibia
ligament/ and fibula.53,58
interosseous Tenderness
ligament/ proximally along
interosseous the interosseous
membrane25,56,57 membrane was
indicative of a longer
time to recovery25
and a more severe
injury59

©Amy Sman

Continued on following page

550 PART IV  Overview of Contemporary Issues in Practice

TABLE 49-1  Summary of Recommended Syndesmosis Clinical Diagnostic Test Protocols (Continued)
Protocol Positive Findings Rationale

Dorsiflexion-external rotation test Leg is stabilized in Reproduction of The test is thought

90° knee flexion, anterolateral to reproduce pain
the ankle in pain over the over the ankle
maximal syndesmosis area syndesmosis
dorsiflexion, and ligaments by
an external mimicking the
rotation stress to commonly described
the injured foot mechanism of
and ankle is injury23,60–62
applied23

©Amy Sman

Squeeze test Patient sitting over Replication of Biomechanical analysis

side of the bed. pain in the area confirmed that the
Compression of of the ankle calf compression
fibula and tibia syndesmosis9,61,63,64 causes separation at
above the the distal tibiofibular
midpoint of the joint.63 It is thought to
calf9,61,63,64 increase tension in
the remaining ankle
syndesmosis
ligament fibres,
resulting in pain
at the ankle65

©Amy Sman

Chronic Ankle Instability measure functional (or perceived) instability are the
Cumberland Ankle Instability Tool32 and the Identifica-
Diagnosis of CAI is relatively straightforward. Patients tion of Functional Ankle Instability.66 A score of ≤27 out
presenting with ongoing problems following an ankle of 30 on the Cumberland Ankle Instability Tool is inter-
sprain, including; pain, recurrent injury, mechanical ankle preted as indicating presence of functional ankle instabil-
instability and functional ankle instability are likely to ity, although a score of ≤24 is recommended for research.
have CAI. There have been a number of methods devel- A score of ≥10 out of 37 for the Identification of Func-
oped to measure these different aspects of CAI. The two tional Ankle Instability is also interpreted as presence of
recommended by the International Ankle Consortium to functional ankle instability.12 A paediatric version of the
 49  Ankle Injury 551

Cumberland Ankle Instability Tool has been developed

for use in people aged 8 years and older.67 For measuring MANAGEMENT
disability related to CAI the Foot and Ankle Ability
measure68 and Foot and Ankle Outcome Score are Evidence and guidelines for the treatment of ankle sprains
recommended.69 has been summarized and published in several countries
over recent years. The reader is directed to these for a
more detailed summary of the literature.101–106 There are
no studies of treatment for the conservative management
IMPAIRMENTS of syndesmosis injuries. Overall, the majority of ankle
sprains can be effectively managed using conservative
Once diagnosed, it is the impairments that are treated treatments.
rather than the actual pathology. Typically, physical Surgery should rarely be considered.107 Lateral sprains
examination of a peripheral injury involves comparison with severe mechanical joint instability, and syndesmosis
of test results with the unaffected limb. However, the injuries that also involve fractures or frank diastasis,
contralateral limb is likely not a useful comparator for require surgery. Currently the most common surgical
determining impairment or monitoring progress. In techniques for severe syndesmosis injury are screws or
addition to the prevalence of bilateral ankle problems, suture buttons.108 While both have excellent outcomes,
there is evidence that deficits are bilateral even after uni- suture buttons appear to provide a more accurate method
lateral injury, e.g. in postural control and various balance of syndesmosis stabilization.109
tests, following an ankle sprain.70
Common impairments following acute ankle sprain
are pain, swelling, reduced range of motion and decreased
Ankle Sprain
balance. Pain and swelling usually resolve quickly. The Conservative treatment in the initial phase after sprain,
volume of swelling is only moderately correlated with usually consists of the (P)RICE regimen for acute soft
injury severity51 and is not associated with self-assessed tissue injuries,106 even though not all individual ele-
function.71 However, swelling that has not resolved within ments have strong evidence to support their use.110
one month is related to ongoing decreased function and Protection in the form of functional support rather
quality of life.71,72 Reduced ankle range of motion occurs than immobilization is effective for most ankle sprains,107
due to pain, swelling or loss of normal accessory joint with the possible exception of severe sprains which
motion in the ankle or subtalar joints.73,74 Dorsiflexion is may benefit from a rigid form of immobilization for
the most commonly impaired motion. Although ankle a short (up to 10 days) period.111 Functional support
laxity improves during the first 6 to 12 weeks, it com- involves the use of a removable device and it appears
monly persists for at least one year post injury.75 The that a semi-rigid brace is better than other supports
extent of ligament laxity is not associated with level of (e.g. an elastic bandage) in terms of functional outcome
self-reported function.76 and total cost.112 The preferred type of functional support
Both strength of the ankle muscles and postural depends on the outcome required. A systematic review
control30,70 are impaired following an ankle sprain. comparing the types of functional support (elastic
Strength may take up to 4 months post injury to bandage, tape, semi-rigid support and lace-up ankle
normalize.77–80 support) found them to be equally effective for reduc-
Chronic ankle instability results in similar impairments ing pain, swelling, ankle instability and preventing
to those of acute ankle sprain. Impairments identified recurrent sprain.113 A semi-rigid support appeared more
from the highest level of evidence (i.e. in systematic effective for earlier return to sport, and tape resulted
reviews) include changes in morphology of the talus,81 in a higher rate of skin complications. A recent com-
muscle weakness,81,82 impaired balance or postural stabil- parison of an Aircast ankle brace with an elastic support
ity,30,70,81,83,84 and decreased proprioceptive ability.84,85 bandage demonstrated a significant improvement in
However, only specific types of muscle contraction or ankle function at 10 days and 1 month when using
strength ratios are affected81,82,84 and, similarly, only some the ankle brace.114 The use of a protective device for
aspects of proprioception are impaired.81,84 Recent find- a prolonged period for lateral ankle sprain is occasion-
ings are indicative of changes in the central organization ally used, but has no research evidence to support its
of movement in people with CAI. Not only are there use, and is not recommended.
bilateral postural deficits,33,86 but also proximal changes Manual therapy has been applied in a number of ways
in muscle patterns,87–90 alterations in planned movement to treat ankle sprains.115 In the acute phase both passive
patterns91–95 and changes in cortical96,97 and peripheral anteroposterior glide of the talus116,117 and osteopathic
sensory excitability.98–100 It is currently thought that there ankle manipulation118 reduced pain and increased dorsi-
may be an association between subgroups of CAI and flexion range of motion in the short term after lateral
various deficits;13,91 however, there is no definitive evi- ankle sprain. For treatment in the subacute phase mobi-
dence to support this proposal. It appears that the deficits lization with movement, as described by Mulligan, a chi-
experienced by people with CAI may be highly individ- ropractic mortise adjustment technique and an
ual.13 Clinicians should therefore take care to examine the anteroposterior glide of the talus were all shown to
presenting patient and not use a routine formula for improve ankle range of motion, reduce pain and improve
treatment. function.115
552 PART IV  Overview of Contemporary Issues in Practice

Medications of various types have been suggested for ‘balance’, ‘neuromuscular’, strength and ‘functional’
ankle sprains. There is strong evidence that the use of training. While there is evidence that some form of exer-
non-steroidal anti-inflammatory drugs (NSAIDs) during cise programme is more effective than no training for
the first 2 weeks following ankle sprain, administered reducing sensorimotor deficits or improving function,130
orally or topically, is more effective than a placebo.102 the size of the effect is moderate at best.131 Furthermore,
Non-steroidal anti-inflammatory drugs (Piroxicam) the variety of combinations of training modes, frequency
reduced pain and swelling and improved function in the and duration of exercise investigated precludes identifica-
short term with continued better functional outcomes tion of the effective component(s).131
than placebo for at least 6 months.119 However, care Manual therapy for CAI is effective for some out-
should be taken to monitor early mobilization levels if comes, but not others. Mobilization techniques to
choosing this option as the study also noted an increase improve ankle range of motion were shown to be mostly
in ankle instability in the treated group. effective.132–135 The techniques improved sports-related
Exercise training includes interventions to restore activities,132 pain and function,134,136 but did not change
range of motion, strength and sensorimotor function.102 dynamic balance or activities of daily living.132
Various forms of exercise training have been shown to Orthotics for treating CAI should be used with caution.
result in more rapid recovery for sprains of any sever- While orthotics have been shown to improve propriocep-
ity,120–123 although one study with apparently contradic- tive and balance abilities137–140 the effect may not be
tory findings found that supervised rehabilitation was not greater than that of an exercise or rehabilitation interven-
superior to conventional treatment for recovery in par- tion alone.140
ticipants in the Netherlands.124 Both groups improved,
potentially because usual care included home exercises in
addition to early mobilization and ankle protection.
There is little evidence for the use of electrophysical
Prevention of Further Ankle Sprain
agents for treatment of acute ankle sprains.103,104,125 Ultra- The use of an external brace or ankle tape has been
sound is not effective and should not be used in the shown to decrease the recurrence of ankle sprains.107,141
treatment of acute ankle sprains.126,127 A recent randomized controlled trial compared an
8-week progressive home-based neuromuscular training
programme with wearing an ankle brace for 12 months
during sports activities, and a combination of the neu-
Syndesmosis Injury romuscular programme and 8 weeks of wearing the
No study to date has evaluated treatment for syndesmosis brace.142 Bracing was more effective than training for
injury, and therefore recommendations must, of neces- reducing ankle sprain recurrence, but not the severity
sity, be based on logic and clinical wisdom. For stable of sprain. While useful for sporting activities, such an
injuries that involve the syndesmosis, the most common intervention does not aid prevention when not wearing
management is protection in a boot or brace for varying the brace during activities of daily living or for those
lengths of time7,21,53,128,129 followed by rehabilitation. Tape who play a sport where braces are not permitted. Tape
has also been suggested when a brace is not suitable, and has also been shown to be effective although the rate
usually consists of a modified circumferential application of skin complications is higher and the long-term cost
placed above the malleoli with or without a modified is greater. It would appear that using a brace or tape
subtalar sling.53 should be considered a long-term protective strategy for
Clinical wisdom and logic would also caution against people participating in sports activities. Their use should
the use of manual therapy techniques at the ankle in the continue after the rehabilitation training programme has
early stages of syndesmosis injury, as dorsiflexion widens finished.
the ankle mortise and places the syndesmotic ligaments
under further stress. It is reasonable to assume that end-
range dorsiflexion and weight-bearing activities also be
avoided in the acute phase due to the potential for widen- CONCLUSION
ing of the ankle mortise.
During later-stage rehabilitation, care should be taken Early accurate diagnosis of ankle injury is essential, in
with return to exercise, and consideration given to delay- particular the identification of a fracture or syndesmosis
ing activities with plyometrics, and cutting or changing injury, to ensure early effective management and to
direction manoeuvres. These activities could force the prevent further harm. Early identification of a syndesmo-
foot into external rotation relative to the tibia, thereby sis injury is important as some common treatment tech-
increasing strain of the syndesmosis. niques should be avoided or modified. While the ‘simple
sprain’ is the most common presenting injury, there is no
treatment ‘recipe’. Treatment must be individualized
according to findings on clinical examination, particu-
Chronic Ankle Instability larly for people who develop chronic ankle instability
Management of CAI encompasses a range of treatment after sprain. However, the most effective treatment
options, all of which have limited evidence for their effi- appears to be an exercise-based programme which
cacy. The most common intervention is exercise, of involves strength, balance, neuromuscular and functional
varying forms, including elements variously described as components.
 49  Ankle Injury 553

24. Sman AD, Hiller CE, Rae K, et al. Prognosis of ankle syndesmosis
REFERENCES injury. Med Sci Sports Exerc 2014;46(4):671–7.
1. Boyce SH, Quigley MA. Review of sports injuries presenting to 25. Nussbaum ED, Hosea TM, Sieler SD, et al. Prospective evalua-
an accident and emergency department. Emerg Med J 2004;21(6): tion of syndesmotic ankle sprains without diastasis. Am J Sports
704–6. Med 2001;29(1):31–5.
2. Bridgman SA, Clement D, Downing A, et al. Population based 26. Miller BS, Downie BK, Johnson PD, et al. Time to return to play
epidemiology of ankle sprains attending accident and emergency after high ankle sprains in collegiate football players: a prediction
units in the West Midlands of England, and a survey of UK prac- model. Sports Health 2012;4(6):504–9.
tice for severe ankle sprains. Emerg Med J 2003;20(6):508–10. 27. Sikka RS, Fetzer GB, Sugarman E, et al. Correlating MRI find-
3. Doherty C, Delahunt E, Caulfield B, et al. The incidence and ings with disability in syndesmotic sprains of NFL players. Foot
prevalence of ankle sprain injury: a systematic review and meta- Ankle Int 2012;33(5):371–8.
analysis of prospective epidemiological studies. Sports Med 28. Witchalls J, Blanch P, Waddington G, et al. Intrinsic functional
2014;44(1):123–40. deficits associated with increased risk of ankle injuries: a systematic
4. Fong DT, Hong Y, Chan LK, et al. A systematic review on ankle review with meta-analysis. Br J Sports Med [Meta-Analysis
injury and ankle sprain in sports. Sports Med [Review] 2007;37(1): Research Support, Non-U.S. Gov’t Review] 2012;46(7):515–23.
73–94. 29. de Noronha M, Refshauge KM, Herbert RD, et al. Do voluntary
5. Marinos G, Giannopoulos A, Vlasis K, et al. Primary care in the strength, proprioception, range of motion, or postural sway
management of common orthopaedic problems. Qual Prim Care predict occurrence of lateral ankle sprain? Br J Sports Med
2008;16(5):345–9. 2006;40(10):824–8, discussion 828.
6. Lebech M, Andersen O, Christensen NC, et al. Feasibility of 30. McKeon PO, Hertel J. Systematic review of postural control and
neonatal screening for toxoplasma infection in the absence of lateral ankle instability, part I: can deficits be detected with instru-
prenatal treatment. Danish Congenital Toxoplasmosis Study mented testing. J Athl Train 2008;43(3):293–304.
Group. Lancet 1999;353(9167):1834–7. 31. Sman AD, Hiller CE, Rae K, et al. Predictive factors for ankle
7. Lin CF, Gross ML, Weinhold P. Ankle syndesmosis injuries: syndesmosis injury in football players: a prospective study. J Sci
anatomy, biomechanics, mechanism of injury, and clinical guide- Med Sport 2014;17(6):586–90.
lines for diagnosis and intervention. J Orthop Sports Phys Ther 32. Hiller CE, Refshauge KM, Bundy AC, et al. The Cumberland
2006;36(6):372–84. ankle instability tool: a report of validity and reliability testing.
8. Hermans JJ, Beumer A, de Jong TA, et al. Anatomy of the distal Arch Phys Med Rehabil [Research Support, Non-U.S. Gov’t]
tibiofibular syndesmosis in adults: a pictorial essay with a multi- 2006;87(9):1235–41.
modality approach. J Anat 2010;217(6):633–45. 33. Hiller CE, Refshauge KM, Herbert RD, et al. Balance and recov-
9. Hopkinson WJ, St Pierre P, Ryan JB, et al. Syndesmosis sprains ery from a perturbation are impaired in people with functional
of the ankle. Foot Ankle 1990;10(6):325–30. ankle instability. Clin J Sport Med [Comparative Study Research
10. Hunt KJ, George E, Harris AH, et al. Epidemiology of syndes- Support, Non-U.S. Gov’t] 2007;17(4):269–75.
mosis injuries in intercollegiate football: incidence and risk factors 34. Brukner P, Khan K, Karlsson J. Acute ankle injuries. In: Brukner
from National Collegiate Athletic Association injury surveillance P, Khan K, editors. Clinical Sports Medicine. 3rd ed. Sydney:
system data from 2004–2005 to 2008–2009. Clin J Sport Med McGraw-Hill.; 2006. p. 612–31.
2013;23(4):278–82. 35. Harper MC, Keller TS. A radiographic evaluation of the tibio-
11. Delahunt E, Coughlan GF, Caulfield B, et al. Inclusion criteria fibular syndesmosis. Foot Ankle 1989;10(3):156–60.
when investigating insufficiencies in chronic ankle instability. Med 36. Oae K, Takao M, Uchio Y, et al. Evaluation of anterior talofibular
Sci Sports Exerc [Review] 2010;42(11):2106–21. ligament injury with stress radiography, ultrasonography and MR
12. Gribble PA, Delahunt E, Bleakley C, et al. Selection criteria for imaging. Skeletal Radiol 2010;39(1):41–7.
patients with chronic ankle instability in controlled research: a 37. Pakarinen H, Flinkkila T, Ohtonen P, et al. Intraoperative assess-
position statement of the international ankle consortium. J Orthop ment of the stability of the distal tibiofibular joint in supination-
Sports Phys Ther 2013;43(8):585–91. external rotation injuries of the ankle: sensitivity, specificity, and
13. Hiller CE, Kilbreath SL, Refshauge KM. Chronic ankle instabil- reliability of two clinical tests. J Bone Joint Surg Am 2011;93(22):
ity: evolution of the model. J Athl Train [Research Support, Non- 2057–61.
U.S. Gov’t] 2011;46(2):133–41. 38. Oae K, Takao M, Naito K, et al. Injury of the tibiofibular
14. Arnold BL, Wright CJ, Ross SE. Functional ankle instability and syndesmosis: value of MR imaging for diagnosis. Radiology
health-related quality of life. J Athl Train 2011;46(6):634–41. 2003;227(1):155–61.
15. Hiller CE, Nightingale EJ, Raymond J, et al. Prevalence and 39. Takao M, Ochi M, Oae K, et al. Diagnosis of a tear of the tibio-
impact of chronic musculoskeletal ankle disorders in the com- fibular syndesmosis. The role of arthroscopy of the ankle. J Bone
munity. Arch Phys Med Rehabil 2012;93(10):1801–7. Joint Surg Br 2003;85(3):324–9.
16. Konradsen L, Bech L, Ehrenbjerg M, et al. Seven years follow-up 40. Cheng Y, Cai Y, Wang Y. Value of ultrasonography for detecting
after ankle inversion trauma. Scand J Med Sci Sports 2002; chronic injury of the lateral ligaments of the ankle joint compared
12(3):129–35. with ultrasonography findings. Br J Radiol 2014;87(1033):20130406.
17. Wikstrom EA, Tillman MD, Chmielewski TL, et al. Self-assessed 41. Hua Y, Yang Y, Chen S, et al. Ultrasound examination for the
disability and functional performance in individuals with and diagnosis of chronic anterior talofibular ligament injury. Acta
without ankle instability: a case control study. J Orthop Sports Radiol 2012;53(10):1142–5.
Phys Ther 2009;39(6):458–67. 42. Mei-Dan O, Kots E, Barchilon V, et al. A dynamic ultrasound
18. Valderrabano V, Hintermann B, Horisberger M, et al. Ligamen- examination for the diagnosis of ankle syndesmotic injury in pro-
tous posttraumatic ankle osteoarthritis. Am J Sports Med 2006; fessional athletes: a preliminary study. Am J Sports Med 2009;
34(4):612–20. 37(5):1009–16.
19. van Rijn RM, van Os AG, Bernsen RM, et al. What is the clinical 43. Gun C, Unluer EE, Vandenberk N, et al. Bedside ultrasonogra-
course of acute ankle sprains? A systematic literature review. Am phy by emergency physicians for anterior talofibular ligament
J Med [Review] 2008;121(4):324–31 e6. injury. J Emerg Trauma Shock 2013;6(3):195–8.
20. Pourkazemi F, Hiller CE, Raymond J, et al. Predictors of chronic 44. Norkus SA, Floyd RT. The anatomy and mechanisms of syndes-
ankle instability after an index lateral ankle sprain: a systematic motic ankle sprains. J Athl Train 2001;36(1):68–73.
review. J Sci Med Sport 2014;17(6):568–73. 45. Stiell IG, McKnight RD, Greenberg GH, et al. Implementation
21. Osbahr DC, Drakos MC, O’Loughlin PF, et al. Syndesmosis and of the Ottawa ankle rules. JAMA 1994;271(11):827–32.
lateral ankle sprains in the national football league. Orthopedics 46. Bachmann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa
2013;36(11):e1378–84. ankle rules to exclude fractures of the ankle and mid-foot: system-
22. Wright RW, Barile RJ, Surprenant DA, et al. Ankle syndesmosis atic review. BMJ [Meta-Analysis Review] 2003;326(7386):417.
sprains in national hockey league players. Am J Sports Med 47. Boutis K, Grootendorst P, Willan A, et al. Effect of the Low Risk
2004;32(8):1941–5. Ankle Rule on the frequency of radiography in children with ankle
23. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. injuries. CMAJ [Clinical Trial Multicenter Study Research
Am J Sports Med 1991;19(3):294–8. Support, Non-U.S. Gov’t] 2013;185(15):E731–8.
554 PART IV  Overview of Contemporary Issues in Practice

48. Koenig MD. Ligament Injuries of the Foot and Ankle in Adult 74. Wolfe MW, Uhl TL, Mattacola CG, et al. Management of ankle
Athletes. In: DeLee JC, Drez D, Miller MD, editors. DeLee and sprains. Am Fam Physician 2001;63(1):93–104.
Drez’s Orthopaedic Sports Medicine. 3rd ed. Philadelphia: Saun- 75. Hubbard-Turner T. Relationship between mechanical ankle
ders/Elsevier.; 2010. p. 1912–60. joint laxity and subjective function. Foot Ankle Int 2012;33(10):
49. Fong DT, Ha SC, Mok KM, et al. Kinematics analysis of ankle 852–6.
inversion ligamentous sprain injuries in sports: five cases from 76. Croy T, Saliba S, Saliba E, et al. Talofibular interval changes after
televised tennis competitions. Am J Sports Med 2012;40(11): acute ankle sprain: a stress ultrasonography study of ankle laxity.
2627–32. J Sport Rehabil [Research Support, Non-U.S. Gov’t] 2013;
50. Croy T, Koppenhaver S, Saliba S, et al. Anterior talocrural joint 22(4):257–63.
laxity: diagnostic accuracy of the anterior drawer test of the ankle. 77. Holme E, Magnusson SP, Becher K, et al. The effect of supervised
J Orthop Sports Phys Ther 2013;43(12):911–19. rehabilitation on strength, postural sway, position sense and re-
51. van Dijk CN, Mol BW, Lim LS, et al. Diagnosis of ligament injury risk after acute ankle ligament sprain. Scand J Med Sci
rupture of the ankle joint. Physical examination, arthrography, Sports 1999;9(2):104–9.
stress radiography and sonography compared in 160 patients after 78. Konradsen L, Olesen S, Hansen HM. Ankle sensorimotor control
inversion trauma. Acta Orthop Scand [Comparative Study] and eversion strength after acute ankle inversion injuries. Am J
1996;67(6):566–70. Sports Med 1998;26(1):72–7.
52. Fong DT, Chan YY, Mok KM, et al. Understanding acute ankle 79. Leanderson J, Bergqvist M, Rolf C, et al. Early influence of an
ligamentous sprain injury in sports. Sports Med Arthrosc Rehabil ankle sprain on objective measures of ankle joint function. A
Ther Technol 2009;1:14. prospective randomised study of ankle brace treatment. Knee Surg
53. Mulligan EP. Evaluation and management of ankle syndesmosis Sports Traumatol Arthrosc [Clinical Trial Randomized Controlled
injuries. Phys Ther Sport 2011;12(2):57–69. Trial] 1999;7(1):51–8.
54. Sman AD, Hiller CE, Refshauge KM. Diagnostic accuracy of 80. Wilkerson GB, Pinerola JJ, Caturano RW. Invertor vs. evertor
clinical tests for diagnosis of ankle syndesmosis injury: a systematic peak torque and power deficiencies associated with lateral
review. Br J Sports Med 2013;47(10):620–8. ankle ligament injury. J Orthop Sports Phys Ther 1997;26(2):
55. Sman AD, Hiller CE, Rae K, et al. Diagnostic accuracy of clinical 78–86.
tests for ankle syndesmosis injury. Br J Sports Med 2013. 81. Hiller CE, Nightingale EJ, Lin CW, et al. Characteristics of
doi:10.1136/bjsports-2013-092787 [Epub ahead of print]. people with recurrent ankle sprains: a systematic review with
56. Taylor DC, Englehardt DL, Bassett Iii FH. Syndesmosis sprains meta-analysis. Br J Sports Med [Meta-Analysis Research Support,
of the ankle. The influence of heterotopic ossification. Am J Sports Non-U.S. Gov’t Review] 2011;45(8):660–72.
Med 1992;20(2):146–9. 82. Arnold BL, Linens SW, de la Motte SJ, et al. Concentric evertor
57. Mullins JF, Sallis JG. Recurrent sprain of the ankle joint with strength differences and functional ankle instability: a meta-anal-
diastasis. J Bone Joint Surg Br 1958;40-B(2):270–3. ysis. J Athl Train 2009;44(6):653–62.
58. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains 83. Arnold BL, De La Motte S, Linens S, et al. Ankle instability is
in athletes. Am J Sports Med 2007;35(7):1197–207. associated with balance impairments: a meta-analysis. Med Sci
59. Alonso A, Khoury L, Adams R. Clinical tests for ankle syndesmo- Sports Exerc 2009;41(5):1048–62.
sis injury: reliability and prediction of return to function. J Orthop 84. Munn J, Sullivan SJ, Schneiders AG. Evidence of sensorimotor
Sports Phys Ther 1998;27(4):276–84. deficits in functional ankle instability: a systematic review with
60. Ogilvie-Harris DJ, Reed SC. Disruption of the ankle syndesmosis: meta-analysis. J Sci Med Sport 2010;13(1):2–12.
diagnosis and treatment by arthroscopic surgery. Arthroscopy 85. Witchalls J, Waddington G, Blanch P, et al. Ankle instability
1994;10(5):561–8. effects on joint position sense when stepping across the active
61. Magee D. Lower Leg, Ankle and Foot. Orthopedic Physical movement extent discrimination apparatus. J Athl Train 2012;
Assessment. 4th ed. Saunders; 2002. p. 765–809. 47(6):627–34.
62. Beumer A, Swierstra BA, Mulder PGH. Clinical diagnosis of syn- 86. Hale SA, Hertel J, Olmsted-Kramer LC. The effect of a 4-week
desmotic ankle instability: evaluation of stress tests behind the comprehensive rehabilitation program on postural control and
curtains. Acta Orthop Scand 2002;73(6):667–9. lower extremity function in individuals with chronic ankle insta-
63. Teitz CC, Harrington RM. A biomechanical analysis of the bility. J Orthop Sports Phys Ther 2007;37(6):303–11.
squeeze test for sprains of the syndesmotic ligaments of the ankle. 87. Brown C, Bowser B, Simpson KJ. Movement variability during
Foot Ankle Int 1998;19(7):489–92. single leg jump landings in individuals with and without
64. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle chronic ankle instability. Clin Biomech (Bristol, Avon) 2012;27(1):
syndesmosis injuries. Foot Ankle Int 2005;26(2):187–8. 52–63.
65. Wataru Miyamoto MT. Management of chronic disruption of the 88. Friel K, McLean N, Myers C, et al. Ipsilateral hip abductor weak-
distal tibiofibular syndesmosis. World J Orthop 2011;2(1):1–6. ness after inversion ankle sprain. J Athl Train 2006;41(1):74–8.
66. Simon J, Donahue M, Docherty C. Development of the Identifi- 89. Gribble PA, Hertel J, Denegar CR. Chronic ankle instability and
cation of Functional Ankle Instability (IdFAI). Foot Ankle Int fatigue create proximal joint alterations during performance of the
2012;33(9):755–63. Star Excursion Balance Test. Int J Sports Med 2007;28(3):
67. Mandarakas M, Hiller CE, Rose KJ, et al. Measuring ankle insta- 236–42.
bility in pediatric Charcot-Marie-Tooth disease. J Child Neurol 90. Sedory EJ, McVey ED, Cross KM, et al. Arthrogenic muscle
2013;28(11):1456–62. response of the quadriceps and hamstrings with chronic ankle
68. Carcia CR, Martin RL, Drouin JM. Validity of the Foot and Ankle instability. J Athl Train 2007;42(3):355–60.
Ability Measure in athletes with chronic ankle instability. J Athl 91. Brown C, Padua D, Marshall SW, et al. Individuals with mechani-
Train 2008;43(2):179–83. cal ankle instability exhibit different motion patterns than those
69. Roos EM, Brandsson S, Karlsson J. Validation of the foot and with functional ankle instability and ankle sprain copers. Clin
ankle outcome score for ankle ligament reconstruction. Foot Biomech (Bristol, Avon) 2008;23(6):822–31.
Ankle Int 2001;22(10):788–94. 92. Delahunt E, Monaghan K, Caulfield B. Altered neuromuscular
70. Wikstrom EA, Naik S, Lodha N, et al. Balance capabilities after control and ankle joint kinematics during walking in subjects with
lateral ankle trauma and intervention: a meta-analysis. Med Sci functional instability of the ankle joint. Am J Sports Med 2006;
Sports Exerc 2009;41(6):1287–95. 34(12):1970–6.
71. Aiken AB, Pelland L, Brison R, et al. Short-term natural recovery 93. Fu SN, Hui-Chan CW. Modulation of prelanding lower-limb
of ankle sprains following discharge from emergency departments. muscle responses in athletes with multiple ankle sprains. Med Sci
J Orthop Sports Phys Ther 2008;38(9):566–71. Sports Exerc 2007;39(10):1774–83.
72. Man IO, Morrissey MC. Relationship between ankle-foot swelling 94. Wikstrom EA, Bishop MD, Inamdar AD, et al. Gait termination
and self-assessed function after ankle sprain. Med Sci Sports Exerc control strategies are altered in chronic ankle instability subjects.
2005;37(3):360–3. Med Sci Sports Exerc 2010;42(1):197–205.
73. Denegar CR, Hertel J, Fonseca J. The effect of lateral ankle sprain 95. Hass CJ, Bishop MD, Doidge D, et al. Chronic ankle instability
on dorsiflexion range of motion, posterior talar glide, and joint alters central organization of movement. Am J Sports Med 2010;
laxity. J Orthop Sports Phys Ther 2002;32(4):166–73. 38(4):829–34.
 49  Ankle Injury 555

96. Needle AR, Palmer JA, Kesar TM, et al. Brain regulation of Australian Regular Army recruits. The Kapooka Ankle Sprain
muscle tone in healthy and functionally unstable ankles. J Sport Study. Am J Sports Med 1997;25(4):544–53.
Rehabil 2013;22(3):202–11. 120. van Rijn RM, van Ochten J, Luijsterburg PA, et al. Effectiveness
97. Pietrosimone BG, Gribble PA. Chronic ankle instability and cor- of additional supervised exercises compared with conventional
ticomotor excitability of the fibularis longus muscle. J Athl Train treatment alone in patients with acute lateral ankle sprains: sys-
2012;47(6):621–6. tematic review. BMJ [Comparative Study Evaluation Studies
98. Needle AR, Charles BBS, Farquhar WB, et al. Muscle spindle Research Support, Non-U.S. Gov’t Review] 2010;341:c5688.
traffic in functionally unstable ankles during ligamentous stress. 121. van Rijn RM, van Heest JA, van der Wees P, et al. Some benefit
J Athl Train 2013;48(2):192–202. from physiotherapy intervention in the subgroup of patients with
99. Hoch MC, McKeon PO, Andreatta RD. Plantar vibrotactile severe ankle sprain as determined by the ankle function score: a
detection deficits in adults with chronic ankle instability. Med Sci randomised trial. Aust J Physiother [Randomized Controlled Trial
Sports Exerc 2012;44(4):666–72. Research Support, Non-U.S. Gov’t] 2009;55(2):107–13.
100. Powell MR, Powden CJ, Houston MN, et al. Plantar cutaneous 122. Bleakley CM, O’Connor SR, Tully MA, et al. Effect of accelerated
sensitivity and balance in individuals with and without chronic rehabilitation on function after ankle sprain: randomised con-
ankle instability. Clin J Sport Med 2014;24(6):490–6. trolled trial. BMJ 2010;340:c1964.
101. McKay G, Cook J. Evidence-Based Clinical Statement: Physio- 123. van Os AG, Bierma-Zeinstra SM, Verhagen AP, et al. Comparison
therapy Management of Annkle Injuries in Sport. Victoria: Aus- of conventional treatment and supervised rehabilitation for treat-
tralian Physiotherapy Association; 2006. ment of acute lateral ankle sprains: a systematic review of the
102. Kaminski TW, Hertel J, Amendola N, et al. National Athletic literature. J Orthop Sports Phys Ther 2005;35(2):95–105.
Trainers’ Association position statement: conservative manage- 124. van Rijn RM, van Os AG, Kleinrensink GJ, et al. Supervised
ment and prevention of ankle sprains in athletes. J Athl Train exercises for adults with acute lateral ankle sprain: a randomised
[Practice Guideline Review] 2013;48(4):528–45. controlled trial. Br J Gen Pract [Multicenter Study Randomized
103. Kerkhoffs GM, van den Bekerom M, Elders LA, et al. Diagnosis, Controlled Trial Research Support, Non-U.S. Gov’t] 2007;57(543):
treatment and prevention of ankle sprains: an evidence-based 793–800.
clinical guideline. Br J Sports Med 2012;46(12):854–60. 125. Lin CW, Hiller CE, de Bie RA. Evidence-based treatment for
104. Martin RL, Davenport TE, Paulseth S, et al. Ankle stability and ankle injuries: a clinical perspective. J Man Manip Ther 2010;
movement coordination impairments: ankle ligament sprains. 18(1):22–8.
J Orthop Sports Phys Ther 2013;43(9):A1–40. 126. van den Bekerom MP, van der Windt DA, Ter Riet G, et al.
105. Seah R, Mani-Babu S. Managing ankle sprains in primary care: Therapeutic ultrasound for acute ankle sprains. Cochrane Data-
what is best practice? A systematic review of the last 10 years of base Syst Rev 2011;(6):CD001249.
evidence. Br Med Bull 2011;97:105–35. 127. Verhagen EA. What does therapeutic ultrasound add to recovery
106. Polzer H, Kanz KG, Prall WC, et al. Diagnosis and treatment of from acute ankle sprain? A review. Clin J Sport Med [Comment
acute ankle injuries: development of an evidence-based algorithm. Research Support, Non-U.S. Gov’t] 2013;23(1):84–5.
Orthop Rev (Pavia) 2012;4(1):e5. 128. Clanton TO, Paul P. Syndesmosis injuries in athletes. Foot Ankle
107. Petersen W, Rembitzki IV, Koppenburg AG, et al. Treatment of Clin 2002;7(3):529–49.
acute ankle ligament injuries: a systematic review. Arch Orthop 129. Miller TL, Skalak T. Evaluation and treatment recommendations
Trauma Surg 2013;133(8):1129–41. for acute injuries to the ankle syndesmosis without associated
108. Hunt KJ. Syndesmosis injuries. Curr Rev Musculoskelet Med fracture. Sports Med 2014;44(2):179–88.
2013;6(4):304–12. 130. de Vries JS, Krips R, Sierevelt IN, et al. Interventions for treating
109. Naqvi GA, Cunningham P, Lynch B, et al. Fixation of ankle syn- chronic ankle instability. Cochrane Database Syst Rev 2011;
desmotic injuries: comparison of tightrope fixation and syndes- (8):CD004124.
motic screw fixation for accuracy of syndesmotic reduction. Am J 131. O’Driscoll J, Delahunt E. Neuromuscular training to enhance
Sports Med 2012;40(12):2828–35. sensorimotor and functional deficits in subjects with chronic ankle
110. van den Bekerom MP, Struijs PA, Blankevoort L, et al. What is instability: a systematic review and best evidence synthesis. Sports
the evidence for rest, ice, compression, and elevation therapy in Med Arthrosc Rehabil Ther Technol 2011;3:19.
the treatment of ankle sprains in adults? J Athl Train 2012; 132. Gilbreath JP, Gaven SL, Van Lunen BL, et al. The effects of
47(4):435–43. Mobilization with Movement on dorsiflexion range of motion,
111. Lamb SE, Marsh JL, Hutton JL, et al. Mechanical supports for dynamic balance, and self-reported function in individuals with
acute, severe ankle sprain: a pragmatic, multicentre, randomised chronic ankle instability. Man Ther 2014;19(2):152–7.
controlled trial. Lancet 2009;373(9663):575–81. 133. Reid A, Birmingham TB, Alcock GK. Efficacy of mobilization
112. Kemler E, van de Port I, Backx F, et al. A systematic review on with movementfor patients with limited dorsiflexion after ankle
the treatment of acute ankle sprain: brace versus other functional sprain: a crossover trial. Physiotherapy Canada 2007;59(3):
treatment types. Sports Med 2011;41(3):185–97. 166–72.
113. Kerkhoffs GMMJ, Struijs PAA, Marti RK, et al. Different func- 134. Pellow JE, Brantingham JW. The efficacy of adjusting the ankle
tional treatment strategies for acute lateral ankle ligament injuries in the treatment of subacute and chronic grade I and grade II
in adults. Cochrane Database Syst Rev 2002;(3):CD002938. ankle inversion sprains. J Manipulative Physiol Ther 2001;24(1):
114. Boyce SH, Quigley MA, Campbell S. Management of ankle 17–24.
sprains: a randomised controlled trial of the treatment of inver- 135. Hoch MC, McKeon PO. Joint mobilization improves spatiotem-
sion injuries using an elastic support bandage or an Aircast poral postural control and range of motion in those with chronic
ankle brace. Br J Sports Med [Clinical Trial Comparative Study ankle instability. J Orthop Res 2011;29(3):326–32.
Multicenter Study Randomized Controlled Trial] 2005;39(2): 136. Hoch MC, Andreatta RD, Mullineaux DR, et al. Two-week joint
91–6. mobilization intervention improves self-reported function, range
115. Loudon JK, Reiman MP, Sylvain J. The efficacy of manual joint of motion, and dynamic balance in those with chronic ankle insta-
mobilisation/manipulation in treatment of lateral ankle sprains: a bility. J Orthop Res 2012;30(11):1798–804.
systematic review. Br J Sports Med 2014;48(5):365–70. 137. Sesma AR, Mattacola CG, Uhl TL, et al. Effect of foot orthotics
116. Cosby NL, Koroch M, Grindstaff TL, et al. Immediate effects of on single- and double-limb dynamic balance tasks in patients with
anterior to posterior talocrural joint mobilizations following acute chronic ankle instability. Foot Ankle Spec [Research Support,
lateral ankle sprain. J Man Manip Ther 2011;19(2):76–83. Non-U.S. Gov’t] 2008;1(6):330–7.
117. Green T, Refshauge K, Crosbie J, et al. A randomized controlled 138. Gabriner ML, Braun BA, Houston MN, et al. The effectiveness
trial of a passive accessory joint mobilization on acute ankle inver- of foot orthotics on improving postural control in individuals with
sion sprains. Phys Ther 2001;81(4):984–94. chronic ankle instability: a critically appraised topic. J Sport
118. Eisenhart AW, Gaeta TJ, Yens DP. Osteopathic manipulative Rehabil 2013;[Epub ahead of print].
treatment in the emergency department for patients with acute 139. Hadadi M, Mousavi ME, Fardipour S, et al. Effect of soft and
ankle injuries. J Am Osteopath Assoc 2003;103(9):417–21. semirigid ankle orthoses on Star Excursion Balance Test perfor-
119. Slatyer MA, Hensley MJ, Lopert R. A randomized controlled mance in patients with functional ankle instability. J Sci Med Sport
trial of piroxicam in the management of acute ankle sprain in 2013;17(4):430–3.
556 PART IV  Overview of Contemporary Issues in Practice

140. Lee HJ, Lim KB, Jung TH, et al. Changes in balancing ability of sprains among elite and recreational players. J Sci Med Sport
athletes with chronic ankle instability after foot orthotics applica- 2010;13(3):309–17.
tion and rehabilitation exercises. Ann Rehabil Med 2013;37(4): 142. Janssen KW, van Mechelen W, Verhagen EA. Bracing superior to
523–33. neuromuscular training for the prevention of self-reported recur-
141. Dizon JM, Reyes JJ. A systematic review on the effectiveness of rent ankle sprains: a three-arm randomised controlled trial. Br J
external ankle supports in the prevention of inversion ankle Sports Med 2014;48(16):1235–9.
 CHAPTER 50 

The Shoulder
CHAPTER OUTLINE

Ch 50.1  Shoulder Assessment  557 Ch 50.4  Posterior Shoulder Tightness  575

Eric Hegedus  •  Jeremy Lewis John Borstad  •  Jeremy Lewis
Ch 50.2  Rotator Cuff Tendinopathy and Subacromial Ch 50.5  Frozen Shoulder Contraction
Pain Syndrome  563 Syndrome  577
Jeremy Lewis  •  Karen Ginn Jeremy Lewis
Ch 50.3  The Unstable Shoulder  568
Lyn Watson  •  Tania Pizzari  • 
Jane Simmonds  •  Jeremy Lewis

CHAPTER 50.1  ■  SHOULDER ASSESSMENT

Eric Hegedus  •  Jeremy Lewis

INTRODUCTION learner or when an experienced examiner is confronted

with an unfamiliar set of signs and symptoms, hypothetical–
Musculoskeletal problems involving the shoulder are deductive reasoning is typified by the gathering of data
common, with a reported lifetime prevalence as high as in a step-wise fashion, from general to specific, to confirm
67%.1 Complaints increase with age and are common in or refute a working hypothesis. The process described in
the fifth to seventh decades.2–4 Of concern is the fact that this chapter is such an approach. This chapter will prog-
40–54% of people with shoulder problems report con- ress systematically from the patient interview, to screen-
tinued symptoms up to 3 years after initial onset.3,5,6 ing, to motion testing and, finally, to orthopaedic tests
These symptoms are frequently associated with substan- where the issue of diagnostic accuracy will be discussed.
tial morbidity. Knowledge of epidemiological data provides valuable
The main role of the shoulder is to position the hand information when examining the shoulder. This will be
to permit the upper limb to perform activities ranging discussed briefly in the following section.
from the performance of high-powered, explosive activi-
ties, such as serving in tennis, to placing the hand within
the visual field to perform highly skilled prehensile tasks The Importance of Epidemiology Data in
such as writing. The shoulder also places the upper limb
and hand to facilitate weight bearing through the upper
Shoulder Assessment and Diagnosis
extremity in activities such as gymnastics. Pain, loss of Certain pathologies and diagnoses have a greater chance
movement, instability, muscle imbalance and loss of of existing in defined patient populations. In other words,
strength and endurance may have a detrimental impact pre-test or pre-assessment probability is higher for certain
on shoulder function. pathologies in specific populations. For example, without
The complexity of the shoulder and its wide spectrum a history of trauma, a rotator cuff tear would be uncom-
of function create challenges in assessment and diagnosis. mon in the average 15-year-old but rotator cuff tendi-
The principal aims of shoulder assessment are to collect nopathy may occur in a young elite swimmer. For a
meaningful information that informs clinical decision person aged between 40 and 60 years there is roughly a
making, aids in diagnosis and directs efficient and effec- 25% chance of a rotator cuff tear which rises to approxi-
tive management of shoulder dysfunction. This chapter mately 50% in people in their 80s.7,8 Two of the stronger
will address the first two aims. diagnostic test clusters for rotator cuff tear incorporate
an age-over-60 component.9,10 Another example pertains
to patients with a first-time traumatic dislocation. The
ASSESSMENT OVERVIEW AND dislocation is almost certain to recur if the individual is
CLINICAL DECISION MAKING under the age of 20 years and almost certain not to
happen again if over the age of 40 years.11–13 Importantly
There are several models of clinical decision making that for diagnosis, individuals over the age of 40 years who
explain how a clinician uses the information gathered in have had a dislocation are likely to have a rotator cuff tear
an assessment. In cases where the examiner is a new in addition to instability and, regardless of age, clinicians
557
558 PART IV  Overview of Contemporary Issues in Practice

should be aware of the possibility of a bony lesion like a supported by research confirming their validity, reliabil-
Hill–Sachs or Bankart. As a final example, degenerative ity and responsiveness. Table 50-1 presents a short list of
changes in the acromioclavicular joint are not likely in physical performance measures for the shoulder, a brief
the young but for those aged 61–88 years, the likelihood description of how to perform them and the population
is 90%.14 Knowing the baseline probability helps the sys- in which they have been studied.
tematic assessment, outlined hereafter, to be more
accurate.
PHYSICAL EXAMINATION
THE PATIENT INTERVIEW, FLAGS AND
ESTABLISHING A BASELINE FOR Observation
OUTCOMES The patient interview helps direct and is followed by a
physical examination. The initial steps of the examination
A systematic examination begins with a review of all rel- include an assessment of posture and identification of any
evant medical records and reports and a patient interview. deviations of posture from an expected norm, as well as
At this stage it is important for the clinician to screen for gathering clinical clues that may later support a diagnosis
Red and Yellow Flags, gain an understanding of how the (e.g. swelling, ecchymosis, muscle atrophy and scapular
shoulder dysfunction is affecting the patient as a whole, dyskinesis). It is important to acknowledge that although
and to determine the patient’s short- and long-term postural assessment is considered to be an integral part
needs. Red Flags are serious conditions that require of the shoulder examination, definitive research evidence
referral. Common Red Flags are reports of trauma, fever providing guidance on how to perform a postural exami-
or chills, unremitting night pain, bilateral symptoms and nation and, importantly, how to interpret findings are
unintentional, substantial weight loss. An affirmative currently unavailable. For example, an increase in the
response to a single Red Flag question may not be a thoracic kyphosis may be observed, and a hypothesis that
reason for an immediate referral but a cluster typically this postural deviation contributes to the patient’s shoul-
would be.15,16 It is essential to continuously monitor der pain has been formulated.35 However, currently this
changes in the individual’s health status for changes to hypothesis has no definitive support.36,37 Similar uncer-
Red Flag status. tainties surround the concept of scapular dyskinesis and
The presence of Yellow Flags such as negative coping discord exists between clinicians. Some suggest that scap-
mechanisms, anxiety, depression and kinesiophobia are ular dyskinesis is an important clinical finding due to its
associated with a negative outcome.17,18 Prognostic factors correlation with pathology,38,39 whereas others have found
associated with a negative outcome in patients with no correlation.40–42 Even when scapular dyskinesis is
shoulder pain include concurrent neck pain, high pain found, there is little agreement about which components
intensity and symptoms greater than 3 months’ dura- and what magnitude constitute dyskinesis.43 What is
tion.3,19,20 Factors correlated with a positive outcome are known currently is that scapular dyskinesis is not diag-
lower disability at baseline and less pain-catastrophizing nostic of any particular pathology but it still may be an
behaviour.21 Psychosocial factors may be more important important impairment to address when treating patients
predictors in those with chronic shoulder pain.21 with shoulder pain.44,45
Self-report outcome measures further enhance patient
history by detailing the effects of the injury or illness on
the patient’s quality of life including function. They may
The Screening Examination
be categorized as generic, disease-specific, site- and After observation, the physical examination involves an
region-specific, and dimension-specific. A review of all appropriate screening examination. For example, the
self-report measures is beyond the scope of this chapter, upper quarter screen (UQS) is used for patients who
but we will touch on a few here. Generic measures for report shoulder pain and radiating symptoms down the
people with musculoskeletal shoulder conditions may arm. The UQS aims to determine whether the source of
include; the single assessment numeric evaluation
(SANE),22 the P4 pain scale,23 and the patient-specific
functional scale (PSFS).24 Shoulder- and region-specific TABLE 50-1  Recommended Upper Extremity
outcome measures that should be considered to inform Physical Performance Measures
assessment and outcome include the nine-item quick dis-
abilities of the arm, shoulder or the Quick-DASH-9,25 the Test Assesses Population
full DASH,26 and the Shoulder Pain and Disability Index FIT-HaNSA 31
Work-specific tasks Younger, working
(SPADI).27 In a throwing athlete with shoulder pain, the CKCUEST32 Single arm stability Mostly young, athletic
Kerlan–Jobe Orthopaedic Clinic Shoulder and Elbow males
Score (KJOC-SES)28 should be considered. UQYBT33 Mobility, stability, College-aged, military
Physical performance measures should be included at endurance population
baseline and are thought to capture a different compo- Single Arm Power Healthy, recreationally
nent of function than self-report measures.29 Physical Shot Put34 active adults
performance measures may be less affected by pain and FIT-HaNSA, Functional impairment test-hand and neck/shoulder/
psychosocial variables than are self-report measures.30 arm; CKCUEST, Closed kinetic chain upper extremity stability
Currently, physical performance measures are not well test; UQYBT, Upper quarter Y-balance test.
 50  The Shoulder 559

the pain is in the neck, shoulder, or other region and performance testing. Methods for measuring impair-
whether the impairments are of neurologic origin. The ments such as range of movement and strength have been
UQS combines active cervical spine motions and func- published.46,47 The known diagnostic accuracies for these
tional movements of the shoulder and, when relevant, components of the shoulder examination can be found in
testing of dermatomes, myotomes, reflexes, vibration Table 50-2. These procedures are followed by orthopae-
sense and upper motoneuron testing. An examination of dic special tests, which are considered to form an integral
vascular status (see Chapter 35) may also be required. It component of the physical examination.
is necessary to appropriately screen the cervical and tho-
racic regions to determine if they are involved with the
presenting shoulder symptoms. Orthopaedic Special Tests and
Diagnostic Accuracy
Active Motion, Passive Motion, Tests have been devised to identify lesions in specific
tissues, such as the labrum, the rotator cuff, the acromio-
Palpation and Muscle Testing clavicular joint, subacromial bursa and the biceps. The
The focused physical examination of the shoulder diagnostic accuracy of a clinical test is determined by
commences with examination of active shoulder range comparing the clinical finding against a ‘gold standard’
of motion (ROM), passive ROM (physiological and comparator. For the shoulder, the comparator would
accessory motions as indicated), palpation and muscle typically be direct observation during surgery (soft tissue

TABLE 50-2  Best Available Evidence of the Diagnostic Accuracy of the Shoulder Examination
Screen (Sc)
Diagnose (D)
Both (B)
Sensitivity/ LR Neither (N)
Test Name Pathology Specificity LR+/LR− Unknown(?)

History Any ? ? ?
Observation
Shrug sign (during elevation)48 OA 91/57 0.16 Sc
Adhesive capsulitis 95/50 0.10
Rotator cuff tendinopathy 96/53 0.08
Motion Testing (Active, Passive, Accessory)
Sulcus sign49 Superior labral tear 17/93 2.43 N
Anterior drawer test50 Anterior instability 53/85 3.53 N
Palpation
Supraspinatus51 Tendinopathy 92/41 0.19 Sc
Biceps51 Tendinopathy 85/48 0.31 N
AC joint52 AC pathology 96/10 0.40 N
Muscle Testing
Infraspinatus test53 Impingement 56/87 4.39 N
Empty can10 Impingement 44/90 4.20 N
Orthopaedic Special Tests
Apprehension54 Anterior instability 72/96 18.0 D
Relocation50 Anterior instability 81/92 10.1/0.1 B
Surprise55 Anterior instability 92/89 8.4/0.08 B
Passive distraction56 SLAP lesion 53/94 8.3 D
Passive compression57 SLAP lesion 82/86 5.7/0.2 B
Dynamic labral shear-modified58 Any labral tear 72/98 36 D
Belly-off59 Subscapularis tendinopathy 86/91 9.7/0.14 B
Belly press60 Subscapularis tendinopathy 40/98 20.0 D
Modified belly press59 Subscapularis tendinopathy 80/88 6.7/0.23 B
Bear hug60 Subscapularis tendinopathy 60/92 7.23 D
Bony apprehension61 Bony instability 94/84 5.9/0.07 B
OMPT62 Bony abnormality 84/99 84.0 D
Lateral Jobe63 Rotator cuff tear (RCT) 81/89 7.4/0.21 B
ERLS64 Full-thickness tear 46/49 7.2 D
AC resisted extension65 AC Joint Pathology 72/85 4.8 D

AC, Acromioclavicular; ERLS, external rotation lag sign; LR, likelihood ratio; OA, osteoarthritis; OMPT, olecranon manubrium percussion
test; SLAP, superior labral anterior to posterior.
560 PART IV  Overview of Contemporary Issues in Practice

TABLE 50-3  Determining the Accuracy of Clinical Tests

‘Gold Standard’ Reference Test
(Examples Include: MRI, US, Arthroscopic Visualization)

Condition/Disorder Present Condition/Disorder Not Present

Clinical test Positive clinical finding True positive False positive

(e.g. pain, weakness, instability) (A) (B)

Negative clinical finding False negative True negative

(e.g. no pain, weakness or instability) (C) (D)

US, ultrasound; MRI, magnetic resonance imaging.

Interpretation:
Sensitivity  =  A/(A + C)  (Ideal 100%)
Specificity  =  D/(B + D)  (Ideal 100%)
Positive likelihood ratio (LR+)  =  Sensitivity/1 – Specificity  >3 = useful, >10 = very useful
Negative likelihood ratio (LR−)  =  1 – Sensitivity/Specificity  <0.33 = useful, <0.1 = very useful

lesions), a radiograph (bony lesions) or injection (impinge- The diagnostic accuracy and use of these tests has been
ment syndrome). The underlying principle is that challenged,45,67,68 as there are a substantial number of
observed structural failure is the cause or is associated people without shoulder symptoms who have identifiable
with symptoms. Table 50-3 details how the accuracy of structural pathology on imaging.69 Published reviews
clinical tests is determined. have discussed this issue in detail.45
Sensitivity, specificity and positive and negative likeli- Clustering tests and measures together, a standard
hood ratios are the most robust metrics in determining procedure in physical examination, helps to improve
diagnostic accuracy. For a clinician to derive confidence diagnosis. Nevertheless studies examining clustered tests
that the findings of an orthopaedic test may help rule in rarely show values better than the most accurate tests, but
or rule out the presence of a condition or specific struc- possibly because the best tests in combination have not
tural pathology the test must be positive if the condition been studied.68 Table 50-2 summarizes the most accurate
is present and negative if not present. The sensitivity and tests from the highest-quality research studies. It is
specificity of any test must be considered together, not important to appreciate that the diagnostic accuracy of
one component in isolation. For example, the Neer sign66 even the best clinical tests is determined by comparison
is a clinical procedure involving scapula stabilization with with observed structural failure (which may be asymp-
shoulder flexion and over-pressure. If the patient informs tomatic and not the cause of symptoms), and as such,
the clinician that the procedure is painful (positive test) interpretation of clinical findings derived from even these
then the presence of subacromial impingement may be best tests must be made in light of all of the other infor-
considered. Alternatively, impingement may be ruled out mation gathered from the patient assessment. Determin-
if no pain (negative test) is reproduced during the proce- ing which structures are involved in the patient’s
dure. The assumption with this interpretation is that the presentation and differentiation between different mus-
orthopaedic test findings for every patient may be classi- culoskeletal shoulder disorders remains difficult.45,70–72
fied as a true positive or a true negative so that both
sensitivity and specificity are 100%. Currently there are
no orthopaedic tests with these stellar metrics. SUMMARY
Likelihood ratios (LR) may be more useful. As dem-
onstrated in Table 50-3, both LR+ and LR− combine The shoulder is a highly complex, multijoint system
sensitivity and specificity into one number. A test with a that has a wide array of functional demands that require
strong LR+ moves the examiner closer to a diagnosis and mobility and stability. Assessment to reach a diagnosis
a test with a strong LR− moves the clinician further away and inform clinical decision making needs to be both
from a diagnosis. At the beginning of this chapter, we thorough and systematic. The assessment process (Fig.
discussed baseline probabilities found in epidemiological 50-1) must also incorporate knowledge of epidemiology
literature. An LR+ of 5.0 or greater and LR− of 0.20 or and baseline probability with best evidence, and an
less are moderately to highly valuable in modifying the appreciation of patient aspirations, desires and values.
baseline probability to the extent of ruling in or ruling Where evidence is unclear, clinicians should rely even
out a pathology, respectively. As either the LR+ or LR− more heavily on clinical decision making, which some
approaches a value of 1.0, the value of the diagnostic test call the ‘art’ of physiotherapy. The clinical decision-
diminishes to the point where it insignificantly modifies making model described in this chapter is the
the baseline probability. hypothetical–deductive model. Although this method
Clinicians should have knowledge of the sensitivity, progresses more rapidly with experience and is most
specificity and positive and negative LRs of clinical tests. comprehensive, it is also the slowest. More experienced
Despite the widespread clinical use of these shoulder clinicians take shortcuts by using pattern-recognition
orthopaedic tests to inform a diagnosis, there is surpris- or heuristic decision making. In order to minimize
ingly little evidence to support their diagnostic utility.45,67,68 false assumptions and misdiagnoses, especially with the
 50  The Shoulder 561

FIGURE 50-1  ■  Components of a systematic, thorough physical examination.

heuristic model, the clinician is obliged to regularly of asymptomatic and symptomatic shoulders. J Bone Joint Surg Am
review research databases to update and synthesize 2006;88(8):1699–704. [Epub 2006/08/03].
8. Yamamoto A, Takagishi K, Osawa T, et al. Prevalence and risk
knowledge. Also, it is important to realize that the factors of a rotator cuff tear in the general population. J Shoulder
assessment process is an ongoing continuum and as the Elbow Surg 2010;19(1):116–20. [Epub 2009/06/23].
patient’s condition changes, additional assessment is 9. Litaker D, Pioro M, El Bilbeisi H, et al. Returning to the bedside:
mandatory. Following the process outlined in this chapter using the history and physical examination to identify rotator cuff
tears. J Am Geriatr Soc 2000;48(12):1633–7. [Epub 2000/12/29].
and summarized in Figure 50-1 ensures a systematic, 10. Park HB, Yokota A, Gill HS, et al. Diagnostic accuracy of clinical
thorough and ongoing assessment process. tests for the different degrees of subacromial impingement syn-
drome. J Bone Joint Surg Am 2005;87(7):1446–55. [Epub
2005/07/05].
REFERENCES 11. Marans HJ, Angel KR, Schemitsch EH, et al. The fate of traumatic
1. Meyers OL, Jessop S, Klemp P. The epidemiology of rheumatic anterior dislocation of the shoulder in children. J Bone Joint Surg
disease in a rural and an urban population over the age of 65 years. Am 1992;74(8):1242–4. [Epub 1992/09/01].
S Afr Med J 1982;62(12):403–51. [Epub 1982/09/11]. 12. Postacchini F, Gumina S, Cinotti G. Anterior shoulder dislocation
2. Bot SD, van der Waal JM, Terwee CB, et al. Incidence and preva- in adolescents. J Shoulder Elbow Surg 2000;9(6):470–4. [Epub
lence of complaints of the neck and upper extremity in general 2001/01/13].
practice. Ann Rheum Dis 2005;64(1):118–23. [Epub 2004/12/21]. 13. Deitch J, Mehlman CT, Foad SL, et al. Traumatic anterior shoul-
3. van der Windt DA, Koes BW, Boeke AJ, et al. Shoulder disorders der dislocation in adolescents. Am J Sports Med 2003;31(5):758–63.
in general practice: prognostic indicators of outcome. Br J Gen [Epub 2003/09/17].
Pract 1996;46(410):519–23. [Epub 1996/09/01]. 14. Needell SD, Zlatkin MB, Sher JS, et al. MR imaging of the rotator
4. Picavet HS, Schouten JS. Musculoskeletal pain in the Netherlands: cuff: peritendinous and bone abnormalities in an asymptomatic
prevalences, consequences and risk groups, the DMC(3)-study. population. AJR Am J Roentgenol 1996;166(4):863–7. [Epub
Pain 2003;102(1–2):167–78. [Epub 2003/03/07]. 1996/04/01].
5. Macfarlane GJ, Hunt IM, Silman AJ. Predictors of chronic shoul- 15. Henschke N, Maher CG, Ostelo RW, et al. Red flags to screen for
der pain: a population based prospective study. J Rheumatol malignancy in patients with low-back pain. Cochrane Database Syst
1998;25(8):1612–15. [Epub 1998/08/26]. Rev 2013;(2):CD008686, [Epub 2013/03/02].
6. Winters JC, Sobel JS, Groenier KH, et al. The long-term course 16. Ross MD, Boissonnault WG. Red flags: to screen or not to
of shoulder complaints: a prospective study in general practice. screen? J Orthop Sports Phys Ther 2010;40(11):682–4. [Epub
Rheumatology (Oxford) 1999;38(2):160–3. [Epub 1999/05/26]. 2010/11/03].
7. Yamaguchi K, Ditsios K, Middleton WD, et al. The demographic 17. Parr JJ, Borsa PA, Fillingim RB, et al. Pain-related fear and cata-
and morphological features of rotator cuff disease. A comparison strophizing predict pain intensity and disability independently
562 PART IV  Overview of Contemporary Issues in Practice

using an induced muscle injury model. J Pain 2012;13(4):370–8. and without shoulder symptoms. BMC Musculoskelet Disord
[Epub 2012/03/20]. 2007;8:64. [Epub 2007/07/11].
18. Cho CH, Jung SW, Park JY, et al. Is shoulder pain for three 38. Ludewig PM, Cook TM. Alterations in shoulder kinematics
months or longer correlated with depression, anxiety, and sleep and associated muscle activity in people with symptoms of
disturbance? J Shoulder Elbow Surg 2013;22(2):222–8. [Epub shoulder impingement. Phys Ther 2000;80(3):276–91. [Epub
2012/06/29]. 2000/03/01].
19. Kuijpers T, van der Windt DA, van der Heijden GJ, et al. System- 39. Kibler WB, Sciascia A, Wilkes T. Scapular dyskinesis and its rela-
atic review of prognostic cohort studies on shoulder disorders. Pain tion to shoulder injury. J Am Acad Orthop Surg 2012;20(6):364–72.
2004;109(3):420–31. [Epub 2012/06/05].
20. Kuijpers T, van der Windt DA, Boeke AJ, et al. Clinical prediction 40. Graichen H, Stammberger T, Bonel H, et al. Three-dimensional
rules for the prognosis of shoulder pain in general practice. Pain analysis of shoulder girdle and supraspinatus motion patterns in
2006;120(3):276–85. patients with impingement syndrome. J Orthop Res 2001;19(6):1192–
21. Reilingh ML, Kuijpers T, Tanja-Harfterkamp AM, et al. Course 8. [Epub 2002/01/10].
and prognosis of shoulder symptoms in general practice. Rheuma- 41. Mell AG, LaScalza S, Guffey P, et al. Effect of rotator cuff pathol-
tology (Oxford) 2008;47(5):724–30. [Epub 2008/04/16]. ogy on shoulder rhythm. J Shoulder Elbow Surg 2005;14(1 Suppl.
22. Williams GN, Gangel TJ, Arciero RA, et al. Comparison of the S):58S–64S. [Epub 2005/02/24].
Single Assessment Numeric Evaluation method and two shoulder 42. Ratcliffe E, Pickering S, McLean S, et al. Is there a relationship
rating scales. Outcomes measures after shoulder surgery. Am J between Subacromial Impingement Syndrome and scapular orien-
Sports Med 1999;27(2):214–21. [Epub 1999/04/02]. tation?: A systematic review. Br J Sports Med 2013;In Press.
23. Stratford PW, Dogra M, Woodhouse L, et al. Validating self-report 43. Ludewig PM, Reynolds JF. The association of scapular kinematics
measures of pain and function in patients undergoing hip or knee and glenohumeral joint pathologies. J Orthop Sports Phys Ther
arthroplasty. Physiother Can 2009;61(4):189–94, discussion 95–6. 2009;39(2):90–104. [Epub 2009/02/06].
[Epub 2010/09/03]. 44. Wright AA, Wassinger CA, Frank M, et al. Diagnostic accuracy of
24. Stratford PW, Gill C, Westaway M, et al. Assessing disability and scapular physical examination tests for shoulder disorders: a sys-
change on individual patients: a report of a patient specific measure. tematic review. Br J Sports Med 2013;47(14):886–92. [Epub 2012/
Physiother Can 1995;47:258–63. 10/20].
25. Gabel CP, Yelland M, Melloh M, et al. A modified QuickDASH-9 45. Lewis JS. Rotator cuff tendinopathy/subacromial impingement
provides a valid outcome instrument for upper limb function. BMC syndrome: is it time for a new method of assessment? Br J Sports
Musculoskelet Disord 2009;10:161. [Epub 2009/12/22]. Med 2009;43(4):259–64. [Epub 2008/10/08].
26. Beaton DE, Katz JN, Fossel AH, et al. Measuring the whole or the 46. Valentine RE, Lewis JS. Intraobserver reliability of 4 physiologic
parts? Validity, reliability, and responsiveness of the Disabilities of movements of the shoulder in subjects with and without symptoms.
the Arm, Shoulder and Hand outcome measure in different regions Arch Phys Med Rehabil 2006;87(9):1242–9. [Epub 2006/08/29].
of the upper extremity. J Hand Ther 2001;14(2):128–46. [Epub 47. Lewis JS, Valentine RE. Intraobserver reliability of angular and
2001/05/31]. linear measurements of scapular position in subjects with and
27. Roach KE, Budiman-Mak E, Songsiridej N, et al. Development of without symptoms. Arch Phys Med Rehabil 2008;89(9):1795–802.
a shoulder pain and disability index. Arthritis Care Res [Epub 2008/09/02].
1991;4(4):143–9. [Epub 1991/12/01]. 48. Jia X, Ji JH, Petersen SA, et al. Clinical evaluation of the shoulder
28. Domb BG, Davis JT, Alberta FG, et al. Clinical follow-up of pro- shrug sign. Clin Orthop Relat Res 2008;466(11):2813–19. [Epub
fessional baseball players undergoing ulnar collateral ligament 2008/06/11].
reconstruction using the new Kerlan-Jobe Orthopaedic Clinic 49. Nakagawa S, Yoneda M, Hayashida K, et al. Forced shoulder
overhead athlete shoulder and elbow score (KJOC Score). Am J abduction and elbow flexion test: a new simple clinical test to detect
Sports Med 2010;38(8):1558–63. [Epub 2010/03/31]. superior labral injury in the throwing shoulder. Arthroscopy
29. Wright AA, Cook CE, Baxter GD, et al. Relationship between the 2005;21(11):1290–5. [Epub 2005/12/06].
Western Ontario and McMaster Universities Osteoarthritis Index 50. Farber AJ, Castillo R, Clough M, et al. Clinical assessment of three
Physical Function Subscale and physical performance measures in common tests for traumatic anterior shoulder instability. J Bone
patients with hip osteoarthritis. Arch Phys Med Rehabil Joint Surg Am 2006;88(7):1467–74. [Epub 2006/07/05].
2010;91(10):1558–64. [Epub 2010/09/30]. 51. Toprak U, Ustuner E, Ozer D, et al. Palpation tests versus impinge-
30. Terwee CB, van der Slikke RM, van Lummel RC, et al. Self- ment tests in Neer stage I and II subacromial impingement syn-
reported physical functioning was more influenced by pain than drome. Knee Surg Sports Traumatol Arthrosc 2013;21(2):424–9.
performance-based physical functioning in knee-osteoarthritis [Epub 2012/03/29].
patients. J Clin Epidemiol 2006;59(7):724–31. [Epub 2006/06/13]. 52. Walton J, Mahajan S, Paxinos A, et al. Diagnostic values of tests
31. Kumta P, MacDermid JC, Mehta SP, et al. The FIT-HaNSA dem- for acromioclavicular joint pain. J Bone Joint Surg Am 2004;86-
onstrates reliability and convergent validity of functional perfor- A(4):807–12. [Epub 2004/04/08].
mance in patients with shoulder disorders. J Orthop Sports Phys 53. Michener LA, Walsworth MK, Doukas WC, et al. Reliability and
Ther 2012;42(5):455–64. [Epub 2012/01/28]. diagnostic accuracy of 5 physical examination tests and combination
32. Goldbeck T, Davies G. Test-retest reliability of the closed kinetic of tests for subacromial impingement. Arch Phys Med Rehabil
chain upper extremity stability test: a clinical field test. Sport 2009;90(11):1898–903. [Epub 2009/11/06].
Rehabil 2000;9(1):35–45. 54. Jia X, Petersen SA, Khosravi AH, et al. Examination of the shoul-
33. Gorman PP, Butler RJ, Plisky PJ, et al. Upper quarter y balance der: the past, the present, and the future. J Bone Joint Surg Am
test: reliability and performance comparison between genders in 2009;91(Suppl. 6):10–18. [Epub 2009/11/26].
active adults. J Strength Cond Res 2012;26(11):3043–8. [Epub 55. Gross ML, Distefano MC. Anterior release test. A new test for
2012/01/10]. occult shoulder instability. Clin Orthop Relat Res 1997;339:105–8.
34. Negrete RJ, Hanney WJ, Kolber MJ, et al. Can upper extremity [Epub 1997/06/01].
functional tests predict the softball throw for distance: a predictive 56. Schlechter JA, Summa S, Rubin BD. The passive distraction test:
validity investigation. Int J Sports Phys Ther 2011;6(2):104–11. a new diagnostic aid for clinically significant superior labral pathol-
[Epub 2011/06/30]. ogy. Arthroscopy 2009;25(12):1374–9. [Epub 2009/12/08].
35. Theisen C, van Wagensveld A, Timmesfeld N, et al. Co-occurrence 57. Kim YS, Kim JM, Ha KY, et al. The passive compression test: a
of outlet impingement syndrome of the shoulder and restricted new clinical test for superior labral tears of the shoulder. Am J
range of motion in the thoracic spine–a prospective study with Sports Med 2007;35(9):1489–94. [Epub 2007/05/05].
ultrasound-based motion analysis. BMC Musculoskelet Disord 58. Ben Kibler W, Sciascia AD, Hester P, et al. Clinical utility of tra-
2010;11:135. [Epub 2010/07/01]. ditional and new tests in the diagnosis of biceps tendon injuries and
36. Lewis JS, Green A, Wright C. Subacromial impingement syn- superior labrum anterior and posterior lesions in the shoulder. Am
drome: the role of posture and muscle imbalance. J Shoulder Elbow J Sports Med 2009;37(9):1840–7. [Epub 2009/06/11].
Surg 2005;14(4):385–92. [Epub 2005/07/15]. 59. Bartsch M, Greiner S, Haas NP, et al. Diagnostic values of clinical
37. Lewis JS, Valentine RE. The pectoralis minor length test: a study tests for subscapularis lesions. Knee Surg Sports Traumatol
of the intra-rater reliability and diagnostic accuracy in subjects with Arthrosc 2010;18(12):1712–17. [Epub 2010/04/09].
 50  The Shoulder 563

60. Barth JR, Burkhart SS, De Beer JF. The bear-hug test: a new and individual tests. Br J Sports Med 2008;42(2):80–92, discussion.
sensitive test for diagnosing a subscapularis tear. Arthroscopy [Epub 2007/08/28].
2006;22(10):1076–84. [Epub 2006/10/10]. 68. Hegedus EJ, Goode AP, Cook CE, et al. Which physical examina-
61. Bushnell BD, Creighton RA, Herring MM. The bony apprehen- tion tests provide clinicians with the most value when examining
sion test for instability of the shoulder: a prospective pilot analysis. the shoulder? Update of a systematic review with meta-analysis
Arthroscopy 2008;24(9):974–82. [Epub 2008/09/02]. of individual tests. Br J Sports Med 2012;46(14):964–78. [Epub
62. Adams SL, Yarnold PR, Mathews JJt. Clinical use of the olecranon- 2012/07/10].
manubrium percussion sign in shoulder trauma. Ann Emerg Med 69. Girish G, Lobo LG, Jacobson JA, et al. Ultrasound of the shoulder:
1988;17(5):484–7. [Epub 1988/05/01]. asymptomatic findings in men. AJR Am J Roentgenol 2011;
63. Gillooly JJ, Chidambaram R, Mok D. The lateral Jobe test: a more 197(4):W713–19. [Epub 2011/09/24].
reliable method of diagnosing rotator cuff tears. Int J Shoulder Surg 70. Luime JJ, Verhagen AP, Miedema HS, et al. Does this patient have
2010;4(2):41–3. [Epub 2010/11/13]. an instability of the shoulder or a labrum lesion? JAMA
64. Miller CA, Forrester GA, Lewis JS. The validity of the lag signs in 2004;292(16):1989–99. [Epub 2004/10/28].
diagnosing full-thickness tears of the rotator cuff: a preliminary 71. de Winter AF, Jans MP, Scholten RJ, et al. Diagnostic classification
investigation. Arch Phys Med Rehabil 2008;89(6):1162–8. [Epub of shoulder disorders: interobserver agreement and determinants
2008/05/28]. of disagreement. Ann Rheum Dis 1999;58(5):272–7. [Epub 1999/
65. Chronopoulos E, Kim TK, Park HB, et al. Diagnostic value of 05/04].
physical tests for isolated chronic acromioclavicular lesions. Am J 72. Norregaard J, Krogsgaard MR, Lorenzen T, et al. Diagnosing
Sports Med 2004;32(3):655–61. [Epub 2004/04/20]. patients with longstanding shoulder joint pain. Ann Rheum Dis
66. Neer CS 2nd. Impingement lesions. Clin Orthop Relat Res 2002;61(7):646–9. [Epub 2002/06/25].
1983;173:70–7. [Epub 1983/03/01].
67. Hegedus EJ, Goode A, Campbell S, et al. Physical examination
tests of the shoulder: a systematic review with meta-analysis of

CHAPTER 50.2  ■  ROTATOR CUFF TENDINOPATHY AND

SUBACROMIAL PAIN SYNDROME
Jeremy Lewis  •  Karen Ginn

INTRODUCTION Uncertainty exists as to the cause of RC pathology

with hypotheses including; extrinsic mechanisms such as
Of the myriad musculoskeletal conditions affecting the subacromial impingement, intrinsic mechanisms such as
shoulder, subacromial impingement (pain) syndrome internal tendon failure, and combinations of the two.
(SIS) and rotator cuff (RC) tendinopathy are considered These hypotheses have been reviewed in detail.3,4 Other
to be the most common. There is uncertainty if SIS potential causes include weakness and recruitment and
represents a primary pathology. The pain, weakness and timing abnormalities, which may lead to anomalous
associated morbidity associated with SIS are hypothe- humeral head translation during movement.5,6
sized to be primarily due to dysfunction of the RC and
not due to a primary mechanical abrasion from the
undersurface of the acromion onto the RC.1 This clinical ROTATOR CUFF FUNCTION
presentation is also known as painful arc syndrome, RC
syndrome and RC disease. All RC muscles produce rotation torque at the shoulder:
The RC tendon is composed of the tendons of the subscapularis (anterior RC) is an internal rotator and
supraspinatus, infraspinatus, teres minor and subscapu- infraspinatus, teres minor and supraspinatus (posterior
laris that interdigitate and fuse together before inserting RC) are external rotators.7–9 Evidence indicates that
onto the humeral tuberosities. This structural arrange- supraspinatus does not initiate shoulder abduction.10,11
ment improves resistance to failure when the RC is The traditional view of the role of the RC muscles to
under load because (a) tension in one muscle may be provide functional shoulder joint stability is that they
distributed over a wider area and (b) it reduces stress contribute in equal proportions12 to compress the humeral
within the tendon during extremes of movement.2 The head into the glenoid fossa during all shoulder move-
RC tendon is confluent, multilayered and interwoven ments to limit humeral head translation.13 In addition,
and the supraspinatus tendon is made up of six to nine they function to depress the humeral head to prevent
structurally independent parallel fascicles separated by potential superior translation of the humerus due to
endotendon and lubricant that facilitates sliding.3 To deltoid activity.14 Recent evidence that the RC muscles
support the wide range of functions demanded of the are recruited at significantly different activity levels
shoulder, the RC contributes to movement, stability during shoulder flexion and extension suggests that this
and sensory–motor control of the glenohumeral joint. explanation of the mechanism whereby the RC provides
The large range of movement implies that during end- dynamic shoulder joint stability may require revision.15,16
range activities different parts of the RC will be rela- Shoulder flexion recruits the posterior RC (infraspinatus
tively compressed and stretched. This may lead to and supraspinatus) at significantly higher levels than
internal friction and compression within the tendons during extension, whereas the subscapularis (anterior
(see Chapters 10.1 and 10.2). RC) is recruited at significantly higher levels during
564 PART IV  Overview of Contemporary Issues in Practice

extension.15,17 This reciprocal recruitment pattern of the instability or osteoarthritis, should be excluded.27 Pain
RC during sagittal plane shoulder movement is not load- associated with RC tendinopathy may extend over the
dependent and occurs at low, medium and high loads.15 shoulder and/or lateral and proximal upper arm. It is
Simultaneous recruitment of all the RC muscles in equal exacerbated by arm movements, particularly overhead
proportions, therefore, does not appear to be an essential activities, and frequently increases at night.27 A recent
requirement to achieve dynamic shoulder joint stability. systematic review reported that the most accurate pain
The direction-specific recruitment pattern of the RC provocation test for detecting RC tendinopathy was the
during sagittal plane shoulder movement was found to be painful arc test: pain occurring in mid-range shoulder
highly synchronous with the muscles producing shoulder abduction had the highest LR and no pain during shoul-
flexion and extension.15 This suggests that the different der abduction the lowest LR.28 As all the RC muscles
parts of the RC function to stabilize the shoulder joint produce rotation torque at the shoulder, assessment of
by counterbalancing potential anterior–posterior humeral active and passive rotation ROM and rotation strength
head translation forces generated by the muscles produc- will aid in diagnosing RC pathology. It is recommended
ing flexion and extension, respectively.15 The RC, there- that, if possible, these tests be performed at 90° abduc-
fore, functions to prevent potential superior translation tion29 where electromyographic studies suggest that RC
of the humeral head due to deltoid activity as well as muscles are more specifically recruited.16 Limitation of
potential anterior and posterior translation due to flexor movement that occurs only with active motion suggests
and extensor muscle activity, respectively. impairment of the RC muscles and although associated
The view that the RC muscles are functioning as sta- with diagnostic uncertainty, external and internal rota-
bilizers of the shoulder joint during all shoulder move- tion lag tests have been identified as the most accurate
ments may also require revision. Maximal isometric clinical tests for identifying full-thickness RC tears.28
shoulder adduction tasks are associated with minimal to Pain and weakness when testing shoulder external rota-
low levels of RC muscle activity,18 suggesting that either tion strength have been found to be the most accurate
activity in shoulder adductor muscles does not produce test for detecting symptomatic RC disease.28 However, it
translation forces on the humeral head, or that muscles is important to reiterate that none of these tests are defin-
other than the RC are functioning to stabilize the shoul- itive and other sources of pain and weakness must be
der joint during adduction. More research is required to considered and excluded.24
better understand the role of the RC as stabilizers. In a recent investigation of individuals with unilateral
Activation of the RC muscles has implications for RC tendinopathy, Roy et al.30 used transcranial magnetic
axio-scapular muscle function. As the RC muscles take stimulation to map both the infraspinatus on the side
their origin from the scapula, contraction of the RC has with symptoms and the asymptomatic side. Their find-
the potential to move the scapula away from the midline.19 ings suggested that decreased corticospinal excitability
Therefore, coordinated contraction of axio-scapular was observed on the symptomatic side and that this asym-
muscles to provide a stable muscular anchor for the metry was related to chronicity, but not to intensity of
scapula is necessary for optimal RC function.19 pain. This investigation is the first to observe this type of
change associated with RC tendinopathy, and it is
extremely relevant for clinicians as it suggests cortical
DIAGNOSIS reorganization occurs in the presence of pain and may
contribute to explaining the poor correlation between
SIS is most probably a collection of clinical symptoms local tendon imaging changes and symptoms.1,24 Further
and not a clinical entity. It is unlikely that the Neer research is needed to determine if the pain associated
sign and Hawkins test are identifying an actual condi- with RC tendinopathy is driving the cortical changes or
tion but are more likely to be reproducing symptoms vice versa and whether exercise as therapy and other
that may include underlying RC pathology. The inci- interventions, such as lifestyle factors (Chapters 11
dence of RC tendinopathy has been reported to range and 37), influence the cortical changes associated with
from 0.3% to 5.5% and the point prevalence from 2.4% RC pathology.
to 21% across all age groups.20 However, many people
choose not to report their symptoms, and as outlined
in Chapter 50.1, deriving a definitive diagnosis of RC TREATMENT
pathology is difficult.21–24 Therefore interpreting epide-
miological data and deriving inferences need to be done The main intervention for treating SIS and RC
with caution. tendinopathy is active exercise therapy.31 The limited
Studies have demonstrated that many people without data available suggest that implementing a programme
symptoms have structural pathology in the region25,26 and of physiotherapist-supervised exercises confers clinical
there is no robust way of determining if the presenting benefit in the short and longer term when compared to
symptoms are due to the observed structural failure.1,24 no treatment or placebo treatment. In patients with
This has implications for clinical decision making, includ- mixed shoulder disorders, including SIS and RC pathol-
ing recommendations for surgery.1,24 ogy, significantly greater recovery, function and ROM
In order to derive a clinical diagnosis of RC pathology was demonstrated in the group receiving exercise after 1
other potential causes of shoulder pain, for example month compared to those receiving no treatment.32
referral from the cervical spine, glenohumeral joint People diagnosed with RC disease who received exercise
 50  The Shoulder 565

therapy demonstrated significant functional benefit at 2.5 stabilizer roles, exercises should be tailored to address
years follow-up compared with a placebo group.33 these different functional roles as well as performed in a
Over the past decade a number of randomized clinical manner related to the specific functional needs of the
trials have been published which clearly demonstrate that patient.
an exercise-based approach should be considered first in Although different rationale have been proposed to
the management of RC tendinopathy and SIS.34,35 Not justify exercise strategies to treat SIS and RC pathol-
only do these studies suggest that no additional benefit is ogy,45,46 a number of common guiding principles emerge.
conferred from surgical intervention, but an exercise- Evidence suggests that shoulder ROM and muscle power
based approach is also associated with substantial savings may improve when pain is reduced.4,5 Pain, weakness
for health funding bodies. Haahr et al.36 reported at and loss of normal function are features associated with
1-year follow-up that there was no difference in out- RC pathology. Pain, which may be irritable and present
comes between subacromial decompression and exercise at night, may be addressed by relative rest and supported
for a group of 90 people diagnosed with SIS. At 4- to by appropriate medication and intra-subacromial bursal
8-year follow-up they again concluded no significant injection therapy.4 Acute or acute on chronic tendon
clinical difference in outcome between the groups with pain may be associated with a proliferation of tendons
more payments for sick leave being required in the surgi- cells and both glucocorticoids and analgesics (e.g. bupi-
cal group.37 Ketola et al. concluded that exercise was as vacaine) have been reported to reduce tenocyte
effective as surgery at 1-year follow-up38 and again at numbers47,48 with possible equal clinical benefit.49,50 Injec-
5-year follow-up,39 arguing that subacromial decompres- tions into the subacromial bursa, as part of an appro-
sion was not cost-effective and exercise should be given priately structured rehabilitation programme, may be
first priority. The average number of physiotherapy treat- beneficial in managing the pain. Weakness may be real
ments ranged from seven to 19 sessions (each lasting 60 or caused by pain inhibition or a combination of both,
minutes), and physiotherapy care pathways should be and may be addressed by pain management and a gradu-
developed using these data as a minimal acceptable stan- ated exercise programme. It may be appropriate to
dard. Specific exercise approaches have demonstrated provide advice to avoid painful shoulder activities and
positive outcomes in patients diagnosed with SIS40 and initially perform exercises in a pain-free manner to
full-thickness41 and massive RC tears.42 Ainsworth et al.42 promote normal muscle function and movement patterns
demonstrated positive outcomes at 3 and 6 months using as part of the management programme.51 The restora-
a specific exercise approach for people with massive RC tion of normal movement patterns is a principal aim of
tears. There is a paucity of research comparing surgical exercise programmes whether they are designed to
repair and exercise for partial- and full-thickness tears of address painful tendons,4 altered scapular kinematics29
the RC. With the exception of those who have sustained or abnormal neuromuscular control.51 Exercise therapy
traumatic tears of the RC, and due to the poor correlation should be performed in a controlled and graduated
between structural failure and symptoms, it would appear manner whether the aim is to exercise an under-loaded
to be advisable to trial exercise therapy first and if desired RC tendon,4 to improve motor control by gradually
outcomes are not being achieved at specific time points increasing the complexity of the exercises51 or to achieve
then an onward referral for a surgical opinion would be conscious scapular control before progressing to scapular
warranted. and RC strengthening exercises.24,29 Patients should be
Although exercise appears to be the most valuable type advised that the exercise programme will need to be
of treatment for SIS and RC pathology, many exercise done regularly over a number of weeks and months to
strategies have been proposed and little evidence is avail- achieve the ongoing mechanical stimulation to restore
able to guide the clinician to the most appropriate and and maintain tendon health or to restore normal RC
effective exercises. Although it is often advocated that and axio-scapular muscle length, strength and/or motor
particular exercises target particular shoulder muscles it control patterns.29,51
is clear from many electromyographic studies that most It is important to recognize that people diagnosed
exercises elicit significant levels of activity in a large with RC pathology who do not respond to exercise
number of shoulder muscles.43,44 This is to be expected therapy and other treatments including medications,
since movements of the humerus and scapula occur injections and surgery may have non-peripherally medi-
simultaneously to produce full-range movement of ated pain mechanisms, with their experience of pain
the shoulder and because the RC and axio-scapular being due to central sensitization.52,53
muscles must also be recruited to prevent muscle forces
from destabilizing the humeral head and scapula,
respectively. WHAT ELSE INFLUENCES OUTCOME?
A thorough examination of shoulder movement quality
and muscle function should determine the choice of Although exercise therapy is the mainstay of the manage-
treatment goals and appropriate exercises.29 All parame- ment for SIS and RC tendinopathy,4 other interventions
ters of muscle function should be considered, including may contribute to improving clinical outcomes. The
active and passive length; isometric, concentric and available evidence from randomized controlled trials
eccentric strength; inner, mid and outer range strength; supports the use of subacromial corticosteroid injection
strength balance; and recruitment pattern/rhythm. As for RC disease, although its effect may be small and
RC and axio-scapular muscles perform both mover and short-lived.54
566 PART IV  Overview of Contemporary Issues in Practice

The evidence to support the inclusion of manual Downward scapular rotation and excessive anterior tilt
therapy with exercise for the treatment of SIS are frequently attributed to shortening of the pectoralis
and RC pathology varies depending on where the minor.77 With the patient supine a distance of greater
passive mobilization/manipulation techniques are applied. than 2.5 cm from the treatment couch to the posterior
Adding manual therapy applied to the cervicothoracic acromion has been attributed to a short pectoralis minor
vertebral region and/or thorax to exercise therapy confers muscle.77 However, the evidence supporting scapular
short- to medium-term clinical benefit compared to exer- posture and muscle imbalance in the aetiology of SIS and
cise therapy alone.55,56 Conversely, the addition of manual RC pathology remains at best equivocal. A recent system-
therapy applied to the shoulder region joints (glenohu- atic review failed to identify evidence for a consistent
meral, acromioclavicular and sternoclavicular joints) to alteration in scapular posture across studies that investi-
exercise therapy and advice does not appear to result in gated SIS and scapular position.78 Research on the pec-
additional clinical benefit.57 The long-term benefit of toralis minor length test failed to identify differences in
adding manual therapy to exercise in the treatment of SIS people with and without shoulder pain, with the distance
and RC pathology is not known. being marginally greater in people with no symptoms.79
The evidence for low-level laser therapy in the man- In addition, if poor posture and a concomitant alteration
agement of RC tendinopathy, although not definitive, in scapular posture does lead to irritation of the RC, the
suggests it may be beneficial.58 The use of therapeutic pathology should occur on the superior (bursal) surface
ultrasound and extracorporeal shock wave therapy for of tendon. A recent narrative review summarizing find-
non-calcific RC tendinosis does not appear to be sup- ings of observational studies reported that the majority
ported; however, there may be some benefit for calcific of RC tendon pathology was observed to occur on the
tendinosis.59,60 Taping may also be beneficial in the short joint side of the tendon or within the tendon, a finding
term61 but again more robust research is required. that largely refutes the acromial abrasion theory.1 As an
Cigarette smoking appears to be a risk factor in RC alternative to the examination of static posture to inform
pathology62 and smoking cessation may be beneficial in management, an approach that assesses dynamic changes
the management of this condition. Future research may to posture may be warranted.24
also establish an improvement in the outcome of RC
pathology with dietary management.63–65
CONCLUSIONS
MEASURING OUTCOME Further research is essential to identify methods of
facilitating more accurate diagnosis of RC pathology
Measuring the effectiveness of clinical intervention is an and exclude other sources of pain experienced in the
essential component of clinical practice to guide treat- shoulder. It is important to appreciate that there is a
ment progression and evaluate treatment outcome. For poor correlation between pain, symptoms and imaging
interventions targeting the RC, outcome measures would findings. The implication is that structural pathology
typically include measuring; pain,38 shoulder range of identified by current imaging modalities may not nec-
movement66 and strength,67 and may include thoracic68 essarily be the cause of symptoms. The tissue changes,
and scapular69 posture. More important than these mea- chemicals or changes in motor recruitment responsible
surements of impairment, are measurements of function for the symptoms remain elusive, and in others the
and disability that should be evaluated using validated symptoms may result from central sensitization. It is
outcome measures such as; the DASH, Quick-DASH and clear that a biopsychosocial approach to assessment
SPADI.70–72 and management is essential. There is mounting evi-
dence supporting exercise therapy in the management
of RC tendinopathy and the challenge is to identify
POSTURE AND MUSCLE IMBALANCE more effective ways to deliver this type of interven-
tion. Patient education and lifestyle management are
Deviations from an ideal posture and associated muscle also important components that support successful
imbalances are considered to be mechanisms that result rehabilitation.
in pain and movement abnormality. Although upper
body postural abnormalities are frequently associated
with SIS and RC tendon pathology,73,74 evidence support- REFERENCES
ing postural abnormalities in the pathogenesis of these 1. Lewis JS. Subacromial impingement syndrome: a musculoskeletal
shoulder pathologies is lacking.75 No study has found that condition or a clinical illusion? Phys Ther Rev 2011;16(5):
treatment directed at improving posture can in fact 388–98.
2. Clark JM, Harryman DT 2nd. Tendons, ligaments, and capsule of
change posture in the long term in people with shoulder the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg
symptoms or that a change in posture is the reason for 1992;74(5):713–25.
long-term improvements in function and reductions in 3. Lewis JS. Rotator cuff tendinopathy. Br J Sports Med 2009;43(4):
pain.76 236–41. [Epub 2008/09/20].
It has been suggested that in the presence of the classic 4. Lewis JS. Rotator cuff tendinopathy: a model for the continuum of
pathology and related management. Br J Sports Med 2010;44(13):
forward head posture, there is an associated increase in 918–23.
the thoracic kyphosis and changes in scapular posture, 5. Chester R, Smith TO, Hooper L, et al. The impact of subacromial
such that the scapula tilts anteriorly and downwards.74 impingement syndrome on muscle activity patterns of the shoulder
 50  The Shoulder 567

complex: a systematic review of electromyographic studies. BMC outcomes following rotator cuff tendinopathy? 12th International
Musculoskelet Disord 2010;11:45. [Epub 2010/03/11]. Congress on Shoulder and Elbow Surgery and 4th International
6. Cools A, Witvrouw E, Declercq G, et al. Scapular muscle recruit- Congress of Shoulder and Elbow Therapists; Nagoya, Japan. 2013.
ment patterns: trapezius muscle latency with and without impinge- 31. van der Heijden GJMG. Shoulder disorders: a state-of-the-art
ment symptoms. Am J Sports Med 2003;31(4):542–9. review. Ballieres Clin Rheumatol 1999;13(2):287–309.
7. Boettcher C, Ginn K, Cathers I. What is the optimal exercise for 32. Ginn K, Herbert R, Khouw W, et al. A randomised, controlled
supraspinatus strengthening? Med Sci Sports Exerc 2009;41(11): clinical trial of a treatment for shoulder pain. Phys Ther
1979–83. 1997;77(8):802–11.
8. Dark A, Ginn K, Halaki M. The effect of increasing resistance on 33. Brox J, Gjengedal E, Uppheim G, et al. Arthroscopic surgery versus
shoulder muscle activity levels during commonly-used rotator cuff supervised exercises in patients with rotator cuff disease (stage ii
exercises. Phys Ther 2007;87(8):1039–46. impingement syndrome): a prospective, randomised, controlled
9. Reinold M, Wilk K, Flesig G, et al. Electromyographis analysis of study in 125 patients with 2.5 year follow-up. J Shoulder Elbow
the rotator cuff and deltoid musculature during common shoulder Surg 1999;8(2):102–11.
external rotation exercises. J Orthop Sports Phys Ther 2004;34(7): 34. Coghlan J, Buchbinder R, Green S, et al. Surgery for rotator cuff
385–94. disease. Cochrane Database Syst Rev 2008;(1):CD005619.
10. van Linge B, Mulder JD. Function of the supraspinatus muscle and 35. Gebremariam L, Hay E, Koes B, et al. Effectiveness of surgical and
its relation to the supraspinatus syndrome: an experimental study postsurgical interventions for subacromial impingment syndrome:
in man. J Bone Joint Surg 1963;45B(4):750–4. a systematic review. Arch Phys Med Rehabil 2011;92:1900.
11. Reed D, Cathers I, Halaki M, et al. Does supraspinatus initiate 36. Haahr JP, Ostergaard S, Dalsgaard J, et al. Exercises versus
shoulder abduction? J Electromyogr Kinesiol 2012. arthroscopic decompression in patients with subacromial impinge-
12. Sharkey N, Marder R, Hansen P. The entire rotator cuff contrib- ment: a randomised, controlled study in 90 cases with a one year
utes to elevation of the arm. J Orthop Res 1994;12:699–708. follow up. Ann Rheum Dis 2005;64(5):760–4.
13. Lippitt S, Matsen F. Mechanisms of glenohumeral joint stability. 37. Haahr JP, Andersen JH. Exercises may be as efficient as subacromial
Clin Orthop 1993;291:20–8. decompression in patients with subacromial stage II impingement:
14. Sharkey N, Marder R. The rotator cuff opposes superior transla- 4–8-years’ follow-up in a prospective, randomized study. Scand J
tion of the humeral head. Am J Sports Med 1995;23(3):270–5. Rheumatol 2006;35(3):224–8.
15. Wattanaprakornkul D, Cathers I, Halaki M, et al. The rotator cuff 38. Ketola S, Lehtinen J, Arnala I, et al. Does arthroscopic acromio-
muscles have a direction specific recruitment pattern during flexion plasty provide any additional value in the treatment of shoulder
and extension exercises. J Sci Med Sport 2011;14:376–82. impingement syndrome?: a two-year randomised controlled trial.
16. Boettcher C, Cathers I, Ginn K. Shoulder muscle recruitment J Bone Joint Surg 2009;91(10):1326–34.
strategies are task specific. J Sci Med Sport 2010;[Epub 10.1016/j. 39. Ketola S, Lehtinen J, Rousi T, et al. No evidence of long-term
jsams.2010.03.008]. benefits of arthroscopicacromioplasty in the treatment of shoulder
17. Wattanaprakornkul D, Halaki M, Boettcher C, et al. A comprehen- impingement syndrome: five-year results of a randomised con-
sive analysis of muscle recruitment patterns during shoulder flexion: trolled trial. Bone Joint Res 2013;2(7):132–9. [Epub 2013/07/10].
an electromyographic study. Clin Anat 2011;24(6):619–26. 40. Holmgren T, Hallgren H, Oberg B, et  al. Effect of specific
18. Reed D, Halaki M, Ginn K. The rotator cuff muscles are activated exercise staregy on need for surgery in patients with subacromial
at low levels during shoulder adduction: an experimantal study. impingement syndrome: randomised controlled study. BMJ 2012;
J Physiother 2010;56(4):259–64. 344:e787.
19. Kibler W. The role of the scapula in athletic shoulder function. Am 41. Kuhn J, Dunn W, Sanders R, et al. Effectiveness of physical therapy
J Sports Med 1998;26(2):325–37. in treating atraumatic full-thickness rotator cuff tears: a multicenter
20. Littlewood C, May S, Walters S. Epidemiology of rotator cuff prospective cohort study. J Shoulder Elbow Surg 2013;22:
tendinopathy: a systematic review. Shoulder Elbow 2013;5(4): 1371–9.
256–65. 42. Ainsworth R, Lewis JS, Conboy V. A prospective randomized
21. Boettcher CA, Ginn KA, Cathers I. The ‘empty can’ and ‘full can’ placebo controlled clinical trial of a rehabilitation programme for
tests do not selectively activate supraspinatus. J Sci Med Sport patients with a diagnosis of massive rotator cuff tears of the shoul-
2009;12(4):435–9. der. Shoulder Elbow 2009;1(1):55–60.
22. Lewis JS, Tennent TD. How effective are diagnostic tests for the 43. Boettcher C, Ginn K, Cathers I. Standard maximum isometric
assessment of rotator cuff disease of the shoulder? In: MacAuley D, voluntary contraction tests for normalizing shoulder muscle EMG.
Best TM, editors. Evidenced Based Sports Medicine. 2nd ed. J Orthop Res 2008;26(12):1591–7.
London: Blackwell Publishing; 2007. 44. Hintermeister R, Lange G, Schultheis J, et al. Electromagnetic
23. Hegedus EJ, Goode AP, Cook CE, et al. Which physical examina- activity and applied load during shoulder rehabilitation exercises
tion tests provide clinicians with the most value when examining using elastic resistance. Am J Sports Med 1998;26(2):210–20.
the shoulder? Update of a systematic review with meta-analysis of 45. Ben-Yishay A, Zuckermann J, Gallagher M, et al. Pain inhibition
individual tests. Br J Sports Med 2012;46(14):964–78. [Epub of shoulder strength in patients with impingement syndrome.
2012/07/10]. Orthopedics 1994;17:685–8.
24. Lewis JS. Rotator cuff tendinopathy/subacromial impingement 46. Brox J, Roe C, Saugen E, et al. Isometric abduction muscle activa-
syndrome: is it time for a new method of assessment? Br J Sports tion in patients with rotator tendinosis of the shoulder. Arch Phys
Med 2009;43(4):259–64. Med Rehabil 1997;78:1260–7.
25. Frost P, Andersen JH, Lundorf E. Is supraspinatus pathology as 47. Scutt N, Rolf CG, Scutt A. Glucocorticoids inhibit tenocyte pro-
defined by magnetic resonance imaging associated with clinical sign liferation and Tendon progenitor cell recruitment. J Orthop Res
of shoulder impingement? J Shoulder Elbow Surg 1999;8(6): 2006;24(2):173–82. [Epub 2006/01/26].
565–8. 48. Scherb MB, Han SH, Courneya JP, et al. Effect of bupivacaine on
26. Girish G, Lobo LG, Jacobson JA, et al. Ultrasound of the shoulder: cultured tenocytes. Orthopedics 2009;32(1):26. [Epub 2009/02/20].
asymptomatic findings in men. AJR Am J Roentgenol 2011; 49. Alvarez CM, Litchfield R, Jackowski D, et al. A prospective,
197(4):W713–19. [Epub 2011/09/24]. double-blind, randomized clinical trial comparing subacromial
27. Gomoll A, Katz J, Warner J, et al. Rotator cuff disorders: recogni- injection of betamethasone and xylocaine to xylocaine alone in
tion and management among patients with shoulder pain. Arth chronic rotator cuff tendinosis. Am J Sports Med 2005;33(2):
Rheum 2004;50(12):3751–61. 255–62.
28. Hermans J, Luime J, Meuffels D, et al. Does this patient with 50. Ekeberg OM, Bautz-Holter E, Tveita EK, et al. Subacromial ultra-
shoulder pain have rotator cuff disease? the rational clinical exami- sound guided or systemic steroid injection for rotator cuff disease:
nation systematic review. JAMA 2013;310(8):837–47. randomised double blind study. Br Med J 2009;338:a3112.
29. Ellenbecker T, Cools A. Rehabilitation of shoulder impingement 51. Ginn K, Cohen M. Exercise therapy aimed at restoring neuromus-
syndrome and rotator cuff injuries: an evidenced-based review. Br cular control for the treatment of shoulder pain: a randomised
J Sports Med 2010;44:319–27. comparative clinical trial. J Rehabil Med 2005;37:115–22.
30. Roy JS, Ngomo S, Mercier C. Is asymmetry in corticospinal excit- 52. Gwilym SE, Oag HC, Tracey I, et al. Evidence that central sensi-
ability of the infraspinatus muscle correlated with shoulder-specific tisation is present in patients with shoulder impingement syndrome
568 PART IV  Overview of Contemporary Issues in Practice

and influences the outcome after surgery. J Bone Joint Surg Br 67. Dollings H, Sandford F, O’Conaire E, et al. Shoulder strength
2011;93(4):498–502. [Epub 2011/04/06]. testing: the intra-and inter-tester reliability of routine clinical
53. Gifford L. The ‘central’ mechanisms. In: Gifford L, editor. Topical tests, using the PowerTrack II Commander. Shoulder Elbow
issues in pain 1. Falmouth: CNS Press; 1998. p. 67–80. 2012;4(2):131–40.
54. Buchbinder R, Green S, Youd J. Corticosteroid injections for shoul- 68. Barrett E, McCreesh K, Lewis J. Reliability and validity of non-
der pain. Cochrane Database Syst Rev 2009. radiographic methods of thoracic kyphosis measurement: a system-
55. Bang M, Deyle G. Comparison of supervised exercise with and atic review. Man Ther 2014;19(1):10–17.
without manual physical therapy for patients with shoulder 69. Lewis JS, Valentine RE. Intraobserver reliability of angular and
impingement syndrome. J Orthop Sports Phys Ther 2000;30(3): linear measurements of scapular position in subjects with and
126–37. without symptoms. Arch Phys Med Rehabil 2008;89(9):1795–802.
56. Bergman G, Winters J, Groenier K, et al. Manipulative therapy in 70. Gabel CP, Yelland M, Melloh M, et al. A modified QuickDASH-9
addition to usual care for patients with shoulder dysfunction and provides a valid outcome instrument for upper limb function. BMC
pain. Ann Intern Med 2004;141:432–9. Musculoskelet Disord 2009;10:161. [Epub 2009/12/22].
57. Yiasemides R, Halaki M, Cathers I, et al. Does passive joint mobi- 71. Beaton DE, Katz JN, Fossel AH, et al. Measuring the whole or the
lization of shoulder region joints provide additional benefit over parts? Validity, reliability, and responsiveness of the Disabilities of
advice and exercise alone for people who have shoulder pain and the Arm, Shoulder and Hand outcome measure in different regions
minimal movement restriction? A randomized controlled trial. of the upper extremity. J Hand Ther 2001;14(2):128–46. [Epub
Phys Ther 2011;91(2). 2001/05/31].
58. Tumilty S, Munn J, McDonough S, et al. Low level laser treatment 72. Roach KE, Budiman-Mak E, Songsiridej N, et al. Development of
of tendinopathy: a systematic review with meta-analysis. Photomed a shoulder pain and disability index. Arthritis Care Res 1991;
Laser Surg 2010;28(1):3–16. [Epub 2009/08/28]. 4(4):143–9.
59. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for 73. Grimsby O, Gray J. Interrelation of the spine to the shoulder
shoulder pain. Cochrane Database Syst Rev 2003;(2):CD004258. girdle. In: Donatelli R, editor. Physical Therapy of the Shoulder.
60. Huisstede B, Gebremariam L, Sande Rvd, et al. Evidence for effec- 3rd ed. New York: Churchill Livingstone; 1997. p. 95–129.
tiveness of extracorporal shock-wave therapy (ESWT) to treat cal- 74. Gray J, Grimsby O. Interrelationship of the spine, rib cage, and
cific and non-calcific rotator cuff tendinosis e A systematic review. shoulder. In: Donatelli R, editor. Physical Therapy of the Shoulder.
Man Ther 2011;16(11):419–33. 4th ed. Edinburgh: Churchill Livingston; 2004. p. 133–85.
61. Teys P, Bisset L, Collins N, et al. One-week time course of the 75. Lewis JS, Green A, Wright C. Subacromial impingement syn-
effects of Mulligan’s Mobilisation with Movement and taping in drome: the role of posture and muscle imbalance. J Shoulder Elbow
painful shoulders. Man Ther 2013;18(5):372–7. [Epub 2013/02/09]. Surg 2005;14(4):385–92.
62. Baumgarten KM, Gerlach D, Galatz LM, et al. Cigarette smoking 76. McClure PW, Bialker J, Neff N, et al. Shoulder function and
increases the risk for rotator cuff tears. Clin Orthop Relat Res 3-dimensional kinematics in people with shoulder impingement
2010;468(6):1534–41. [Epub 2009/03/14]. syndrome before and after a 6-week exercise program. Phys Ther
63. Radak Z, Takahashi R, Kumiyama A, et al. Effect of aging and late 2004;84(9):832–48.
onset dietary restriction on antioxidant enzymes and proteasome 77. Sahrmann S. Diagnosis and treatment of movement impairment
activities, and protein carbonylation of rat skeletal muscle and syndromes. London: Mosby; 2002.
tendon. Exp Gerontol 2002;37(12):1423–30. 78. Ratcliffe E, Pickering S, McLean S, et al. Is there a relationship
64. Fallon K, Purdam C, Cook J, et al. A ‘polypill’ for acute tendon between subacromial impingement syndrome and scapular orienta-
pain in athletes with tendinopathy? J Sci Med Sport Med Aust tion? A systematic review. Br J Sports Med 2013;[Epub 2013/11/01].
2008;11(3):235–8. [Epub 2007/12/14]. 79. Lewis JS, Valentine RE. The pectoralis minor length test: a study
65. Lewis JS, Sandford FM. Rotator cuff tendinopathy: is there a role of the intra-rater reliability and diagnostic accuracy in subjects with
for polyunsaturated Fatty acids and antioxidants? J Hand Ther and without shoulder symptoms. BMC Musculoskelet Disord
2009;22(1):49–56. 2007;8(1):64.
66. Valentine RE, Lewis JS. Intraobserver reliability of 4 physiologic
movements of the shoulder in subjects with and without symptoms.
Arch Phys Med Rehabil 2006;87(9):1242–9.

CHAPTER 50.3  ■  THE UNSTABLE SHOULDER

Lyn Watson  •  Tania Pizzari  •  Jane Simmonds  • 
Jeremy Lewis

INTRODUCTION GHJ instability represents a spectrum of disorders

with overlapping syndromes that range from complete
The glenohumeral joint (GHJ) requires a large range of dislocation of the joint to excessive uncontrolled transla-
multi-planar motion to enable the upper limb to perform tion of the humeral head leading to secondary shoulder
multiple and complex functional tasks that range from symptoms.1,3–7 Although a number of classification
precision activities such as writing to high-powered systems for shoulder instability have been proposed,
explosive activities commonplace in sport. Passive and none have gained universal acceptance. This creates
dynamic structures are required to maintain congruence difficulties not only for diagnosis and inter-professional
between the humeral head and glenoid fossa in order to communication, but also for evaluation and comparisons
stabilize the GHJ during all shoulder movements and of treatments across trials.1,8 The FEDS system, which
activities.1 Deficits in these structures may lead to GHJ evaluates the patient perception of frequency, aetiology,
instability and be associated with substantial disability direction and severity of the instability, is the only system
due to loss of normal movement, pain and kinesiophobia, to date that has been tested for reliability and content
resulting in compromised function and reduced quality validity.8 However, this system has been criticized for
of life.2 eliminating multidirectional instability and pain in the
 50  The Shoulder 569

overhead athlete from the classification, and for failing ASSESSMENT

to address voluntary instability.9
Shoulder instability may occur as a result of trau- Interview
matic injury, repetitive use, or be inherited.1 In the
absence of an accepted classification system, it may The FEDS classification system identifies the patient
be appropriate to use an individual or algorithmic interview as the most important component of the exami-
approach to the diagnosis and management of insta- nation.8 Many features of the patient’s history may alter
bility.10 A well-structured clinical examination that the clinicians’ decision-making process for both the clini-
systematically documents the factors associated with cal examination and treatment strategies. A history of
each individual suffering from instability enables the trauma increases the likelihood of a structural lesion such
clinician to determine the direction, severity, functional as a labral tear, and this might place the patient at risk of
impact and most appropriate management pathway. recurrence and the possible need for surgery. A sudden
In this chapter, instability will be classified according increase or worsening of symptoms may suggest the onset
to direction, and will cover unidirectional instabilities of a structural lesion associated with repetitive micro-
(anterior, posterior or inferior) and multidirectional trauma in a person who has been classified with atrau-
instability. matic instability. However, as discussed in Chapter 50.1
Anterior shoulder instability is the predominant (Shoulder Assessment) not all structural lesions are
direction of instability. The incidence of anterior shoul- symptomatic.33,34
der dislocation is estimated to range from 8.2 to 56.3 The frequency of instability impacts on treatment
dislocations per 100 000 people per year,11–14 with an esti- planning, and people with recurrent dislocations that
mated prevalence of 1.7%.8 These data almost certainly substantially affect function are more likely to require
underestimate the prevalence of instability as they relate surgical stabilization. The direction of instability experi-
to joint dislocations and not to other forms of instability enced by the individual is also important to establish, as
such as subluxations, which may occur at rates five times this will influence rehabilitation strategies. Some indi-
higher than dislocations in young athletes.15 viduals are able to clearly define and even demonstrate
Although posterior dislocation is less common than the direction(s) of their shoulder instability and may even
anterior, there is a higher rate of associated bone and soft be able to reduce a dislocation of the GHJ independently.
tissue injury.16 Posterior dislocations are considered to Others may sense that the shoulder is unstable but may
account for only 2–3% of all shoulder instabilities. not be able to accurately describe the direction(s) of the
However, the majority of posterior dislocations are instability.20,25,35
missed on initial examination,16 and posterior subluxation Pain patterns may vary1 although the most likely
or translational instability may be easily overlooked and description is global shoulder pain, ill-defined and rather
misdiagnosed as ‘impingement’ pain or tight posterior vague in location, that is often activity- or position-
capsule. Assessment of humeral head translation during specific.19,20,25 In patients with an inferior component to
flexion and horizontal flexion may help identify excessive their instability pattern, paraesthesia may develop, par-
posterior translation of the humeral head. Posterior ticularly with use of the arm by the side, such as when
instabilities may be associated with increased joint laxity carrying or writing.35
and with multidirectional instability. Increased retrover-
sion of the glenoid fossa may also be associated with
posterior instability.17
Multidirectional instability (MDI) may be defined as
Physical Examination
symptomatic glenohumeral subluxation or dislocation in In standing, active ranges of movement are performed to
more than one direction as a result of repetitive micro- ascertain where in the ROM the instability occurs. In par-
trauma, muscle incoordination and congenital differences ticular, abduction, flexion, horizontal flexion (in varying
in the joint.18–21 The quintessential finding of this clinical ranges of flexion) and external rotation (through varying
condition is the presence of symptomatic inferior insta- ranges of abduction) are observed since these commonly
bility (sulcus sign) in addition to anterior and posterior demonstrate through-range subluxations.24,36–38
dislocations or subluxations of the shoulder.22–24 The lit- Treatment direction tests involve determining the
erature presents varying opinions on whether two or influence of changing the thoracic kyphosis, scapular
three directions of instability are required to be classified position and humeral head position on symptoms, in iso-
as MDI, whether the onset is always atraumatic23,25–29 or lation or combination.34,39–41 Decreasing the thoracic
whether MDI exists at all.8 kyphosis is associated with a concomitant posterior
Following traumatic dislocations, the shoulder joint scapular tilt. These procedures may be applied to any
is more susceptible to recurrent dislocation due to insta- movement, posture and orthopaedic test that reproduce
bility. Two-thirds of all anterior dislocations are reported the individual’s symptoms.34,40,41
to recur in patients aged less than 20 years old.30,31 These These types of correction techniques will help deter-
rates drop slightly (to approximately 40%) in those aged mine whether the patient’s instability symptoms will
between 20 and 40 years and are further reduced (less respond to rehabilitation and help direct the direction of
than 15%) in people aged over 40 years.31 With respect the rehabilitation protocol. One specific suggestion
to posterior dislocations, an overall recurrence rate of involves positioning the scapula in a combination of
17.7% has been reported and is highest in younger slight (10°) upward rotation, elevation (1–2 cm) and 5°
people.32 posterior tilt (Fig. 50-2).40,41
570 PART IV  Overview of Contemporary Issues in Practice

MANAGEMENT
Anterior Dislocation
Following dislocation, management typically involves
reduction and immobilization, followed by rehabilitation
to strengthen the shoulder.45 Historically, surgery has
been reserved for recurrent dislocations, associated GHJ
trauma, or the presence of ongoing symptoms.46 However,
robust evidence supports surgical intervention over con-
servative management for the prevention of recurrence
in young active males following primary anterior disloca-
tion.26,45,46 Surgery is associated with few complications
and has also been shown to produce superior functional
outcomes in comparison to conservative management.45
FIGURE 50-2  ■  Scapular positioning in a combination of slight The high risk of recurrent dislocations in young active
(10°) upward rotation, elevation (1–2 cm) and 5° posterior tilt. males, combined with evidence that recurrence poten-
tially leads to damage of the passive stabilizing struc-
tures47 and that cumulative trauma may result in higher
degrees of osteoarthritis,48 suggests a surgical approach
as first-line treatment should be considered.49,50
The reluctance to adopt surgical intervention as the
primary management approach possibly stems from a
lack of confidence in the research evidence and the
limited generalizability of the findings to the general
population.50 Variations in the types of surgical interven-
tions and conservative management provision exist in the
literature.45,46,50 It is therefore impossible to conclude that
the studies to date have compared ‘best practice’ surgical
intervention with ‘best practice’ conservative interven-
tion. It should also be considered that some individuals
will have success with conservative management, while
others may require stabilization. While respecting patient
values and understanding their aspirations, identifying
those that may benefit from the most appropriate con-
servative treatment51 will help avoid unnecessary surgery.52
FIGURE 50-3  ■  Manually applied anteriorly directed force on the The best surgical technique following anterior dislo-
humeral head.
cation remains a matter of debate.53 Although arthroscopic
surgery is becoming increasingly popular,54 a recent
Cochrane review55 reported no definitive differences in
outcome between arthroscopic and open surgery to ante-
Humeral head procedures that involve an anteriorly riorly stabilize the shoulder.
(Fig. 50-3) or posteriorly directed force may be achieved A bony (non-anatomical) procedure (e.g. Latarjet–
manually,34,40,41 with seatbelts or neoprene straps. The Bristow) is advocated for patients at high risk of recur-
advantage of a neoprene shoulder fixation belt34 is that rence56 in preference to a soft tissue, arthroscopic repair.
they may be applied with varying force and directions as Currently, there is no consensus as to what constitutes
well as during functional activities such as weight bearing best post-surgical rehabilitation.
(push up) and throwing and may also be used in treatment Following an acute dislocation where no fracture has
(Fig. 50-4). occurred, immobilization is generally prescribed (typi-
cally for 2 weeks) until pain is reduced. The duration and
position of immobilization after anterior dislocation have
Orthopaedic Instability Tests been debated.57 For people under the age of 30 years
Shoulder assessment including the orthopaedic instabil- there may be no difference in recurrence rates when
ity tests has been discussed in Chapter 50.1, and a com- immobilized in internal rotation for less than 1 week
prehensive review has been published.42 There is a when compared to 3 weeks or even longer periods of
possible risk of dislocation when performing the tests immobilization.58 Additionally, duration of immobiliza-
designed to assess instability and as such they must be tion in internal rotation does not appear to impact on
performed cautiously. When performing these tests a outcome.51,52,59 Similar recurrence rates are reported fol-
positive finding for instability is increased translation lowing immobilization in external rotation for 0, 3, or 6
associated with reproduction of the patient’s symptoms weeks.60 Compliance rates for immobilization in both
(pain, guarding or apprehension).20,43,44 internal and external rotation are typically low.61
 50  The Shoulder 571

& ' (

FIGURE 50-4  ■  Humeral head ‘positioning’ procedures applied with a purpose-built neoprene shoulder fixation strap. Anterior (A) and
posterior (P) glides with varying pressures and inclinations may be applied during weight-bearing and non-weight-bearing activities
of variable speeds and complexities. Examples shown: (A) A–P glide during shoulder flexion; (B) A–P superior glide during shoulder
abduction-external rotation; (C) A–P glide during weight bearing; (D) P–A glide during flexion; and (E) A–P/superior during shoulder
rehabilitation. (Shoulder Fixation Belt: www.LondonShoulderClinic.com)

Immobilization in external rotation has gained attention and rotator cuff muscles compensates for the lack of
in the past decade with cadaveric and magnetic resonance passive stability and assists in active control of the shoul-
studies demonstrating greater approximation of the ante- der.20,70 Poor muscle patterning is uncoordinated muscle
rior soft tissue to the glenoid when compared to internal activation strategies that result in aberrant scapulo-
rotation.62–64 However, subsequent randomized con- humeral movement patterns that compromise humeral
trolled trials comparing immobilization in internal rota- head control and may increase the risk of GHJ sublux-
tion with external rotation have produced equivocal ation. Muscle patterning is recognized as a contributing
findings.61,65–67 Appropriately designed research is factor in MDI71 and rehabilitation is considered the
required to advance knowledge in these areas. primary treatment option. Despite this recommendation,
the evidence for exercise-based management of MDI
remains uncertain due to studies of low quality and a
Posterior Dislocation high risk of bias.72 When conservative treatment is unsuc-
There is a paucity of research evidence guiding the cessful, surgery, usually to tighten the inferior capsule,
management of posterior dislocations.68 Conservative may be considered.19,20 Studies that have compared surgi-
management is recommended for at least 6 months fol- cal intervention with conservative treatment for MDI
lowing successful reduction with no substantial fracture, have demonstrated improvements in favour of surgery
rotator cuff tear or ongoing instability.16,17 for impairment outcomes and improvements in favour
of conservative management for patient-focused
Anterior or Posterior Subluxation and outcomes.73–76 Definitive conclusions are not available
due to a lack of appropriately designed research.72
Multidirectional Instability (MDI)
Anterior and posterior subluxations occur when the
humeral head translates excessively but does not dislo-
Conservative Rehabilitation Principles
cate. This may result from structural lesions (such as Currently there are no randomized controlled trials that
labral tears or capsule and ligament attenuation) or as compare conservative management to control or sham
a result of weakened or decreased muscular control.1 treatment. A number of protocols have been published77
Exercise therapy is commonly recommended as the and these are based on physiological and biological evi-
initial treatment strategy for these instabilities.18–20,69 This dence of shoulder joint stability. Table 50-4 outlines con-
is based on the rationale that strengthening the scapular servative management, including the acute phase where
 TABLE 50-4  Management Guidelines Post Reconstruction Surgery or Dislocation
Acute Management Acute Stage 3: Stage 5:
Immediately Management Stage 1: Stage 2: Posterior Coronal/ Stage 6: Stage 7:
Stage of Post-Surgery or Approximately 2–6 Scapula Setting Coronal Plane Musculature 0–45° Stage 4: Sagittal Plane Isolated Overhead/
Rehabilitation Dislocation Weeks Phase 0–45° Abduction Abduction Flexion 45–90° Strength Drills Functional
Components Shoulder Passive and active Upward Standing ER with Shrugs Forward punch ER and IR at Posterior deltoid Deltoid >90°
immobilization assisted range of rotation light band Side lie ER in scapula 90° abduction Anterior deltoid IR >90°
Pain relief motion shrug resistance Standing ER with plane Flexion at 90° Middle deltoid ER >90°
Elbow/wrist Isometric scapula (0° abduction) heavier band Horizontal (short lever Flexion >90°
exercises muscle strength Standing IR with Standing row (0° flexion/ abduction) Sport-specific
band resistance abduction extension part drills
(0° abduction) progress to 45°
abduction)
Dosage Continual Scapula setting: Goal: Goal: Goal: Goal: Goal: Goal: Control of drill
immobilization for 20 repetitions 3 × 0.5 kg–1 kg × ER/IR: full arc 3 × Shrugs 3 × 20 reps × 20 reps up to ER/IR: full arc × All exs: 3–4 kg × 20 reps
approximately 2 per day 20 reps in 20 reps against with 2 kg 45° with light 20 reps at arc of Strength drills ×
weeks post- standing medium Side lie ER with 1 kg to moderate against motion 12 (increased
surgery, resistance ER 3 × 20 moderate band medium required for load)
immobilization to heavy resistance as resistance × function Low load high
time may vary by resistance able to 20 reps up to reps for
surgeon Row: 45° abduction, control 90° with endurance,
heavy band 3 × 20 moderate high load
reps band high reps for
resistance strength
HF/HE × 20 reps
pain-free
light
resistance
Progression Commence passive Commence upward Start with no Commence ER Regress to Higher-level Commence Progress to
movement when rotation shrug weight in approximately 1 stage 3 if resistance post. deltoid strength drills
pain allows or when able to standing, if week prior to IR poor control, bands/ first, progress as required
according to control setting unable to If unable to pain or weights can from standing and whole
surgeon protocol drill perform complete posterior be prescribed rows to bent practice of
complete standing ER with subluxation if required for over sports-specific
shrugs in control perform during sport or Then introduce drills
side lying standing exercise function and mid. deltoid
shoulder can be (standing
extension controlled punch to
initially flexion 90°)
Then commence
ant. deltoid
Precautions Avoid positions of If predisposed, Continue upward Care must be Ensure humeral
risk individuals rotation shrug, taken in head is
Anterior instability: may only progress flexion for articulating in
abduction experience an stage when patients with a central
combined with increase in individual has posterior position in
external rotation neck pain good scapular instability abduction/
Posterior performing and humeral external
instability: the shrug. head control rotation
flexion with Deep neck Exercises should positions at
horizontal flexion flexor not elicit 90°
+/− internal exercises symptoms
rotation may be
required, or
supine/
side-lying
shrugs
initially

ant. deltoid, anterior deltoid; ER, external rotation; exs, exercises; IR, internal rotation; mid. deltoid, middle deltoid; post. deltoid, posterior deltoid; reps, repetitions.
 50  The Shoulder 573

an individual is post-surgery or post-dislocation, followed BOX 50-1  Brighton Criteria

by the stages of rehabilitation for individuals with MDI
or subluxing instabilities or for individuals following the MAJOR CRITERIA
acute phase post injury or surgery. • A Beighton score of 4/9 or greater (either currently or
historically)
GENERALIZED JOINT HYPERMOBILITY, • Arthralgia for longer than 3 months in four or more
joints
JOINT HYPERMOBILITY SYNDROME
MINOR CRITERIA
AND SHOULDER INSTABILITY
• A Beighton score of 1, 2, or 3/9 (0, 1, 2 or 3 if aged 50+)
Generalized joint hypermobility (GJH) is a unifying • Arthralgia (for 3 months or longer) in one to three
joints or back pain for (for 3 months or longer), spon-
feature of Ehlers–Danlos syndrome (EDS), Marfan syn-
dylosis, spondylolysis/spondylolisthesis
drome and osteogenesis imperfecta which are all herita- • Dislocation/subluxation in more than one joint, or in
ble disorders of connective tissue (HDCT) that affect the one joint on more than one occasion. Soft tissue rheu-
connective tissue matrix proteins.78 In recent decades matism: three or more lesions (e.g. epicondylitis, teno-
joint hypermobility syndrome (JHS), a more common synovitis, bursitis)
connective tissue disorder with a mixed phenotype of the • Marfanoid habitus (tall, slim, span/height ration 1.03
heritable disorders of connective tissues, has been identi- upper: lower segment ration less than 0.89, arachno-
fied. JHS is considered to be an atypical HDCT, sharing dactyly (positive Steinberg/wrist signs)
overlapping features with EDS, Marfan syndrome and • Abnormal skin striae, hyperextensibility, thin skin,
osteogenesis imperfecta.78 Many authorities now con- papery scarring
• Eye signs: drooping eyelids or myopia or antimongol-
sider JHS to be indistinguishable from EDS (hypermo-
oid slant
bility type).79 The term JHS is used in this section to • Varicose veins or hernia or uterine/rectal prolapse
describe these inseparable entities. A diagnosis is made on the basis of:
The reported point prevalence of GJH and JHS in the • Two major criteria
adult general population is 10 to 30% and 0.75% respec- • One major plus two minor criteria
tively.78,80 The point prevalence of JHS reported in mus- • Four minor criteria
culoskeletal rheumatology and physiotherapy outpatient • Two minor criteria and unequivocally affected first-
settings ranges from 30–60%.81–83 degree relative in family history
Currently there is no biomedical test to diagnose JHS • JHS is excluded by the presence of Marfan or Ehlers–
and therefore the diagnosis is based on clinical examina- Danlos syndromes other than the EDS hypermobility
type (formerly EDS III).
tion. The Brighton Criteria (Box 50-1) may be used to
NB: Criteria Major 1 and Minor 1 are mutually exclusive,
reach a diagnosis in both adults and children.84 Symptoms as are Major 2 and Minor 2.
of JHS frequently commence in early childhood, are
amplified during adolescence and may continue into (Grahame et al.84)
adult life.84,85 The predominant presenting complaints are EDS, Ehlers–Danlos syndrome; JHS, joint hypermobility syndrome.
musculoskeletal dysfunction and pain. Numerous extra-
articular manifestations are also reported.78,85,86
Individuals with GJH and JHS may present with a aquatic rehabilitation and a graduated strength, endur-
wide range of shoulder pathologies. Pain is often more ance and plyometric functional rehabilitation programme
profound in those with JHS. Muscular weakness, fatigue, may be implemented. More challenging cases often
altered scapular position,87 scapular dyskinesia, poor pro- require additional pain management and input from a
prioception, maladaptive postural changes and subse- multidisciplinary team.
quent chronic pain states are common88,89 and may
cascade towards regional chronic pain states.
Although individuals with GJH and JHS are suscep- REFERENCES
tible to traumatic instability,90,91 they also commonly 1. Lewis A, Kitamura T, Bayley JIL. (ii) The classification of shoulder
present with multidirectional and unidirectional instabil- instability: new light through old windows! Curr Orthop
ity unrelated to trauma.88 Very minor events may create 2004;18(2):97–108.
recurring episodes of shoulder displacement and ongoing 2. Gartsman GM, Brinker MR, Khan M, et al. Self-assessment of
general health status in patients with five common shoulder condi-
pain, resulting in increasing disability. Correct and early tions. J Shoulder Elbow Surg 1998;7(3):228–37.
recognition and classification of the instability in this 3. Garth WP Jr, Allman FL Jr, Armstrong WS. Occult anterior sub-
patient population will lead to appropriate management luxations of the shoulder in noncontact sports. Am J Sports Med
and avoid unnecessary surgery, which in some cases may 1987;15(6):579–85.
4. Jobe CM, Iannotti JP. Limits imposed on glenohumeral motion by
exacerbate symptoms and disability.88 joint geometry. J Shoulder Elbow Surg 1995;4(4):281–5.
Management requires a multifaceted approach due to 5. Salomonsson B, Sforza G, Revay S, et al. Atraumatic shoulder
the nature of the condition. Initial rehabilitation should instability. Discussion of classification and results after capsular
focus on education, joint protection and training the imbrication. Scand J Med Sci Sports 1998;8(6):398–404.
motor control system.92 Closed kinetic chain exercises, 6. Walch G, Boileau P, Noel E, et al. Impingement of the deep surface
of the supraspinatus tendon on the posterosuperior glenoid rim: an
using biofeedback to enhance proprioception from arthroscopic study. J Shoulder Elbow Surg 1992;1(5):238–45.
mirrors, tape, exercise balls and hands-on facilitation may 7. Yamaguchi K, Flatow EL. Management of multidirectional insta-
be helpful in the early stages.92 Later, hydrotherapy/ bility. Clin Sports Med 1995;14(4):885–902.
574 PART IV  Overview of Contemporary Issues in Practice

8. Kuhn JE. A new classification system for shoulder instability. Br J 34. Lewis JS. Rotator cuff tendinopathy/subacromial impingement
Sports Med 2010;44(5):341–6. syndrome: is it time for a new method of assessment? Br J Sports
9. Shea KP. ISAKOS Consensus shoulder instability classification Med 2009;43(4):259–64.
system. Shoudler Concepts 2013: Consensus and Concerns 35. VandenBerghe G, Hoenecke HR, Fronek J. Glenohumeral joint
ISAKOS Upper Extremity Committees 2009–2013. Springer; instability: the orthopedic approach. Semin Musculoskelet Radiol
2013. 2005;9(1):34–43.
10. Murray IR, Ahmed I, White NJ, et al. Traumatic anterior shoulder 36. Ozaki J. Glenohumeral movements of the involuntary inferior and
instability in the athlete. Scand J Med Sci Sports 2013;23(4): multidirectional instability. Clin Orthop Relat Res 1989;238:
387–405. 107–11.
11. Liavaag S, Svenningsen S, Reikeras O, et al. The epidemiology of 37. Inui H, Sugamoto K, Miyamoto T, et al. Three-dimensional rela-
shoulder dislocations in Oslo. Scand J Med Sci Sports 2011; tionship of the glenohumeral joint in the elevated position in shoul-
21(6):e334–40. ders with multidirectional instability. J Shoulder Elbow Surg
12. Nordqvist A, Petersson CJ. Incidence and causes of shoulder girdle 2002;11(5):510–15.
injuries in an urban population. J Shoulder Elbow Surg 38. Jobe FW, Kvitne RS, Giangarra CE. Shoulder pain in the overhand
1995;4(2):107–12. or throwing athlete. The relationship of anterior instability and
13. Simonet WT, Melton LJ 3rd, Cofield RH, et al. Incidence of ante- rotator cuff impingement. Orthop Rev 1989;18(9):963–75.
rior shoulder dislocation in Olmsted County, Minnesota. Clin 39. Magarey ME, Jones MA. Specific evaluation of the function of
Orthop Relat Res 1984;186:186–91. force couples relevant for stabilization of the glenohumeral joint.
14. Kroner K, Lind T, Jensen J. The epidemiology of shoulder disloca- Man Ther 2003;8(4):247–53.
tions. Arch Orthop Trauma Surg 1989;108(5):288–90. 40. Watson LA, Pizzari T, Balster S. Thoracic outlet syndrome part 1:
15. Owens BD, Duffey ML, Nelson BJ, et al. The incidence and char- clinical manifestations, differentiation and treatment pathways.
acteristics of shoulder instability at the United States Military Man Ther 2009;14(6):586–95.
Academy. Am J Sports Med 2007;35(7):1168–73. 41. Watson LA, Pizzari T, Balster S. Thoracic outlet syndrome part 2:
16. Rouleau DM, Hebert-Davies J. Incidence of associated injury in conservative management of thoracic outlet. Man Ther 2010;
posterior shoulder dislocation: systematic review of the literature. 15(4):305–14.
J Orthop Trauma 2012;26(4):246–50. 42. Hegedus EJ, Goode AP, Cook CE, et al. Which physical examina-
17. Tannenbaum E, Sekiya JK. Evaluation and management of poste- tion tests provide clinicians with the most value when examining
rior shoulder instability. Sports Health 2011;3(3):253–63. the shoulder? Update of a systematic review with meta-analysis of
18. An YH, Friedman RJ. Multidirectional instability of the glenohu- individual tests. Br J Sports Med 2012;46(14):964–78.
meral joint. Orthop Clin North Am 2000;31(2):275–85. 43. Kuhn JE, Helmer TT, Dunn WR, et al. Development and reli-
19. Bahu MJ, Trentacosta N, Vorys GC, et al. Multidirectional insta- ability testing of the frequency, etiology, direction, and severity
bility: evaluation and treatment options. Clin Sports Med 2008; (FEDS) system for classifying glenohumeral instability. J Shoulder
27(4):671–89. Elbow Surg 2011;20(4):548–56.
20. Guerrero P, Busconi B, Deangelis N, et al. Congenital instability 44. Tennent TD, Beach WR, Meyers JF. A review of the special tests
of the shoulder joint: assessment and treatment options. J Orthop associated with shoulder examination. Part II: laxity, instability, and
Sports Phys Ther 2009;39(2):124–34. superior labral anterior and posterior (SLAP) lesions. Am J Sports
21. Mallon WJ, Speer KP. Multidirectional instability: current con- Med 2003;31(2):301–7.
cepts. J Shoulder Elbow Surg 1995;4(1 Pt 1):54–64. 45. Godin J, Sekiya JK. Systematic review of rehabilitation versus
22. Ide J, Maeda S, Yamaga M, et al. Shoulder-strengthening exercise operative stabilization for the treatment of first-time anterior
with an orthosis for multidirectional shoulder instability: quantita- shoulder dislocations. Sports Health 2010;2(2):156–65.
tive evaluation of rotational shoulder strength before and after the 46. Handoll HH, Almaiyah MA, Rangan A. Surgical versus non-
exercise program. J Shoulder Elbow Surg 2003;12(4):342–5. surgical treatment for acute anterior shoulder dislocation. Cochrane
23. McFarland EG, Kim TK, Park HB, et al. The effect of variation Database Syst Rev 2004;(1):CD004325.
in definition on the diagnosis of multidirectional instability of the 47. Habermeyer P, Gleyze P, Rickert M. Evolution of lesions of the
shoulder. J Bone Joint Surg Am 2003;85-A(11):2138–44. labrum-ligament complex in posttraumatic anterior shoulder insta-
24. Neer CS 2nd, Foster CR. Inferior capsular shift for involuntary bility: a prospective study. J Shoulder Elbow Surg 1999;8(1):
inferior and multidirectional instability of the shoulder. A prelimi- 66–74.
nary report. J Bone Joint Surg Am 1980;62(6):897–908. 48. Ogawa K, Yoshida A, Ikegami H. Osteoarthritis in shoulders with
25. Fischer SP. Arthroscopic treatment of multidirectional instability. traumatic anterior instability: preoperative survey using radiogra-
Sports Med Arthrosc 2004;12(2):127–34. phy and computed tomography. J Shoulder Elbow Surg 2006;
26. Chahal J, Marks PH, Macdonald PB, et al. Anatomic Bankart repair 15(1):23–9.
compared with nonoperative treatment and/or arthroscopic lavage 49. Boone JL, Arciero RA. First-time anterior shoulder dislocations:
for first-time traumatic shoulder dislocation. Arthroscopy has the standard changed? Br J Sports Med 2010;44(5):355–60.
2012;28(4):565–75. 50. Monk AP, Garfjeld Roberts P, Logishetty K, et al. Evidence in
27. Gerber C, Nyffeler RW. Classification of glenohumeral joint insta- managing traumatic anterior shoulder instability: a scoping review.
bility. Clin Orthop Relat Res 2002;400:65–76. Br J Sports Med 2013 Aug 21;doi:10.1136/bjsports-2013-092296;
28. Joseph TA, Williams JS Jr, Brems JJ. Laser capsulorrhaphy for [Epub ahead of print].
multidirectional instability of the shoulder. An outcomes study and 51. Van Tongel A, Rosa F, Heffernan G, et al. Long-term result after
proposed classification system. Am J Sports Med 2003;31(1): traumatic anterior shoulder dislocation: what works best? Muscu-
26–35. loskelet Surg 2011;95(Suppl. 1):S65–70.
29. Throckmorton TW, Dunn W, Holmes T, et al. Intraobserver and 52. Hovelius L, Olofsson A, Sandstrom B, et al. Nonoperative treat-
interobserver agreement of International Classification of Diseases, ment of primary anterior shoulder dislocation in patients forty
Ninth Revision codes in classifying shoulder instability. J Shoulder years of age and younger. a prospective twenty-five-year follow-up.
Elbow Surg 2009;18(2):199–203. J Bone Joint Surg Am 2008;90(5):945–52.
30. Hovelius L, Augustini BG, Fredin H, et al. Primary anterior dislo- 53. Randelli P, Taverna E. Primary anterior shoulder dislocation in
cation of the shoulder in young patients. A ten-year prospective young athletes: fix them! Knee Surg Sports Traumatol Arthrosc
study. J Bone Joint Surg Am 1996;78(11):1677–84. 2009;17(12):1404–5.
31. Simonet WT, Cofield RH. Prognosis in anterior shoulder disloca- 54. Malhotra A, Freudmann MS, Hay SM. Management of traumatic
tion. Am J Sports Med 1984;12(1):19–24. anterior shoulder dislocation in the 17- to 25-year age group: a
32. Robinson CM, Seah M, Akhtar MA. The epidemiology, risk of dramatic evolution of practice. J Shoulder Elbow Surg 2012;21(4):
recurrence, and functional outcome after an acute traumatic poste- 545–53.
rior dislocation of the shoulder. J Bone Joint Surg Am 2011; 55. Pulavarti RS, Symes TH, Rangan A. Surgical interventions for
93(17):1605–13. anterior shoulder instability in adults. Cochrane Database Syst Rev
33. Miniaci A, Mascia AT, Salonen DC, et al. Magnetic resonance 2009;(4):CD005077.
imaging of the shoulder in asymptomatic professional baseball 56. Balg F, Boileau P. The instability severity index score. A simple
pitchers. Am J Sports Med 2002;30(1):66–73. pre-operative score to select patients for arthroscopic or open
 50  The Shoulder 575

shoulder stabilisation. J Bone Joint Surg Br 2007;89(11): 74. Kiss J, Damrel D, Mackie A, et al. Non-operative treatment of
1470–7. multidirectional shoulder instability. Int Orthop 2001;24(6):
57. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann 354–7.
R Coll Surg Engl 2009;91(1):2–7. 75. Kiss RM, Illyes A, Kiss J. Physiotherapy vs. capsular shift and
58. Paterson WH, Throckmorton TW, Koester M, et al. Position and physiotherapy in multidirectional shoulder joint instability. J Elec-
duration of immobilization after primary anterior shoulder disloca- tromyogr Kinesiol 2010;20(3):489–501.
tion: a systematic review and meta-analysis of the literature. J Bone 76. Tillander B, Lysholm M, Norlin R. Multidirectional hyperlaxity of
Joint Surg Am 2010;92(18):2924–33. the shoulder: results of treatment. Scand J Med Sci Sports
59. Scheibel M, Kuke A, Nikulka C, et al. How long should acute 1998;8(6):421–5.
anterior dislocations of the shoulder be immobilized in external 77. Gibson K, Growse A, Korda L, et al. The effectiveness of rehabili-
rotation? Am J Sports Med 2009;37(7):1309–16. tation for nonoperative management of shoulder instability: a sys-
60. Itoi E, Hatakeyama Y, Itoigawa Y, et al. Is protecting the healing tematic review. J Hand Ther 2004;17(2):229–42.
ligament beneficial after immobilization in external rotation for an 78. Hakim A, Grahame R. Joint hypermobility. Best Pract Res Clin
initial shoulder dislocation? Am J Sports Med 2013;41(5): Rheumatol 2003;17(6):989–1004.
1126–32. 79. Tinkle BT, Bird HA, Grahame R, et al. The lack of clinical distinc-
61. Liavaag S, Brox JI, Pripp AH, et al. Immobilization in external tion between the hypermobility type of Ehlers-Danlos syndrome
rotation after primary shoulder dislocation did not reduce the risk and the joint hypermobility syndrome (a.k.a. hypermobility syn-
of recurrence: a randomized controlled trial. J Bone Joint Surg Am drome). Am J Med Genet A 2009;149A(11):2368–70.
2011;93(10):897–904. 80. Klemp P, Williams SM, Stansfield SA. Articular mobility in Maori
62. Liavaag S, Stiris MG, Lindland ES, et al. Do Bankart lesions heal and European New Zealanders. Rheumatology 2002;41(5):554–7.
better in shoulders immobilized in external rotation? Acta Orthop 81. Clark CJ, Simmonds JV. An exploration of the prevalence of hyper-
2009;80(5):579–84. mobility and joint hypermobility syndrome in Omani women
63. Miller BS, Sonnabend DH, Hatrick C, et al. Should acute anterior attending a hospital physiotherapy service. Musculoskeletal Care
dislocations of the shoulder be immobilized in external rotation? A 2011;9(1):1–10.
cadaveric study. J Shoulder Elbow Surg 2004;13(6):589–92. 82. Connelly E. The prevalence of joint hypermobility and joint hyper-
64. Itoi E, Sashi R, Minagawa H, et al. Position of immobilization after mobility syndrome (JHS) in patients presenting to a London neu-
dislocation of the glenohumeral joint. A study with use of magnetic romusculoskeletal triage clinic and the impact of JHS on quality of
resonance imaging. J Bone Joint Surg Am 2001;83-A(5):661–7. life. UK: Master of Science: University of Herfordshire; 2013.
65. Itoi E, Hatakeyama Y, Kido T, et al. A new method of immobiliza- 83. Grahame R, Hakim A. High prevalence of joint hypermobility
tion after traumatic anterior dislocation of the shoulder: a prelimi- syndrome in clinic referrals to a north London community hospital.
nary study. J Shoulder Elbow Surg 2003;12(5):413–15. Rheumatology 2004;43(3 Suppl. 1):198.
66. Itoi E, Hatakeyama Y, Sato T, et al. Immobilization in external 84. Grahame R, Bird HA, Child A. The revised (Brighton 1998) crite-
rotation after shoulder dislocation reduces the risk of recurrence. ria for the diagnosis of benign joint hypermobility syndrome
A randomized controlled trial. J Bone Joint Surg Am 2007; (BJHS). J Rheumatol 2000;27(7):1777–9.
89(10):2124–31. 85. Murray KJ. Hypermobility disorders in children and adolescents.
67. Finestone A, Milgrom C, Radeva-Petrova DR, et al. Bracing in Best Pract Res Clin Rheumatol 2006;20(2):329–50.
external rotation for traumatic anterior dislocation of the shoulder. 86. Engelbert RHH, Scheper MC. Joint hypermobility with and
J Bone Joint Surg Br 2009;91(7):918–21. without musculoskeletal complaints: a physiotherapeutic approach.
68. Paul J, Buchmann S, Beitzel K, et al. Posterior shoulder dislocation: Int Musculoskelet Med 2011;33(4):146–50.
systematic review and treatment algorithm. Arthroscopy 2011; 87. Moghadam AN, Salimee MM. A comparative study on scapular
27(11):1562–72. static position between females with and without generalized joint
69. Burkhead WZ Jr, Rockwood CA Jr. Treatment of instability of the hyper mobility. Med J Islam Repub Iran 2012;26(3):97–102.
shoulder with an exercise program. J Bone Joint Surg Am 88. Jaggi A, Lambert S. Regional complications in joint hypermobility
1992;74(6):890–6. syndrome: the shoulder joint. In: Hakim A, Keer R, Grahame R,
70. Beasley L, Faryniarz DA, Hannafin JA. Multidirectional instability editors. Hypermobility, fibromyalgia, and chronic pain. Edinburgh:
of the shoulder in the female athlete. Clin Sports Med 2000; Churchill Livingstone/Elsevier; 2010. p. 197–205.
19(2):331–49. 89. Simmonds JV, Keer RJ. Hypermobility and the hypermobility syn-
71. Jaggi A, Lambert S. Rehabilitation for shoulder instability. Br J drome. Man Ther 2007;12(4):298–309.
Sports Med 2010;44(5):333–40. 90. Cameron KL, Duffey ML, DeBerardino TM, et al. Association of
72. Warby SA, Pizzari T, Ford JJ, et al. The effect of exercise-based generalized joint hypermobility with a history of glenohumeral
management for multidirectional instability of the glenohumeral joint instability. J Athl Train 2010;45(3):253–8.
joint: a systematic review. J Shoulder Elbow Surg 2014;23(1): 91. Muhammad AA, Jenkins P, Ashton F, et al. Hypermobility a risk
128–42. factor for recurrent shoulder dislocations. Br J Sports Med
73. Illyes A, Kiss J, Kiss RM. Electromyographic analysis during pull, 2013;47(10):e3.
forward punch, elevation and overhead throw after conservative 92. Keer R, Simmonds J. Joint protection and physical rehabilitation
treatment or capsular shift at patient with multidirectional shoulder of the adult with hypermobility syndrome. Curr Opin Rheumatol
joint instability. J Electromyogr Kinesiol 2009;19(6):e438–47. 2011;23(2):131–6.

CHAPTER 50.4  ■  POSTERIOR SHOULDER TIGHTNESS

John Borstad  •  Jeremy Lewis

muscles, or a combination of both. Increased humeral

OVERVIEW retroversion may also contribute to a decrease in ROM,
but is distinct from posterior shoulder tightness.1 The
Posterior shoulder tightness is suspected when glenohu- first published account of posterior shoulder tightness
meral internal rotation and/or horizontal adduction was described in association with shoulder ROM altera-
ROM are decreased. This reduction of normal move- tions in baseball pitchers.2 Posterior shoulder tightness
ment may result from decreased extensibility of the pos- occurs frequently in throwing athletes but may also occur
terior glenohumeral joint capsule, the posterior shoulder in the general population.3 Many uncertainties exist
576 PART IV  Overview of Contemporary Issues in Practice

regarding posterior shoulder tightness, including whether comparison to asymptomatic shoulders was not per-
or not it is even a real phenomenon related to soft tissue formed. While these associations provide validity to pos-
structure or mechanics. terior shoulder tightness as an impairment, direct
evidence that verifies the existence of posterior shoulder
tightness is lacking.
MECHANISMS
In throwing athletes, it is proposed that posterior shoul- DIAGNOSIS
der tightness is caused by reduced posterior capsule
extensibility.4 During the deceleration phase of throwing, Posterior shoulder tightness is currently assessed by
the posterior shoulder muscles contract eccentrically to quantifying glenohumeral joint internal rotation and/or
absorb energy created during the acceleration phase. horizontal adduction ROM. Intra- and inter-rater reli-
However, muscle function may decline with fatigue, such ability of each method is reported as good to excel-
that the posterior capsule shares deceleration loads. Over lent,23–25 yet construct validity has not been established.
time, cyclic capsule loading leads to contracture and Both measurements produced lower strain on the poste-
fibrosis, decreased capsule extensibility and altered rior capsule of cadavers than a position of 60° flexion and
motion.5 It is hypothesized that tensile loading triggers passive internal rotation.18 This measurement also accu-
cellular and metabolic processes that synthesize tissue in rately identifies capsule tightness in throwers and has
an effort to protect the capsule against further loading.4 high intra-rater reliability. Motion must be compared to
Increased muscle stiffness, a short-term consequence the contralateral shoulder motion to determine if tight-
of fatiguing eccentric contractions, may also contribute ness exists. A concern with all posterior shoulder tight-
to posterior shoulder tightness in throwing athletes.6 ness measurements is their inability to distinguish
However, this mechanism remains speculative because between capsule tightness, muscle tightness and humeral
long-term eccentric exercise results in increased ROM retroversion. In addition, the influence of scapula posi-
and protection against further muscle adaptations.7 Adhe- tion on these measurements may affect their interpreta-
sions between the posterior capsule and shoulder external tion and this has not been examined.
rotators have also been described and may contribute to
motion loss.5
Other hypotheses for the development of posterior MANAGEMENT
shoulder tightness include adaptations resulting from
ageing or activity. Changes associated with ageing such Alleviating posterior shoulder tightness appears possible
as increased collagen cross-links, variations in collagen through stretching and/or manual therapy. Two stretch
expression and reduced elasticity may reduce capsular positions are commonly used and both are effective.14
extensibility.8 Osteoarthritis involving the posterior The ‘sleeper stretch’ is performed by passively internally
glenoid fossa may result in local tissue changes.9 Labour- rotating the shoulder when side lying on the affected
ers may develop tightness through work demands that side with the arm flexed to near 90°. The cross-body
repetitively load the posterior cuff and capsule complex.10 stretch is performed by elevating the arm to 90° and
For muscle, increased cross-bridge engagement or stiff- passively adducting the humerus towards the chest.
ness of the parallel or series elastic components may cause Both stretches can be administered by the clinician or
tightness.11 Importantly, all these proposed mechanisms the patient. The cross-body stretch may be more effec-
remain hypothetical. tive than the sleeper stretch, while both improved
tightness more than a non-stretch control group.14
Contract–relax techniques may also reduce posterior
EVIDENCE shoulder tightness.15
Several studies have demonstrated that manual inter-
Evidence of posterior shoulder tightness is based primar- ventions focused on increasing posterior capsule extensi-
ily on clinical observation. Characteristic motion loss bility, when added to stretching and strengthening
patterns are consistently noted in throwing athletes, and exercises, may decrease tightness.13,16,26 Manual therapy
interventions to increase posterior shoulder extensibility may be more effective if initially applied in the open
often reverse these patterns.12–16 Similarly, increased position of the glenohumeral joint and progressed to
internal rotation ROM is reported after cutting the pos- more flexed and internally rotated positions.27
terior capsule in cadaver experiments17 and releasing the
capsule arthroscopically in vivo.7 Likewise, experimental
shortening of cadaver posterior capsules results in motion RECOMMENDATIONS
losses similar to those exhibited by throwing athletes,18,19
but it is not known if shortening is equivalent to contrac- Despite evidence that posterior shoulder tightness is
ture and fibrosis in vivo. The characteristic motion associated with shoulder injury in throwing athletes,
losses are associated with thickened posterior shoulder the relative importance of the impairment remains
structures20,21 including the capsule,22 but no studies have unknown. Specifically, prevalence rates in symptomatic
correlated motion loss with muscle extensibility. non-throwers, the degree of tightness that is clini-
Arthroscopic evaluation identified visible posterior cally meaningful and the risk of developing shoulder
capsule contracture and fibrosis, but quantification or pain when posterior shoulder tightness is present are
 50  The Shoulder 577

key unknown factors. Longitudinal studies that verify mobilization for posterior shoulder tightness measured by internal
the development of posterior shoulder tightness are rotation motion loss. Sports Health2010;2(2):94–100.
14. McClure P, Balaicuis J, Heiland D, et al. A randomized controlled
warranted, as are studies that establish the mecha- comparison of stretching procedures for posterior shoulder tight-
nisms by which capsule or muscle tightness occur. ness. J Orthop Sports Phys Ther 2007;37(3):108–14.
The optimum posterior shoulder measurements must 15. Moore SD, Laudner KG, McLoda TA, et al. The immediate effects
be determined, with an emphasis on discerning capsule of muscle energy technique on posterior shoulder tightness: a ran-
domized controlled trial. J Orthop Sports Phys Ther 2011;
from muscle, controlling for the influence of humeral 41(6):400–7.
retroversion and establishing validity. Finally, the most 16. Tyler TF, Nicholas SJ, Lee SJ, et al. Correction of posterior shoul-
effective interventions for reversing posterior shoulder der tightness is associated with symptom resolution in patients with
tightness, including treatment dose, still need to be internal impingement. Am J Sports Med 2010;38(1):114–19.
determined. 17. Moskal MJ, Harryman DT 2nd, Romeo AA, et al. Glenohumeral
motion after complete capsular release. Arthroscopy 1999;
15(4):408–16.
REFERENCES 18. Borstad JD, Dashottar A. Quantifying strain on posterior shoulder
tissues during 5 simulated clinical tests: a cadaver study. J Orthop
1. Crockett HC, Gross LB, Wilk KE, et al. Osseous adaptation and
Sports Phys Ther 2011;41(2):90–9.
range of motion at the glenohumeral joint in professional baseball
19. Grossman MG, Tibone JE, McGarry MH, et al. A cadaveric model
pitchers. Am J Sports Med 2002;30(1):20–6.
of the throwing shoulder: a possible etiology of superior labrum
2. Pappas AM, Zawacki RM, McCarthy CF. Rehabilitation of the
anterior-to-posterior lesions. J Bone Joint Surg Am 2005;
pitching shoulder. Am J Sports Med 1985;13(4):223–35.
87(4):824–31.
3. Ticker JB, Beim GM, Warner JJ. Recognition and treatment of
20. Tehranzadeh AD, Fronek J, Resnick D. Posterior capsular fibrosis
refractory posterior capsular contracture of the shoulder. Arthros-
in professional baseball pitchers: case series of MR arthrographic
copy 2000;16(1):27–34.
findings in six patients with glenohumeral internal rotational
4. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing
deficit. Clin Imaging 2007;31(5):343–8.
shoulder: spectrum of pathology Part I: pathoanatomy and biome-
21. Tuite MJ, Petersen BD, Wise SM, et al. Shoulder MR arthrography
chanics. Arthroscopy 2003;19(4):404–20.
of the posterior labrocapsular complex in overhead throwers with
5. Yoneda M, Nakagawa S, Mizuno N, et al. Arthroscopic capsular
pathologic internal impingement and internal rotation deficit. Skel-
release for painful throwing shoulder with posterior capsular tight-
etal Radiol 2007;36(6):495–502.
ness. Arthroscopy 2006;22(7):801.e1–e5, –.
22. Thomas SJ, Swanik CB, Higginson JS, et al. A bilateral comparison
6. Oyama S, Myers JB, Blackburn JT, et al. Changes in infraspinatus
of posterior capsule thickness and its correlation with glenohumeral
cross-sectional area and shoulder range of motion with repetitive
range of motion and scapular upward rotation in collegiate baseball
eccentric external rotator contraction. Clin Biomech (Bristol, Avon)
players. J Shoulder Elbow Surg 2011;20(5):708–16.
2011;26(2):130–5.
23. Laudner KG, Stanek JM, Meister K. Assessing posterior shoulder
7. Potier TG, Alexander CM, Seynnes OR. Effects of eccentric
contracture: the reliability and validity of measuring glenohumeral
strength training on biceps femoris muscle architecture and knee
joint horizontal adduction. J Athl Train 2006;41(4):375–80.
joint range of movement. Eur J Appl Physiol 2009;105(6):939–44.
24. Myers JB, Oyama S, Wassinger CA, et al. Reliability, precision,
8. Freemont AJ, Hoyland JA. Morphology, mechanisms and pathol-
accuracy, and validity of posterior shoulder tightness assessment in
ogy of musculoskeletal ageing. J Pathol 2007;211(2):252–9.
overhead athletes. Am J Sports Med 2007;35(11):1922–30.
9. Madry H, Luyten FP, Facchini A. Biological aspects of early osteo-
25. Tyler TF, Nicholas SJ, Roy T, et al. Quantification of posterior
arthritis. Knee Surg Sports Traumatol Arthrosc 2012;20(3):
capsule tightness and motion loss in patients with shoulder impinge-
407–22.
ment. Am J Sports Med 2000;28(5):668–73.
10. Kim SG, Akaike T, Sasagaw T, et al. Gene expression of type I and
26. Tate AR, McClure PW, Young IA, et al. Comprehensive
type III collagen by mechanical stretch in anterior cruciate ligament
impairment-based exercise and manual therapy intervention for
cells. Cell Struct Funct 2002;27(3):139–44.
patients with subacromial impingement syndrome: a case series.
11. Kragstrup TW, Kjaer M, Mackey AL. Structural, biochemical, cel-
J Orthop Sports Phys Ther 2010;40(8):474–93.
lular, and functional changes in skeletal muscle extracellular matrix
27. Cools AM, Declercq G, Cagnie B, et al. Internal impingement in
with aging. Scand J Med Sci Sports 2011;21(6):749–57.
the tennis player: rehabilitation guidelines. Br J Sports Med
12. Laudner KG, Sipes RC, Wilson JT. The acute effects of sleeper
2008;42(3):165–71.
stretches on shoulder range of motion. J Athl Train 2008;43(4):
359–63.
13. Manske RC, Meschke M, Porter A, et al. A randomized controlled
single-blinded comparison of stretching versus stretching and joint

CHAPTER 50.5  ■  FROZEN SHOULDER CONTRACTION

SYNDROME
Jeremy Lewis

adhesions within the axillary fold and to the anatomic

INTRODUCTION neck of the humerus. However, more recent evidence
supports thickening and contracture of the inferior GHJ
The term frozen shoulder was introduced by Codman in capsule, without adhesions to the humerus.3 As such, the
19341 describing it as a condition of unknown aetiology, term adhesive capsulitis may not appropriately describe
being difficult to treat but certain to resolve. In 1945, the condition. Terminology has evolved to include
Neviaser,2 based on a case series of ten patients, suggested primary frozen shoulder, which is used when the cause of
the term adhesive capsulitis better described the pathol- the condition is of idiopathic origin, and secondary frozen
ogy, due to the observations of inflammation, fibrosis and shoulder when it is deemed to have occurred following a
578 PART IV  Overview of Contemporary Issues in Practice

specific event such as trauma, following surgery or is characterized by the onset of pain that generally
associated with an underlying condition such as calcific becomes severe and disabling, and is often described as
tendinosis. Zuckerman and Rokito4 have further classi- excruciating when the shoulder moves suddenly. Pain is
fied secondary frozen shoulder into systemic, extrinsic present at night and is usually severe and disrupts sleep.
and intrinsic categories. In Japan and China the term ‘the In association with the pain, the shoulder becomes pro-
50-year-old shoulder’ is used reflecting the mean age of gressively stiff and movement substantially reduced.
onset. Yang et al.5 used the term frozen shoulder syn- Clinically, the severity of pain will vary as will the degree
drome and Bunker6 advocated use of the term ‘contrac- of stiffness between individuals. Codman1 described that
tion of the shoulder’ arguing this best encompasses the recovery will occur and should be expected. Reeves15
clinical and histological presentation. The myriad termi- reported that the average duration of the condition is
nology reflects poor understanding of the patho-aetiology 30.1 months (range 1 to 3.5 years), observing that the
and lack of clinical consensus. The term frozen shoulder longer the second or stiff/frozen stage, the longer the
has been described as a ‘waste-can diagnosis’7 as it is often third or thawing/recovery phase. Other studies suggest
applied to any stiff and painful presentation of the shoul- substantially longer duration of symptoms. Shaffer et al.8
der. Additionally, current use of the term frozen shoulder reported that 50% of people diagnosed with idiopathic
may be ambiguous and lead to complacency as it suggests frozen shoulder had ongoing shoulder pain and/or shoul-
the shoulder will ‘thaw’ and return to normal with or der stiffness at an average 7-year follow-up. In contrast,
without treatment. This may be incorrect as research Miller et al.16 reported in a retrospective analysis that all
suggests recovery may not be complete even after 11 patients achieved pain-free shoulder movement during
years post onset.8 The suggestion by Bunker6 for the term activities of daily living. These conflicting data suggest
‘contracture of the shoulder’ may be more suitable, but that the natural history of frozen shoulder may be vari-
this does not take into account the often severe pain able. They may also reflect different diagnostic criteria,
associated with the condition. As such, the term frozen variation in outcome measurements and procedures, bias
shoulder contraction syndrome (FSCS) may be more and the possibility of concomitant shoulder presenta-
appropriate. tions. Routinely informing people diagnosed with FSCS
that the condition always resolves with or without treat-
ment, may be inaccurate and misleading. The natural
EPIDEMIOLOGY history may follow the shape of a bell curve with the
majority of people taking 2 to 3 years for the symptoms
Uncertainty remains as to the lifetime prevalence and to resolve and a percentage on either side of the peak
annual incidence of FSCS. Nevasier and Hannifan9 pre- experiencing symptoms for considerably shorter or
sented epidemiological data from published studies that longer durations. Although the pain may settle and the
suggested FSCS occurs in 2–5% of the population, with function may return, this does not necessarily mean full
women more commonly affected than men, with the range of movement is always restored. Kanbe et al.17
non-dominant hand more frequently involved, and that described adhesions of the long head of biceps to the
20–30% will develop the condition bilaterally. Although rotator interval, which may contribute to ongoing move-
these data have been cited in publications for many ment restriction.
decades, considerable uncertainty persists as to the accu-
racy of these statistics. Issues such as diagnosis and inclu-
sion criteria in the original studies may have possibly DIAGNOSIS
resulted in over-reporting and misinterpretation of the
epidemiology. Bunker6 has described that the condition There is no definitive diagnostic test for FSCS, and
is equally distributed between men and women and the diagnosis is based on physical examination and the
incidence is 0.75%. This may be comparable with an absence of radiographic abnormalities. Cyriax and
estimated annual incidence of 0.24% reported in general Cyriax18 described FSCS as being a capsular restriction
practice in the Netherlands.10 Diabetes, hypothyroidism, of the shoulder involving some limitation of internal
lower body mass index and a family history of frozen rotation, with a greater limitation of passive abduction,
shoulder may be risk factors for idiopathic frozen shoul- with the greatest limitation of passive external rotation.
der.11 Smith et al.12 identified diabetes and a sibling with Zuckerman and Rokito4 published a consensus document
frozen shoulder as risk factors for developing FSCS in describing frozen shoulder as a restriction of both active
those undergoing arthroscopic capsular release. Others and passive shoulder motion with shoulder radiographs
have also identified a genetic predisposition13,14 and eth- being essentially normal except for the possible presence
nicity may also be involved, as people born in the British of osteopenia or calcific tendinosis. They further
Isles or having parents/grandparents born in the British described primary frozen shoulder as idiopathic in origin
Isles, may be at greater risk of suffering from the and secondary when the underlying aetiology was iden-
condition.11 tifiable. Intrinsic secondary frozen shoulder occurred in
the presence of rotator cuff and biceps tendinopathy
and calcific tendinosis, and extrinsic secondary frozen
NATURAL HISTORY shoulder being associated with pathology remote from
the shoulder such as ipsilateral breast surgery, cervical
FSCS is typically described as progressing through three radiculopathy, chest wall tumour, cerebrovascular acci-
phases: freezing, frozen and thawing. In most cases FSCS dent and humeral or clavicular fracture. Systemic
 50  The Shoulder 579

secondary frozen shoulder occurred in the presence of and assessment criteria for FSCS were not specified other
conditions such as diabetes and thyroid abnormalities. than patient’s being classified with the ICD-9 code 726.0.
However, a definitive relationship between many of these Mobilization therapy may be beneficial in the manage-
conditions and frozen shoulder remains uncertain. ment of FSCS. A randomized comparison of high- (Mai-
The importance of a radiograph cannot be underesti- tland grade III-IV) and low-(grade II) grade glenohumeral
mated as many conditions affecting the shoulder manifest inferior, anterior and posterior mobilization procedures
with pain and stiffness.6,19 Locked glenohumeral disloca- in 100 people with frozen shoulder for an average of 20
tions, substantial glenohumeral degenerative changes, treatments over 12 weeks suggested that significant
avascular necrosis of the humeral head, fractures, osteo- improvements occurred in both groups over 12 months.
sarcomas and calcific tendinosis are examples of condi- A trend for greater clinical improvement (movement and
tions that would usually be associated with reduced joint pain) was observed in the high-grade mobilization
movement and pain. In these conditions, the radiological group.23 In a study of 28 people with frozen shoulder,
presentation would demonstrate pathology. Bunker6 both end-range mobilizations and mobilization with
argued that a diagnosis of frozen shoulder should be movement demonstrated greater clinical effectiveness
considered if clinically there is an equal restriction of than mid-range mobilizations over a 12-week period.5 A
active and passive shoulder external rotation range and control group was not included in either study and as
that radiologically the shoulder radiograph is reported as such, without a ‘no treatment’ control group it is not
normal. This remains the simplest diagnostic procedure clear if improvement was due to natural recovery.
and research is required to fully validate this method. It In a small pilot randomized clinical study (n = 27) no
may be necessary to test external rotation range in a significant difference in pain and functional ability as
number of positions to ensure that there are no compen- measured by the SPADI was identified between an osteo-
satory movements for lost glenohumeral external rota- pathic (Neil-Asher) deep soft tissue technique and a
tion.20 Clinic assessment for FSCS may need to be tested group given manual therapy and exercise, and another
over time as the condition may not have declared itself (termed placebo) comprised of breathing exercise, pain-
in the initial clinical visit. Additionally, the presence of free range of movement exercises and effleurage. Gains
pain, for reasons other than FSCS, may lead to the indi- in shoulder abduction range were greatest in the deep
vidual rigidly fixing the shoulder, possibly due to fear of soft tissue group. This study only reported short-term
increased pain on movement and this may be misdiag- results (12 weeks) post-intervention and the number and
nosed as a FSCS. details of interventions were not described.24 The SPADI
involves five questions concerning pain and eight pertain-
ing to functional movement. As no difference in outcome
MANAGEMENT was detected in SPADI between the groups, the impor-
tance of an increase in abduction range must be inter-
FSCS is difficult to treat and there is little consensus as preted cautiously and more research is required.
to what constitutes optimal evidence-based treatment In a small, short-term follow-up randomized clinical
and as mentioned FSCS is frequently described in three trial, deep heating (12 sessions over 4 weeks) involving
stages: (a) frozen or pain; (b) freezing or stiffness; and short-wave diathermy followed by stretching appeared to
(c) thawing or recovery phase.15 Others have described it produce favourable results in people diagnosed with
as a four-stage process.7 Once diagnosis has been con- frozen shoulder.25 There may also be some short-term
firmed, an alternative approach used by the author is to benefit with 12 laser treatments administered over 12
divide the condition into two phases: (a) more pain than weeks combined with home exercises.26
stiff and (b) more stiff than pain. Acupuncture is commonly used to treat FSCS;
People suffering with FSCS require education detail- however, the quality of the evidence supporting its effec-
ing what is known about the natural history and expected tiveness is generally poor. Maund et al.27 concluded that
outcomes, as well as being made aware of treatment alter- there is insufficient evidence to make definitive recom-
natives and outcomes of each in an unbiased and patient- mendations regarding the use of acupuncture in the treat-
focused manner. It is incumbent upon the clinician to be ment of frozen shoulder. However, on the basis of one
aware of the research evidence, its generalizability, as well randomized controlled trial deemed to be of high
as its quality. People with FSCS are frequently informed quality,28 two systematic reviews29,30 concluded that acu-
that the condition will get better with or without treat- puncture combined with exercise may confer moderate
ment and supervised neglect is preferable to physiother- benefit in the short term.
apy. This was the conclusion reported in a non-randomized Although popular, there is a paucity of definitive evi-
investigation employing a quasi-experimental design with dence for the use of corticosteroid (CS) injections in the
a high risk of bias,21 and as such these recommendations management of FSCS. A synthesis of the evidence sug-
must be interpreted cautiously. In addition, the treatment gests that CS injections may reduce pain and improve
offered in the ‘supervised neglect’ group should also be function in the short term,27,31,32 and that the benefit may
considered as physiotherapy. be enhanced in both the short term and medium term
Data from 2370 people diagnosed with frozen shoul- when guided intra-articular CS injections are combined
der suggested that therapeutic benefit may be achieved with physiotherapy.27,32 Carette et al.32 reported best out-
with procedures such as joint mobilization and exercise, comes in a group randomized to receive image-guided
and poorer outcomes may be associated with ultrasound injections up to 1 year post onset and physiotherapy,
and massage.22 A limitation of these data is that inclusion which involved twelve, 1-hour sessions over 4 weeks.
580 PART IV  Overview of Contemporary Issues in Practice

TABLE 50-5  Frozen Shoulder Contraction Syndrome: Injection Therapy and Physiotherapy
Care Pathway
Stage I to Early Stage II (Pain > Stiffness)
Corticosteroid Injection and Late Stage II to Stage III: (Stiffness > Pain)
Assessment Physiotherapy Hydro-Distension and Physiotherapy
• Sexes are affected equally • Screen for contraindications and special • Screen for CI and SP to image guided GHJ
with approximate peak onset precautions for an intra-articular intra-articular lidocaine and large-volume
of 52 years for men and 55 for small-volume corticosteroid and NaCl injection (i.e. hydro-distension)
women lidocaine injection • Consider USGI as no radiation associated
• Full patient interview and • If no CIs/SPs, explain risks and benefits, with ultrasound
physical examination. Screen gain consent, proceed with ultrasound- • If no CIs/SPs, explain risks and benefits,
for Yellow and Red Flags and guided small-volume corticosteroid and gain consent, proceed with hydro-
monitor during treatment lidocaine injection distension procedure if:
• Equal restriction of active and (strong evidence short term and • ROM not restored from CS and lidocaine
passive external rotation moderate evidence medium term) injection, or
• Radiographs normal • Perform the injection as an ultrasound- • First presentation to clinic when in
• Organize blood tests to screen guided procedure (or use another stiffness > pain stage
for diabetes and other related imaging guidance). No radiation (moderate evidence; NNT-pain 2,
health conditions associated with ultrasound NNT-ROM/function: 3)
• Outcome measures • RCTs have not demonstrated a • Immediately following the procedure:
Consider: ROM, Pain, Function, difference between location, dosage and Passive movements and PNF
SPADI, DASH, Quick-DASH, volume of injection • Instruct home programme involving regular
EQ-5D-5L, PGIC, Patient • During the first week gentle self-assisted (hourly if possible) active movements,
Satisfaction and active movements self-assisted active movements and
• Fully inform patient. • Second to fourth weeks, mobilization, stretching on day of procedure and
Determine care pathway based soft tissue massage, passive regularly on following days
on evidence and patient's movements, self-assisted movements, • In clinic: mobilization, PNF, progress home
values. Consider following as exercises as tolerated programme
possible pathway • Consider re-injecting at 4/52 if pain not • If required repeat hydro-distension at one
under control. No more than three times week
in 1 year and at least 1 month between • Injection procedures may overlap across
injections the stages and be performed concomitantly
• Injection procedures may overlap across Main references: Favejee et al.,30 Buchbinder
the stages and be performed et al.35
concomitantly. If unable to inject Notes:
consider: [need to screen for CIs] • Monitor outcome measures
• Laser, mobilization, soft tissue massage, • Ensure adequate physiotherapy is
passive movements, acupuncture, embedded within care pathway
exercise, short-wave diathermy • For physiotherapists not currently providing
• Oral steroid and suprascapular nerve ultrasound-guided injections, develop care
blocks are also procedures associated pathways with orthopaedic and radiology
with clinical benefit colleagues
Main references: Maund et al.,27 Favejee • In refractory cases and if improvement not
et al.30 as expected, consider orthopaedic referral
for opinion on capsular release

CI, contraindication; CS, corticosteroid; DASH, Disability of the Arm Shoulder and Hand; GHJ, glenohumeral joint; NNT, numbers needed
to treat for benefit; PGIC, patient global impression of change; PNF, proprioceptive neuromuscular facilitation; Quick-DASH, Quick
Disability of the Arm Shoulder and Hand; ROM, range of movement; SP, special precaution; SPADI, Shoulder Pain and Disability Index;
USGI, ultrasound-guided injection. Adapted from www.LondonShoulderClinic.com (01/2014).

Physiotherapy treatments varied according to the stage appropriately skilled physiotherapists in the United
of the frozen shoulder and included active and assisted Kingdom.34 A systematic review35 concluded that the
range of movement exercises, ultrasound, mobilization, procedure was associated with a numbers needed to treat
ice and strengthening. In an attempt to elucidate the for benefit of 2 for pain reduction, and a numbers needed
optimal dose of ultrasound-guided intra-articular CS to to treat of 3 for improvement in function in patients
treat FSCS (freezing or stiff stage) Yoon et al.33 reported diagnosed with FSCS. Range of shoulder movement (but
significant improvement in the CS groups when com- not pain and function) is enhanced when physiotherapy
pared to the placebo group (analgesic only) but no dif- (manual therapy and exercise) is provided after the
ference between the CS groups using the SPADI, shoulder hydro-distension procedure.36
pain and shoulder range of movement as outcome mea- Manipulation under anaesthetic involves scapular sta-
sures, and recommended the use of low-dose CS. bilization with shoulder flexion, abduction and adduc-
Arthrographic hydro-distension is a technique that tion, followed by maximal shoulder internal and external
involves injecting large volumes of sodium chloride into rotation (with the elbow flexed). Tearing of the con-
the glenohumeral joint under imaging guidance. The tracted capsule may be felt or heard. The evidence sup-
aim of the procedure is to distend the contracted joint porting manipulation under anaesthetic is poor. Kivimaki
capsule. It is a procedure that is now performed by et al.37 randomized 127 people with frozen shoulder to
 50  The Shoulder 581

manipulation under anaesthetic and physiotherapy- to physiotherapist-led care pathways for FSCS that
directed exercises and to physiotherapy exercises alone. include ultrasound-guided CS injections and hydro-
They did not detect any difference at 6, 12, 26 and 52 distension procedures embedded within physiotherapy
weeks. Of concern, in a study of 30 people undergoing exercise and mobilization treatment (Table 50-5). Much
manipulation under anaesthetic, arthroscopy revealed is still to be learnt about frozen shoulder and a better
haemarthrosis in all patients following the procedure, name for this disorder may be FSCS.
and in addition to other iatrogenic intra-articular damage;
four people (13%) were observed to have suffered SLAP
(superior labral anterior to posterior) lesions, partial tears REFERENCES
of the subscapularis were detected in three people, and 1. Codman E. The Shoulder: rupture of the supraspinatus tendon and
anterior labral detachment were detected in four people, other lesions in or about the subacromial bursa. Boston: Thomas
with an associated osteochondral lesion detected in one Todd Company; 1934.
person.38 2. Neviaser J. Adhesive capsulitis of the shoulder. A study of the
Arthroscopic capsular release of the shoulder involves pathological findings in periarthritis of the shoulder. J Bone Joint
Surg (Am) 1945;27(2):211–22.
combinations of glenohumeral joint distension, capsular 3. Wiley AM. Arthroscopic appearance of frozen shoulder. Arthros-
debridement, ligament splitting, loosening of adhe- copy 1991;7(2):138–43. [Epub 1991/01/01].
sions, shoulder movement, shoulder manipulation and 4. Zuckerman JD, Rokito A. Frozen shoulder: a consensus definition.
post-surgical physiotherapy. Usually following surgery J Shoulder Elbow Surg 2011;20(2):322–5. [Epub 2010/11/06].
there is a need to take a week or longer off work. 5. Yang JL, Chang CW, Chen SY, et al. Mobilization techniques
in subjects with frozen shoulder syndrome: randomized
The procedure is not supported by robust research multiple-treatment trial. Phys Ther 2007;87(10):1307–15. [Epub
and conclusions from published case series are there- 2007/08/09].
fore at high risk of bias.39,40 Grant et  al.41 concluded 6. Bunker T. Time for a new name for frozen shoulder-contracture
that the quality of evidence available is low and the of the shoulder. Shoulder Elbow 2009;1:4–9.
7. Neviaser RJ, Neviaser TJ. The frozen shoulder. Diagnosis and
current available data demonstrate little benefit for management. Clin Orthop Relat Res 1987;223:59–64. [Epub
a capsular release instead of, or in addition to, a 1987/10/01].
manipulation under anaesthetic. 8. Shaffer B, Tibone JE, Kerlan RK. Frozen shoulder. A long-term
Health funding bodies are appropriately demanding follow-up. J Bone Joint Surg 1992;74(5):738–46.
ways of reducing the cost of health-care delivery while 9. Neviaser AS, Hannafin JA. Adhesive capsulitis: a review of current
treatment. Am J Sports Med 2010;38(11):2346–56. [Epub
maintaining and improving outcomes. Chapter 40 2010/01/30].
(Advanced roles in musculoskeletal physiotherapy) dis- 10. van der Windt DA, Koes BW, Deville W, et al. Effectiveness of
cusses a physiotherapy-led initiative for the management corticosteroid injections versus physiotherapy for treatment of
of FSCS. The pathway comprises assessment, imaging, painful stiff shoulder in primary care: randomised trial. BMJ
1998;317(7168):1292–6. [Epub 1998/11/07].
ultrasound-guided CS injection and hydro-distension 11. Wang K, Ho V, Hunter-Smith DJ, et al. Risk factors in idiopathic
procedures, embedded within a physiotherapy rehabilita- adhesive capsulitis: a case control study. J Shoulder Elbow Surg
tion programme, entirely led and performed by physio- 2013;22(7):e24–9. [Epub 2013/01/29].
therapists.34 This treatment package is provided at a 12. Smith CD, White WJ, Bunker TD. The associations of frozen
fraction of the cost of the surgical procedures used to shoulder in patients requiring arthroscopic release. Shoulder Elbow
2012;4(2):87–9.
treat FSCS. It would be beneficial to appropriately 13. Hakim AJ, Cherkas LF, Spector TD, et al. Genetic associations
compare the physiotherapy-led programme and capsular between frozen shoulder and tennis elbow: a female twin study.
release procedure for clinical outcomes, adverse events, Rheumatology 2003;42(6):739–42. [Epub 2003/05/06].
economic analysis and patient satisfaction. Additionally, 14. Hirschhorn P, Schmidt JM. Frozen shoulder in identical twins.
Joint Bone Spine 2000;67(1):75–6. [Epub 2000/04/25].
hydro-distension is performed in a clinic and the patient 15. Reeves B. The natural history of the frozen shoulder syndrome.
is free to go home soon after the procedure and is not Scand J Rheumatol 1975;4(4):193–6. [Epub 1975/01/01].
associated with additional time off work. 16. Miller MD, Wirth MA, Rockwood CA Jr. Thawing the frozen
shoulder: the ‘patient’ patient. Orthopedics 1996;19(10):849–53.
[Epub 1996/10/01].
17. Kanbe K, Inoue K, Inoue Y. Dynamic movement of the long head
CONCLUSION of the biceps tendon in frozen shoulders. J Orthop Surg (Hong
Kong) 2008;16(3):295–9. [Epub 2009/01/08].
FSCS may be less common than suggested in the lit- 18. Cyriax J, Cyriax P. Cyriax’s Illustrated Manual of Orthopaedic
erature; however, when present it is associated with Medicine. 2nd ed. Oxford: Butterworth Heinemann; 1993.
19. Sano H, Hatori M, Mineta M, et al. Tumors masked as frozen
substantial pain, movement restriction and morbidity. shoulders: a retrospective analysis. J Shoulder Elbow Surg
The literature is beset with studies that are frequently 2010;19(2):262–6. [Epub 2009/07/04].
small and have high levels of bias, from which conclu- 20. Valentine RE, Lewis JS. Intraobserver reliability of 4 physiologic
sions to underpin clinical practice are difficult to extract movements of the shoulder in subjects with and without symptoms.
with confidence. There is a paucity of literature sup- Arch Phys Med Rehabil 2006;87(9):1242–9.
21. Diercks RL, Stevens M. Gentle thawing of the frozen shoulder: a
porting physiotherapy interventions for FSCS, but it prospective study of supervised neglect versus intensive physical
is potentially incorrect to state that supervised neglect therapy in seventy-seven patients with frozen shoulder syndrome
is preferential to physiotherapy. Manipulation under followed up for two years. J Shoulder Elbow Surg 2004;13(5):
anaesthetic appears to be no more effective than phys- 499–502.
22. Jewell DV, Riddle DL, Thacker LR. Interventions associated with
iotherapy and is associated with possible joint damage. an increased or decreased likelihood of pain reduction and improved
Capsular release is not supported by robust scientific function in patients with adhesive capsulitis: a retrospective cohort
evidence and has not been comprehensively compared study. Phys Ther 2009;89(5):419–29. [Epub 2009/03/10].
582 PART IV  Overview of Contemporary Issues in Practice

23. Vermeulen HM, Rozing PM, Obermann WR, et al. Comparison placebo-controlled trial. Am J Sports Med 2013;41(5):1133–9.
of high-grade and low-grade mobilization techniques in the man- [Epub 2013/03/20].
agement of adhesive capsulitis of the shoulder: randomized con- 34. O’Connaire E, Lewis JS. Arthrographic hydrodistension for
trolled trial. Phys Ther 2006;86(3):355–68. frozen shoulder. A physiotherapy-led initiative in primary care.
24. Greenhalgh S, Self J. Red flags: A guide to identifying serious Available from: <http://www.health.org.uk/media_manager/public
pathology of the spine. Edinburgh: Churchill Livingstone Elsevier; /75/programme_library_docs/Central%20London%20-%20
2006. Frozen%20Shoulder.pdf>; 2011.
25. Leung MS, Cheing GL. Effects of deep and superficial heating in 35. Buchbinder R, Green S, Youd JM, et al. Arthrographic distension
the management of frozen shoulder. J Rehabil Med 2008;40(2):145– for adhesive capsulitis (frozen shoulder). Cochrane Database Syst
50. [Epub 2008/05/30]. Rev 2008;(1):CD007005, [Epub 2008/02/07].
26. Stergioulas A. Low-power laser treatment in patients with frozen 36. Buchbinder R, Youd JM, Green S, et al. Efficacy and cost-
shoulder: preliminary results. Photomed Laser Surg 2008;26(2):99– effectiveness of physiotherapy following glenohumeral joint disten-
105. [Epub 2008/03/18]. sion for adhesive capsulitis: a randomized trial. Arthritis Rheum
27. Maund E, Craig D, Suekarran S, et al. Management of frozen 2007;57(6):1027–37. [Epub 2007/08/01].
shoulder: a systematic review and cost-effectiveness analysis. Health 37. Kivimaki J, Pohjolainen T, Malmivaara A, et al. Manipulation
Technol Assess 2012;16(11):1–264. [Epub 2012/03/13]. under anesthesia with home exercises versus home exercises alone
28. Sun KO, Chan KC, Lo SL, et al. Acupuncture for frozen shoulder. in the treatment of frozen shoulder: a randomized, controlled trial
Hong Kong Med J 2001;7(4):381–91. [Epub 2002/01/05]. with 125 patients. J Shoulder Elbow Surg 2007;16(6):722–6. [Epub
29. Jain TK, Sharma NK. The effectiveness of physiotherapeutic inter- 2007/10/13].
ventions in treatment of frozen shoulder/adhesive capsulitis: a sys- 38. Loew M, Heichel TO, Lehner B. Intraarticular lesions in primary
tematic review. J Back Musculoskeletal Rehabil 2013;27(3):247–73. frozen shoulder after manipulation under general anesthesia.
30. Favejee MM, Huisstede BM, Koes BW. Frozen shoulder: J Shoulder Elbow Surg 2005;14(1):16–21. [Epub 2005/02/22].
the effectiveness of conservative and surgical interventions– 39. Fernandes MR. Arthroscopic capsular release for refractory shoul-
systematic review. Br J Sports Med 2011;45(1):49–56. [Epub der stiffness. Rev Assoc Med Bras 2013;59(4):347–53. [Epub
2010/07/22]. 2013/07/16].
31. Blanchard V, Barr S, Cerisola FL. The effectiveness of corticoste- 40. Dattani R, Ramasamy V, Parker R, et al. Improvement in quality
roid injections compared with physiotherapeutic interventions for of life after arthroscopic capsular release for contracture of the
adhesive capsulitis: a systematic review. Physiotherapy 2010; shoulder. Bone Joint J 2013;95-B(7):942–6. [Epub 2013/07/03].
96(2):95–107. [Epub 2010/04/28]. 41. Grant JA, Schroeder N, Miller BS, et al. Comparison of manipula-
32. Carette S, Moffet H, Tardif J, et al. Intraarticular corticosteroids, tion and arthroscopic capsular release for adhesive capsulitis: a
supervised physiotherapy, or a combination of the two in the treat- systematic review. J Shoulder Elbow Surg 2013;22(8):1135–45.
ment of adhesive capsulitis of the shoulder: a placebo-controlled [Epub 2013/03/21].
trial. Arthritis Rheum 2003;48(3):829–38.
33. Yoon SH, Lee HY, Lee HJ, et al. Optimal dose of intra-articular
corticosteroids for adhesive capsulitis: a randomized, triple-blind,
 CHAPTER 51 

Elbow
Brooke Coombes • Leanne Bisset • Bill Vicenzino

are important to clarify, particularly in the throwing

INTRODUCTION athlete. The presence and location of any numbness or
paraesthesia may help determine potential sites of com-
Anatomically, the elbow is a complex joint with a large pression or irritation of nerves around the elbow. Given
range of motion, many musculotendinous attachments most sites around the elbow involve dynamic structures,
and several traversing neurovascular structures. Its elabo- their temporal nature and relationship to throwing or
rate design allows this joint to position the hand in space occupational tasks provides important information.3 Pat-
and act as a stabilizer for lifting, carrying, pushing, pulling terns of symptoms or behaviours that indicate an urgent
and throwing. The complex anatomy and biomechanics medical or psychological problem should be highlighted
of the elbow, combined with a large spectrum of pathol- during the clinical interview. For example, symptoms
ogy, presents a challenge for the treating clinician. This of sudden swelling may indicate infection, inflammation
chapter presents an overview of contemporary issues in or compartment syndrome, while malignancy may be
examination and differential diagnosis, along with the considered if severe progressive pain is unrelated to
conservative rehabilitation programmes for various elbow activity.
injuries, synthesizing the current evidence with clinical
reasoning. Functional Demands
It is essential to determine if any limitations on daily
activities, work, sport or hobbies exist. For the throwing
CLINICAL INTERVIEW athlete, specific information should be obtained about
History symptoms while throwing, including what phase, after
how many throws, and the presence of paraesthesia or
Establishing the mechanism of injury is important fol- symptoms of instability. Questioning should extend to
lowing traumatic injuries to gain an understanding of the details of work status and timing for return to work.
original injury, any concomitant injuries and timeframes Failure to gain information about the functional demands
for healing. For the post-surgical patient, additional placed on the elbow may limit diagnosis and effective
information should be gained from the surgeon to under- treatment planning.
stand the surgical procedure, and any limitations in range
of motion due to joint stability or fixation. For non-
traumatic injuries, it is equally important to question the
Co-morbidity
nature, duration and evolution of symptoms, including There is strong evidence that musculoskeletal co-
exposure to repetitive occupational or sporting risks. A morbidity has an adverse impact on the overall prognosis
combination of physical exertion and repetitive elbow of musculoskeletal problems4,5 and may influence treat-
and wrist movements is a strong risk factor for epicon- ment planning. For these reasons, examination of the
dylalgia and other non-specific elbow disorders in spine, shoulder, wrist and hand is also essential. Con-
working populations.1 Lateral epicondylalgia is more comitant pathology may exist, for example trauma-
common in racket sports,2 whereas overhead throwing associated fractures or soft tissue injuries at the wrist,
athletes are predisposed to medial elbow injury. It is or pain secondary to the use of substitution patterns
important to ascertain if the condition has occurred when elbow range of motion (ROM) or strength is
before or if there is a history of other upper extremity insufficient.
injury or surgery.
Outcome Measures
Symptoms There is a need for greater consensus and standardization
Thorough questioning of the location, quality, intensity of outcomes concerning the elbow to allow comparison
and behaviour of pain is insightful. Snapping or clicking between trials and clinical practice. Patient-reported out-
during supination/extension with associated pain over comes are advocated over observer-based scoring systems
the posterolateral elbow region may implicate postero- for examination of elbow pain and function because
lateral rotatory instability. Other symptoms of instability, of lack of agreement and heterogeneous weighting of
including clumsiness, heaviness, fatigue or loss of control, outcomes.6–8 Patient-rated instruments vary in specificity
583
584 PART IV  Overview of Contemporary Issues in Practice

or focus, some are joint-specific (e.g. Oxford Elbow Diagnosis of elbow instability is usually made with a
Score), or condition-specific (e.g. the Patient-Rated combination of history, physical examination, imaging
Tennis Elbow Evaluation), while others are applicable to and arthroscopic examination. Several clinical tests to
the whole upper limb (e.g. Disability of Arm Shoulder or elucidate symptoms of instability are described in Table
Hand). An advantage of using a specific outcome measure 51-1. However, it is important to recognize that findings
that is focused on the condition (or anatomical site), is it on physical examination are commonly subtle and exami-
is likely to be the most responsive to change in that con- nation of instability may need to be performed with the
dition. However, kinesiological theory suggests that the patient under sedation or with stress radiography.13,14
upper extremity operates as a single functional unit and
the latter may be more relevant for examining conditions
Lateral Instability
that tend to affect more than one joint or are associated
with many co-morbidities. A recent systematic review of Under acute axial loading (e.g. a fall on an outstretched
the validity, reliability and responsiveness of elbow- hand), there is progressive involvement of soft and bony
specific clinical rating systems found the Oxford Elbow structures about the elbow. Initially, the lateral ulnar
Score was the only outcome with good or excellent rotates posterolaterally, injuring the lateral collateral and
quality methods based on the COSMIN checklist.9 lateral ulnar collateral ligaments, while the integrity of
Research into the use of rating scales in patients follow- the anterior band of the medial collateral ligament (MCL)
ing traumatic elbow injury is currently lacking.10 remains intact.13 This injury results in valgus and pos-
terolateral rotatory instability (PLRI, stage 1). PLRI is
rarely seen as an overuse injury, but rather as a conse-
quence of acute trauma20 and may be combined with
PHYSICAL EXAMINATION secondary radio-capitellar joint compression and pos-
OF THE ELBOW teromedial impingement in people with long-standing
instability. PLRI is diagnosed through the patient history
Many elbow conditions and associated investigations and and through the lateral pivot-shift manoeuvre of the
tests used to differentiate between conditions have yet to elbow (see Table 51-1). Patients may complain of recur-
be evaluated for their accuracy (i.e. the sensitivity and rent snapping or clicking during supination/extension
specificity). In the following paragraphs, we provide a with associated pain over the posterolateral elbow region.
description of key physical tests for examination of the The patient may report difficulty or a feeling of instabil-
elbow, highlighting the diagnostic and prognostic rele- ity while performing activities such as pushing up from a
vance of findings. chair or attempting a push up with forearm supination.
When demonstrating these tasks, the patient will be
reluctant to fully extend the elbow in weight bearing. In
Range of Motion addition, they may also report painful catching, clicking
Goniometry is useful, especially for monitoring the effec- or a feeling of instability during elbow flexion/extension,
tiveness of treatments to improve ROM. The measure- particularly around 40° of elbow flexion with forearm
ment error for this instrument is estimated to be 5° for supination. Posterolateral subluxation usually reduces in
elbow flexion–extension and 9° for forearm rotation.11 pronation, which is thought to be due to greater contact
The patterns of loss of elbow motion and passive exami- at the radio-humeral joint and therefore greater trans-
nation, including assessment of the end feel and accessory mission of axial forces across the radio-humeral joint in
movements, are also informative and may direct the clini- pronation compared with supination,21 particularly in the
cian to the structures limiting motion. For example, presence of an intact MCL.
motion deficits secondary to capsular joint stiffness Stage 2 instability involves incomplete elbow disloca-
should be differentiated from that secondary to two-joint tion that results in tearing of the lateral collateral liga-
muscle length, such as the biceps, triceps or forearm ment (LCL) complex as well as anterior and posterior
muscles. When assessing forearm rotation it is essential soft tissue disruption. Lastly, stage 3 involves a full elbow
to examine accessory movements at both proximal and dislocation that may involve rupture to some or all of the
distal radio-ulnar joints, as both may contribute to limited MCL as well as fractures of the radial head and/or coro-
pronation and supination.12 noid process.13 The terrible triad injury of the elbow
involves a combination of coronoid process and radial
head fractures, and elbow dislocation. It often results in
Elbow Stability recurrent instability, development of degenerative
Elbow instability can be viewed on a continuum from changes and persistent long-term disability.13,22–24 Often
mild laxity to severe and recurrent dislocation that pro- a trauma seen in younger people, long-term complica-
gresses from the lateral to the medial side of the elbow tions include persistent instability, non-union, malunion
and may involve soft tissue and/or bone.13 Elbow instabil- and radio-ulnar fusion.13
ity can be classified according to the following:13
• articulations involved (radial head, elbow) Medial Instability
• direction of displacement (valgus, varus, anterior,
posterolateral rotatory) Medial instability may also be approached on a spectrum,
• degree of displacement (subluxation, dislocation) from micro tears of the MCL in response to repetitive
• timing (acute, chronic, recurrent) overload that eventually leads to partial or full ligament
• presence or absence of fractures. tears.25,26 The chronic valgus overload that leads to valgus
 51  Elbow 585

TABLE 51-1  Clinical Tests for Elbow Instability

Indication Test Description Positive Result
Ulnar collateral Abduction stress Patient’s elbow in 90° flexion Pain
ligament test Examiner applies valgus force while Medial joint space opening of 2 mm
injury15 palpating the medial joint line greater than the uninjured elbow
Moving valgus Patient’s shoulder in 90° abduction and Pain between 120° and 70° of elbow
stress test external rotation flexion
Examiner applies valgus stress to flexed Sensitivity 100%, specificity 75%16
elbow, then extends the elbow while
maintaining the valgus elbow/external
shoulder rotation force
Modified milking Patient’s shoulder in adduction and Pain
manoeuvre maximum external rotation and elbow Medial joint space opening
flexed to 70°
Examiner applies valgus stress by pulling
down on patient’s thumb and palpating
the medial joint line with their other
hand
Posterolateral Lateral pivot shift18 Patient supine with shoulder flexed and Skin dimple or prominent radial
rotatory externally rotated and forearm supinated head
instability Examiner flexes the elbow while applying Apprehension/pain at 40° flexion
(PLRI)17 valgus, supination and axial Clunk or relief with further flexion
compression (joint reduced)
Posterolateral rotary Examiner pulls the proximal lateral Skin dimple
drawer test14 forearm posteriorly Apprehension
Table top relocation Patient standing in front of a table with
test19 affected hand on the lateral edge of the
table
(a) Patient performs a press-up with the (a) Apprehension/pain at
elbow pointing laterally (forearm approximately 40° flexion
supinated)
(b) Above repeated while the examiner (b & c) Relief and recurrence of
prevents posterior subluxation of the symptoms, respectively
radial head
(c) Removal of examiner support

instability is most common in throwing athletes. The late extended fully, while resisted elbow flexion and supina-
cocking and early acceleration phases of throwing, when tion is used to test for distal biceps tendinopathy.
the elbow is in flexion, create excessive repetitive valgus
forces generated by high angular velocities.27–29 There are Palpation
significant negative consequences associated with chronic
valgus instability, including compression stress in the Systematic palpation of local elbow structures may be
radio-humeral joint, traction stress in the medial com- useful in the differential diagnosis of the source of local-
partment (flexor-pronator muscles, medial epicondyle ized pain in some elbow conditions. For example, tender-
epiphysis, ulnar nerve) and posteromedial impingement, ness of the lateral epicondyle and/or common extensor
all of which can lead to chronic pain and be career-ending tendon origin is typical of lateral epicondylalgia, whereas
for an athlete.20 In contrast, an acute injury to the MCL pain over the posterolateral elbow, particularly in the
may be associated with a compression fracture of the younger patient, may implicate involvement of the syno-
radial neck, and ligament injury should be suspected if a vial plica. Patients with medial epicondylalgia experience
radial head fracture is identified radiographically. pain that is localized just anterior and distal to the
common flexor muscle origin, whereas patients with
ulnar collateral ligament injury typically have point ten-
Muscle–Tendon Function derness approximately 2 cm distal to the medial epicon-
Physical evaluation of musculotendinous function is dyle. However, forearm tenderness is found in lateral
useful for determining the presence and extent of both epicondylalgia, fibromyalgia and cervical referred pain,
acute, traumatic injuries and chronic degenerative condi- reducing the specificity of palpation as a stand-alone
tions, including tendinopathy. Patients with lateral epi- diagnostic test.
condylalgia present with lateral elbow pain with resisted
wrist extension test (Cozens test), resisted middle finger
extension test and/or the Mills test, in which the exam-
Nerve Function
iner passively pronates the forearm, flexes the wrist and Examination of nerve function associated with elbow
extends the elbow. Patients with medial epicondylalgia injury is multifaceted and should proceed in a systematic
have pain with resisted wrist flexion when the elbow is fashion based on clinical interview. Table 51-2 presents a
586 PART IV  Overview of Contemporary Issues in Practice

TABLE 51-2  Clinical Tests for Provocation of Peripheral Nerves at the Elbow
Indication Test Description Positive Result
33
Ulnar neuropathy Tinel’s test Examiner taps lightly at the ulnar Tingling radiating to fourth or
nerve at medial epicondylar groove fifth digits
Flexion compression Patient’s elbow maximally flexed Tingling in the ulnar nerve
test33 with wrist in neutral, sustained for distribution within 60 seconds
60 seconds while the examiner
applies compression proximal to
the cubital tunnel
Elbow flexion test34 Maximal elbow flexion combined Reproduction of paraesthesia or
with maximal wrist extension, pain
sustained for 5 seconds Sensitivity 25%, specificity 100%
Shoulder internal Patient positioned in 90° abduction, Reproduction of symptoms
rotation elbow 10° flexion and maximal internal within the ulnar nerve
flexion test34 rotation of the shoulder, maximal distribution
supination, wrist and finger Sensitivity 87%, specificity 98%
extension sustained for 5 seconds
Radial tunnel Resisted supination Resisted supination with elbow Pain distal to lateral epicondyle
syndrome extended

selection of nerve provocation tests. In the general popu- syndrome. The features of radial tunnel syndrome are
lation, the presence of pain about the elbow and sensory similar to lateral epicondylalgia, with patients reporting
loss or associated paraesthesias is often the first diagnostic pain over the proximal dorsal aspect of the forearm that
clue to a nerve problem, whereas motor weakness is a is aggravated by repetitive or resisted forearm supination/
much later finding.3 In throwing athletes, the first symp- pronation and middle finger extension, localized tender-
toms can be fatigue and loss of velocity or control. Several ness on palpation over the lateral epicondyle, with a
neural provocation tests of the upper extremity have been history of repetitive manual activity.38–41 The difficulty in
described, in which a series of positions are sequentially differentiating radial tunnel syndrome from lateral epi-
applied to increase or decrease stress on nerve branches condylalgia is reflected in the low level of accuracy (37–
at the elbow.30,31 The reader is referred to other texts or 52%) using history and physical tests in the diagnosis of
chapters for description of these tests.32 There is consid- radial tunnel syndrome.42,43
erable debate regarding the diagnostic validity of neural
provocation tests, and results should be combined with
findings from the interview, imaging and other physical
Strength
tests.32 Others have shown that provocative tests provide Clinically useful measures of elbow and grip strength
marginal value over routine clinical examination for diag- may be obtained using hand-held isometric devices and
nosing ulnar neuropathy at the elbow.33 compared to either the contralateral arm, or in cases of
The ulnar nerve is the most commonly affected nerve bilateral involvement, to normative values.44 The domi-
around the elbow and the second most common neuropa- nant arm is reported to be 6–8% stronger than the non-
thy in the upper limb, after carpal tunnel syndrome.35 dominant arm for gripping and forearm rotation and 4%
Ulnar neuropathy at the elbow may occur after traumatic stronger for elbow flexion and extension strength.44 A
rupture of the MCL or secondary to chronic medial standardized test position of 90° of elbow flexion and
elbow instability, as seen in throwing athletes. Symptoms neutral forearm position is recommended45 for testing
are commonly related to repetitive or prolonged elbow of elbow strength, because reduced ROM in some con­
flexion, resulting in neural traction rather than dynamic ditions precludes positioning in full pronation or
compression in the cubital tunnel.34 Subluxation of the supination.44
ulnar nerve is reported in 11% of healthy individuals and Maximal grip strength has been found to be of limited
may not be related to a higher incidence of ulnar neu- use in clinical populations, such as lateral epicondylalgia
ropathy at the elbow.36 Subluxation of the ulnar nerve or arthritic disease, where pain interferes with maximal
may be examined by palpating the nerve as the elbow is voluntary effort.46,47 The pain-free grip test, which mea-
flexed. sures the amount of force that the patient generates to
Nerve compression may occur anywhere within the the onset of pain, is commonly performed in patients
radial tunnel.37,38 However, the posterior interosseus with lateral epicondylalgia and correlates more strongly
nerve (PIN), a motor branch of the common radial nerve, with pain and disability and perceived improvement than
is most commonly compressed as it passes between two maximal strength in this population.48,49 Most protocols
portions of the superior border of supinator at the arcade recommend testing with the elbow in relaxed extension
of Froshe. Motor weakness of the finger and thumb and forearm pronation, three times with 1-minute inter-
extensors and abductor pollicis longus has traditionally vals, using the average of these repetitions to compare
been considered the primary clinical feature of PIN between affected and unaffected sides.50 An alternative
involvement.38,39 An alternative, sometimes disputed syn- testing position with the elbow flexed 90° and forearm in
drome associated with PIN dysfunction is radial tunnel neutral forearm rotation is also used.
 51  Elbow 587

Diagnostic Imaging Ultrasound may also be useful in diagnosing nerve

compression (Fig. 51-1) by detecting swelling and
Radiographs remain the initial imaging choice following hypoechogenicity of the nerve or identifying secondary
traumatic elbow injuries to establish the initial injury, any causes such as cysts.59–62 Follow-up of patients with ulnar
associated fractures or displacement, as well as to evaluate neuropathy at the elbow after a median of 14 months
post-reduction alignment and bony healing. The elbow found pronounced ulnar nerve thickening at the time of
extension test51 has been proposed as a simple test to the diagnosis was associated with poor outcome, espe-
effectively rule out the need for radiography. Patients cially in conservatively treated cases, indicating that
with a recent elbow injury who cannot fully extend their sonography provides prognostic as well as diagnostic
elbow after injury should be referred for radiography, as information.63
they have a nearly 50% chance of fracture. For those able Electrophysiological testing is reported to be benefi-
to fully extend their elbow, radiography can be deferred cial in evaluating ulnar neuropathy and PIN syndrome,
but the patients should return if symptoms have not while is difficult to perform and rarely helpful for exam-
resolved within 7–10 days. Caution should be used in ining the median nerve at the elbow or radial tunnel
children and in patients with suspected olecranon syndrome.3 Throwing-related nerve injuries are typically
fracture. exertional, so electrodiagnostic testing immediately after
Magnetic resonance imaging (MRI) has been reported throwing may be helpful.3
to be highly specific (100% specificity, 57% sensitivity)
for detecting ulnar collateral ligament tears.52 Complete
or large tears on MRI respond more poorly to rehabilita- CONSERVATIVE MANAGEMENT
tion than partial tears, indicating MRI plays a role in both OF THE ELBOW
diagnosis and predicting outcomes.53 Computed tomog-
raphy and MRI arthrography have been shown to be very The elbow must have mobility, stability and strength and
sensitive for the detection of full or partial articular car- be pain-free to allow independent function in daily activi-
tilage lesions of the elbow.54 ties including the physical demands of work and recre-
Reports on the accuracy of ultrasound for diagnosis of ation. Optimal outcome after elbow injury requires the
lateral epicondylalgia are variable. Some studies have therapist to address all aspects of elbow function. In order
found relatively high sensitivity but low specificity in the to effectively treat a patient with an acute traumatic
detection of symptomatic lateral epicondylalgia,55 whereas injury, an understanding of tissue healing, potential
others have found high specificity using a combination of stresses to tissues and treatment techniques to protect the
grey-scale changes and power Doppler examination of injured structures is essential. Early and continued com-
neovascularity.56 The latter study concluded that ultra- munication with the surgeon regarding the injured struc-
sound can be used to conclusively rule out lateral epicon- tures, specifics about any surgical intervention, stability
dylalgia as a diagnosis and should prompt the clinician to of fracture fixation and joint stability may be required.
consider other causes for lateral elbow pain. If the patient For non-traumatic injuries, an understanding of the onset
complains of clicking or locking, MRI and computed of pathology as well as the individual’s premorbid func-
tomography or magnetic resonance arthrography may be tional level are important. The following paragraphs and
used to detect other pathologies, such as loose bodies, Table 51-3 describe the current evidence for conservative
instability, annular ligament injury or elbow synovial fold rehabilitation of acute traumatic and non-traumatic inju-
syndrome.57,58 Clarke et al.59 found large tears of the ries of the elbow.
common extensor tendon and tears of the lateral collat-
eral ligament were significantly correlated with poorer Acute Traumatic Injuries
response to conservative treatment. The presence of neo-
vascularity demonstrated no correlation with change in
of Bone and Ligaments
pain or disability suggesting it may be a poor indicator While several systematic reviews are available for treating
of prognosis. acute traumatic injuries of the elbow, few offer guidance

$ %

FIGURE 51-1  ■  Posterior interosseus nerve impingement at the arcade of Froshe. (From Qld XRay Pty Ltd, Australia.)
TABLE 51-3  Elbow Conditions and Treatments
Injury/Condition Timing Treatment Precautions and Indications
Simple acute First 3–5 days Closed reduction, rest in an elbow Forearm supination facilitates radial head
dislocation 6–8 weeks splint, followed by active ROM in subluxation posterolaterally, therefore
pronation to avoid subluxing pronation may protect against PLRI.65
positions Careful monitoring of the patient’s
Rehabilitation when both MCL and progress is necessary, and presence of
LCL are injured should use active subluxation or dislocation during the
motion with the humerus in either rehabilitation phase (particularly in the
the horizontal or vertical first 3 weeks following reduction) may
orientations, irrespective of forearm indicate the need for an elbow brace
rotation, to minimize valgus and that limits supination and varus/valgus
varus loads64 forces13
Passive motion should be avoided in early
rehabilitation phases as it may cause
alterations in varus–valgus angulation
and internal–external rotation of the
ulna relative to the humerus64
Stable injury either Immediately Active ROM of all unaffected joints, Safe limits to ROM should be determined
post-reduction or including shoulder, wrist and hand, at surgery or post-reduction of
post-surgery and the unaffected arm dislocation, to avoid stress to healing
MCL and LCL, particularly end-of-range
extension66
Begin as early as Commence active ROM through the
pain and safe (stable) zone, in a gravity-
inflammation assisted position for elbow flexion/
allow, on extension
average 1–5 days Early triceps activation included to
post-surgery or minimize possible scarring of the
relocation12,22,90–92
posterior capsule67
Progress to anti-gravity as tolerated
4–6 weeks, with Elbow passive ROM: gentle 20-second Painful stretching should be avoided as it
good fracture sustained holds end of range, elicits guarding and spasm and limits
healing and joint repeated four to five times to avoid progression
stability12 the stretch reflex67 When there is significant elbow or
Passive force should be directed forearm instability, strengthening may
through the distal radius and ulna be delayed until 6–8 weeks. The ability
and not the wrist or hand, to avoid of the scapular musculature to form a
stressing the passive restraints of stable base for the upper extremity is
the wrist12 important to regain ROM and strength
Progressive resistance exercises: for at the elbow, forearm and wrist. Correct
elbow flexors and extensors, form should be emphasized to prevent
strengthening should begin in stresses to healing ligaments or
pain-free arcs of motion with light fractures. For example, a patient may
resistance with hand or cuff weights compensate for limited supination by
or resistive bands with progression shoulder adduction and external
of ROM and resistance as tolerated. rotation, which causes a valgus stress
Strengthening in pronation and on the elbow
supination begins with the elbow in
90° of flexion using a weighted bar
Strengthening of muscles at
uninvolved joints may be started
within the first week as tolerated
Once good ROM and strength of the
upper extremity are achieved,
work- and sport-specific conditioning
may begin as necessary to allow the
patient to safely and confidently
return to activity. Suggested
exercises for rehabilitation of elbow
injuries and principles guiding
prescription can be found
elsewhere68
Once adequate Manual therapy techniques (e.g. Passive joint mobilizations are never used
fracture and soft passive accessory glides if capsular on an unstable elbow
tissue healing is tightness is limiting motion) Manual force should be specifically
achieved and the Grade I or II mobilizations to decrease applied to each structure identified as
joint is pain and oedema, grade III or IV being involved, recognizing that joints
considered stable mobilizations carefully applied to outside the elbow may contribute to
increase motion limited elbow motion. For example,
Simple distraction may be more both anterior mobilization of the radial
helpful than accessory glides, as head and posterior mobilization of the
intra-articular translation during distal radius on the ulnar may be
normal elbow flexion and extension applied to improve supination, whereas
is minimal69 the reverse is appropriate for
pronation69
 51  Elbow 589

TABLE 51-3  Elbow Conditions and Treatments (Continued)

Injury/Condition Timing Treatment Precautions and Indications

Acute medial 0–6 weeks Following surgical repair, patient is in

collateral protective bracing for 6 weeks70
ligament
mid-substance
tear
Subacute or chronic It is recommended that throwing be Throwing athletes with complete tears
isolated ulnar avoided for the first 2–3 months, found on MRI are less likely to be
collateral during which night splitting and rehabilitated successfully and surgical
ligament injury ROM exercises for the elbow flexors intervention might be considered earlier
and forearm pronators is in these patients15
commenced.93 Strengthening of the
elbow extensors should be avoided
because of potential valgus stress.
Once pain-free, a progressive
strengthening programme for all
muscle groups about the elbow and
shoulder can be commenced. Active
flexion/extension motion in
supination stabilizes the MCL-
deficient elbow71,72
Posterolateral Active flexion/extension motion in
rotatory pronation stabilizes the LCL-deficient
instability elbow, even in the presence of
disruption to the common extensor
origin64,73–76
Biceps, triceps and forearm muscles
should be strengthened
Medial elbow musculature promotes
elbow stability in forearm supination
and the lateral musculature in
pronation77
Anconeus activation should be
included as a stabilizer for the
posterolateral corner14
Ulnar neuropathy Active rest, in which gentle physical Avoid prolonged movements or positions
therapy, icing and anti- that provoke symptoms
inflammatories are given. Night splinting and nerve gliding
Immobilization is used only for exercises did not produce additional
severe cases and is very brief, improvement78
only until acute symptoms
subside. After approximately
4 weeks, a graduated throwing
programme is started3
Radial neuropathy Throwing athletes: activity Throwing athletes often do strenuous
modification, ice, anti- wrist extensor exercises, and these
inflammatories and splinting to should be reduced during the recovery
support both the elbow and the phase to diminish the irritation of the
wrist3 radial nerve and its branches3
Lateral At diagnosis Mobilization with movement, manual
epicondylalgia therapy in combination with
pain-free grip, isometric,
concentric68,79,80 or eccentric wrist
extension, and supination/
pronation81
Cervical spine manual and exercise
therapy techniques, particularly in
patients reporting cold hyperalgesia,
severe pain and disability82
Global upper limb strength and
conditioning
Retraining sensorimotor function,
including attention to re-establishing
optimal wrist posture during
gripping tasks, as well as proximal
strength conditioning83,84

LCL, lateral collateral ligament; MCL, medial collateral ligament; PLRI, posterolateral rotatory instability; ROM, range of motion.
590 PART IV  Overview of Contemporary Issues in Practice

on conservative management options. Two Cochrane sys- the lateral musculature in pronation, where the passive
tematic reviews of treatments for elbow fractures85,86 did tension in the respective muscles is increased. Anconeus,
not identify any randomized controlled trial (RCT) of which originates near the lateral epicondyle and inserts
conservative treatments, while systematic review of treat- broadly onto the ulnar in a fan shape, seems designed
ments for elbow dislocation87 identified only two, small to serve its major function as a dynamic stabilizer, par-
underpowered RCTs. One trial88 found no significant ticularly in the prevention of lateral or posterolateral
differences between early mobilization of the elbow instability.14
versus 3 weeks of cast immobilization, while the other
trial89 found no significant differences between surgical
repair of torn ligaments versus 2 weeks of cast
immobilization.
Lateral Epicondylalgia
For a stable fracture and/or a stable reduction post- Several high-quality RCTs have evaluated the efficacy of
dislocation, early active ROM has been shown to result a multimodal programme of elbow mobilization with
in better outcomes versus prolonged immobiliza- movement and exercise for lateral epicondylalgia, finding
tion.12,22,90–92 Acute fracture dislocations require open evidence of short-term benefit on pain and function.46,94
reduction internal fixation, which involves stabilizing the No difference was found in the long term compared to
fracture sites and repair of ligaments to facilitate early either wait-and-see or placebo injection, in which approx-
active ROM (Table 51-3).13 Information obtained from imately 93–100% of individuals enrolled in the trials
the surgeon regarding healing status will determine if it reported complete recovery or much improvement at
is appropriate. Simple dislocations, in the absence of 1 year.
associated fractures, have a good long-term prognosis. Systematic review of the effectiveness of manipulative
Specific exercises for rehabilitation of elbow injuries therapy in treating lateral epicondylalgia95 found the use
and principles guiding prescription can be found of Mulligan’s mobilization with movement effective in
elsewhere.68 providing immediate, short-term and long-term benefits.
A comprehensive description of techniques can be found
in the following review papers, along with discussion of
potential physiological rationales for immediate improve-
Elbow Instability ments in pain-free grip.96,97 Immediate benefits have also
Management of PLRI requires surgical repair, as they are been demonstrated using manipulative therapy directed
unlikely to correct in the long term, once established. at the cervical spine compared to placebo or control con-
Avulsion of the MCL from the medial epicondyle may be ditions,95 while its addition to local elbow treatments was
managed through direct surgical reattachment. It is found to improve pain and disability at 6 weeks and 6
important to note the importance of the radial head as a months compared to local elbow treatment alone.95,98 A
secondary stabilizer against valgus forces in the elbow, cross-sectional study of individuals with lateral epicon-
and saving the radial head after dislocation should be dylalgia but without significant neck pain identified
considered to maintain valgus stability.13,70 impairment on manual examination at C4–C5, C5–C6
There is no published literature comparing surgical and C6–C7 segmental levels in comparison to healthy
and conservative management of ulnar collateral liga- controls.99
ment injury. Generally, localized injury to the ulnar col- Several systematic reviews can be found evaluating
lateral ligament is initially treated non-surgically. exercise interventions for lateral epicondylalgia.100–102
However, throwing athletes with complete tears found While they are in agreement that resistance exercise
on MRI are less likely to be rehabilitated successfully and results in substantial improvement in pain and grip
surgical intervention might be considered earlier in these strength, optimal mode and dosing remains undefined.
patients.15 In their study of the outcome of conservative Eccentric exercise has been the most studied; however,
management of athletes with ulnar collateral ligament there is no conclusive evidence of its superiority over
injury, Rettig et al.93 found 42% were able to return to other protocols.102 A protocol of progressive resistance
pre-injury level of competition after a minimum of 3 exercises is recommended as a part of a multimodal
months rest and rehabilitation exercises, an average of therapy programme and described in detail else-
24.5 weeks after diagnosis (Table 51-3). where.68,79,80 The rationale for progressive loading is
Much less is known about the role of conservative to improve local muscular strength and endurance as
management of PLRI. If injury to the lateral collateral well as stimulating tendon remodelling.103 It is recom-
ligament complex is present, patients should avoid mended that loading commence in a pain-free capacity.
placing the arm in an abducted or internally rotated This may be particularly important for individuals with
position to prevent varus opening of the elbow, which severe pain and disability, who demonstrate widespread
may impair ligament healing. Exercises in prone lying mechanical hyperalgesia and bilateral cold hyperalgesia.82
with external rotation of the shoulder should be avoided Evidence of bilateral sensorimotor impairments and
for the same reason. Study of the role of muscle con- global upper limb weakness can be found in unilateral
tributions to elbow stability, indicates that biceps, triceps lateral epicondylalgia.83,84,104,105 Based on these findings,
and the forearm muscles contribute to dynamic elbow a comprehensive exercise programme should incorporate
stability by producing joint compression forces. Recent retraining of wrist positioning during gripping, as well
findings77 suggest the medial elbow musculature mostly as address proximal strength deficits and scapulothoracic
affects elbow stability with the arm in supination and conditioning.
 51  Elbow 591

Posterolateral Impingement that patients undergoing surgery more frequently

reported a remission or improvement (61%) than those
Posterolateral impingement can be clinically confused treated conservatively (35%).
with lateral epicondylalgia, potentially resulting in mis- Keefe and Lintner3 provide guidelines for conservative
management and failure to respond to treatment. In con- treatment of early ulnar neuropathy in the throwing
trast to lateral epicondylalgia, posterolateral impingement athlete. If symptoms recur despite an adequate period of
is more common in young adult athletes. The symptoms conservative care, then surgery should be considered.
are non-specific, with pain located posterolaterally to the They advise that the chance for success with conservative
elbow, not directly over the lateral epicondyle or common measures is smaller in individuals with multiple recur-
extensor origin or muscle/tendon tissue, with or without rences, and thus advocate decompression and ulnar nerve
symptoms of clicking or locking. If the patient does com- transposition sooner rather than later for the throwing
plain of clicking or locking, then other pathologies must athlete with multiple recurrences or chronic symptoms.
be ruled out (e.g. loose bodies, instability or annular liga- Treatment of ulnar nerve injuries should start with con-
ment injury).57,58 MRI and computed tomography or sideration of the status of the ulnar collateral ligament as
magnetic resonance arthrography may be useful in the even minor laxity has been shown to contribute to ulnar
diagnosis of elbow synovial fold syndrome. Late diagno- nerve injuries in throwing athletes, and must be addressed
sis may result in mechanical degeneration of articular to prevent recurrence.3
cartilage.106,107 While several case reports describe suc-
cessful outcomes following surgical removal of an
inflamed or hypertrophied synovial fold,106,107 few discuss
Radial Nerve Entrapment
conservative treatment options or prognosis. Anti- In radial tunnel syndrome, the patient complains of pain
inflammatory medication, manual therapy and avoidance that is deep and characterized as an ache. The pain is
of aggravating activities, such as tennis or throwing, fol- worse at night or after throwing, and is located just distal
lowed by a graduated return to these tasks are recom- to the lateral epicondyle in the extensor muscle mass.
mended. As in rehabilitation of epicondylalgia, exercise There are rarely sensory or motor changes. In contrast
programmes should emphasize scapulothoracic posture to radial tunnel syndrome, PIN entrapment often occurs
and shoulder strength. after a long history of lateral forearm or elbow pain fol-
lowed by notable loss of PIN-supplied muscles, causing
weak wrist extension with radial deviation. The differen-
Medial Epicondylalgia tiating feature between radial tunnel syndrome and PIN
In the systematic review of manual therapy and exercise syndrome is the presence or absence of motor weakness.
interventions by Hoogvliet et al.,108 no study of medial Given that motor weakness may be more a function of
epicondylalgia was found. Exercise prescription is cur- the severity rather than the location of compression,
rently based on that of lateral epicondylalgia, with these two syndromes may be considered to be variants on
emphasis on the wrist flexors and pronators rather than the same pathology.38
extensors. If present, concomitant ligament laxity or Neurogenically mediated lateral elbow/forearm pain
ulnar nerve irritation should be addressed. may be defined as a vague, diffuse, aching pain in the
extensor muscles of the proximal forearm, possibly radi-
ating into the dorsal aspect of the hand, or as a sharp
Ulnar Neuropathy shooting pain along the dorsal aspect of the forearm.37
The ulnar nerve is the most commonly affected nerve Pain is increased by resisted supination of the extended
around the elbow and the second most common com- elbow. Tenderness can be elicited by palpation over the
pression neuropathy in the upper limb, after carpal tunnel supinator muscle, approximately 4–5 cm distal to the
syndrome.35 Compression of the nerve resulting in neu- lateral epicondyle. Electrophysiological tests are often
ropraxia or neuropathic signs and symptoms is commonly inconclusive;37 however, compression of the nerve as it
related to repetitive or prolonged elbow flexion. Ulnar passes through the supinator bundle may be confirmed
nerve involvement may occur secondary to medial elbow through skilled ultrasound imaging (Fig. 51-1). A recent
instability, after traumatic rupture of the MCL or chronic systematic review110 found no RCTs concerning radial
laxity as seen in throwing athletes. tunnel syndrome. As PIN entrapment may lead to per-
Cochrane systematic review of treatments for ulnar manent injury, the threshold for surgical release of the
neuropathy109 found only one randomized trial of conser- nerve is reported to be lower for this disorder than radial
vative treatment. This trial found that information on tunnel syndrome.3 Non-operative treatment has been
avoiding prolonged movements or positions that provoke described for the throwing athlete (Table 51-3).3 If there
symptoms was effective in improving subjective discom- is no improvement after 3 months of conservative man-
fort78 (Table 51-3). None of the conservative treatments agement, then surgical release can be undertaken.
improved muscle strength. In another prospective study
of patients with ulnar neuropathy, Beekman52 found only
16% of affected arms were in complete remission, 28% CONCLUSION
had improved, 34% were stable and 22% were progres-
sive after a median follow-up of 14 months. While not Given the expanding knowledge base of the unique bio-
designed to investigate the most optimal treatment for mechanics of the elbow complex and the physiological
patients with ulnar neuropathy at the elbow, they found changes that occur with both acute and chronic injuries,
592 PART IV  Overview of Contemporary Issues in Practice

a review in this area is timely. This chapter identifies a 24. Ring D, Jupiter J. Current concepts review. Fracture-dislocation
need for more RCTs comparing different conservative of the elbow. J Bone Joint Surg Am 1998;80:566–80.
25. Azar F, Andrews J, Wilk K, et al. Operative treatment of ulnar
approaches using standardized outcomes to optimise collateral ligament injuries of the elbow in athletes. Am J Sport
rehabilitation after elbow injury. Med 2000;28:16–23.
26. Jobe F, Stark H, Lombardo S. Reconstruction of the ulnar
collateral ligament in athletes. J Bone Joint Surg Am
Acknowledgement 1986;68:1158–63.
27. Feltner M. Three-dimensional interactions in a two-segment
Dr Sanjay Dhupelia and Qld XRay (Australia) for provi- kinetic chain. Part II: application to the throwing arm in baseball
sion of Figure 51-1 and technical advice on ultrasound pitching. Int J Sport Biomech 1989;5:420–50.
imaging. 28. Fleisig G, Andrews J, Dillman C, et al. Kinetics of baseball pitch-
ing with implications about injury mechanisms. Am J Sport Med
REFERENCES 1995;23:233–9.
29. Werner SL, Fleisig GS, Dillman CJ, et al. Biomechanics of the
1. Herquelot E, Bodin J, Roquelaure Y, et al. Work-related risk elbow during baseball pitching. J Orthop Sports Phys Ther
factors for lateral epicondylitis and other cause of elbow pain in 1993;17:274–8.
the working population. Am J Ind Med 2013;56:400–9. 30. Butler D. Mobilisation of the Nervous System. Melbourne:
2. Hsu S, Moen T, Levine W, et al. Physical examination of the Churchill Livingstone; 1991.
athlete’s elbow. Am J Sport Med 2012;40:699–708. 31. Elvey RL. Physical evaluation of the peripheral nervous system in
3. Keefe DT, Lintner DM. Nerve injuries in the throwing elbow. disorders of pain and dysfunction. J Hand Ther 1997;10:122–9.
Clin Sports Med 2004;23:723–42. 32. Nee RJ, Jull G, Vicenzino B, et al. The validity of upper-limb
4. Mallen CD, Peat G, Thomas E, et al. Prognostic factors for mus- neurodynamic tests for detecting peripheral neuropathic pain.
culoskeletal pain in primary care: a systematic review. Br J Gen J Orthop Sports Phys Ther 2012;42:413–24.
Pract 2007;57:655–61. 33. Beekman R, Schreuder AH, Rozeman CA, et al. The diagnostic
5. Smidt N, Lewis M, Van Der Windt D, et al. Lateral epicondylitis value of provocative clinical tests in ulnar neuropathy at the elbow
in general practice: course and prognostic indicators of outcome. is marginal. J Neurol Neurosurg Psychiatry 2009;80:1369–74.
J Rheumatol 2006;33:2053–9. 34. Ochi K, Horiuchi Y, Tanabe A, et al. Shoulder internal rotation
6. MacDermid JC, Michlovitz SL. Examination of the elbow: linking elbow flexion test for diagnosing cubital tunnel syndrome.
diagnosis, prognosis, and outcomes as a framework for maximizing J Shoulder Elbow Surg [AM] 2012;21:777–81.
therapy interventions. J Hand Ther 2006;19:82–97. 35. Bonzentka D. Cubital tunnel syndrome pathophysiology. Clin
7. Riedel K, Beaton DE. Update on the state of outcome measure- Orthop Relat Res 1998;351:90–4.
ment in total elbow arthroplasty research: identifying a need for 36. Van Den Berg PJ, Pompe SM, Beekman R, et al. Sonographic
consensus. J Bone Joint Surg Am 2013;95:e97 91–8. incidence of ulnar nerve (sub)luxation and its associated clinical
8. Turchin DC, Beaton DE, Richards RR. Validity of observer-based and electrodiagnostic characteristics. Muscle Nerve 2013;47:
aggregate scoring systems as descriptors of elbow pain, function, 849–55.
and disability. J Bone Joint Surg Am 1998;80:154–62. 37. Kotnis NA, Chiavaras MM, Harish S. Lateral epicondylitis and
9. The B, Reininga IH, El Moumni M, et al. Elbow-specific clinical beyond: imaging of lateral elbow pain with clinical-radiologic cor-
rating systems: extent of established validity, reliability, and relation. Skeletal Radiol 2012;41:369–86.
responsiveness. J Shoulder Elbow Surg 2013;22:1380–94. 38. Tennent T, Woodgate A. Posterior interosseous nerve dysfunction
10. Dowrick AS, Gabbe BJ, Williamson OD, et al. Outcome instru- in the radial tunnel. Curr Orthop 2008;22:226–32.
ments for the assessment of the upper extremity following trauma: 39. Vrieling C, Robinson P, Geertzen J. Posterior interosseous nerve
a review. Injury 2005;36:468–76. syndrome: literature review and report of 14 cases. Eur J Plast
11. Armstrong AD, MacDermid JC, Chinchalkar S, et al. Reliability Surg 1998;21:196–202.
of range-of-motion measurement in the elbow and forearm. 40. Lawrence T, Mobbs P, Fortems Y, et al. Radial tunnel syndrome.
J Shoulder Elbow Surg 1998;7:573–80. A retrospective review of 30 decompressions of the radial nerve.
12. Bano KY, Kahlon RS. Radial head fractures – advanced techniques J Hand Surg B 1995;20:454–9.
in surgical management and rehabilitation. J Hand Ther 41. Lister G, Belsole R, Kleinert H. The radial tunnel syndrome.
2006;19:114–35. J Hand Surg [Am] 1979;4:52–9.
13. O’Driscoll S, Jupiter J, King G, et al. The unstable elbow. J Bone 42. Ferdinand B, Rosenberg Z, Schweitzer M, et al. MR imaging
Joint Surg Am 2000;82:724–38. features of radial tunnel syndrome: initial experience. Radiology
14. O’Driscoll SW. Classification and evaluation of recurrent instabil- 2006;240:161–8.
ity of the elbow. Clin Orthop Relat Res 2000:34–43. 43. Ritts G, Wood M, Linscheid R. Radial tunnel syndrome. A
15. Freehill MT, Safran MR. Diagnosis and management of ulnar ten-year surgical experience. Clin Orthop Relat Res 1987;
collateral ligament injuries in throwers. Curr Sports Med Rep 219:201–5.
2011;10:271–8. 44. Askew LJ, An KN, Morrey BF, et al. Isometric elbow strength in
16. O’Driscoll SWM, Lawton RL, Smith AM. The ‘moving valgus normal individuals. Clin Orthop Relat Res 1987;261–6.
stress test’ for medial collateral ligament tears of the elbow. Am J 45. Fess E. Grip strength. In: Casanova J, editor. Clinical Assessment
Sport Med 2005;33:231–9. Recommendations. Chicago: American Society of Hand Thera-
17. Anakwenze OA, Kancherla VK, Iyengar J, et al. Posterolateral pists; 1992. p. 41–5.
rotatory instability of the elbow. Am J Sport Med 46. Bisset L, Beller E, Jull G, et al. Mobilisation with movement and
2014;42:485–91. exercise, corticosteroid injection, or wait and see for tennis elbow:
18. O’Driscoll SW, Horii E, Carmichael SW, et al. The cubital tunnel randomised trial. Br Med J 2006a;333:939–41.
and ulnar neuropathy. J Bone Joint Surg Br 1991;73:613–17. 47. Helliwell PS, Howe A, Wright V. An evaluation of the dynamic
19. Arvind CH, Hargreaves DG. Table top relocation test – New qualities of isometric grip strength. Ann Rheum Dis 1988;
clinical test for posterolateral rotatory instability of the elbow. J 47:934–9.
Shoulder Elbow Surg 2006;15:500–1. 48. Smidt N, van der Windt DAWM, Assendelft WJ, et al. Interob-
20. Cain E, Dugas J, Wolf R, et al. Elbow injuries in throwing server reproducibility of the assessment of severity of complaints,
athletes: a current concepts review. Am J Sport Med grip strength, and pressure pain threshold in patients with lateral
2003;31:621–35. epicondylitis. Arch Phys Med Rehabil 2002;83:1145–50.
21. Morrey B, An K, Stormont T. Force transmission through the 49. Stratford P, Levy D. Assessing valid change over time in patients
radial head. J Bone Joint Surg 1988;70–A:250–256. with lateral epicondylitis at the elbow. Clin J Sport Med
22. Broberg M, Morrey B. Results of treatment of fracture-dislocations 1994;4:88–91.
of the elbow. Clin Orthop 1987;216:109–19. 50. Lim EC. Pain free grip strength test. J Physiother 2013;59:59.
23. Hotchkiss R. Fractures and Dislocations of the Elbow. Philadel- 51. Appelboam A, Reuben AD, Benger JR, et al. Elbow extension test
phia USA: Lippincott-Raven; 1996. to rule out elbow fracture: multicentre, prospective validation and
 51  Elbow 593

observational study of diagnostic accuracy in adults and children. 78. Svernlov B, Larsson M, Rehn K, et al. Conservative treatment
BMJ 2008;337:a2428. of the cubital tunnel syndrome. J Hand Surg Eur Vol
52. Timmerman LA, Schwartz ML, Andrews JR. Preoperative evalu- 2009;34:201–7.
ation of the ulnar collateral ligament by magnetic resonance 79. Coombes B, Bisset L, Connelly L, et al. Optimising corticosteroid
imaging and computed tomography arthrography. Evaluation in injection for lateral epicondylalgia with the addition of physio-
25 baseball players with surgical confirmation. Am J Sport Med therapy: a protocol for a randomised control trial with placebo
1994;22:26–32. comparison. BMC Musculoskelet Disord 2009;10:doi:10.1186/
53. Kim NR, Moon SG, Ko SM, et al. MR imaging of ulnar collateral 1471-2474-1110-1176.
ligament injury in baseball players: value for predicting rehabilita- 80. Pienimaki TT, Tarvainen TK, Siira PT, et al. Progressive strength-
tion outcome. Eur J Radiol 2011;80:e422–6. ening and stretching exercises and ultrasound for chronic lateral
54. Waldt S, Bruegel M, Ganter K, et al. Comparison of multislice epicondylitis. Physiotherapy 1996;82:522–30.
CT arthrography and MR arthrography for the detection of artic- 81. Navsaria R, Ryder D, Lewis J, et al. The Elbow-EpiTrainer: a
ular cartilage lesions of the elbow. Eur Radiol 2005;15:784–91. method of delivering graded resistance to the extensor carpi radia-
55. Levin D, Nazarian LN, Miller TT, et al. Lateral epicondylitis of lis brevis. Effectiveness of a prototype device in a healthy popula-
the elbow: US findings. Radiology 2005;237:230–4. tion. Br J Sports Med 2013.
56. du Toit C, Stieler M, Saunders R, et al. Diagnostic accuracy of 82. Coombes B, Bisset L, Vicenzino B. Thermal hyperalgesia distin-
power Doppler ultrasound in patients with chronic tennis elbow. guishes those with severe pain and disability in unilateral lateral
Br J Sports Med 2008;42:572–6. epicondylalgia. Clin J Pain 2012;28:595–601.
57. Cerezal L, Rodriguez-Sammartino M, Canga A, et al. Elbow 83. Alizadehkhaiyat O, Fisher AC, Kemp GJ, et al. Upper limb
synovial fold syndrome. Am J Roentgenol 2013;201:W88–96. muscle imbalance in tennis elbow: a functional and electromyo-
58. Huang G, Lee C, Lee H, et al. MRI, arthroscopy, and histologic graphic assessment. J Orthop Res 2007;25:1651–7.
observations of an annular ligament causing painful snapping of 84. Bisset LM, Russell T, Bradley S, et al. Bilateral sensorimotor
the elbow joint. Am J Roentgenol 2005;185:397–9. abnormalities in unilateral lateral epicondylalgia. Arch Phys Med
59. Clarke A, Ahmad M, Curtis M, et al. Lateral elbow tendinopathy. Rehabil 2006;87:490–5.
Correlation of ultrasound findings with pain and functional dis- 85. Gao Y, Zhang W, Duan X, et al. Surgical interventions for treating
ability. Am J Sport Med 2010;38:1209–14. radial head fractures in adults. Cochrane Database Syst Rev 2013.
60. Beekman R, Schoemaker M, van der Plas J, et al. Diagnostic value doi:10.1002/14651858.CD008987.pub2.
of high-resolution sonography in ulnar neuropathy at the elbow. 86. Wang Y, Zhuo Q, Tang P, et al. Surgical interventions for treating
Neurology 2004;62:767–73. distal humeral fractures in adults. Cochrane Database Syst Rev
61. Konin G, Nazarian L, Walz D. US of the elbow: indications, 2013;doi:10.1002/14651858.CD009890.pub2.
technique, normal anatomy, and pathologic conditions. Radio- 87. Taylor F, Sims M, Theis J-C, et al. Interventions for treating acute
graphics 2013;33:E125–47. elbow dislocations in adults. Cochrane Database Syst Rev
62. Yoon J, Hong S-J, Kim B-J, et al. Ulnar nerve and cubital tunnel 2012;doi:10.1002/14651858.CD007908.pub2.
ultrasound in ulnar neuropathy at the elbow. Arch Phys Med 88. Rafai M, Largab A, Cohen D, et al. Pure posterior luxation of the
Rehabil 2008;89:887–9. elbow in adults: immobilization or early mobilization. A random-
63. Beekman R, Wokke JH, Schoemaker MC, et al. Ulnar neuropathy ized prospective study of 50 cases. Chir Main 1999;18:272–8.
at the elbow: follow-up and prognostic factors determining 89. Josefsson PO, Gentz CF, Johnell O, et al. Surgical versus non-
outcome. Neurology 2004;63:1675–80. surgical treatment of ligamentous injuries following dislocation of
64. Alolabi B, Gray A, Ferreira LM, et al. Rehabilitation of the the elbow joint. A prospective randomized study. J Bone Joint Surg
medial- and lateral collateral ligament-deficient elbow: an in vitro Am 1987;69:605–8.
biomechanical study. J Hand Ther 2012;25:363–72. 90. Kuntz DG Jr, Baratz ME. Fractures of the elbow. Orthop Clin
65. Dodds S, Fishler T. Terrible triad of the elbow. Orthop Clin North Am 1999;30:37–61.
North Am 2013;44:47–58. 91. Liow RY, Cregan A, Nanda R, et al. Early mobilisation for mini-
66. King G, Morrey B, An K. Stabilizers of the elbow. J Shoulder mally displaced radial head fractures is desirable. A prospective
Elbow Surg 1993;2:165–74. randomised study of two protocols. Injury 2002;33:801–6.
67. Davila SA, Johnston-Jones K. Managing the stiff elbow: operative, 92. Saati AZ, McKee MD. Fracture-dislocation of the elbow: diagno-
nonoperative, and postoperative techniques. J Hand Ther sis, treatment, and prognosis. Hand Clin 2004;20:405–14.
2006;19:268–81. 93. Rettig AC, Sherrill C, Snead DS, et al. Nonoperative treatment
68. Vicenzino B, Hing W, Rivett D, et al., editors. Mobilisation with of ulnar collateral ligament injuries in throwing athletes. Am J
Movement: The Art and the Science. Chatswood NSW: Elsevier; Sport Med 2001;29:15–17.
2011. 94. Coombes BK, Bisset L, Brooks P, et al. Effect of corticosteroid
69. Lockard M. Clinical biomechanics of the elbow. J Hand Ther injection, physiotherapy, or both on clinical outcomes in patients
2006;19:72–80. with unilateral lateral epicondylalgia: a randomized controlled
70. Morrey B. Instructional course lectures: complex instability of the trial. J Am Med Assoc 2013;309:461–9.
elbow. J Bone Joint Surg 1997;79-A:460–9. 95. Herd C, Meserve B. A systematic review of the effectiveness of
71. Armstrong A, Dunning C, Faber K, et al. Rehabilitation of the manipulative therapy in treating lateral epicondylalgia. J Man
medial collateral ligamentdeficient elbow: an in vitro biomechani- Manip Ther 2008;16:225–37.
cal study. J Hand Surg [Am] 2000;25:1051–7. 96. Vicenzino B. Lateral epicondylalgia: a musculoskeletal physio-
72. Pichora J, Fraser G, Ferreira L, et al. The effect of medial col- therapy perspective. Man Ther 2003;8:66–79.
lateral ligament repair tension on elbow joint kinematics and sta- 97. Vicenzino B, Cleland JA, Bisset L. Joint manipulation in the man-
bility. J Hand Surg [Am] 2007;32:1210–17. agement of lateral epicondylalgia: a clinical commentary. J Man
73. Dunning C, Zarzour Z, Patterson S, et al. Muscle forces and Manip Ther 2007;15:50–6.
pronation stabilize the lateral ligament deficient elbow. Clin 98. Cleland JA, Flynn TW, Palmer JA. Incorporation of manual
Orthop Relat Res 2001;388:118–24. therapy directed at the cervicothoracic spine in patients with
74. Fraser G, Pichora J, Ferreira L, et al. Lateral collateral ligament lateral epicondylalgia: a pilot clinical trial. J Man Manip Ther
repair restores the initial varus stability of the elbow: an in vitro 2005;13:143–51.
biomechanical study. J Orthop Trauma 2008;22:615–23. 99. Coombes BK, Bisset L, Vicenzino B. Bilateral cervical dysfunction
75. McKee M, Schemitsch E, Sala M, et al. The pathoanatomy of in patients with unilateral lateral epicondylalgia without concomi-
lateral ligamentous disruption in complex elbow instability. tant cervical or upper limb symptoms: a cross-sectional case-
J Shoulder Elbow Surg 2003;12:391–6. control study. J Manipulative Physiol Ther 2014;37:79–86.
76. O’Driscoll S, Morrey B, Korinek S, et al. Elbow subluxation 100. Cullinane FL, Boocock MG, Trevelyan FC. Is eccentric exercise
and dislocation. A spectrum of instability. Clin Orthop 1992; an effective treatment for lateral epicondylitis? A systematic
280:186–97. review. Clin Rehabil 2014;28:3–19.
77. Seiber K, Gupta R, McGarry MH, et al. The role of the elbow 101. Raman J, MacDermid JC, Grewal R. Effectiveness of different
musculature, forearm rotation, and elbow flexion in elbow stabil- methods of resistance exercises in lateral epicondylosis – a system-
ity: an in vitro study. J Shoulder Elbow Surg 2009;18:260–8. atic review. J Hand Ther 2012;25:5–25.
594 PART IV  Overview of Contemporary Issues in Practice

102. Woodley BL, Newsham-West RJ, Baxter GD. Chronic tendi- three cases and review of literature. Arch Orthop Trauma Surg
nopathy: effectiveness of eccentric exercise. Br J Sports Med 2010;130:347–51.
2007;41:188–99. 108. Hoogvliet P, Randsdorp MS, Dingemanse R, et al. Does effective-
103. Coombes BK, Bisset L, Vicenzino B. A new integrative model of ness of exercise therapy and mobilisation techniques offer guid-
lateral epicondylalgia. Br J Sports Med 2009b;43:252–8. ance for the treatment of lateral and medial epicondylitis? A
104. Bisset LM, Coppieters MW, Vicenzino BT. Sensorimotor deficits systematic review. Br J Sports Med 2013;47:1112–19.
remain at 12 months despite conservative treatment in patients 109. Caliandro P, La Torre G, Padua R, et al. Treatment for ulnar
with tennis elbow. Arch Phys Med Rehabil 2009;90:1–8. neuropathy at the elbow. Cochrane Database Syst Rev
105. Coombes B, Bisset L, Vicenzino B. Elbow flexor and extensor 2011;CD006839.
muscle weakness in lateral epicondylalgia. Br J Sports Med 110. Rinkel WD, Schreuders TA, Koes BW, et al. Current evidence for
2012a;46:449–53. effectiveness of interventions for cubital tunnel syndrome, radial
106. Antuna S, O’Driscoll S. Snapping plicae associated with radiocapi- tunnel syndrome, instability, or bursitis of the elbow: a systematic
tellar chondromalacia. Arthroscopy 2001;17:491–5. review. Clin J Pain 2013;29:1087–96.
107. Steinert A, Goebel S, Rucker A, et al. Snapping elbow caused by
hypertrophic synovial plica in the radiohumeral joint: a report of
 CHAPTER 52 

Wrist/Hand
Anne Wajon

Achieving the best possible functional outcome following treatment strategy will need to consider all pathologies
hand injury requires careful understanding of anatomy affecting the hand, particularly ensuring that any newly
and pathology, together with a team approach involving prescribed exercise programme will not aggravate a pre-
the patient, therapist and surgeon. This chapter will inte- vious condition.
grate clinical reasoning into the assessment, diagnosis
and management of a variety of common hand and wrist Clinical Context
conditions. Emerging issues and new advances in the care
of the hand-injured patient, providing directions that Considering the importance of the hand in everyday life,
reflect advances in practice, will also be discussed. particularly in relation to the patient’s hand dominance,
While some hand conditions require immobilization knowledge of their occupation, hobbies and sports is
for adequate tissue healing, many others will suffer from essential.
persistent stiffness if the hand is not permitted to move Does the individual have any special requirements
during the healing period. that will help determine appropriate management? For
example, will a young mother presenting with de Quer-
vains syndrome be able to modify her postures and hand-
holds when managing the baby to allow the condition to
PRINCIPLES OF ASSESSMENT resolve?
History
When assessing a patient with a hand or wrist complaint,
Examination
it is essential to take a detailed history. This will enable It is essential to have a thorough understanding of the
the clinician to develop ‘hypotheses about the probable anatomical structures likely to be involved. It is beyond
location and type of pathology, the clinical symptoms to the scope of this text to review all structures involved;
be treated, possible strategies to manage the problem, however, they will be discussed where relevant to the
contraindications or precautions to examination and pathology being presented.
treatment procedures’ (p 117).1
Inspection
Mechanism of Injury Observing the hand at rest and during use will provide
Identifying the mechanism of injury will help to establish an invaluable insight. Considering that there is very little
the general direction and force applied to the hand during muscle or fat coverage on the hand and wrist, any local
an injury, and identify the potential structures involved. pathology can be identified by areas of discoloration
Other patients will not be able to identify a mechanism (bruising/redness) and swelling. Further, inspecting for
of injury and may describe an insidious onset of symp- wasting of intrinsic muscles, presence of wounds and
toms. Careful questioning might reveal a contributing scars, and general bony alignment will be important.
factor in their activities of daily living, such as a sudden
increase in computer use or caring for a new child. Iden-
tification of these contributing factors will provide guid-
Sensation
ance for patient education in the long-term relief of It is important to determine the location of any paraes-
symptoms. thesia or numbness, as location of areas of altered sensa-
tion may be helpful in assessing for involvement of
peripheral nerves. Further, it is possible to map recovery
Previous Injuries of sensation following peripheral nerve injury by using
It is also important to identify whether the patient has sensibility and manual muscle tests.2
any underlying pathology or had suffered previous inju-
ries to the affected hand. A history of waking with tin-
gling in the fingers at night, joint stiffness following
Range of Motion
previous fracture, or pre-existing pain condition (or It is helpful to develop a routine sequence of movements
arthritis) will need to be taken into consideration when in assessing the hand and wrist. This sequence may be
planning treatment goals and functional outcomes. The altered if the patient complains of any exacerbation of
595
596 PART IV  Overview of Contemporary Issues in Practice

symptoms. A finger goniometer is particularly useful in Additional individual muscle tests may be indicated
measuring the small joints of the hand. following a peripheral nerve laceration, in the presence
The fingers should be measured for gross range of of suspected nerve compression, or in the presence of
extension and flexion. However, if there is local pathol- limited range of motion in the hand. It may be appropri-
ogy at the proximal interphalangeal joint of one digit, it ate to perform a full manual muscle test of the upper limb
might be appropriate to measure both gross and isolated in certain conditions. Comprehensive texts are available
range of motion. For isolated proximal interphalangeal which detail how this may be performed.7
joint measurements, measure proximal interphalangeal
joint flexion with the metacarpophalangeal joint extended, Palpation and Provocative Tests
and conversely, measure proximal interphalangeal exten-
sion with the metacarpophalangeal joint flexed. This will Palpation provides information regarding temperature,
help eliminate involvement of the long forearm extensors swelling, bony involvement, soft tissue thickening and
and flexors in restricting joint range of motion. pain, and will be useful in determining which structure(s)
Measurements of the thumb are more complicated might be contributing to the patient’s symptoms. This
because of the flexibility afforded by the carpometacarpal will further assist in determining which provocative tests
joint. The interphalangeal and metacarpophalangeal are appropriate.
joints should be measured for extension and flexion, and A number of provocative tests have been described
the carpometacarpal joint measured for palmar and radial to assist in the diagnosis of specific pathological condi-
abduction, retropulsion (ability to lift thumb off the tions in the hand, wrist and elbow. To determine the
table) and opposition (ability to touch tip of little finger usefulness of these tests, Valdes and LaStayo8 performed
and slide down to distal palmar crease of little finger). a literature review and determined positive (LR+) and
Measurements of the wrist include extension, flexion, negative (LR−) likelihood ratios. They proposed that
radial and ulnar deviation. It is helpful to allow the fingers provocative tests with a LR+ ≥2.0, or a mean LR− of
to curl while measuring wrist extension, and for the ≤0.5, from two or more studies that scored ≥ 812 on the
fingers to straighten when measuring wrist flexion, oth- MacDermid rating scale9 would be highly recommended.
erwise the long finger flexors and extensors will limit Tests that met this criteria include Phalen’s, Tinel’s and
range of wrist motion. Additionally, measures of forearm modified compression test for carpal tunnel syndrome,10
rotation, pronation and supination, should be taken with the scaphoid shift test for scapholunate instability,11 and
the elbow positioned next to the waist. Either an incli- Tinel’s and elbow flexion test for cubital tunnel
nometer or regular small joint goniometer may be used. syndrome.12
Assessment of range of motion will contribute to It is important to remember that provocative tests are
determining whether the restriction is due to joint stiff- not used in isolation, but considered in a clinical reason-
ness and muscle tightness, and additionally whether any ing framework that incorporates subjective assessment,
of these movements reproduce the patient’s pain. clinical intuition and experience.

Strength Investigations
Muscles are tested for isometric strength. The hand-held Plain radiographs are useful for assessing fractures, dis-
dynamometer is a reliable way to measure isometric locations and osteoarthritis. Complex fracture anatomy
forearm strength,3 however it does not necessarily relate is more clearly identified with computed tomography,
to overall hand function and task performance.4 Standard whereas magnetic resonance imaging is indicated when
assessment of grip strength involves the patient being there is a suspected subtle fracture or soft tissue involve-
seated with the arms by their side, the elbow flexed at ment. In particular, magnetic resonance imaging is useful
90°, and the forearm and wrist in neutral.5 Traditionally, for investigations for scapholunate instability, triangular
a hydraulic hand dynamometer is used, and the mean of fibrocartilage complex (TFCC) trauma or occult gangli-
three trials recorded. However a study comparing the ons. Ultrasound is helpful in the analysis of suspected soft
reliability of one versus three grip strength trials found tissue problems such as digital pulley injuries, tendon
that one maximal trial is ‘as reliable as, and less painful ruptures, ganglions or tendinopathy. Nevertheless, one
than, either the best of, or mean of, three trials’ (p. 318).6 should be cautious when interpreting imaging results as
Pinch strength may be tested in three positions: tip there can be a poor correlation between clinical symp-
pinch (two point), chuck pinch (three point) and lateral toms and radiological findings.13
pinch. Results will vary according to the patient’s age, sex,
occupation and hand dominance. The dominant hand is
usually stronger than the non-dominant hand, and it
would be expected that patient’s strength would improve
PRINCIPLES OF MANAGEMENT
as they progress through their rehabilitation. Hand Therapy
Specific manual muscle testing can be performed to
determine whether there is peripheral nerve involve- Hand therapists are physical therapists or occupational
ment. A simple test for radial nerve function involves therapists who incorporate patient education, exercise
resistance of the extensor carpi radialis and extensor carpi prescription, custom-made splints and casts, modalities,
ulnaris; for the median nerve abductor pollicis brevis, and and attention to ergonomic and postural issues in their
for the ulnar nerve abductor digiti minimi. treatments. Their goal is to improve patient function and
 52  Wrist/Hand 597

independence with work tasks, sports, hobbies and other digitorum profundus and flexor digitorum superficialis
activities of daily living. (Fig. 52-1). It is important to educate patients to perform
exercises carefully and accurately to avoid inadvertently
compensating with unaffected joints.
Immobilization
Prolonged immobilization after finger fractures or joint
injuries may result in persistent stiffness, chronic pain MANAGING COMMON CONDITIONS
and deformity. It is recommended that an early motion
programme that avoids re-stressing injured structures, be Fractures
encouraged to prevent joint contracture and adhesions of Metacarpal and Phalangeal Fractures
the gliding soft tissues of the extensor and flexor tendons.14
It is recommended that the hand be supported in the Metacarpal and phalangeal fractures are relatively
intrinsic plus position, known as the ‘position of safe common in sporting injuries, and may result in consider-
immobilization’, during fracture healing. This position able functional impairments, including pain, stiffness and
involves metacarpophalangeal joint flexion of 60–90°, weakness, if not managed well. It is essential to consider
interphalangeal extension at 0° and the wrist in approxi- whether the fracture is stable, is in correct anatomical
mately 30° extension. The thumb should be positioned alignment, and whether there are any other associated
in mid palmar/radial abduction and the forearm in soft tissue injuries. Mal-alignment of the fracture will
neutral, unless otherwise indicated. This position mini- result in mal-rotation of the digits, and this may interfere
mizes contracture of collateral ligament and joint capsu- with the ability to return to full function.
lar structures and addresses the ‘ultimate functional Conservative treatment is appropriate if the fracture
demands of the hand requiring length and extensibility is stable, in good alignment and only minimally displaced.
of the dorsal skin’ (p. 6).15 Not only is it essential that any The hand may be splinted in the position of safe immo-
splinting or casting does not include joints that do not bilization, supporting the adjacent digit and the joints
need to be immobilized, but it is important that the frac- above and below the fracture site.
ture is sufficiently stable to allow early motion, otherwise Acute swelling may be controlled by cryotherapy,
complications of pain and persistent stiffness are likely to elevation and compression. The patient is instructed to
arise.16 As swelling begins to subside it is important begin pain-free active range of motion exercises immedi-
to reassess if the applied immobilization is continuing to ately, and by 4 weeks, it is likely that a set of buddy straps
provide adequate support or needs remoulding to ensure will replace the splint for light activities. Generally it is
fit and avoid pressure areas. advisable that the patient is instructed to continue using
the splint for any sporting or at-risk activities until the
Oedema Control 6-week time period. At this time, any residual stiffness or
weakness should be resolved by specific blocking exer-
A fracture to the hand will injure adjacent and surround- cises, appropriate splinting and progression of a resisted
ing soft tissues, resulting in oedema that may contribute strengthening programme.
to persistent swelling and stiffness if not appropriately Blocking exercises attempt to isolate the movement to
managed. Cold therapy has been shown to reduce pain the involved joint, and involve supporting the phalanx or
at rest and with movement, and reduce functional dis- metacarpal below the stiff joint. For example, holding the
ability when compared with placebo in a prospective ran- proximal interphalangeal joint in extension will facilitate
domized controlled trial of 74 patients with a sports-related isolated distal interphalangeal joint flexion exercise, alter-
soft tissue injury.17 Additionally, rest, compression, eleva- natively holding the metacarpophalangeal joint flexed
tion and protected mobilization can help to reduce will facilitate active proximal interphalangeal joint exten-
oedema following acute injury or surgery. sion. By 8 to 10 weeks, any persistent joint stiffness may
be addressed by applying a dynamic splint that holds the
Scar and Wound Care stiff joint at the end of available range, for an extended
period of time.19
Massage is performed to reduce adhesion of scars, assist If the fracture is unstable or rotated, or intra-articular
in oedema reduction and reduce hypersensitivity. Patients at the proximal interphalangeal joint, it is advisable to
are instructed to perform massage four to six times per refer the patient to a hand surgeon to discuss whether
day to the affected area. Additionally, various silicone internal fixation is required.
products can be useful to flatten raised or thickened scars.
Silicone gel sheets are available commercially and patients Distal Radius Fractures
are instructed to wear them if appropriate at night for up
to 3 months following surgery. Distal radius fractures are common in the elderly,
although they may occur in any age group. A dorsally
displaced fracture is known as a Colles fracture, whereas
Exercises a volarly displaced fracture is referred to as a Smith’s type
Exercises are designed to regain full range of motion fracture.20 Stable fractures in good alignment may be
without causing any increase in pain or inflammation. managed in a short arm cast; however, comminuted frac-
Specific tendon gliding exercises18 may be useful for tures with intra-articular involvement may require either
maximizing differential tendon glide between flexor closed or open reduction with internal fixation.
598 PART IV  Overview of Contemporary Issues in Practice

A B C

D E

FIGURE 52-1  ■  Tendon gliding exercises.

During the period of immobilization, it is important and/or wrist, particularly falls onto an outstretched hand’
that the patient exercises the uninvolved digits and is able (p. 1370).22 Initial radiographic findings may be reported
to move the thumb, fingers and elbow freely within the as normal; however, tenderness in the anatomical snuff-
cast. Once the cast is removed (usually at around 6 weeks box, accompanying swelling and loss of grip strength are
post fracture) the patient should be instructed to perform suggestive of a scaphoid fracture and warrant presump-
a routine set of exercises, aiming to regain wrist extension tive casting and repeat radiography or a magnetic reso-
and flexion, and forearm pronation and supination. Often nance imaging investigation after 10 to 14 days. Acute
the use of heat with stretch can facilitate the early return stable or incomplete fractures may be treated conserva-
of motion once the cast is removed, and a graded pro- tively23 by immobilization for 6 to 8 weeks. Subsequent
gramme of grip and forearm strengthening is helpful to radiographs must confirm fracture union before immo-
improve strength and confidence with return to func- bilization is discontinued and the patient started on a
tional tasks. programme of exercises for regaining range of motion
and strength. Although options for immobilization of
scaphoid fractures include a long arm cast, a below-elbow
Scaphoid Fractures
cast or a scaphoid cast including the thumb carpometa-
The scaphoid is the most commonly fractured carpal carpal and metacarpal joints, current evidence suggests
bone, accounting for 60% of carpal fractures and 11% of there is no advantage of any one particular cast over
hand fractures in Norway.21 Scaphoid fractures should be another,24 and no significant difference in the rate of non-
suspected in any cases where ‘trauma involved the hand union between the various types of cast.25 Based on the
 52  Wrist/Hand 599

information available to date, it would seem reasonable joint extension splint. A recent comparative study between
for surgeons and therapists to continue to follow their these two different style splints identified an improved
casting preference. Alternatively, some patients may con- extension lag of 5° in the cylindrical group in comparison
sider surgical treatment of non-displaced or minimally to the 9° lag after immobilization in a lever-type thermo-
displaced fractures to achieve an earlier return to work, plastic splint.29 The amount of oedema, the patient’s con-
even though these short-term benefits may be associated tribution to skin care and compliance with splint wearing,
with an increased risk of osteoarthritis.26 and the expertise of the therapist will determine which
Unfortunately, the diagnosis of scaphoid fracture may style of splint is appropriate for any given patient.
be delayed, and non-union or malunion can result. This
may lead to chronic pain, weakness and stiffness, ulti- Boutonniere
mately leading to early osteoarthritis.27 Internal fixation
is appropriate in these individuals, as well as those A true boutonniere deformity of the finger presents with
with displaced scaphoid waist fractures, proximal pole proximal interphalangeal flexion and distal interphalan-
fractures and fractures resulting in loss of carpal geal hyperextension. It occurs following rupture of the
alignment.28 central slip (extensor apparatus) on the dorsum of the
proximal interphalangeal joint. The distal interphalan-
geal joint hyperextends as the lateral bands of the
Tendon Injury extensor mechanism sublux volarly at the proximal inter-
phalangeal joint, and their extension force is transmitted
Mallet Injury
to the distal interphalangeal joint. Acutely, the proximal
The most common injury to the distal interphalangeal interphalangeal joint is passively correctable into full
joint of the digits is a mallet finger injury. Commonly extension, but left untreated, will ultimately develop into
people will complain that they were struck on the tip of a flexion contracture with increasing proximal interpha-
the finger by a ball, or they ‘caught’ the finger when langeal joint flexion. Patients presenting with this condi-
tucking in the sheets. The traumatic incident may be tion should be treated conservatively with 4 weeks in a
insignificant. The resultant loss of active extension of the splint that holds their proximal interphalangeal joint in
distal interphalangeal joint (Fig. 52-2) is due to either a full extension, while allowing the distal interphalangeal
small avulsion fracture of the insertion of the extensor joint to flex. Subsequently, they may be managed with a
tendon, or a rupture of the tendon itself. Capener splint30 that takes the extension load off the
The mallet finger injury responds well to a period of proximal interphalangeal joint, and allows the joint to
conservative splinting. In the absence of a fracture, the move through a protected range of flexion.
distal interphalangeal joint is held in constant slight
hyperextension for up to 8 weeks. If there is an avulsion Flexor Tendon – Flexor Digitorum
fracture, the distal interphalangeal joint is held in neutral Profundus Avulsion
extension for 6 weeks. It is essential to remind the patient
to continue to exercise the uninvolved proximal interpha- The flexor digitorum profundus tendon may be avulsed
langeal joint and to care for the skin. During the 6- to at its insertion to the distal phalanx when a player is grab-
8-week period of immobilization, the patient must main- bing an opponent’s jersey during a game of rugby or
tain the extension force to the distal interphalangeal joint American football. As the opponent pulls or runs away,
at all times, even if the splint is removed for skin care. the distal interphalangeal joint is forcibly hyperextended,
Splinting options include a cylindrical-style thermoplas- resulting in rupture of the flexor digitorum profundus
tic splint or a dorsally based static distal interphalangeal tendon. The patient will report that they are unable to
actively flex the distal interphalangeal joint. Active flexion
of the proximal interphalangeal joint should not be
affected due to the action of the FDS tendon. Patients
presenting with this injury should be immediately referred
to a hand surgeon for surgical intervention.

Joint Injury
Volar Plate Injury at the Proximal
Interphalangeal Joint
The volar plate is a mobile, thick and fibrocartilaginous
structure attached to the anterior margin of the base of
the middle phalanx.31 It is commonly injured when the
joint is forced into hyperextension while attempting to
catch a ball, and this results in a small avulsion fracture
of the volar plate. Trauma to the volar plate may be suc-
cessfully managed by a dorsal blocking splint to prevent
the joint from being fully straightened for the first 3
FIGURE 52-2  ■  Mallet finger deformity. weeks. Initially, the splint will be moulded to prevent the
600 PART IV  Overview of Contemporary Issues in Practice

joint from extending in the last 20 to 30° of range, while

the patient is encouraged to actively flex towards the
palm. Alternatively, a custom-made thermoplastic figure-
of-eight splint may be fitted.32
Each week, the splint is remoulded to allow a further
10° extension. By 3 weeks, the patient is encouraged to
wear either the straightened dorsal splint or buddy straps
for protection during sport and physical activities, until
the 6-week time period. It is important that flexion exer-
cises are performed during the early healing phase. By 6
weeks, blocked extension exercises can be added. Unfor-
tunately, some people complain of persistent stiffness and
may require dynamic splinting to regain full range of
proximal interphalangeal joint extension.

Swan-neck Deformity
Chronic injury to the volar plate may result in a patient FIGURE 52-3  ■  Stress testing of ulnar collateral ligament injury.
presenting with a ‘swan-neck’ deformity. This deformity
of proximal interphalangeal joint hyperextension and
distal interphalangeal flexion can lead to considerable (Fig. 52-3) on stress testing.33 If it is associated with a
functional handicap, making it difficult to flex at the Stener lesion, whereby the proximal end of the torn liga-
proximal phalangeal joint during grasping activities. It ment flips out over the adductor aponeurosis, surgical
can be managed by the application of a small ‘figure-of- repair will be required.34 A postero-anterior stress radio-
eight’ splint that prevents the proximal interphalangeal graph with a difference of more than 15 degrees should
joint from fully extending, while still allowing full flexion be surgically explored for a Stener lesion.35
range. If there is laxity on stress testing, but a firm and painful
end feel, it may be assumed that the patient has suffered
a partial tear and can be managed with a custom-made
Collateral Ligament Injury
thumb splint which prevents any radial force being trans-
The collateral ligaments of the proximal interphalangeal mitted to the metacarpophalangeal joint. It should be
joint protect the joint from lateral force, and become worn for up to 6 weeks, depending on the degree of laxity
increasingly tense with flexion of the joint.31 Collateral and pain with stress testing. The splint may be removed
ligament injuries are common with ball sports, and will for gentle pain-free active range of motion and proprio-
result in a swollen, stiff and painful joint. Stress testing ceptive exercises. After the 6-week period of splinting the
of the collateral ligament will reproduce pain and confirm patient may be instructed to wean out of the splint, and
whether there is any joint laxity. It is useful to assess while being careful to avoid any lateral stress to the meta-
integrity of the collateral ligaments at the proximal inter- carpophalangeal joint when out of the splint, they could
phalangeal joint in full extension and slight flexion to begin pinch and grip strengthening with exercise putty.
help determine at which angle the joint is least stable. At this stage, they should be advised to continue with the
Conservative management includes oedema control with splint during heavy lifting or gym work, or to use strap-
a compressive bandage, tendon gliding exercises and ping tape to provide an intermediate amount of support
buddy straps to maintain the proximal interphalangeal while resuming sporting activities, possibly for up to 3
joint in neutral deviation during motion. Although it may months.
take 12 to 24 months for morning stiffness and residual
swelling to resolve, most people will manage with little
functional deficit.
Wrist Instabilities
Patients may present with wrist pain following either
acute trauma or with a history of chronic pain related to
Ulnar Collateral Ligament
overuse. The pain may be local or diffuse, and taking a
Injury of the Thumb
thorough history and performing a careful examination
The metacarpophalangeal joint of the thumb is most will assist in determining which structures are contribut-
commonly injured when a radially directed impact forces ing to their symptoms.
the thumb into abduction and hyperextension. The resul- There are various degrees of instability and many
tant injury to the ulnar collateral ligament is referred to structures that may cause pain, but for the purpose of this
as skier’s thumb, as this is a common injury in this sport. chapter, only scapholunate and ulnar carpal instabilities
Symptoms include local swelling, pain and tenderness to will be presented.
palpation, instability and weakness during pinch. Pain
will be reproduced when stressing the ulnar collateral Scapholunate Ligament
ligament by applying a valgus force to the metacarpopha-
langeal joint in extension and at 30° of flexion. A com- The scapholunate ligament is commonly injured in a fall
plete tear is diagnosed when there is no solid endpoint on an outstretched hand and will result in central dorsal
 52  Wrist/Hand 601

wrist pain. Patients frequently complain that this pain is

aggravated by weight bearing on an extended wrist. The
scaphoid shift test11 is commonly used to test for scapho­
lunate instability. The examiner moves the wrist from
ulnar deviation towards radial deviation while maintain-
ing pressure with their thumb on the scaphoid tubercle.
This stresses the scapholunate ligament and restricts the
normal flexion that occurs during the movement from
radial to ulnar deviation.36
As the scapholunate interosseous ligament is supplied
by mechanoreceptors and ligamentomuscular reflexes, a
new approach to rehabilitation for dynamic instability
will incorporate proprioceptive retraining, specifically
conscious training of muscles that protect the scapholu-
nate joint and unconscious neuromuscular training incor-
porating joint stability and posture.37 It has been identified
that the dart-throwing motion is a stable and controlled
plane of motion that results in less scaphoid and lunate
motion than pure wrist flexion–extension,38 while being
a more functional plane of motion for most activities of
daily living.
Rehabilitation of patients with a scapholunate liga-
ment injury initially includes splinting for pain relief,
and education regarding avoiding aggravating activities.
Once the initial pain has begun to settle, it is appropriate
to introduce proprioceptive awareness training including
joint position sense and kinaesthesia. It is important to
avoid any strong resisted gripping at this stage as this
is only likely to increase gapping of the scapholunate
ligament as the hand is compressed onto the carpus.
FIGURE 52-4  ■  Slosh pipe for scapholunate ligament instability.
Progression of proprioceptive and strengthening exer-
cises will include isometric training, eccentric training,
isokinetic training and co-activation based on Hagert’s a recent study investigating the accuracy of provocative
principles of conscious neuromuscular rehabilitation.37 tests for diagnosing wrist ligament injuries suggests that
Late-stage rehabilitation should aim to ‘restore the neu- these tests have limited value,36 although when combined
romuscular reflex patterns that exist in a normal joint’ with magnetic resonance imaging, the proportion of
(p. 11) and may include training with a Powerball or correct diagnoses improved by 13%.
slosh pipe (Fig. 52-4). These devices provide an unpre- Depending on the severity of symptoms, patients with
dictable and multidirectional stimulus to the wrist, which ulnar-sided wrist pain may be managed with an ulnar
requires a coordinated unconscious contraction of wrist carpal support attached to a soft wrist splint, which
agonists and antagonists.37 attempts to pronate the subluxed carpus.40 Others find a
‘WristWidget™’ may be sufficient support, especially for
those who find that wearing the brace while weight
Distal Radio-ulnar Joint and
bearing through an extended wrist relieves their pain
Ulnocarpal Complex
(http://www.wristwidget.com/protocol.html). For those
Ulnar-sided wrist pain may occur following a sudden with more persistent symptoms, it may be necessary to
twisting injury to the wrist, with or without a fall. Stabil- support the wrist and forearm in a thermoplastic wrist
ity of the distal radio-ulnar joint relies on both muscular splint until symptoms begin to settle.
and ligamentous restraints. Structures include pronator Patients with ulnar carpal instability should be
quadratus, extensor carpi ulnaris, interosseous membrane instructed in the importance of activity modification, spe-
and the triangular fibrocartilage complex.39 cifically to prevent loading the wrist in ulnar deviation,
Aggravating activities may include tennis or golf; or extension and radial deviation which can place exces-
however, it is not uncommon to develop ulnar-sided wrist sive traction on the ulnocarpal ligaments.41 Exercises
pain following distal radius fracture. Additionally, occu- should aim to improve dynamic neuromuscular stability
pational, degenerative or anatomical factors may contrib- of the TFCC.
ute to ulnar-sided wrist pain. Considering the natural tendency when making a
Provocative tests for the TFCC include the TFCC closed fist is for the carpal bones to supinate, increasing
stress test and the TFCC stress test with compression.36 tension at the TFCC, treatment should concentrate on
Both tests involve ‘placing the wrist in ulnar deviation muscles that result in pronation of the carpus. A recent
while applying a shear force across the ulnar complex of cadaveric study42 concluded that the extensor carpi ulnaris
the wrist’ (p. 249), while the TFCC stress test with com- tendon and its sheath offer dynamic stability for the wrist
pression additionally applies axial compression. However by providing a pronation effect on the distal carpal row.
602 PART IV  Overview of Contemporary Issues in Practice

Further, extensor carpi ulnaris may be considered the opponens splint will be helpful for those with scapho-
only dynamic stabilizer on the ulnar side of the wrist.43 trapezotrapezoidal joint involvement as it supports the
Exercises for neuromuscular control may include iso- wrist, while the short opponens splint should suffice if
kinetic, isometric, eccentric, co-activation and reactive the pain is limited to the carpometacarpal joint. Alterna-
muscle activation exercises.37 tively, the Colditz ‘push’ splint50 or the three-point strap
splint51 may be useful for more specific task performance
activities, including writing, stringed instrument playing
Osteoarthritis and crafts.
The development of osteoarthritis may be considered the While there is no evidence to support the superiority
‘end-stage of a disease that originates in the tissues sup- of one exercise programme over another, there is a
porting the joint’ (p. 278).44 These structures include the general consensus that exercise may improve function,
cartilage, subchondral bone, synovium, ligaments, nerves pain and strength.49,52 Guidelines for the performance of
and peri-articular muscles. Osteoarthritis frequently exercises may be found in a recent narrative review by
affects the small joints of the hand, and while most people Valdes and Heyde.53 They suggest that exercises should
over the age of 55 will have some radiographic changes be pain-free and not lead to an aggravation of pain for
consistent with osteoarthritis,13 the correlation between more than 2 hours after the activity. A retrospective
severity of symptoms and radiographic changes is low.45 review of a dynamic stability approach to the treatment
of this common condition reported a reduction in pain
and disability scores with a combination of splinting, web
Thumb Carpometacarpal Joint
space release, mobilizations to provide distraction and
Pain at the base of the thumb is particularly common in to reduce dorsal subluxation, first dorsal interosseous
postmenopausal women in the fifth to seventh decades of strengthening and taping.54
life.46 It is frequently located either at the palmar surface Anatomical studies have recently identified the pres-
of the trapeziometacarpal joint, or more dorsally, between ence of mechanoreceptors in the dorsal carpometacarpal
the base of the first and second metacarpals. The pain is joint ligaments,55 supporting their proprioceptive role in
most often aggravated by opening jars, writing, turning enhancing joint stability. This has led the author to
taps and sustained grip activities; however, in cases of develop specific exercises for neuromuscular retraining,
more advanced arthritis, it can also result in a constant particularly concentrating on activities that address insta-
dull aching pain. Radiographs may reveal joint space nar- bility. These exercises include improving the patient’s
rowing, sclerosis, articular debris and joint subluxation.47 awareness and control of the alignment of their thumb
Severe (stage IV) joint degeneration will be associated while tracing along the line of a tennis ball with the tip
with scaphotrapezotrapezoidal joint involvement and of the thumb. It may be necessary to wear the small three-
these patients will often complain of wrist pain along with point strap splint51 to prevent hyperextension of the
pain at the base of the thumb. Careful palpation of the metacarpophalangeal joint if they are unable to control
scaphotrapezotrapezoidal joint and trapezium, just distal this themselves (Fig. 52-5). Similarly, they may practice
to the scaphoid, will assist in determining the source of tearing sheets of paper while ‘maintaining the thumb
symptoms.48 Further, axial compression and rotation of joints in an ideal arc’,56 incorporate use of chopsticks to
the first metacarpal on a stabilized trapezium (the grind improve joint position sense and neuromuscular control,
test) is a recommended manoeuvre8 for reproducing pain or enhance stability by rotating a credit card in exercise
and crepitus at the joint.48 putty.
A variety of splinting options are available for patients The specific intervention that is appropriate for
with pain at the base of the thumb; however, there is no any given patient will depend on the severity of the
evidence to support the superiority of one over another.49 patient’s symptoms at the time, and their response to
In general, a more flexible neoprene style splint is appro- treatment provided. Failure of symptom relief with such
priate for those with mild symptoms, and the rigid ther- conservative interventions may lead the therapist to con-
moplastic style splint is useful for those with more severe sider whether graded motor imagery could be useful
pain that limits most activities of daily living. The long for chronic pain, as recent research has suggested

A B

FIGURE 52-5  ■  Trace line on tennis ball for proprioceptive training (A), but consider using three-point splint to control metacarpo-
phalangeal joint alignment if necessary (B).
 52  Wrist/Hand 603

sensitization mechanisms may contribute to symptoms in prevent return of symptoms. Referral to a hand surgeon
this population.57 Surgery may be an appropriate inter- should be considered following failure of conservative
vention for ongoing debilitating pain and limitation of intervention over a 6- to 12-week period, or the presence
function. of bilateral symptoms. Other options include a cortico-
steroid injection or surgical release of the first dorsal
compartment for more persistent and severe cases.
Soft Tissue Conditions
Carpal Tunnel Syndrome Trigger Finger
Carpal tunnel syndrome is the most common neuropa- Trigger finger is more common in women in the fifth to
thy,58 affecting 3.8% of the population. Personal risk sixth decades of life64 and most commonly affects the
factors include being female, increased basal metabolic thumb, middle and ring fingers in otherwise healthy indi-
rate and age, while workplace risk factors included high viduals. The onset of triggering may be insidious, yet it
job strain.59 Patients usually present with nocturnal pins has also been associated with direct trauma, de Quervain’s
and needles and numbness in the median nerve distribu- disease, diabetes mellitus and osteoarthritis.65
tion. Various tests may be used to assess for carpal tunnel Patients report a triggering or snapping sensation
syndrome, including Phalen’s test, the hand elevation when they attempt to straighten their fingers from a full
test, Hoffman-Tinel’s sign, the carpal compression test fist, but in more severe cases, find they are unable to
and the tourniquet test.10 An electrodiagnostic study of straighten their finger without assistance from their other
the median nerve may be considered the reference stan- hand. Most cases are due to thickening of the digit’s
dard and is useful to exclude other diagnoses and stage annular (A1) pulley, restricting the smooth glide of the
the severity of carpal tunnel syndrome.60 flexor tendon through the fibro-osseous tunnel, and
Treatment approaches include nocturnal splinting resulting in a nodule forming on the tendon sheath. This
with the wrist in neutral, and while it may be necessary nodule moves proximally during flexion, but gets caught
to continue this for 6 weeks, it is likely that night splint- at the A1 pulley on extension.
ing will provide immediate relief. Additionally, nerve and Conservative management involves splinting the digit
tendon gliding,61 and median nerve sliding exercises58 are to prevent the friction of the tendon gliding through the
considered helpful, as is education regarding aggravating A1 pulley. A small metacarpophalangeal joint blocking
postural factors. Constant tingling and numbness in the splint that permits IP joint flexion may be sufficient;
median nerve distribution, wasting of abductor pollicis however, if this small splint does not prevent clicking or
brevis or failure of symptom relief with conservative mea- locking with movement, a dorsal finger splint that immo-
sures will necessitate surgical review for consideration of bilizes the proximal interphalangeal and distal interpha-
decompression. langeal joints may be required. Failure of a 6-week trial
of splinting may indicate the need for a corticosteroid
injection, which is considered effective and safe in the
De Quervain’s Disease
management of trigger finger.66 Those who fail to achieve
De Quervain’s disease is the result of thickening of the long-lasting relief with either splinting or a repeat steroid
first extensor tendon sheath, and is considered the result injection may require surgical release.
of intrinsic degenerative mechanisms.62 It is common in
young mothers and home renovators who perform
repeated unaccustomed activities requiring sustained
Complex Regional Pain Syndrome
pinch or grasp with radio-ulnar deviation. The diagnosis Complex regional pain syndrome type 1 describes a
of de Quervain’s disease is made by history and physical population of patients who have incapacitating pain and
examination. Symptoms include pain over the radial impairment in function without an identifiable peripheral
styloid, with tenderness and swelling of the first extensor nerve injury. The resulting pain is often disproportionate
compartment and reproduction of pain with resisted to the severity of the injury and is associated with
thumb extension or the Finkelstein’s manoeuvre.63 The abnormal sensory, motor, sudomotor, vasomotor and/
Finkelstein’s manoeuvre will reproduce pain at the radial or trophic changes.67 Emerging approaches to treatment
styloid in affected people and involves the patient making include graded motor imagery,68 incorporating left /right
a fist over a flexed thumb, and then moving the wrist into judgements, imagined movements and mirror therapy.
ulnar deviation. Other approaches include sensorimotor retraining,69
Conservative intervention includes splinting in a functional active exercises and neuroscience education.70
custom-made thermoplastic splint, which immobilizes A recent systematic review of neuroscience education
the wrist and thumb but allows interphalangeal joint has found positive effects on pain perception, disability
motion, education regarding avoidance of aggravating and catastrophization, and may give patients the con-
activities and postures, and tendon and nerve glides. fidence to move without anxiety about causing further
Gradual improvement in symptoms over a 4- to 6-week tissue injury.70
period of conservative intervention should be expected,
and may lead the therapist to wean the patient into a
flexible neoprene thumb and wrist support and progress REFERENCES
into a neuromuscular rehabilitation programme. It is 1. Refshauge K, Latimer J, Maher C. The History. In: Refshauge K,
essential that activity modifications are maintained to Gass E, editors. Musculoskeletal Physiotherapy. Clinical Science
604 PART IV  Overview of Contemporary Issues in Practice

and Evidence-Based Practice. 2nd ed. Butterworth Heinemann; intervention for closed mallet fingers: a randomized clinical trial.
2004. p. 117–63. J Hand Ther 2013;26(3):191–201.
2. Skirven T, Osterman AL, Fedorczyk J, et al. Sensibility Assessment 30. Pratt A, Burr N, Grobbelaar AO. A prospective review of open
for Nerve Lesions-in-Continuity and Nerve Lacerations. 6th ed. central slip laceration repair and rehabilitation. J Hand Surg [Am]
Philadelphia, PA: Elsevier Mosby; 2011. 2002;27B(6):530–4.
3. Bohannon R. Testing isometric limb muscle strength with dyna- 31. Palastanga N, Field D, Soames R. Anatomy and Human Move-
mometers. Crit Rev Phys Rehabil Med 1990;2:75–86. ment: Structure and Function. 5th ed. Butterworth Heinemann
4. Herzberg G. Muscle Testing. In: Refshauge K, Gass E, editors. Elsevier; 2006.
Musculoskeletal Physiotherapy. Clinical Science and Evidence- 32. Laporte J, Berrettoni B, Seitz W, et al. The figure-of-eight splint
Based Practice. Butterworth Heinemann; 2004. for prominal interphalangeal joint volar plate injuries. Orthop Rev
5. Fess E. Grip Strength. 2nd ed. Chicago: American Society of Hand 1992;21(4):457–62.
Therapists; 1992. p. 41–5. 33. Ritting A, Baldwin P, Rodner C. Ulnar collateral ligament injury
6. Codham F, Lewis J, Lee H. The reliability of one vs. three grip of the thumb metacarpophalangeal joint. Clin J Sport Med 2010;
trials in symptomatic and asymptomatic subjects. J Hand Ther 20(2):106–12.
2006;19(3):318–26. 34. Samora J, Harris J, Greiesser M, et al. Outcomes after injury to the
7. Hislop H, Avers D, Brown M. Daniels and Worthingham’s Muscle thumb ulnar collateral ligament – a systematic review. Clin J Sport
Testing. Techniques of Manual Examination and Performance Med 2013;23(4):247–54.
Testing. 9th ed. St Louis, Missouri: Elsevier Saunders; 2014. 35. Fujiwara H, Oda R, Kubo T. Re-evaluation of stress radiographic
8. Valdes K, LaStayo P. The value of provocative tests for the findings for preoperative diagnosis of Stener lesion. J Hand Surg
wrist and elbow: a literature review. J Hand Ther 2013;26(1):32–42, 2013;38(8):906–7.
quiz 43. 36. Prosser R, Harvey L, LaStayo P, et al. Provocative wrist tests and
9. MacDermid JC, Wessel J. Clinical diagnosis of carpal tunnel syn- MRI are of limited diagnositc value for suspected wrist ligament
drome: a systematic review. J Hand Ther 2004;17(2):309–19. injuries: a cross-sectional study. J Physiother 2011;57(4):247–52.
10. Amirfeyz R, Clark D, Parsons B, et al. Clinical tests for carpal 37. Hagert E. Proprioception of the wrist joint: a review of current
tunnel syndrome in contemporary practice. Arch Orthop Trauma concepts and possible implications on the rehabilitation of the
Surg 2010;131(4):471–4. wrist. J Hand Ther 2010;23:2–17.
11. Watson H, Ashmead D, Makhlouf V. Examination of the scaphoid. 38. Moritomo H, Apergis EP, Herzberg G, et al. IFSSH Committee
J Hand Surg 1988;13:657–60. Report of Wrist Biomechanics Committee: biomechanics of the
12. Kroonen LT. Cubital tunnel syndrome. Orthop Clin North Am so-called dart-throwing motion of the wrist. J Hand Surg 2007;
2012;43(4):475–86. 32(9):1447–52.
13. Dahaghin S, Bierma-Zeinstra S, Ginai AZ, et al. Prevalence and 39. Hagert E, Chim H, Moran SL. Anatomy of the distal radioulnar
pattern of radiographic hand osteoarthritis and association with joint and ulnocarpal complex. In: Greenberg JA, editor. American
pain and disability (the Rotterdam study). Ann Rheum Dis Society for Surgery of the Hand. 2013. p. 11–21.
2005;64(5):682–7. 40. Prosser R. Conservative management of ulnar carpal instability.
14. Oetgen ME, Dodds SD. Non-operative treatment of com­ Aust J Physiother 1995;41(1):41–6.
mon finger injuries. Curr Rev Musculoskelet Med 2007;1(2): 41. Moritomo H, Murase T, Arimitsu S, et al. Change in length of the
97–102. ulnocarpal ligaments during radiocarpal motion: possible impact on
15. Wilton J. Hand Splinting. Principles of design and fabrication. Bath triangular fibrocartilage complex foveal tears. J Hand Surg [Am]
Press, Avon: WB Saunders Company Ltd; 1997. 2008;33(8):1278–86.
16. Putnam M. Posttraumatic stiffness in the hand. Clin Orthop Relat 42. Salva-Coll G, Garcia-Elias M, Leon-Lopez M, et al. Role of the
Res 1996;327:182–90. extensor carpi ulnaris and its sheath on dynamic carpal stability.
17. Airaksinen OV, Kyrklund N, Latvala K, et al. Efficacy of cold gel J Hand Surg 2011;37:544–8.
for soft tissue injuries: a prospective randomized double-blinded 43. Leon-Lopez M, Salva-Coll G, Garcia-Elias M, et al. Role of the
trial. Am J Sports Med 2003;31(5):680–4. extensor carpi ulnaris in the stabilization of the lunotriquetral joint.
18. Wehbe MA. Tendon gliding exercises. Am J Occup Ther An experimental study. J Hand Ther 2013;26(4):312–17.
1987;41(3):164–7. 44. Hagert ELJ, Ladd A. Innervation patterns of thumb trapeziometa-
19. Glasgow C, Tooth LR, Fleming J, et al. Dynamic splinting for the carpal joint ligaments. J Hand Surg 2012;37A:706–14.
stiff hand after trauma: predictors of contracture resolution. J Hand 45. Zhang W, Doherty M, Leeb BF, et al. EULAR evidence based
Ther 2011;24(3):195–206. recommendations for the management of hand osteoarthritis:
20. Prosser R. The Wrist. In: Prosser R, Conolly WB, editors. Reha- Report of a Task Force of the EULAR Standing Committee for
bilitation of the Hand and Upper Limb. Butterworth Heinemann; International Clinical Studies Including Therapeutics (ESCISIT).
2003. p. 109–75. Ann Rheum Dis 2007;66(3):377–88.
21. Hove L. Epidemiology of scaphoid fractures in Bergen, Norway. 46. Swigart C, Eaton R, Glickel S, et al. Splinting in the treatment of
Scandinavian. Scand J Plast Reconstr Surg Hand Surg 1999;33(4): arthritis of the first carpometacarpal joint. J Hand Surg [Am] 1999;
423–6. 24A:86–91.
22. Baldassarre R, Huges T. Investigating suspected scaphoid fracture. 47. Eaton R, Glickel S. Trapeziometacarpal osteroarthritis. Staging as
Br Med J 2013;346:1370. a rationale for treatment. Hand Clin 1987;3(4):455–71.
23. Geissler W, Adams J, Bindra R, et al. Scaphoid fractures: what’s 48. Skirven T. Clinical examination of the wrist. J Hand Ther 1996;
hot, what’s not. Instr Course Lect 2012;61:71–84. 9(2):96–107.
24. Alshryda S, Shah A, Odak S, et al. Acute fractures of the scaphoid 49. Wajon A, Ada L. No difference between two splint and exercise
bone: systematic review and meta-analysis. Surgeon 2012;10(4): regimens for people with osteoarthritis of the thumb: a randomised
218–29. controlled trial. Aust J Physiother 2005;51:245–9.
25. Doornberg J, Buijze G, Ham S, et al. Nonoperative treatment for 50. Colditz J. The biomechanics of a thumb carpometacarpal immo-
acute scaphoid fractures: a systematic review and meta-analysis of bilisation splint. J Hand Ther 2000;13(3):228–35.
randomized controlled trials. J Trauma 2011;71(4):1073–81. 51. Wajon A. The thumb strap splint for dynamic instability of the
26. Buijze G, Doornberg J, Ham S, et al. Surgical compared with trapeziometacarpal joint. J Hand Ther 2000;13(3):236–7.
conservative treatment for acute nondisplaced or minimally dis- 52. Davenport BJ, Jansen V, Yeandle N. Pilot randomized controlled
placed scaphoid fractures. J Bone Joint Surg 2010;92:1534–44. trial comparing specific dynamic stability exercises with general
27. Meyer C, Chang J, Stern P, et al. Complications of distal radial and exercises for thumb carpometacarpal joint osteoarthritis. Hand
scphoid fracture treatment. J Bone Joint Surg 2013;95A(16): Therapy 2012;17(3):60–7.
1518–26. 53. Valdes K, Von der Heyde R. An exercise program for carpometa-
28. Meermans G, Verstreken F. Influence of screw design, sex, and carpal osteoarthritis based on biomechanical principles. J Hand
approach in scaphoid fracture fixation. Clin Orthop Relat Res Ther 2012;25:251–63.
2012;470(6):1673–81. 54. O’Brien VH, Giveans MR. Effects of a dynamic stability approach
29. Tocco S, Boccolari P, Landi A, et al. Effectiveness of cast immobi- in conservative intervention of the carpometacarpal joint of the
lization in comparison to the gold-standard self-removal orthotic thumb: a retrospective study. J Hand Ther 2013;26(1):44–52.
 52  Wrist/Hand 605

55. Hagert E, Mobargha N. The role of proprioception in osteoarthri- clinical diagnosis and management. Musculoskeletal Care 2008;
tis of the hand and wrist. Curr Rheumatol Rev 2012;8:278–84. 6(3):168–80.
56. Colditz JC. Dynamic loading posture of the thumb: the Colditz 64. Makkouk AH, Oetgen ME, Swigart CR, et al. Trigger finger: etiol-
tear test. J Hand Ther 2013;26(4):360–2. ogy, evaluation, and treatment. Curr Rev Musculoskelet Med
57. Chiarotto A, Fernandez-de-Las-Penas C, Castaldo M, et al. Bilat- 2007;1(2):92–6.
eral pressure pain hypersensitivity over the hand as potential sign 65. Nimigan A, Ross D, Gan B. Steroid injections in the management
of sensitization mechanisms in individuals with thumb carpometa- of trigger fingers. Am J Phys Med Rehabil 2006;85(1):36–43.
carpal osteoarthritis. Pain Med 2013;14(10):1585–92. 66. Peters-Veluthamaningal C, van der Windt D, Winters D, et al.
58. Coppieters MW, Alshami AM. Longitudinal excursion and strain Corticosteroid injection for de Quervain’s tenosynovitis. Cochrane
in the median nerve during novel nerve gliding exercises for carpal Database Syst Rev 2009;(3):1–19.
tunnel syndrome. J Orthop Res 2007;25(7):972–80. 67. Harden RN, Bruehl S, Stanton-Hicks M, et al. Proposed new diag-
59. Harris-Adamson C, Eisen EA, Dale AM, et al. Personal and work- nostic criteria for complex regional pain syndrome. Pain Med
place psychosocial risk factors for carpal tunnel syndrome: a pooled 2007;8(4):326–31.
study cohort. Occup Environ Med 2013;70:529–37. 68. Moseley GL. Graded motor imagery is effective for long-standing
60. Boland RA, Kiernan MC. Assessing the accuracy of a combination complex regional pain syndrome: a randomised controlled trial.
of clinical tests for identifying carpal tunnel syndrome. J Clin Pain 2004;108(1–2):192–8.
Neurosci 2009;16(7):929–33. 69. Flor H, Diers M. Sensorimotor training and cortical reorganiza-
61. Rozmaryn LM, Dovelle S, Rothman ER, et al. Nerve and tendon tion. NeuroRehabilitation 2009;25:19–27.
gliding exercises and the conservative management of carpal tunnel 70. Louw A, Diener I, Butler DS, et al. The effect of neuroscience
syndrome. J Hand Ther 1998;11(3):171–9. education on pain, disability, anxiety, and stress in chronic
62. Clarke M, Lyall H, Grant J, et al. The histopathology of de musculoskeletal pain. Arch Phys Med Rehabil 2011;92(12):
Quervain’s disease. J Hand Surg [Am] 1998;23(6):732–4. 2041–56.
63. Batteson R, Hammond A, Burke F, et al. The de Quervain’s
screening tool: validity and reliability of a measure to support
This page intentionally left blank
 PA RT V

FUTURE DIRECTIONS

607
This page intentionally left blank
 CHAPTER 53 

Future Directions in
Research and Practice
Gwendolen Jull  •  Ann Moore  •  Deborah Falla  • 
Jeremy Lewis  •  Christopher McCarthy  •  Michele Sterling

For much of the 20th century, musculoskeletal conditions contributing to high-quality musculoskeletal research
were not the pre-eminent concern of Western govern- that is being used to address these issues and inform
ments or health-funding bodies nor were they a funding health-care policy. The work presented in this text is
priority area for health-care research. This is understand- testament to some of the research currently being under-
able as other diseases such as diphtheria, chicken pox, taken internationally. However, there is still a significant
small pox, measles, tuberculosis, pertussis, pneumococcal amount of work to be completed across the spectrum of
disease, polio, tetanus, thyroid and others were of far health-care provision (primary, secondary and tertiary
more concern. We now live in a very different world. rehabilitation) to provide more effective management
Vaccines have controlled many of the diseases of the early and treatments for musculoskeletal conditions.
part of the century. Life expectancy in the United States Physiotherapists working with other health-care col-
at the beginning of the 20th century was 47 years and by leagues need to develop innovative ways to prevent mus-
the end was approaching 78 years. The impact of mus- culoskeletal disease to reduce the burden and detriment
culoskeletal disorders grew. of musculoskeletal disease experienced by individuals and
The magnitude of the problem of musculoskeletal society, with primary prevention being the ideal. Physio-
conditions was effectively brought to prominence, and therapists in clinical, community, work, sport, education
the World Health Organization (WHO) established the or research environments are well placed to contribute
Bone and Joint Decade 2000–2010 which, notably, has to population health initiatives such as promoting active
been extended for another decade (Bone and Joint Decade lifestyles to optimize musculoskeletal health at all stages
2010–2020). As one outcome of this worldwide initiative, of life. However, there are still substantial gaps in our
the Global Burden of Disease study confirmed the knowledge regarding both the optimal and valid methods
immense burden associated with musculoskeletal condi- of physical screening towards primary prevention of
tions across all developed and developing countries.1 injury or overuse syndromes for a range of individuals,
Such evidence as well as WHO initiatives has drawn from those trying to maintain the desired fitness level and
attention to musculoskeletal disorders internationally, healthy lifestyle to those involved in competitive sport.
generated momentum in research and is changing health Likewise conclusive knowledge as to what constitutes the
attitudes and policies. Musculoskeletal disorders are a safest and the most effective means of staying active and
major cause of pain, physical disability and attendant promoting musculotendinous health across all ages and
distress. Frequently they have a profound and detrimen- co-morbidities without detrimentally impacting on these
tal impact on an individual’s quality of life. They are a tissues remains elusive.
major reason for health-related work absence and as such, Physiotherapists have a large stake in secondary pre-
have a substantial detrimental impact on countries’ econ- vention of painful musculoskeletal disorders and much
omies, both in terms of lost productivity and the percent- laboratory and clinical research has already been under-
age of gross domestic product spent on managing these taken into the neurosciences, pathokinesiology and
conditions. Musculoskeletal conditions are rarely a direct pathophysiology towards development of optimal man-
cause of death, but as exercise is considered to be essential agement methods. Knowledge has grown enormously
in the treatment of common illnesses such as obesity, and therapeutics have improved. However, the results
diabetes, cancer, depression, anxiety and stress and car- from randomized controlled trials reveal that the effect
diorespiratory disease, the lack of mobility associated sizes of most treatments are, at best, modest for most
with musculoskeletal pathology will directly contribute conditions. The heterogeneity of patient presentations
to the morbidity and mortality associated with these dis- within a diagnostic category (e.g. subacute low back pain,
eases. With an ageing and more sedentary population the shoulder impingement syndrome) is held to contribute
impact of these problems experienced by the individual to these poor to modest mean group outcomes when all
will increase exponentially. individuals are managed with the same treatment regimen.
Physiotherapists with their body of knowledge, clini- It is now well known that the relative contribution of
cal and research expertise are perfectly placed to rise to sensory, motor, psychological and social mechanisms in a
the challenges and make a significant contribution to patient’s pain condition will vary considerably between
enhancing the prevention and management of musculo- individuals, and different mechanisms will have different
skeletal disorders. Many have already done so by weighting at any point in time. This heterogeneity has
609
610 PART V  Future Directions

spurred interest into concepts of subgrouping and, over are understood, recognized and articulated in order for
the last decade, creation of clinical prediction rules to try self-management programmes to be more effectively
to best fit the intervention to the patient. The notion that utilized and tailored to particular needs. There are many
one treatment fits all sizes has been dispelled. However, ‘topics’ within education but it still remains to be deter-
it could be questioned if we are yet even aware of all of mined what is the most effective education/advice that
the criteria on which individuals should be characterized individuals require for certain conditions or circum-
towards prescribing a particular intervention. More stances and which produce best outcomes, especially in
research is required across the spectrum ‘from bench top terms of enhanced quality of life. Likewise, there is a
to bedside’. More knowledge is required about, for range of face-to-face and electronic channels to deliver
example, the role of genetics and an individual’s biologi- education at a group or individual basis, but the best
cal make-up with respect to propensity for musculoskel- ways and the best times to deliver this intervention for
etal disorders and chronic pain; how biological and education or self-management strategies to have the
psychosocial features interrelate and how they might greatest impact has not yet been established. It is like-
moderate or mediate a painful musculoskeletal disorder. wise not known which models of care best slow mus-
In persistent spinal pain, there has been somewhat of a culoskeletal disease progression, but it is anticipated that
dismissal of the presence of ongoing peripheral sources it will be a multimodal model, for example, education,
of nociception. Yet, for instance, in the case of chronic exercise, various aides/supports and pharmacological
whiplash-associated disorders, this position is proving to interventions. How delivery affects models of care needs
be inaccurate. Nevertheless further research is necessary to be questioned. For example, will extended personal
to understand the role that peripheral sources of nocicep- contact with patients with chronic musculoskeletal dis-
tion play in a patient’s pain, disability and psychological orders decrease distress and increase their compliance
distress. This is becoming more feasible with advanced with activity and exercise. Benefits of this low-cost
imaging and diagnostic techniques continuing to develop. approach to-long-term care have been shown with other
Physiotherapy management is not the panacea for all chronic diseases, but is yet to be proven with muscu-
musculoskeletal ills and more clarity is required to clearly loskeletal disorders.
understand which sensory, movement, neuromuscular Research may inform new directions in management,
and sensorimotor features are able to be modified by but ensuring that the evidence translates to a change in
physiotherapy management strategies and what features practice is a challenge faced by all professionals. It
may mitigate against a successful outcome from these behoves institutions training future generations of phys-
treatment approaches. iotherapists to design and deliver contemporary curricula
There has been a tendency to regard each episode of and ensure that their graduates are intelligent consumers
musculoskeletal pain as a new acute episode. What has of research and well skilled in communication, educa-
become clear is that musculoskeletal disorders and espe- tional approaches and research-informed therapeutics.
cially spinal pain are usually recurrent in nature over Knowledge is being generated at a rapid pace. As well as
several decades of an individual’s life, if not a lifetime. research to generate knowledge, research is also required
Similarly, it is well recognized that when a joint such as to determine the best methods of delivery of continuing
the knee is subjected to significant trauma, the arthritic professional development for practicing clinicians to
process may be initiated prematurely. Thus it is consid- ensure this knowledge is translated into practice, and
ered a necessary step to view musculoskeletal disorders as results in changes in practice behaviour and improved
likely recurrent and progressive disorders, not as repeti- patients outcomes. Continuing professional development
tions of an acute episode, if effective rehabilitation pro- for physiotherapists has some unique challenges espe-
grammes are to be designed. Thus an important focus for cially regarding expert physical skill acquisition to imple-
future rehabilitation practices and research is the preven- ment new assessment or management practices.
tion of recurrence or transition to chronicity and, with This fourth edition of Grieve’s Modern Musculoskeletal
our ageing population, effective methods to slow disease Physiotherapy is evidence of a vibrant research and clinical
progression. This opens questions such as what can phys- culture in the field of musculoskeletal disorders interna-
ical interventions achieve against certain disease markers, tionally. There is no doubt that mechanistic and clinical
what ‘dosages’ of exercise are required to achieve the research have progressed the field substantially in the last
required change in neuromuscular control, will the train- decade. The aim for the next decade of research is to
ing produce permanent change, or does the brain have to build on this knowledge and further refine practices so
be constantly tuned with a maintenance programme? that the outcome is a notable reduction in the burden of
Tertiary prevention is a vital area to optimize an musculoskeletal disease across all developed and develop-
individual’s quality of life and lower the personal and ing countries.
financial burden of persistent or progressive musculo-
skeletal disorders in our ageing populations. The areas
of education, self-management programmes and main-
REFERENCE
tenance care become important strategies to refine and
optimize their effect. More attention needs to be given 1. Lim SS, Vos T, Flaxman AD, et al. A comparative risk assessment
of burden of disease and injury attributable to 67 risk factors and
to patient perspectives through qualitative research. For risk factor clusters in 21 regions, 1990–2010: a systematic analysis
example, there is a need to ensure that differences in for the Global Burden of Disease Study 2010. Lancet 2012;
therapists’ and patients’ perspectives of self-management 380(9859):2224–60.
 Index

A Acute traumatic injuries, of bone and Anti-pronation foot taping, 532, 532f
Aα fibres, 78, 79t ligaments, 587–590 Anxiety, 329
Aβ fibres, 78 Adaptations, in sensorimotor dysfunction, pain and, 411
Aδ fibres, 8–9, 78, 79t 56–59, 57f–61f Aponeurotic fibres, 98
information, 418 long-term consequences of, 59–62 Apophyseal joints, 102, 102f
A-mode (amplitude mode) ultrasound, 145t Adaptive care, 244 Apoptosis, theory of ageing, 127t
Abdominal muscles, lumbar spine and, 104 Adductor squeeze test, 390t–391t Arterial occlusion, dynamic upper limb, 350b
Absolute risk (AR), 259 Adenosine diphosphate (ADP), 68 Arthralgia, 435
Acceleration injury, 522 Adhesive capsulitis, 577–578 Arthrogenic muscle inhibition (AMI), 524
Accessory arthrokinematic motion, 474 Adopted patterns, of activity, 58–59 Arthrogenic temporomandibular disorders,
Accountability, in advanced practice roles, ADP. see Adenosine diphosphate (ADP) 435
401 Adult learning, 255 arthralgia in, 435
Accuracy, good-quality data, 228 Advice/brief education, 266 disc displacements in, 435
Acetabular labral pathology, 507 Afferent feedback, 44–45 hypermobility and dislocation in, 435
Acetabular labrum, 506 Age, physical work capacity and, 379 Arthrographic hydro-distension, for frozen
Achilles tendinopathy, 114 Ageing shoulder contraction syndrome, 580
Achilles tendon, 106 influences on intervertebral disc associated Articular cartilage, 507–508
Actin, 68 with, 129f Articular dysfunction, 461b
Action possibilities, generation of, 33, 33f of musculoskeletal system, 126–128 Assessment
Action potential osteoarthritis and, 127t guide for therapeutic exercise, 298–300
decomposing of, 23 spine, 128–133, 129f of motor control, 299
propagation of, 22–24, 23f–24f theories of, 127t of movement quality, in exercise, 299
Activation signals, 24, 174 Akt/mTOR signalling pathway, 71, 72f of muscle fatigue, 300
Active exercise therapy, for rotator cuff Alar ligaments, 94, 95f of muscle structure, 299–300
tendinopathy and subacromial integrity of, tests for, 354 of strength parameters, 300
impingement (pain) syndrome, 564–565 Amperes, 19–20 Atlanto-axial joint (A-A joint), 93, 93f
Active motion, in shoulder assessment, 559, Amplitude synovial folds in, 94
559t EMG, 171 Atlanto-occipital joint (A-O joint), 93
Active motor threshold, 180 motor evoked potential, 180–181 synovial folds in, 94
Active proprioception, 31–32 Amygdala, 162 Auditing, 227–231
Active straight leg raise (ASLR) test, 502 pain and, 11–12, 11f Autonomic nervous system, pain and,
Active transporters, 22 Anabolism, muscle, 71, 72f 14–16
Actuator system, 44f Analgesia, exercise-induced endogenous, 11 Autonomy, in advanced practice roles,
Acupuncture, 336–338 Angiogenesis, in endurance training, 74 401
adequacy of, 337 Ankle, 547–556 Axial rotation, 93
applications of, 337 Ankle dorsiflexion lunge test, 390t–391t Axioscapula muscle control, thoracic
clinical efficacy of, 337 Ankle fracture, diagnosis of, 548 musculoskeletal pain and, 448–449
dose of, 337 Ankle injuries, 547 Axio-scapular muscle, RC muscles
effects of, 337–338 diagnosis of, 548–551 implications for, 564
evolution of, 338 epidemiology of, 547 Axonal transport, 82
for frozen shoulder contraction syndrome, impairments and, 551 mild nerve compression in, 86–87
579 management of, 551–552
for knee osteoarthritis, 543 prognosis of, 547–548
for musculoskeletal pain, 337–338 risk factors of, 548 B
physiological effects of, 336–337 Ankle sprain B-mode (brightness mode) ultrasound,
Acute ankle sprains, epidemiology of, 547 diagnosis of, 548–549 145t
Acute back pain, development of, 189f management of, 551–552 speckle tracking, 148–149, 149f
Acute knee injuries, 522–527 prevention of, 552 motion, 148–149
common, 522 Annulus fibrosus, 98, 102–103, 103f Back muscles, of lumbar spine, 104
nature of loads in, 522–523, 523f Antagonistic pleiotropy, theory of ageing, Back pain, 189
neuromuscular control development in, 127t acute, development of, 189f
524–525, 526f Anterior cingulate cortex, pain and, 13 Back schools, 265–266
strengthening for, 524 Anterior cruciate ligament (ACL), injury to, Balance, exercises for, 313t
muscle inhibition, 524 522 Balance test, single leg, 390t–391t
strength, power and work capacity Anterior dislocation, management of, Basal ganglia, 34f
development, 524, 525f 570–571 in selection mechanisms, 33–34, 33f–35f
Anterior longitudinal ligament, 97–98, 104 Behaviour
Anterior shear test, 353–354, 353t health, change of
Anterior shoulder instability, 569 5 As and 5 Rs in, 374, 375b
Page numbers followed by ‘f ’ indicate Anterior subluxation, management of, 571 histories of, 374
figures, ‘t’ indicate tables, and ‘b’ indicate Anterolateral muscles, of lumbar spine, 104 interventions for, 371–377
boxes. Anticipation, of pain, 13 motivating patient in, 364
611
612 Index

physiotherapy-directed, 375–377, 375f, C Cervical spine, 190

376t C fibres, 78, 79t application of mechanical diagnosis and
process of, 375f afferent information, inhibition of, 418 therapy in, 463–464
readiness in, 374, 375t C nerve fibres, 8–9 functional anatomy of, 93–101
strategies of, 374 CAD. see Cervical arterial dysfunction intervertebral disc, 98
lifestyle-related health (CAD) intervertebral foramina, 99
assessment of, 365, 366f–367f Calcium (Ca2+), in muscle contraction, 68 ligaments, 97–98
unhealthy, clustering of, 364 Cam lesions, 507, 507f mid to low, 96–99
modification of, 371 x-ray for, 508 spinal nerves, 99
promotion of, change in, 331 Canadian Diabetes Risk Questionnaire vertebral arch, 97
single motor unit, 174–175, 174f (CANRISK), 365, 368f–369f vertebral body, 96–97
Behaviour change CANRISK. see Canadian Diabetes Risk idiopathic neck pain and, 410–422
in implementation research, 234–235 Questionnaire (CANRISK) effectiveness of, 417
theoretical framework for, 237 Capsule, mechanoreceptor stimulation in, localization of, 417
Behavioural graded activity, approaches in, 321t mobilization and manipulation of,
330–331 Capsuloligamentous mechanoreceptors, 416–418
Beighton score, 390t–391t 322 neurophysiological mechanisms of,
Biering-Sorenson test, 390t–391t Carpal tunnel syndrome, 603 417–418
Biology education, of pain, 266 Case-mix adjustment, 208 risks of, 418
Biomechanical model, of spinal musculoskeletal, 208f summary of, 418
manipulation, 278–279 Case series study. see Case study impairments in
inducing cavitation within the joint and, Case study, 221 exercise approach based on, tailored,
278–279 Case-control studies, 221 311–312, 313t–314t
limitations in, 279–280 Cauda equina syndrome (CES), 343–345 local treatment for, tailored, 311
reducing muscle hypertonicity/stiffness, complete (CES-R), 344 overall management approach to,
279 confusion in, 345 310–311
stretching/tearing tissue and, 278 description of, 343–344 recommendations, and progression of
Biomechanics, in knee osteoarthritis, 538 diagnosis of, 344–345 treatment of, 312–313
Biomedical education, 265–266 emerging issues in, 345 reported complaints and, 310, 311f
Biopsychosocial education, 266 important issues in, 344–345 magnetic resonance images of, 154f
Biopsychosocial model, 247, 247b incidence of, 343 model, 191f
Blood circulation, neural, nerve interface of, incomplete (CES-I), 344 and simulation, 190–191
80–82, 81f new advances in, 345 predicted reaction forces between
Blood-nerve interface, 81 sexual dysfunction associated with, 344b vertebrae, 192f
Blood oxygenation level differences symptom progression in, 345 three-dimensional musculoskeletal model,
(BOLD), 157 Causation through analogy, 427t 190–191
Body, configuration of, 28 Cause and effect Cervical zygapophysial joints, 97
Body composition, 120 criteria for, 427t Cervicothoracic pain, in COPD, 456
Body scan relaxation, 329 nature of, 426 CES. see Cauda equina syndrome (CES)
BOLD. see Blood oxygenation level CBT. see Cognitive behavioural therapy Chemical synapses, 25
differences (BOLD) (CBT) Chemicals, in nociceptors, 8
Bone, mineralization, 120 Cell models, of tendinopathy, 113 Chronic ankle instability (CAI), 547
Bone digital model, 138 Cellular level, of ageing, 127t diagnosis of, 550–551
Bone-tendon junction, 113 Cellular Senescence Theory of ageing impairments and, 551
Boutonniere deformity, 599 (1965), 126, 127t management of, 552
Bracing Central nervous system Chronic musculoskeletal conditions,
for ankle sprain, 552 lesions, motor relearning in, 48f, 49–50, management of, 341
for knee osteoarthritis, 541–542 50f Chronic obstructive pulmonary disease,
in pelvic girdle pain, 490–491 peripheral nervous system and, 82 455
Bradford-Hill, Sir Austin, 426 changes in, 87 management of, to improve flexibility,
Brain in tendon pain, 113–114 456–458
network for pain, 161–164 Central neuropathic pain, 9b exercise in, 457–458, 457b, 458f
nociceptive inputs to, 161 Central sensitization, 13–14 manual therapy in, 456–457
training of, 503 in pain, 340–341 symptomatic features of, 456
Brain stem, pain and, 12–13 recognition of, 14b Chronic pain, 328
Brain stimulation, non-invasive, Centralization negative thoughts in, 330
musculoskeletal disorders, 179–186 in physiotherapy examination procedures, states, motor relearning in, 49
Brain-orchestrated pain modulation, 462 Chronic systemic low-grade inflammation,
9–11 in specific exercise classification, 472 120
Breathing Centre of pressure (CoP), 44–45 Chronic valgus overload, 584–585
control, thoracic musculoskeletal pain Cervical arterial dysfunction (CAD), 348 Cigarette smoking, in rotator cuff pathology,
and, 448 clinical presentations related to, in 566
retraining, 329 different stages of pathologies, 348t Cingulate cortex, anterior, pain and, 13
‘Breathing fish’, 440, 440f Cervical facet joint Classic electrodes for surface EMG, 168
Brighton Criteria, 573, 573b nociception from, 424 Clinical decision making, shoulder
Bruxism, 434, 435t radiofrequency neurotomy of, 424, assessment and, 557–558
Building common ground, 251–253, 424f Clinical instability, in motor control
251b whiplash-associated disorders and, training, 483
explaining reasons for treatments and 423–424 Clinical management, models for, 242–249
recommendations, 253 Cervical joint position error, exercises for, Clinical practice, implications for,
making recommendations, 253 311, 313t 194–201
online commentary, 253 Cervical movement sense, exercises for, clinical utility of quantitative sensory
stepwise building of agreement, 251–253, 311–312, 311f, 313t testing in physiotherapy, 199
252b Cervical proprioception, assessment and importance of standardizing protocols,
‘you tell me first’ sequences, 253 treatment of, 310 194–195
Bursitis, tendinopathy and, 113 Cervical rotation, 93 test parameters, 195–198
 Index 613

test site and interpretation of quantitative Contraction Derangement, 461b

sensory testing data, 198–199 muscle, neural control of, 68 Descending modulation, facilitation of, 293
thermal quantitative sensory testing, of the shoulder, 577–578 Descending nociceptive facilitation, 10
197–198 Control parameters, 43 Descending nociceptive inhibition, 10–11
Clinical prediction rules, 244–245 Controlled trial, 222 Descriptive implementation research, 233,
Clinical profiling, 227–231 Coordination and balance training, for 233t
Clinical reasoning. see Reasoning, clinical patellofemoral pain, 530 Descriptive study, 221–222
Closed-loop control systems, 42 Cortical potential, movement-related, 49 Detection threshold
Cochrane Effective Practice and Cortical representation mapping, 179–180 cold, 195t
Organization of Care (EPOC) Review Cortical silent period, 183 mechanical, 195t, 196, 196f
Group, 234 Corticosteroid (CS) injection, for frozen warm, 195t
Cochrane systematic reviews, 214f shoulder contraction syndrome, Diamond design, 215, 215f
Codon restriction, theory of ageing, 127t 579–580 Diffusion weighted imaging (DWI),
Cognitive behavioural therapy (CBT), 371 COSMIN guidelines, 207 156–157
skills and procedures of, relevant to definitions, 203t Direct current stimulation, transcranial, 184
physiotherapy practice, 329–330 Costovertebral joint degeneration, Disability, 263
Cognitive coping skills, 330 zygapophysial and, 131–132 relief from, motor control training for,
Coherence, 427t Cranial neural tissue testing, for 486
Cohort study, 221 temporomandibular disorders, 439 Disc degeneration, 130, 131f, 132
Cold detection threshold, 195t Craniocervical angle, 437 Disc displacement, in temporomandibular
Cold pain threshold, 195t Craniocervical extension, 440, 440f disorder, 435
Collaborative patient education learning Craniocervical flexor, 94–95, 95f with reduction, 435
cycle, 256, 256f Craniocervical instabilities without reduction, 435
Collagen fibrils, in tendon, 107 screening for, 352–354, 353t Disc prolapse, intervertebral, 133
Collagen-tearing models, of tendinopathy, anterior shear test, 353–354, 353t Disease, in neuropathic pain, 9b
113 distraction test, 353t, 354 Dislocation, in temporomandibular
Collateral ligament injury, 600 rotation stress test, 353t, 354 disorders, 435
Collecting outcome measures, practical Sharp-Purser test, 353, 353t Disposable soma, theory of ageing, 127t
issues in, 207–209 side-bending stress test, 353t, 354 Distal radio-ulnar joint, 601–602
decide on timing, 207–208 signs and symptoms of, 352–353, 352t Distal radius fractures, 597–598
set a clear purpose, 207 Craniocervical ligament, integrity of Distraction test, for tectorial membrane,
Colour Doppler, 145t controversies in testing, 354–355 353t, 354
Communication pre-manipulative screening for, 352–356 Distributed processing module (DPM), 35f
asking question, for patients, 251–253 stress tests for, 353t ‘Dog follows boss’, 440, 440f
building common ground, 251–253, Craniocervical muscles, clinical significance ‘Doppler imaging of vibrations’, 150
251b of, 94–96, 95f Dorsal horn neurons, in pain, 14
explaining reasons for treatments and Craniocervical spine Dorsiflexion-external rotation test, 550f
recommendations, 253 movements in, 93–94 Dose-response relationship, 427t
making recommendations, 253 stability of, 94–96 Dosing
online commentary, 253 craniocervical muscles in, 94–96, 95f of exercise, 269
stepwise building of agreement, ligamentous system in, 94, 95f of transcutaneous electrical nerve
251–253, 252b synovial folds in, 94 stimulation, 271
‘you tell me first’ sequences, 253 Cross-body stretch, for posterior shoulder Double-blind controlled trial, 222
in clinical setting, 250–254 tightness, 576 Downward scapular rotation, in shortening
concluding remarks, 253 Cross-over design, 215f, 222 of pectoralis minor, 566
key features of, 251, 251b Cross-sectional studies, 221 DPM. see Distributed processing module
and language, in assessment of pelvic Cryotherapy, for arthrogenic muscle (DPM)
girdle pain, 492, 493t inhibition, 524 Dry needling, 336–338. see also Acupuncture
patient education and, 254–258 Cumberland Ankle Instability Tool, 548, ‘Dynamic’ elastography techniques, 150
patient-focused practice and, 250–254 550–551 Dynamic mechanical, 195t
with patients, 250–261, 250b Current, 19–20 allodynia, 196
risk, 258–261, 261b Current evidence, summary of, 427–428, 428b Dynamic progression, in motor control
tools, 259, 260f Cutaneous sensory fibre, types of, 79t training, 484
Comorbidities, pelvic girdle pain and, 492 Cytokines, spinal manipulation and, 418 Dynamic systems theory, of motor control,
Completeness, good-quality data, 228 43
Complex interventions, 234 Dynamic upper limb arterial occlusion,
development of, theory in, 236 D 350b
Complex regional pain syndrome, 603 Data Dynamic valgus collapse, 522–523, 523f
Compressive loads, in tendinopathy, 113 good-quality, 228 Dysdifferentiation, theory of ageing, 127t
Computerized tomography, of use of, in research, 231
patellofemoral pain, 529 Data collection method, 209
Conductance, 20 De Quervain’s disease, 603 E
Conduction test, for temporomandibular Decision balance analysis, 374 EDs. see Emergency departments (EDs)
disorders, 439 Deconditioning, 467 Education, in knee osteoarthritis, 539
Conduction velocity (CV), 170 Decussate fibres, 98 Educator, 257–258
Connective tissue, neural, innervation of, 80, Deductive-based clinical reasoning models, Elastography, ultrasound imaging,
81f 243, 247b 149–150
Consequences, of sensorimotor adaptations, Deductive reasoning, 243–244, 247b Elbow, 583–594
59–62, 61f Deep cervical flexor, specific training of, clinical interview of, 583–584
Consistency of findings, 427t 415, 416f co-morbidity, 583
Constant current. see Transcranial direct ‘Degenerative joint disease’, 537 functional demands, 583
current stimulation Delphi process, 228–229 history, 583
Contract, learning, 255 Demyelination, due to entrapment outcome measures, 583–584
Contract-relax techniques, for posterior neuropathies, 83–84, 83f symptoms, 583
shoulder tightness, 576 Depression, 329 conservative management of, 587–591,
Contractile dysfunction, 461b pain and, 411 588t–589t
614 Index

acute traumatic injuries of bone and in large and small diameter nerve fibres, Extracellular matrix, tendon, 107
ligaments, 587–590 84, 85f Extracorporeal shock wave therapy, for
instability, 590 pathophysiology of, 82–87 non-calcific RC tendinosis, 566
lateral epicondylalgia, 590 EPAs. see Electrophysical agents (EPAs) Extraneural oedema, reduction of, 292
medial epicondylalgia, 591 Epineurium, 80, 81f Extraneural pressure, reduction of, 292
posterolateral impingement, 591 EQ-5D, used for generic instruments, 204f, Extrapyramidal motor system, 36–37
radial nerve entrapment, 591 205 Eye follow, exercises for, 313t
ulnar neuropathy, 591 Equilibrium Eye-head-body coordination, exercises for,
physical examination of, 584–587 horizontal, 188 312–313
diagnostic imaging, 587, 587f moment, about spinal joint, 188 Eye-head coordination, exercises for, 312,
muscle-tendon function, 585 vertical, 188 313t
nerve function, 585–586, 586t Ergonomics human-technology systems Eye-tragus-horizontal angle, 437, 437f
palpation, 585 model, 381, 381f
range of motion, 584 efficacy of, 382
stability, 584–585, 585t Error catastrophe, theory of ageing, 127t F
strength, 586 Evaluative implementation research, Facet joint capsule, 97
Elbow flexion test, 586t 233–234, 233t Factorial design, 215, 216t
Electrical current, 179f Evidence special fractional, 216, 216t
Electrical potential, 19–20 self-management and, 359–360 Failed load transfer, 496, 499f
Electrical stimulation techniques, 183 sources of, 242–243, 243f, 243t Falling, ageing and, 128
Electrical synapse, 24, 25f Evidence-based practice, 242 Fascia, mechanoreceptor stimulation in, 321t
Electrode systems, of electromyography, Evidence-practice gaps, 232, 235–236 ‘Fascicles’, 68
168, 169f Evolutionary level, of ageing, 127t Fast loop, 28–29, 36
Electrodiagnostic testing, 84 Excessive anterior tilt, in shortening of Fast pain, 8–9
Electromotive force, 19–20 pectoralis minor, 566 Fat pad, mechanoreceptor stimulation in,
Electromyographic bio-feedback, for Exercise(s) 321t
arthrogenic muscle inhibition, 524 basic mechanisms of, 270 Fat separation, 154–155, 156f
Electromyography (EMG), 168 additional, 270 Fatigue, 183
advances in measurement methods, central, 270 muscle, assessment of, 300
168–178 peripheral, 270 myoelectric manifestations of, 170–171
amplitude, 171 for chronic whiplash-associated disorder, Fatigue plot, 170f
applications in, 169–175 429–430 Fear avoidance
amplitude, 171 interventions based on, 430 in mechanical neck pain, 411
distribution of muscle activity, clinical studies of, 269 pain-related disability and, 340–341
172 in descending nociceptive inhibition, 11 FEDS system, 568–569
muscle synergies, 172–174 dosing of, 269 Feedback, in neuromuscular rehabilitation,
myoelectric manifestations of fatigue, for knee osteoarthritis, 539–541, 524–525
170–171 542b Feedback control, 43–44
single motor unit behaviour, 174–175 for neck pain, 413 Feedback loop, 30, 32, 35f
timing of muscle activity, 169 neuromuscular adaptations to, 68–77 Feedforward control, 43–44
tuning curves, 171–172 endurance training, 74–75 Femoroacetabular impingement, 507, 507f,
electrode systems, 168, 169f high-resistance strength training, 514
high-density, 168, 174f 70–74, 70f cam lesion in, 507, 507f
limitations in, 175 hormonal influences to, 73–74 pincer impingement, 507
monitoring change with rehabilitation, overload principle in, 69–70 Fibre composite, 107–108
175 for pain management, 269–270 Fibre-composite theory, 111
single motor unit behaviour, 174–175, for patellofemoral pain, 529–531 Field-expedient screening tests, 390t–391t
174f rehabilitative, 415–416 Financial interventions, 235t
tuning curves, 171–172, 172f–173f with spinal manipulation, 417 Fitted recruitment curve, 181
USI against, 146 therapeutic, 298–309 Flexion compression test, 586t
Electrophysical agents (EPAs), 334–336 assessment to guide for, 298–300 Flexion-extension, abduction-adduction,
effectivity of, 335 clinical prescription of, 298, 299f 141–142
fundamental approaches to, 335 indications for, 298 Flexor digitorum profundus avulsion,
home-based, 334–335 principles of management, 298–301 599
reviews of, 335 selectivity of, 300–301 Flexor tendons, 106, 599
Electrophysiological testing, of elbow, 587 specificity of, 300–301 fMRI. see Functional magnetic resonance
Emergency departments (EDs), advanced timing of, 301 imaging (fMRI)
roles in, 401 variability in response to, 301 FMS. see Functional Movement Screen
End-organ model, 262 for wrist/hand, 597, 598f (FMS)
Endogenous analgesia, exercise-induced, 11 Exercise therapy Focus On Therapeutic Outcomes system,
Endplates, vertebral, 103 definition of, 323 245
Endurance building, for patellofemoral pain, sensorimotor system and, 323, 324f Foot, 547–556
530 Exercise training Foot orthoses
Endurance training, 69–70, 74–75 for ankle sprain, 552 for knee osteoarthritis, 542–543
angiogenesis in, 74 for chronic ankle instability, 552 for patellofemoral pain, 532, 532f
in exercise, 304 Exocytosis, 25 Footwear, for knee osteoarthritis, 542–543
mitochondrial adaptations to, 74 Expectations, of pain, 13 Force, 68–69, 69f
muscle changes in, 75t Experimental evidence, 427t muscle, alteration of, 190f
neural adaptations to, 75 Experimental studies, 221 Force-plate, 141f
substrate utilization in, 74–75 Expertise-based designs, 217f Force progressions, in McKenzie method,
Enthusiastic user, of self-management Extensor tendons, 106 462
website, 360 External forces, measure of, 141, 141f 4D mode ultrasound, 145t
Entrapment neuropathy, 78, 89f External knee adduction moment (KAM), Fractures, of wrist/hand, 597–599
demyelination due to, 83–84, 83f for knee osteoarthritis, 538 Free nerve endings, 78
immune system in, 84–85, 86f–88f Extinction training, long-term pain Free radical, theory of ageing, 127t
ischaemia and, 82–83 memories and, 12b Free-standing postural control, 31
 Index 615

Frozen shoulder contraction syndrome Health assessment of, 508

(FSCS), 577–582 definition of, 118b conservative management of
diagnosis of, 578–579 musculoskeletal, 117–125 advice, 508–510
epidemiology of, 578 nutrition and, 119–120 effectiveness of, 510, 516
injection therapy and physiotherapy for, patient control of, 359 exercise in, 510, 511f–512f
580t Health advocates, physiotherapists as, 364 manual therapy for, 510, 513f
management of, 579–581 Health assessment, 364–365 imaging in, 514–515
natural history of, 578 Health behaviour joint-related, 507–514
Functional activities, retraining of, for change of background of, 507–508
patellofemoral pain, 530–531 5 As and 5 Rs in, 374, 375b chondropathy of the hip, 507–508
Functional anatomy, 93–105 histories of, 374 conservative management of, 508–510
Functional magnetic resonance imaging interventions for, 371–377 controversies in, 514
(fMRI), 157 physiotherapy-directed, 375–377, 375f, femoroacetabular impingement, 507,
Functional movement patterns, screening of, 376t 507f
392 processes required in, 331 future directions of, 514
Functional Movement Screen (FMS), readiness in, 374, 375t imaging in, 508
395–396 strategies for, 374 key clinical diagnostic features of, 508,
Functional Movement Systems, 395, 395f lifestyle-related 509t
‘Functional pathology’, 339 assessment of, 365, 366f–367f medical and surgical management of,
Functional re-education, in motor control unhealthy, clustering of, 364 510–514
training, 484 Health care, screening in, 388–399, 388b red flags in, 508
Health Improvement Card, 371, 372f–373f treatment for, 508–514
Health outcome measure, 202 uncertainties in, 514
G Health promotion, definition of, 118b tendinopathy-related, 514–516
Gain-framing, 259–260 Health risks, lifestyle-related assessment of, 514–515
Gait aids, for knee osteoarthritis, 543 assessment of, 365 background, 514
Gait retraining, for knee osteoarthritis, unhealthy, clustering of, 364 controversies in, 516
543 Health status exercise for, 516, 517f
Galvanism. see Transcranial direct current lifestyle-related health behaviours future directions in, 516
stimulation associated with, 365 gluteal, 515–516
Gamma-aminobutyric acid (GABA), in tools for assessing, 365b key clinical diagnostic features of, 514,
overactive pain neuromatrix, 14 Health-based physiotherapy practice, 117 515t
Gap junction, 24, 25f Heat pain threshold, 195t treatment of, 515–516
‘Gate control theory’, 336–337 Hebbian rule of associativity, 49 uncertainties, 516
Gaze stability, exercises for, 312, 313t Hemispheric regions, 162–164, 163f Horizontal equilibrium, 188
Gene regulation, theory of ageing, 127t Hemodynamics, 347–352 Human brain, musculoskeletal pain in,
Generalized joint hypermobility (GJH), altered, 347 161–167
573 considerations for manual therapists, 349b network, 161–164
German Research Network on Neuropathic Hierarchical theory, of motor control, 42–43 Human functional brain imaging studies,
Pain (DFNS), 195 ‘High’ ankle sprain. see Syndesmosis sprain 162
Glenohumeral joint (GHJ), 568 High-frequency TENS, 271 Humeral head ‘positioning’, 570, 571f
Glenohumeral joint instability, 568–569 High-load resistance training, for β-hydroxyl-β-methylbutyrate, 71
Glide technique, for neuropathic disorders, arthrogenic muscle inhibition, 524 Hyperalgesia, 121–122, 197
289, 291f High-load strength training, 413–414 in neck pain, 410
Global Burden of Disease study, 609 High-resistance strength training, 69–70 Hyperexcitability, of neurons, 85
Global Postural Re-education (GPR®), adaptations to, 70–74, 70f Hypermobility
457 hormonal influences in, 73–74 taping for, 340, 340f
Gluteal tendinopathy, 514–516 muscular, 70–73 in temporomandibular disorders, 435
Gluteals, lumbar spine and, 104 neural, 70 Hyperpolarization, of action potential, 23
Goldman equation, 22 muscle changes in, 75t Hypertrophy, in resistance training, 71
Golgi tendon organ, 323 High-resolution bone digital model, 138–139 Hypoalgesia, spinal manipulation-induced,
Goniometry, 584 Hip 417–418
Good-quality data, 228 articular and muscle control in, 506 Hypomobility, taping for, 340, 340f
Graded exercise approach, 330 bony morphology in, 506 Hypothalamus, 162
Graded exposure, 330–331 passive joint structures in, 506
Grieve’s Modern Musculoskeletal Physiotherapy, chondropathy of, 507–508
610 ligaments of, 506 I
Ground referenced information, for postural musculature of, 506 ICF. see International Classification of
control, 31 stabilizers of, 506 Functioning, Disability and Health
Growth hormone, 73 Hip arthroscopy, 510–514 Idiopathic scoliosis, 132
Guarding behavior, 315–316 Hip lateral rotation test, 480–481 IFOMPT. see International Federation of
Hip muscle control, thoracic musculoskeletal Orthopaedic Manipulative Physical
pain and, 449 Therapists (IFOMPT)
H Hip muscle dysfunction, 533 Iliofemoral ligament, 506
H-reflex, 46 Hip muscle retraining, for patellofemoral Iliolumbar ligaments, 104
Habitual-reflexive (fast) loop, 28–29 pain, 530, 531f Image display, types of, 145f
Hamstring bridge test, single leg, 390t–391t Hip muscle strength test, with HHD, Imaging
Hand therapy, 596–597 390t–391t of ankle injury, 548
Hand-held dynamometer, 596 Hip osteoarthritis (OA), physical human functional brain, studies of,
Head, position of performance measures for, 541t 162
altered, temporomandibular disorders and, Hip-related pain, 506–521 for tendinopathy, 115
437 acetabular labral pathology in, 507 USI against, 146
measurement of, 437, 437f articular and muscle control in, 506 Immobilization, of wrist/hand, 597
Head referenced information, for postural bony morphology in, 506 Immune cells, of nervous system, 82
control, 31 hip musculature in, 506 Immune response, musculoskeletal health,
Headache, acupuncture for, 337 passive joint structures in, 506 120
616 Index

Immune system, in entrapment of lumbar vertebrae, 102–103 role of biomechanics and neuromuscular
neuropathies, 84–85, 86f–88f nerve supply of, 103 factors in, 538
Immunity, musculoskeletal health, 120 Intervertebral disc prolapse, 133 treatment strategies of, 539–543
Immunologic, theory of ageing, 127t Intervertebral foramina, 99 Knee pain, chronic, acupuncture for, 337
Impairments Intervertebral ligaments, 104 Kolb’s classic learning cycle, 256, 256f
ankle and, 551 Interview, motivational, 371–374, 374b Kyphosis, 446, 447f
definition of, 474–475 action plan for, 374b
Implementation interventions, 234 follow-up strategy for, 374b
Implementation research, 232–238 questions for, 374b L
conceptual framework of, 235, 235f Intra-articular inclusions, 97 Labrum, mechanoreceptor stimulation in,
description of, 233 Intramuscular EMG, 175 321t
interventions of signals, 168 Lactate, accumulation of, 74
for clinical practice, 234, 235t Intraneural inflammation, 84–85 Laminae, 97
for increase of, 234–236 Intraneural oedema, evacuation of, 292 Large diameter nerve fibres, entrapment
process of, 232 Inverse dynamics neuropathies in, 84
theory used in, 236–237 basics of musculoskeletal modelling based Lateral epicondylalgia, 583, 590
types of, 233–234, 233t on, 187–189 Lateral instability, of elbow, 584
descriptive, 233 process of finding forces from motions, Lateral nucleus, ventroposterior, 162
evaluative, 233–234 188f–189f Lateral passive support, of patellofemoral
methodological, 234 Inversion sprain, diagnosis of, 548–549 joint, 528
Inactivity, deleterious effects of, 121 Ischaemia, entrapment neuropathies and, Lateral wedge insoles, for knee
Inductive reasoning, 243–244 82–83 osteoarthritis, 542
Inferior articular processes, 97 Isthmic spondylolisthesis, 461b Latissimus dorsi, lumbar spine and, 104
Inflammation Learning agreement, for patient education,
knee osteoarthritis and, 537 255, 256t
neurogenic, 85–86 J Leg balance test, single, 390t–391t
nociceptors and, 8 Job Requirements and Physical Demands Leg hamstring bridge test, single, 390t–391t
in tendinopathy, 113 Scale, 384 Lesions
Inflammatory mediators, dispersal of, 292 Joint(s) central nervous system, motor relearning
Initial depolarization, of action potential, 23 ageing, 126 in, 48f, 49–50, 50f
Injection(s), by physiotherapists, 402 cavitation within, spinal manipulation and, in neuropathic pain, 9b
Injection therapy, for frozen shoulder 278–279 Lifestyle management, for tendinopathy,
contraction syndrome, 580t spinal, moment equilibrium about, 188, 115
Injury 188f Lifestyle-related health behaviours
as cause of sensorimotor dysfunction, Joint hypermobility syndrome (JHS), assessment of, 365, 366f–367f
55–56, 55f 573 unhealthy, clustering of, 364
subtle and major adaptations in, 56–59, Joint injury, 599–600 Lifestyle-related health risks
57f–60f Joint kinematics, 141–142 assessment of, 365
multifactorial aetiology of, 389 Joint kinetics, 142 unhealthy, clustering of, 364
musculoskeletal, research into, 389 Joint manual therapy, sensorimotor system Ligament, mechanoreceptor stimulation in,
risk factors and, 389 and, 322 321t
sensorimotor system and, 320 Joint mechanics, movement analysis and, Ligamentous system, craniocervical, 94,
Instability, of elbow, 584, 585t, 590 141–142, 142f 95f
Insula, pain and, 13 Joint mobilizations, in descending Ligamentum flavum
Insulin-like growth factor 1 (IGF-1), 73 nociceptive inhibition, 11 of cervical spine, 98
pathway, 71 Joint stability, definition of, 319 of lumbar spine, 104
Integrated systems model for disability and Joules, 19–20 Ligamentum nuchae, 98
pain, 496–497 Jump landing training, 525 Ligamentum teres, 506
Intensity coding, spinothalamic pathways, Light touch, 196
164 Likelihood ratios (LR), 560
Intentional (slow) loop, 28–29 K Limb loading, 525
Intermittent control, 28–29 Keele Musculoskeletal Patient Reported ‘Limit in replicative capacity’, 126
Internal-external rotation, 141–142 Outcome Measure (MSK-PROM), 205, Load, tendinopathies and, 514
International Classification of Functioning, 206f Local motor control, evidence for
Disability and Health, 118f Kerlan-Jobe Orthopaedic Clinic Shoulder impairments in, in patellofemoral pain,
on health assessment, 364–365 and Elbow Score (KJOC-SES), 558 528–529
International Federation of Orthopaedic Kessler Psychological Distress Scale (K10), Locomotion, sensory feedback during,
Manipulative Physical Therapists 329 44–46, 45f
(IFOMPT), 347, 348b, 418 Kinematics, joint, 141–142 Long-latency stretch response, 37f
Interpolation by a factor 8, of EMG, 173f Kinesiopathological model, movement Long polysegmental back muscles, 104
Interpretability, COSMIN guidelines, 203t syndrome and, 474–476, 476f Long-term consequences, of sensorimotor
Intersegmental back muscles, 104 Kinesiophobia, 12b adaptations, 59–62, 61f
Interspinous ligaments, 104 ‘Kinetic chains’, 457 Long-term memories, of pain, 12b
Interventions Kinetics, joint, 142, 142f Longitudinal ligaments, 104
complex, 234 Knee, 522–546 Longitudinal or repeated measures studies,
financial, 235t Knee hyperextension test, 390t–391t 221
implementation, 234 Knee osteoarthritis (OA), 536–546 Longus capitis, 95, 95f
organizational, 235t assessment of, 538–539 Loss-framing, 259–260
pharmaceutical, 234 beyond diagnosis of, 539 Low back pain (LBP)
professional, 235t concepts of, 537 acupuncture for, 337
regulatory, 235t diagnosis of, 538–539, 539b behaviour modification for, 371
Interventions studies, 221 holistic assessment of, 540t biopsychosocial principles for, 3
Intervertebral disc impact on individuals and society of, classification of patients with, 501–502,
blood supply of, 103 536 501f
of cervical spine, 98 physical performance measures for, 541t excessive muscle activity during tasks,
internal mechanical function of, 103, 103f risk factors for, 537–538, 537f 502, 502f
 Index 617

mixed behaviour, 502 M Mechanical pain thresholds, 197

reduced muscle activity during task, M-mode (motion mode) ultrasound, 145t, evaluation, 197f
502, 502f 148 Mechanoreceptors, 320
disability associated with, 395 Magic user, of self-management website, 360 capsuloligamentous, 322
impaired sensorimotor control in, 316 Magnetic and inertial measurement units stimulation of, 321t
motor behavior in, 315–316 (MIMU), 140–141 superficial cutaneous, 322–323
motor control and, 315–316 Magnetic resonance imaging (MRI) Medial epicondylalgia, 591
multidimensional classification system for, contrasts, 153, 154f, 154t Medial instability, of elbow, 584–585
465–470 of elbow, 587 Mediators, inflammatory, dispersal of, 292
classification-based cognitive functional fat/water separation, 154–155, 156f Medication
therapy, 467–468 functional, 157–158 musculoskeletal side effects of, 346t
current practice, failure of, 465 muscle, 155–156 in physiotherapy, 346
skills required to implement, 468 for lateral ligament or syndesmosis injury, Membrane potential, experimentally
summary of, 468 548 measuring, 21, 21f
targeted management of, clinical measures, advances in, 153–160 Memory, long-term, of pain, 12b
reasoning framework for, 467 microscopic evaluation of muscle and Meniscal injury, 522
patient education for nervous systems, 156–158 Meniscus, mechanoreceptor stimulation in,
content of interventions for, 265 in musculoskeletal clinical practice, 321t
effectiveness of, 265–266 158 Mental health, musculoskeletal health and,
proprioceptive impairments in, 316–317 of patellofemoral pain, 529 122
research on, as work-related MSD, structural, 157–158 Mental hygiene, beneficial effects of, 122
384–385 three-dimensional semi-automated Mental ill health, deleterious effects of, 122
self-management of, 360 segmentation, 155f Mental illness, 328
sensorimotor control in, 316–317 Magnetic stimulation techniques, 183 Mesencephalic pontine reticular formation,
assessment of, 317 Magnetization transfer ratios (MTRs), 156, pain and, 12–13
management of, 317 157f Metacarpal fractures, 597
stabilization exercises for, 360 ‘Major’ adaptations, in sensorimotor Metastatic spinal cord compression (MSCC),
Low-frequency TENS, 271–272 dysfunction from pain, 56–59, 57f–60f 345–346
Low-level laser therapy, for rotator cuff long-term consequences of, 59–62, 61f confusion in, 345
tendinopathy, 566 Maladaptive beliefs, patient education and, description of, 345
Low-load coordination training, 413–414 266 diagnosis of, 345
Lower limb Mallet finger injury, 599, 599f early detection of, 345
muscle strengthening, for patellofemoral Mandible, laterotrusion of, 440, 440f emerging issues in, 346
pain, 530 Mandibular jaw jerk, 439 important issues in, 345
sensorimotor system and, 319–327 Manipulative therapy, concepts of, 3 incidence of, 345
Lower motor neurons, 36–37 Manual therapy new advances in, 346
Lumbar flexion syndromes, 476–478 for ankle sprain, 551 Methodological implementation research,
Lumbar proprioception, assessment of, 317 for chronic ankle instability, 552 233t, 234
Lumbar spine, 460–487, 460b for knee osteoarthritis, 541 mfMRI. see Muscle functional MRI (mfMRI)
alignment, sensorimotor system and, for patellofemoral pain, 532, 532f MI. see Motivational interviewing (MI)
315–319 for posterior shoulder tightness, 576 Mild nerve compression, 85, 88f
combined movement examination of, 130f for rotator cuff tendinopathy and in axonal transport, 86–87
functional anatomy of, 101–105, 101f subacromial impingement (pain) Mitochondrial adaptations, to endurance
intervertebral discs, 102–103, 103f syndrome, 566 training, 74
intervertebral ligaments, 104 science mechanisms of, 272 Mixed methods research (MMR), 224–225
lumbar vertebrae, 102 systematic reviews, 215t difficulties associated with, 225
muscles in, 104 Mapping, cortical representation, methodology and methods, 225
McKenzie method of mechanical 179–180 using of, 225
diagnosis and therapy, 460–464 Masqueraders, 343–347 ‘Mobility’ shoes, for knee osteoarthritis,
motor control training, role of, 482–487 clinical severity of, 343 542–543
movement system impairment syndromes, definition of, 343b Model of form and force closure, 500
of the lower back, 474–482 Maximal isometric shoulder adduction tasks, Model of muscular spinal control, 500–501
multidimensional classification system, for 564 Modern electrode technology, 168
low back pain, 465–470 McKenzie method of mechanical diagnosis Modern pain neuroscience, translating of, to
sensorimotor control of, 316 and therapy, 460–464 practice, 15b
treatment-based classification system, application of, in the cervical spine, Modified Thomas test, 390t–391t
470–474 463–464 Modulation, descending, facilitation of, 293
Lumbar spine radiculopathy, 155f assessment in, 461–462 Modulus, of tendon, 108
Lumbar vertebrae, 102 evidence regarding, 462 Molecular level, of ageing, 127t
Lumbopelvic pain, models, testing and conclusions for, 464 Moment equilibrium, about spinal joint, 188
treatment of, critical viewpoint on, force progressions in, 462 Morphology, assessment of muscle, 144–146
500–505 introduction to, 460–461 Morphometry, assessment of muscle,
diagnostic process in, 501 management in, 462–463 144–146
interventions for, 503 evidence regarding, 463, 463t Motion capture, movement analysis and,
introduction to, 500 mechanical syndromes, operational 137–141
low back pain in, classification of patients definitions for, 461b Motions, process of finding forces from,
with, 501–502, 501f other syndromes in, 463 188f–189f
excessive muscle activity during tasks, prognosis, evidence regarding, 462 Motivation, in behaviour change, 331
502, 502f repeated movements in, 461–462 Motivational interviewing (MI), 371–374,
mixed behaviour, 502 Meaningful Task Analysis (MTA), 451–452 374b
reduced muscle activity during task, Measure of external forces, 141, 141f action plan for, 374b
502, 502f Mechanical allodynia, 196 follow-up strategy for, 374b
theoretical models in, 500–501 Mechanical detection thresholds, 195t, 196, questions for, 374b
model of form and force closure in, 500 196f Motor control, 36–38, 42–52
model of muscular spinal control in, Mechanical Diagnosis and Therapy in exercise, assessment of, 299
500–501 approach, 247 hypothesis in, 172–174
618 Index

in sensorimotor integration, 29f, 30 general pattern and distribution of, Muscle imbalance, rotator cuff tendinopathy
sensory feedback as part of, 43–44 476–478 and subacromial impingement (pain)
tests, for orofacial region, 439–440, 440f human movement system, 475f syndrome and, 566
theories of, 42–43 kinesiopathological model in, 474–476, Muscle inhibition, in acute knee injuries,
training of, 302–304, 302f 476f 524
neuromuscular adaptations, 303–304 repeated movements and prolonged Muscle patterning, multidirectional
training principles of, 303 alignment, tissue adaptations instability and, 571
Motor control training, role of, 482–487 associated with, 475–476 Muscle protein synthesis, 71, 72f
clinical application of, 484–486 research for, 478–481 Muscle spindle, 323
assessment in, 484, 485f versus system syndromes, 474 in postural control, 31
correction of motor control faults in, treatment for, 478 Muscle stiffness, increased, 576
484 Movement therapy, in musculoskeletal pain, Muscle stimulation, for arthrogenic muscle
progression of exercise in, 484 12 inhibition, 524
recovery in, potential barriers to, 486 MSCC. see Metastatic spinal cord Muscle synergies, 172–174
clinical framework for, 483–486, 483f compression (MSCC) Muscle-tendon function, in elbow, 585
basic principles in, 483–484 MSDs. see Musculoskeletal disorders Muscle-tendon unit, measuring tissue
common misconceptions in, 486 (MSDs) motion and mechanical properties of,
conclusion for, 487 MTRs. see Magnetization transfer ratios 146–148, 148f
evidence for, 486–487 (MTRs) Muscle testing, in shoulder assessment, 559,
effectivity of, 486 Multidimensional classification system, for 559t
motor control, change in, 487 low back pain, 465–470 Musculoskeletal conditions, 609
in pain and disability, 486 classification-based functional therapy in, magnitude of problem of, 609
patients to likely respond to, 467–468 prevalence rates of, 401
identification of, 486 clinical reasoning framework in, 467 Musculoskeletal disorders (MSDs), 609
introduction to, 482–483 cognitive factors in, 467 non-invasive brain stimulation in
Motor cortex, mapping of, 181f current practice, failure of, 465 measurement and treatment, 179–186
Motor evoked potential, 180f framework for, 466f safety considerations, 184
amplitude, 180–181 health and pain co-morbidities in, pain network in, 164–165
latency, 180 467 painful, concepts of, 3
Motor function, variability of, 54 individual factors in, 467 screening for, 388–394
Motor learning, 42–52 lifestyle factors in, 467 assumption of, 389–391
sensory feedback in, 49–50 neurophysiological factors in, 465 benefits of, 389
Motor neurons, 36–37 psychological factors in, 467 clinical, 392
Motor output, 37–38 skills required to implement, 468 components of, 391
Motor primitives, 28–29 social and cultural factors in, 467 conduction of, 392
Motor programming theory, of motor summary of, 468 cost benefit of, 389–391
control, 43 time course of the disorder in, 465 difficulties of, 389
Motor system, 36–37 triage in, 465 functional movement patterns, 392
mechanisms of, 62–63, 64f work-related factors in, 467 importance of, 389
Motor threshold, resting and active, 180 Multidirectional instability (MDI), interpretation of, 389
Motor unit, 68 569 prevention and, 389–391
Motoric system, altering output of, 503 management of, 571 protocols for, 389, 391
Motor-related areas, pain and, 13b Multisystem review, 365, 370f risk factors and injury, 389, 390t–391t
Movement Muscle(s) tool for, development of, 391
ageing and beneficial effects of, 128 ageing, 126–127 work-related, 380
in exercise, quality assessment of, anabolism of, 71, 72f body regions involved in, 380
299 assessment of clinical syndromes in, 380
in motor control training, 483 fatigue, 300 hazards for, 381
neural control of, from EMG, 174–175 morphometry and morphology, risk control in, 382
neuro-electrochemistry of, 19–27, 19b 144–146 Musculoskeletal health
action potential in, 22–24, 23f–24f structure, 299–300 inactivity/activity and, 121
fundamental principles of, 19–20 contracted, 146 lifestyle and, 117–125
resting membrane potential in, 20–22 contraction of, neural control of, 68 modifiable risk factors, 119t
synaptic transmission in, 24–25, 25f function of, 68–69, 69f mental health and, 122
patterns of, 394–395 hypertonicity/stiffness, reducing of, in nutrition and, 119–120
functional, screening of, 392 spinal manipulation, 279 sleep and, 121–122
screening, testing and assessment of, of lumbar spine, 104 smoking and, 118–119
394–399 macroscopic structure of, 154–155 beneficial effects of quitting, 119
skeletal muscle in, 68 mechanoreceptor stimulation in, 321t deleterious effects of, 118–119
and stiffness, sensorimotor control and, microscopic activation and function of, in workplace, 379–387
53–54 155–156 prevention of, 380–385
Movement analysis, 137–143 microscopic evaluation of, 156–158 Musculoskeletal injury, sensorimotor system
joint mechanics and, 141–142 size and strength, 146 and, 320
magnetic and inertial measurement units, Muscle activity Musculoskeletal modelling, 187–193
140–141 distribution of, 172 advantage of, 192
measure of external forces, 141, 141f onset of, 169f basics of, based on inverse dynamics,
mechanical model of musculoskeletal spatial distribution of, 172 187–189
system, 137, 138f timing of, 169 results of, 191–192
motion capture and, 137–141 topographical mapping of, 173f semispinalis cervicis muscle using,
reconstruction of bone during, 139f Muscle fibres, 68 190–192
stereophotogrammetry and, 138–140, length of, 506 simulated changes in lumbar muscle
140f types of, 69 activation from pelvic tilt, 189–190,
Movement system impairment syndromes, switching of, 75 190f
of the lower back, 474–482 Muscle forces, alteration of, 190f Musculoskeletal pain
conclusions for, 481 Muscle functional MRI (mfMRI), 155–156 acupuncture for, 337–338
examination of, 478, 479t–480t Muscle hypertrophy, 475, 477f disorders, persistent, 199
 Index 619

episode of, 610 Neck muscles hormonal influences to, 73–74

syndromes, 339 behaviour of, change in, 414, 415f overload principle in, 69–70
Musculoskeletal (MSK) physiotherapy, 220, EMG tuning curves of, 171 Neuromuscular control, development of, in
400–405 Neck pain, idiopathic, 410–422 acute knee injuries, 524–525
aims of, 403 exercise dosage in, to address recurrence, Neuromuscular function, restoration of,
aspects of, 402 415–416, 416f training for, 413–414, 414f
background of, 400 incidence of, 410 Neuromuscular training, sole aim of,
case studies on, 349–351, 350b profiling patients with, 410–413 524
definitions of, 401 biological perspectives in, 410–411 Neuronal synapses, long-term potentiation
drivers of, 400–401 in clinical practice, 412 of, 14
evaluation of, 402–403 psychological perspectives, 411 Neurons, peripheral, anatomy and
diagnostic accuracy in, 402 social perspectives, 411–412 physiology of, 78–79, 79f
patient satisfaction/experience in, responses to, 411 Neuropathic pain, definition of, 9b
402 summary of, 416 Neuropathy, entrapment, 78, 89f
professional issues in, 403 summary statement, 413 demyelination due to, 83–84, 83f
treatment effectiveness in, 402 training for, 413–416 immune system in, 84–85, 86f–88f
impacts on health services, 402–403 pain relief, 413, 413f ischaemia and, 82–83
health economic, 403 restoration of neuromuscular function, in large and small diameter nerve fibres,
process/organizational, 402–403 413–414, 414f 84, 85f
models of, 401–402 variability in response to, 415, 416f pathophysiology of, 82–87
emergency departments, 401 transfer to function, 414–415 Neurophysiological mechanisms, of spinal
neurosurgery, 401 Neer sign, 560 manipulation, 279–281, 280f
orthopaedics, 401 ‘Negotiated learning agreement’, 255 peripheral, 280
primary care settings, 401–402 Neoprene or elastic sleeves, for knee spinal cord mediated, 280–281
rheumatology, 401 osteoarthritis, 541–542 supraspinally mediated, 281
and pain processing, 165–166 Nernst equation, 20–22 Neurophysiology, of pain, 266
requirements for, 401 Nerve, movement of, normalization of, education, 267
research methods in, 220–226, 220b–221b 291–292 and pain modulators, 8–18
approaches to research, 224–226 Nerve compression, 586 Neurosurgery, in hospital-based services,
qualitative research, 223–224 mild, 85, 88f 401
quantitative research, 221–222 in axonal transport, 86–87 Newton-Euler equations, 187
theory and practice of, 3 Nerve function, in elbow, 585–586 Newton’s second law, 187
titles for, 401 provocation tests, 586t Nociceptive facilitation, descending, 10
Musculoskeletal practice Nerve supply, in tendon, 114 Nociceptive inhibition, descending,
cautions in, 342–356, 342b Nerve trunk palpation, for 10–11
outcome measures in, 202–210 temporomandibular disorders, 439 Nociceptors, 8
acting on information, 209 Nervi nervorum, 80 Nodes of Ranvier, 79, 80f
case-mix adjustment, 208, 208f Nervous system Nominal group technique, 229–231
data collection method, 209 ageing, 127 developmental process of, 230f
development and validation of, 207, microscopic evaluation of, 156–158 findings from, 229–230
207b as source of nociception and pain, 9b protocol, 229–231
practical issues in collecting, Neural arch, 102 standardized data collection and,
207–209 Neural container, treating of, neurodynamic 229
types of, 202–205 management of, 289 Non-communicable diseases, 117–118
Musculoskeletal Services Framework, Neural regulation, in postural control, 28–29 Non-contact deceleration injuries,
401–402 Neurodynamic management 522–523
Musculoskeletal system considerations of, 294 Non-invasive brain stimulation,
ageing of, 126–128 contraindications of, 289–291 measurement and treatment, in
impairment measures of, 394 indications of, 289–291 musculoskeletal disorders, 179–186
mechanical model of, 137, 138f influences on pathobiological processes, Non-steroidal anti-inflammatory drugs
pulmonary function and, 456 291–293 (NSAIDs), for ankle sprain, 552
Mutation accumulation, theory of ageing, peripheral nervous system, 287–297 Nottingham Cervical Arterial Dysfunction
127t clinical trial evidence of, 293–294 (nCAD) sub-classification system,
Myelin sheath, 79, 80f mobilization of surrounding structures, 348–349, 349f
Myoelectric manifestations of fatigue, 289, 291f Nucleus pulposus, 102, 103f
170–171 sliding techniques, 289, 290f–291f Number needed to harm (NNH), 259
Myofascial pain, acupuncture for, 337 tensioning techniques, 289, 290f–291f Numeric Rating Scale and Neck Disability
Myofascial trigger points, acupuncture for, treating neural container, 289 Index, 212
337 of peripheral nervous system, 287–297 Nutrition
Myofibril, 68 Neurodynamic tests guidelines on, for prevention of all-cause
Myogenic temporomandibular disorders, of nervous system, 287–289, 288f premature mortality and related
433–435 for temporomandibular disorders, 439 morbidity, 367b
dental occlusal factors of, 434 Neuroendocrine, theory of ageing, 127t musculoskeletal health and, 119–120
increased muscle activity during rest in, Neurogenic inflammation, 85–86 optimizing, 376t
434–435 Neurogenic temporomandibular disorders,
neuroendocrine and genetic factors of, 435–436
434 proposed features of, 436t O
parafunctions of, 434 Neuro-immune response, influence on, O-AA complex. see Occipito-atlantoaxial
Myosin, 68 neurodynamic management, 292–293 (O-AA) complex
Myostatin, 73–74 Neuromodulation, 183–184 Obesity, musculoskeletal health, 120
Neuromuscular activation patterns, 476 Oblique capitis superior, 96, 96f
Neuromuscular adaptations, to exercise, Observational study, 221–222
N 68–77 Occipito-atlantoaxial (O-AA) complex, 93
N-of-1 trial designs endurance training, 74–75 Oculomotor system
clinical treatment, 217f high-resistance strength training, 70–74, control of, exercises for, 312
withdrawal, 218, 218f 70f impairments in, 310
620 Index

Odds ratios (OR), 259 as cause of sensorimotor dysfunction, Paravertebral muscle vibration, for low back
Oedema 55–56, 55f pain, 316
control of, 597 subtle and major adaptations in, 56–59, Passive motion, in shoulder assessment, 559,
extraneural, reduction of, 292 57f–60f 559t
intraneural, evacuation of, 292 definition of, 262b, 339 ‘Passive space fillers’, 94
Off-cells, pain and, 12–13 disability and, 263 Passive stabilization, in postural control,
Ohm, 20 evoked, in musculoskeletal disease, 28
Ohm’s law, 20 164–165 Patella, 528
On-cells, pain and, 12–13 experience, components of, 161 Patellar taping, for patellofemoral pain, 531
One leg standing (OLS) test, 496–497, inhibition of, spinal manipulation and, Patellar tendinopathy, 112
497f–498f 418 Patellar tendon, 106
Online commentary, 253 management of, 262–276 Patellofemoral chondral/cartilage lesions,
Open-loop control systems, 42 educational approaches to, 269–276 533
Operant conditioning, physiotherapy- exercise for, 269–270 Patellofemoral joint (PFJ)
provided, 371 manual therapy, 272 anatomy and motor control of, 528
Optimal sleep, beneficial effects of, 122 physical interventions of, 265–269 anatomy of remote structures and impact
Optoelectronic stereophotogrammetry, 138 transcutaneous electrical nerve on, 528
Orebro Musculoskeletal Pain Screening stimulation, 270–272 articular and muscle control of, 528
Tool, 205 musculoskeletal Patellofemoral pain (PFP), 528–533
Organizational interventions, 235t forms of exercise for, 301–306 assessment of, 529
Orofacial pain, 433 human brain in, 161–167 controversies, uncertainties and future
Orthopaedic instability tests, in unstable neurophysiology of, 8–9, 266 directions of, 533
shoulder, 570 patellofemoral, 528–533 emerging issues and new advances of,
Orthopaedic physiotherapy, evidence- patient experiencing, 262–264 533
informed, 117–118 persistent, 263, 340–341 evidence for impairments in
Orthopaedic special tests, in shoulder personal changes in, 263 local motor control in, 528–529
assessment, 559–560 potential processes, 265–269 remote contributors to, 529
Orthopaedics, in hospital-based services, relief from, motor control training for, key clinical diagnostic features of, 529,
401 486 530t
Orthotics, for chronic ankle instability, 552 sensitization and, 486 role of imaging in, 529
Osteoarthritic process, 474 sensorimotor control and, 53–67 treatment of, 529–533
Osteoarthritis (OA), 602–603 sensorimotor system and, 320 effectiveness of, 532–533
ageing and contribution to, 127t social changes in, 263 Patient
knee, 536–546 spontaneous, central processing of, 165 communicating with, 250–261, 250b
Osteophytosis, 130–131 susceptibility to, 339 as learner
Osteoporosis, 132–133 temporal summation of, 197 characteristics of, 255–256
Osteoporotic fracture, 132–133 tendon learning needs of, 255
Otoliths, in postural control, 31 causes of, 114 personal characteristics of, 255–256,
Ottawa Ankle Rules (OAR), 548 source of, 113–114 256f
Outcome measures threshold evaluation, 197f learning
acting on information, 209 tissue loading and, 486 approaches to facilitate, 256–257,
case-mix adjustment, 208, 208f Pain communicative behaviours, 467 257t
data collection method, 209 Pain-free grip test, 586 assessment of, 257
development and validation of, 207, Pain gate mechanism, 320–322 Patient care, clinical reasoning models for,
207b Pain modulation 246–247
in musculoskeletal practice, 202–210, brain-orchestrated, 9–11 Patient care continuum, 361
202b neurophysiology of, 8–18 Patient education, 254–258
practical issues in collecting, 207–209 Pain neuromatrix, 11–13, 11f, 13b beliefs targeted by, 267
recommendations for, 209b in central sensitization pain, 14 biopsychosocial, 266
types of, 202–205 tissue nociception to, 8–9 defined, 254
Outcome prediction, clinical relevance of, Pain perception, cultural differences in, delivery of, 265
426–428 whiplash-associated disorders and, maladaptive beliefs and, 266
cause and effect and 425 pain and, 265
criteria for, 427t Pain processing, musculoskeletal patient-centred approach to, 257, 257t
nature of, 426 physiotherapy and, 165–166 self-management and, 358–359, 362
characteristics of, 426 Pain relief, training for, 413, 413f for tendinopathy, 115
predictor variable in, 427 Pain states, chronic, motor relearning in, 49 therapist-centred approach to, 257,
Overload principle, 69–70 Pain thresholds 257t
Overshoot, 23 cold, 195t Patient empowerment, 359
Ownership, perceptual sense of, 32 heat, 195t Patient selection, in spinal manipulation,
Oxford Elbow Score, 583–584 mechanical, 197 282–283
evaluation, 197f Patient-centred approach, to patient
in musculoskeletal health, 120 education, 257, 257t
P Painful arc test, 564 Patient-focused practice, communication
PAG. see Periaqueductal grey (PAG) Painful musculoskeletal disorders, concepts and, 250–254
Pain of, 3 Patient-reported outcome measures (PRO),
adjunct modalities for, 334–341, 334b Paired-pulse transcranial magnetic 202, 212
adopting a role in health and social care stimulation, 183 Patterns, adopted, of activity, 58–59
system, 263–264 Palpation Pedagogy, 255
ageing and, 128 in elbow, 585 Pedicles, 97
associated with rotator cuff tendinopathy, in shoulder assessment, 559, 559t Pelvic girdle, 495–500
564 in wrist/hand, 596 case report for, 497–499, 497f–499f
biology education, 266 Paper-based aides, for clinical reasoning, conclusion for, 499
brain network for, 161–164 245, 245t integrated systems model for disability
functional components of, 161–164 Parabrachial nuclei, nociceptive inputs to, and pain in, 496–497
in musculoskeletal disorders, 164–165 162 one leg standing (OLS) test in, 496–497
 Index 621

Pelvic girdle pain, assessment and Physical examination Postural control, 28–29
management of, person-centred of elbow, 584–587 exercises for, 312
biopsychosocial approach to, in shoulder assessment, 558–560 neck pain and, 310
488–495, 490f of unstable shoulder, 569–570, principles of, for physiotherapeutic
clinical framework for, 491f 570f–571f practice, 38
comorbidities and, 492 Physical interventions, of pain management, sensorimotor integration in, 29–30, 29f
conclusion for, 493 265–269 sensory integration in, 30–36, 30f
genetic and individual factors in, 492 Physiological cross-sectional area (PCSA), Postural syndrome, 461b
key considerations in, 492–493 506 Posture, 28
cognitive-functional approach to Physiotherapist(s), 609 assessment of, in thoracic musculoskeletal
management in, 492–493 in advanced roles, 400, 402 pain, 446, 446f
communication and language in, 492, as health advocate, 364 correction of, in thoracic musculoskeletal
493t Physiotherapy pain, 448, 448f
risk profiling in, 492 acupuncture and, 338 rotator cuff tendinopathy and subacromial
lifestyle factors in, 490 clinical utility of quantitative sensory impingement (pain) syndrome and,
motor control factors in, 490–492 testing in, 199 566
neurophysiological factors in, 489 cognitive and behavioural influences on, Potassium (K+), equilibrium potential for, 22
passive treatments for, 493 328–333 ‘Potential difference’, 19–20
pelvis, challenging health-care practitioner behavioural graded activity approaches, Power, 68–69, 69f
beliefs regarding, 488–489 330–331 Power Doppler, 145t
physical restoration in, 492 body scan relaxation, 329 Practical issues, associated with, in spinal
psychosocial factors in, 489–490 breathing retraining, 329 manipulation, 281–283
Pelvic tilt, lumbar muscle activation from, coping skills, 330 Practice, future directions in, 609–610
189–190, 190f integrating psychological factors in to Prefrontal cortex
Pelvis, facts regarding, 489b clinical practice, 331–332, 332b, pain and, 13
Perception 332f in selection mechanisms, 34
in sensorimotor integration, 29, 29f problem solving, 330 Premotor cortex, in selection mechanisms,
in sensory integration, 32–33 promoting behaviour change, 331 34
Periaqueductal grey (PAG), 161 psychological co-morbidity, 328–329 Pre-participation examination, 388–389
Perimuscular connective tissue thickness, skills and procedures, 329–330 Pressure, extraneural, reduction of, 292
146 understanding problem presentation, Pressure pain threshold, 195t, 196–197, 196f
Perineurium, 80, 81f 328 tests, for temporomandibular pain, 438
Peripheral mechanisms, of spinal for frozen shoulder contraction syndrome, Prevention, stages of, 380
manipulation, 280 579–580, 580t Primary prevention, definition of, 380
Peripheral nervous system, 78–92 musculoskeletal PRO. see Patient-reported outcome
anatomy and physiology of, 78–82 advanced roles in, 400–405 measures (PRO)
axonal transport in, 82 and pain processing, 165–166 Probabilities, understanding, 259
blood circulation in, 80–82, 81f theory and practice of, 3 Problem solving, 330
central nervous system and, 82 role in lifestyle and health promotion in ‘Procedural justice’, 384
changes in, 87 musculoskeletal conditions, 364–378 Professional interventions, 235t
connective tissue in, 80, 81f clustering of unhealthy lifestyle-related Progressive resistance training, 70
immune cells of, 82 behaviours and risks, 364 Prone passive hip external rotation test,
myelin sheath in, 79, 80f health and risk assessments and 390t–391t
neurodynamic management of, interventions, 364–371, 365b Prone passive hip internal rotation test,
287–297 health behaviour change interventions, 390t–391t
mobilization of surrounding structures, 371–377 Proprioception, 320, 322–323
289, 291f physiotherapists as health advocates, cervical, assessment and treatment of,
sliding techniques, 289, 290f–291f 364 310
tensioning techniques, 289, 290f–291f for temporomandibular disorders, impaired, 317
treating neural container, 289 439–440 lumbar, assessment of, 317
neurons in, 78–79, 79f for whiplash-associated disorders, in postural control, 31
Schwann cells in, 79 428–429 ‘Proprioceptive chain’, 31
Peripheral neuropathic pain, 9b Pinch strength, 596 Proprioceptive feedback, 43
Peripheral sensitization, 13 Plausibility, 427t in lumbar spine, 316
Peroxisome proliferator-activated receptor Pogonion-tragus-C7 angle, 437, 437f Proprioceptive training, 602f
gamma co-activator 1α (PGC-1α), Polysegmental back muscles, 104 Prospective cohort study, 221
74 Population ageing, 379 Protective pain memory, 12
Persistent lower back pain (PLBP), 465 Positional tendons, 109–110 Protocol, nominal group technique,
brain changes and, 465–467 ‘Positive’ neurodynamic test, 287 229–231
Persistent musculoskeletal pain disorders, Post-traumatic stress disorder, and Protraction, 463–464
199 whiplash-associated disorders, 425 Proximal interphalangeal joint, volar plate
Persistent tendinopathy, 112 Posterior dislocation, 569 injury at, 599–600
Personal changes, of pain, 263 management of, 571 Psoas major, 104
Personal risk, 261 Posterior interosseus nerve (PIN), 586 Psychological co-morbidity, 328–329
‘Perspective display’ sequences, 253 impingement of, 587f Psychological factors, integration of, to
PGC-1α. see Peroxisome proliferator- Posterior longitudinal ligament, 98, clinical practice, 331–332, 332b, 332f
activated receptor gamma co-activator 104 Psychosocial factors, sensorimotor changes
1α (PGC-1α) Posterior RC muscles, 564 and, 63–64
Phalangeal fractures, 597 Posterior shoulder tightness, 575–577 Pubofemoral ligament, 506
Pharmaceutical interventions, 234 Posterior subluxation, management of, Pulmonary rehabilitation
Physical activity 571 for COPD, 456
guidelines on, for prevention of all-cause Posterolateral impingement, 591 evaluation of, 457–458
premature mortality and related Posterolateral rotatory instability (PLRI), Pulsed-wave (PW) Doppler, 145t
morbidity, 367b 585t Punctate pain thresholds, 195t
motivation for, 376t Postural components, sensorimotor control Pure tendinopathy, 113
regular, beneficial effects of, 121 and, 53 Pyramidal motor system, 36–37
622 Index

Q Recalcitrant tendinopathy, 112 Rheumatology, in hospital-based services,

Quadratus lumborum, 104 Recruitment curves, 181–182, 182f 401
Quadriceps muscle weakness, 524 Rectus capitis anterior muscle, 95f, 96 (P)RICE regimen, for ankle sprain, 551
Qualitative research, 223–224 Rectus capitis lateralis muscle, 96 Risk
description of, 223 Rectus capitis posterior major, 96, 96f framing, 259–261
findings, 224 Rectus capitis posterior minor, 96, 96f personal, 261
methodology and methods, 223–224 Red flag, definition of, 343b understanding, 258–259
ontological and epistemological Red herring, definition of, 343b Risk communication, 258–261, 261b
assumptions, 223 Redistribution, of muscle activity, due to probabilities versus natural frequencies,
using of, 224 pain, 56–58, 57f–60f 259
Quality Adjusted Life Years (QALYs), 402 Reflex(es), 42–43, 322 relative versus absolute, 259
Quantitative movement analysis, 137 inhibition of, 62–63 Risk profiling, for pelvic girdle pain, 492
Quantitative research, 221–222 Reflex loop, sensory feedback as part of, Risk-management
description of, 221 46–49, 46f–47f efficacy of, 382
findings, 222 Reflex theory, of motor control, 42–43 model, 381–382, 381f
methodology and methods, 221–222 Refractoriness, 35f, 36 tools for, 381–382
Quantitative sensory testing (QST), 194 Refractory period, of action potential, 23 Rotation motions, 476–478
clinical utility of, in physiotherapy, Regulatory interventions, 235t Rotation stress test, 353t, 354
199 Rehabilitation Rotator cuff (RC)
mechanical, 195–197 for chronic whiplash-associated disorders, direction-specific recruitment pattern of,
modalities, receptors and testing methods, 430 564
195t for tendinopathy, 115 function of, 563–564
reliability of, 194–195 Rehabilitative ultrasound imaging (RUSI), Rotator cuff (RC) tendinopathy, 563–568
for temporomandibular disorders, 439 144 diagnosis of, 564
test site and interpretation of, 198–199 Relative flexibility, 475, 480–481 measuring outcome of, 566
thermal, 197–198 Relative risk (RR), 259 outcome of, 565–566
Quasi-experimental research, 222 Relative stiffness, 475 posture and muscle imbalance and, 566
Quitting smoking, beneficial effects of, 119 Relaxation, body scan, 329 treatment of, 564–565
Relevance, good-quality data, 228 Rotator cuff (RC) tendon, 563
Reliability RTW. see Return to work (RTW)
R COSMIN guidelines, 203t Rubrospinal tract, 36–37
Radial nerve entrapment, 591 good-quality data, 228 Rydel-Seiffer graded tuning fork, 195–196
Radiofrequency neurotomy (RFN), for Repetitive transcranial magnetic stimulation,
whiplash-associated disorders, 423–424, 183–184
424f Repolarization, of action potential, 23 S
Radiographs Research Safety issues, associated with, in spinal
of frozen shoulder contraction syndrome, approaches to, 224–226 manipulation, 281–283
579 defined, 227 Satellite cells, 71–73
of patellofemoral pain, 529 findings, different types of, 243 Scaphoid fractures, 598–599
‘Rain collector’, 440, 440f future directions in, 609–610 Scapholunate ligament, 600–601
Randomized controlled trials (RCTs), 212, implementation, 232–238 instability of, 601f
222 methods in, 220–226, 220b–221b Scar, care of, 597
classic multiple group parallel design, mixed methods, 224–225 Schmorl’s nodes, 131, 132f
213f–214f qualitative, 223–224 Schwann cells, 79
for redesign considerations, 213t–214t quantitative, 221–222 Science, advances in, musculoskeletal
Randomized withdrawal use of data in, 231 physiotherapy and, 3
design, 216f Resistance, 20 Science mechanisms
Range of motion (ROM) Resistance training, 69–70, 304–306 of manual therapy, 272
in elbow, 584 adaptations to, 70–74, 70f of transcutaneous electrical nerve
neurodynamic test, 287–288 hormonal influences in, 73–74 stimulation, 271–272
of wrist/hand, 595–596 muscular, 70–73 Secondary prevention, definition of, 380
Rate-of-living, theory of ageing, 127t neural, 70 Selection
RCD/TMD classification, 433 clinical prescription of, 305–306 executive function of, 35–36
RCTs. see Randomized controlled trials duration of, 305 in sensorimotor integration, 29–30, 29f
(RCTs) frequency of, 305 in sensory integration, 33–36, 34f
Reaction resultant load, 141 intensity of, 304–305 Selective Functional Movement Assessment
Readiness, in behaviour change, 331 muscle changes in, 75t (SFMA), 396–398, 397f
Reasoning, clinical, 242–249, 243f volume of, 305 clinical measurement of, 396
biopsychosocial model, 247, 247b Resisted supination, 586t flowcharts for, 397
clinical prediction rules, 244–245 Respiratory muscle stretch gymnastics, 457, regional interdependence in, 396
evidence-based, 242, 242b 457b, 458f Selective user, of self-management website,
health-care environment, 242 Responsiveness, COSMIN guidelines, 360
future directions for, and management, 203t Self-care, self-management versus, 359
248 Resting membrane potential, 20–22 Self-efficacy, 359, 361–362
inductive and deductive, 243–244 action potential and, 23 in behaviour change, 331
Mechanical Diagnosis and Therapy measurement of, 21, 21f Self-help, overview of, 358–363
approach, 247 sodium-potassium pump and, 21–22, 22f Self-management
models, challenge of, 246–247, Resting motor threshold, 180 categories of, 359–360
247b Reticular formation, mesencephalic pontine, in chronic illness, 359–360
in motor control training, 483 pain and, 12–13 concept of, 358
in spinal manipulation, 282–283 Reticulospinal tract, 36–37 definition of, 358
stepped care and adaptive care, 244 Retraction, 463–464 discussion in, 361–362
stratified health care and treatment effect Retrospective cohort studies, 221 evidence and, 359–360
modification, 246, 247b Return to work (RTW), 382 interesting component of, 359
technology and paper-based aides, 245, Return to Work Self-Efficacy Scale, 384 patient education and, 358–359, 362
245t Reversibility, 427t patients’ and clinicians’ viewpoint of, 361
 Index 623

programmes, 359 SFMA. see Selective Functional Movement Social systems, whiplash-related disorders
versus self-care, 359 Assessment (SFMA) and, 425
strategies of, 359 Sharp-Purser test, 353, 353t Socratic method, in cognitive behavioural
successful, 362 Short polysegmental back muscles, 104 therapy, 371
supported, 358–363 Shoulder, 557–582 Sodium (Na+), 22
website users, 360 arthroscopic capsular release of, 581 Sodium-potassium pump, 21–22, 22f
Semicircular canals, in postural control, 31 assessment of, 557–563, 561f Somatic mutation, theory of ageing, 127t
Semispinalis cervicis muscle active motion, passive motion, palpation Somatosensory, definition of, 9b
predicted activity of, 191f and muscle testing, 559, 559t Somatosensory cortex, 11
predicted force in, 192f clinical decision making and, 557–558 Spatial heterogeneity, 172
using musculoskeletal modelling, importance of epidemiology data in, Special fractional factorial design, 216, 216t
190–192 557–558 Specificity of the relationship, 427t
Sensation, of wrist/hand, 595 observation, 558 Spinal cord mediated mechanisms, of spinal
Sensitization orthopaedic special tests and diagnostic manipulation, 280–281
central, 13–14 accuracy, 559–560, 560t Spinal curvature anomalies, degenerative,
pain and, 486 patient interview, flags and establishing 132, 133f
peripheral, 13 baseline for outcomes, 558, 558t Spinal joint, moment equilibrium about,
Sensitizing factors, pelvic girdle pain and, physical examination, 558–560 188, 188f
489 screening examination, 558–559 Spinal manipulation (SM), 277–286
Sensorimotor control frozen shoulder contraction syndrome of, clinical reasoning and patient selection,
changes in, in musculoskeletal conditions, 577–582 282–283
62–64, 64f posterior shoulder tightness of, 575–577 definition of, 277–278, 278f, 283
definition of, 319 unstable, 568–575 inducing cavitation within the joint and,
dysfunction of, 53–64 Shoulder flexion, 563–564 278–279
adaptations in, 56–59, 57f–60f Shoulder instability, 569, 573 international context, 283
pain/injury as cause of, 55–56 Shoulder internal rotation elbow flexion test, for lower back pain, 470–472
individual variation of, 54 586t minimizing risk, in application of,
pain, injury and, relationship between, SI joint (pelvic pain), models of assessment 281–282
54–64, 55f and management of, 488–505, 488b muscle hypertonicity/stiffness, 279
pain and, 53–67 facts regarding, 489b objectives of
principles of, 53, 54b inter-tester reliability of commonly used biomechanical, 278–279
Sensorimotor integration, 29–30, 29f tests for mobility of, 496t neurophysiological, 279–281
overall scheme of, 35f lumbopelvic pain, models, testing and safety and practical issues associated with,
principles of, for physiotherapeutic treatment of, critical viewpoint on, 281–283
practice, 38 500–505 stretching/tearing tissue and, 278
Sensorimotor system pelvic girdle, 495–500 Spinal nerves, 99
cervical region, impairments in, 310–315 pain, assessment and management of, Spinal pain, management of, use of tape in,
exercise approach based on, tailored, person-centred biopsychosocial 339–341, 340f
311–312, 313t–314t approach to, 488–495 Spinal stenosis, 461b
local treatment for, tailored, 311 Side-bending stress test, 353t, 354 Spine, ageing of, 128–133, 129f
overall management approach to, Single leg balance test, 390t–391t disc degeneration, 130, 131f
310–311 Single leg hamstring bridge test, osteophytosis, 130–131
recommendations, and progression of 390t–391t Spinobulbar pathways, 161–162, 162f
treatment of, 312–313 Single leg squat, for quadriceps weakness, Spinothalamic pathways, 162–164, 163f
reported complaints and, 310, 311f 524, 525f Spontaneous pain, central processing of,
components of, 319–320, 322 Single motor unit behaviour, EMG, 165
activation of, 323 174–175, 174f Squeeze test, 550f
effects of injury on, 320 Single-blind controlled trial, 222 Stability, of elbow, 584–585
exercise therapy and, 323, 324f Single-pulse transcranial magnetic Stabilization exercises, for low back pain,
lower limb and, 319–327 stimulation, 179–183 360
lumbar spine alignment control by, Single-subject design, 217–218, 217f Standardized data collection, 227–231
315–319 Skeletal muscle, in movement, 68 advantages of, 231
manual therapy and, 320–322, 322f Skin, mechanoreceptor stimulation in, 321t importance of, 227–228
review of, 319–320 Sleep nominal group technique in, 229
sensory component of, 320 musculoskeletal health and, 121–122 tool, development of, 228
taping and bracing and, 322–323, 323f optimizing, 376t STarT Back Tool, 245
Sensory feedback reduced, pelvic girdle pain and, 490 Static progression, in motor control
during locomotion, 44–46, 45f Sleep deprivation, deleterious effects of, training, 484
in motor learning, 49–50 121–122 Static stabilization test, 440, 440f
as part of motor control, 43–44 ‘Sleeper stretch,’ for posterior shoulder Stepped care, 244
as part of reflex loop, 46–49, 46f–47f tightness, 576 Stereophotogrammetry, 138–140, 140f
Sensory integration, 30–36, 30f Sliding techniques, for peripheral nervous Stiffness
action possibilities and, generation of, 33, system, in neurodynamic management, in motor control training, 483
33f 289, 290f–291f movement and, sensorimotor control and,
perception in, 32–33 Slow loop, 28–29, 36 53–54
selection in, 33–36, 34f Small diameter nerve fibres, entrapment Stratified health care, 246, 247b
Sensory loss, 194 neuropathies in, 84, 85f Strength
Sensory nerve endings, in skin, Smoking of elbow, 586
322–323 beneficial effects of quitting, 119 of wrist/hand, 596
Sensory profiling, 198f deleterious effects of, 118–119 Strength of association, 427t
Sensory system musculoskeletal health and, 118–119 Strength parameters, assessment of, 300
mechanisms of, 62 Smoking cessation, 376t Strength training, 69–70
redundancy of, 54 rotator cuff pathology and, 566 adaptations to, 70–74, 70f
Serious pathology, definition of, 343b Smooth pursuit, exercises for, 312, 312f hormonal influences in, 73–74
Sexual dysfunction, associated with cauda Social changes, of pain, 263 muscular, 70–73
equina syndrome, 344b Social environment, pain and, 503 neural, 70
624 Index

in exercise, 304 Technology-assisted aids, for clinical Testosterone, 73

muscle changes in, 75t reasoning, 245, 245t Thalamus, pain and, 12
Strengthening, for acute knee injuries, Tectorial membrane, 94 Theoretical framework, for behaviour
524 distraction test for, 353t, 354 change, 237
Stress Temporal summation of pain, 9, 10b, 10f, Therapeutic exercise, 298–309
exposure to, 340–341 197 assessment to guide for, 298–300
management of, 329, 376t Temporality, 427t clinical prescription of, 298, 299f
pain and, 14–15 Temporomandibular disorders indications for, 298
pelvic girdle pain and, 490 altered posture of head and, 437 principles of management, 298–301
Stress-strain behaviour, of tendon, 108–109, arthrogenic, 435 selectivity of, 300–301
109t arthralgia in, 435 specificity of, 300–301
Stress test disc displacements in, 435 timing of, 301
for alar ligament integrity, 353t, 354 hypermobility and dislocation in, 435 variability in response to, 301
rotation, 353t, 354 assessment of, 436–439 Therapeutic pain neuroscience, 15b
side-bending, 353t, 354 physical examination of, 436–437 Therapeutic ultrasound, for non-calcific RC
for transverse ligament integrity, 353–354, subjective examination in, 436 tendinosis, 566
353t clinical diagnostic process of, 433, 434f Therapist-centred approach, to patient
of ulnar collateral ligament injury, 600, clinical diagnostic testing of, 437–439 education, 257, 257t
600f multi-test scores in, 437, 438t Thermal detection, 197f
Stress X-rays, for lateral ligament or muscle testing in, 438 Thermal quantitative sensory testing,
syndesmosis injury, 548 nervous system and, 438–439 197–198
‘Stressors,’ categories of, 340–341 neuromuscular tests chosen for, 438 Thermode, 197
Stretch reflex, 46, 47f and peripheral nerve sensitization, 438 Thick myelinated fibres, 78, 79t
Stroke, motor relearning and, 49 physiological and accessory movements Thinly myelinated fibres, 78, 79t
Structure-pathology model, 262 in, 438 Thixotropy, 32
‘Student-centred’ approaches, in patient quality of, 437–438 Thoracic extension, 440, 440f
education, 255 head position, measurement of, 437, 437f Thoracic musculoskeletal pain, clinical
Subacromial decompression, for rotator cuff management of, 439–440 examination and targeted management
tendinopathy and subacromial physiotherapy in, 439–440 of, 444–449
impingement (pain) syndrome, 565 myogenic, 433–435 anatomical and biomechanical
Subacromial impingement syndrome (SIS), dental occlusal factors of, 434 considerations of, 445
563–568 increased muscle activity during rest in, assessment and diagnosis of, 445–448
diagnosis of, 564 434–435 diagnosis of, 447–448, 447b
measuring outcome of, 566 neuroendocrine and genetic factors of, history of, 445–446
outcome of, 565–566 434 red flags in, 445
posture and muscle imbalance and, 566 parafunctions of, 434 spinal pathologies in, 445, 446f
treatment of, 564–565 neurogenic, 435–436 yellow flags in, 445–446
Suboccipital muscle group, 96, 96f proposed features of, 436t management of, 448–449
Subscapularis (anterior RC), 563 neuromusculoskeletal assessment and contributing impairments, addressing,
Substrate utilization, in endurance training, management of, 433–443 448–449
74–75 summary of, 440–441 muscle function, optimization of, 448
Subtalar joint pronation, excessive, 529 Tendinopathy, 106–116 postural correction in, 448, 448f
‘Subtle’ adaptations, in sensorimotor assessment of, 114–115 thoracic spine mobility, improvement
dysfunction from pain, 56–59, 57f–60f imaging for, 115 of, 448
long-term consequences of, 59–62, 61f management of, 115 manual examination of, 447
Superior articular processes, 97 pathoaetiology of, 113 physical examination of, 446–447
Supine passive hip external rotation test, at persistent, 112 motion assessment in, 446–447
90°, 390t–391t physical examination of, 114–115 muscle system assessment in, 447
Supine passive hip internal rotation test, at prevalence of, 112 posture, 446, 446f
90°, 390t–391t questioning for, 114 subjective examination of, 445
Supraspinally mediated mechanisms, of recalcitrant, 112 area of symptoms, 445
spinal manipulation, 281 risk factors of, 114 behaviour of symptoms, 445
Supraspinous ligaments, 104 source of pain in, 113–114 Thoracic ring, 497, 498f
Surgery treatment for, 115 Thoracic ring approach ™, 449–455, 450f
for ankle sprains, 551 Tendon, 106–116 categories to consider for, 454t
for anterior dislocation, 570 composition and structure of, 106–108, multimodal treatment program in, 453
Swan-neck deformity, 600 107f non-optimal force vectors in, 453
Synaptic transmission, 24–25 function of, 106 summary for, 453–454
Syndesmosis injury injuries and repair of, 110–111, 111f thoracic ring behaviour, modification of,
diagnosis of, 549, 549t–550t loss of function of, 112 452, 452f
management of, 552 mechanical behaviour of, 108–110, thoracic ring driver, treatment of, 453
Syndesmosis ligament palpation, 549f 108f–110f, 109t thoracic spine and ribcage, connection of,
Syndesmosis sprain, epidemiology of, 547 pain 450
Synovial folds, in craniocervical spine, 94 causes of, 114 whole body function, connecting the
System level, of ageing, 127t source of, 113–114 thorax to, 450–452, 451t
pathology, 112–114 Thoracic ‘ring palpation’, 450
Tendon gliding exercises, 598f ‘Thoracic ring stack and breathe’, 453, 454f
T Tendon injury, 599 Thoracic spine, 444–459, 444b
Taping Tenocyte, 106–108 management of, in patients with COPD,
for patellofemoral pain, 531–532, 532f TENS. see Transcutaneous electrical nerve 455–459
for rotator cuff tendinopathy and stimulation (TENS) anatomy and biomechanics in, 456
subacromial impingement (pain) Tensile overload, in tendinopathy, 113 exercise in, 457–458, 457b, 458f
syndrome, 566 Tensioning techniques, for peripheral to improve flexibility, 456–458
Task imagination, 49–50, 50f nervous system, in neurodynamic manual therapy in, 456–457
‘Teacher-centred’ approaches, in patient management, 289, 290f–291f musculoskeletal system and pulmonary
education, 255 Tertiary prevention, 380, 610 function, relationship between, 456
 Index 625

and symptomatic features of COPD, Treatment effects, clinical research to test, V

456 212–219, 212b, 218b Vaccines, 609
Three-dimensional musculoskeletal model, classic multiple group parallel design Valgus bracing, for knee osteoarthritis,
of cervical spine, 190–191 randomized controlled trial, 214f 541–542
3D mode ultrasound, 145t cross-over design, 215f Validity
Thumb carpometacarpal joint, 602–603 diamond design, 215f COSMIN guidelines, 203t
proprioceptive training for, 602f expertise-based designs, 217f good-quality data, 228
Time series, 222 factorial design, 215, 216t ‘Variable stiffness’ soles, for knee
Timelines, good-quality data, 228 N-of-1 trial designs, 217f osteoarthritis, 542–543
Tinel’s test, 586t randomized withdrawal, 216f Vascular dysfunction, descriptors associated
Tissue, stretching/tearing, in spinal Trigger finger, 603 with, in peripheral regions, 349t
manipulation, 278 Trunk-head coordination, exercises for, 312, Vascular endothelial growth factor (VEGF),
Tissue Doppler imaging, 145t, 148 313f, 313t in endurance training, 74
motion tracking using, 148–149, 149f Tuning curves, EMG, 171–172, 172f Vasti retraining, for patellofemoral pain,
Tissue loading, pain and, 486 Type I muscle fibres, 69, 69f, 75 529–530, 531f
Tissue nociception, to pain neuromatrix, Type II muscle fibres, 69, 69f, 75 Vastus medialis, 528
8–9 Vastus medialis obliquus (VMO), 528
TMS. see Transcranial magnetic stimulation inadequate motor control of, 528–529
(TMS) U VEGF. see Vascular endothelial growth
Tongue, protrusion of, 440, 440f Ulnar collateral ligament injury, 585t factor (VEGF)
‘Toolkit,’ in learning, 256–257 of thumb, 600, 600f Velocity, 68–69, 69f
Tracer techniques, 71 Ulnar nerve, in elbow, 586 Ventroposterior lateral nucleus, 162
Tragus-C7-shoulder angle, 437, 437f Ulnar neuropathy, of elbow, 586, 591 Vertebral arch, 97
Training Ulnocarpal complex, 601–602 Vertebral body
endurance, 304 Ultrasound imaging (USI), 144 of cervical spine, 96–97
of motor control, 302–304, 302f biofeedback of muscle function, 146, of lumbar vertebrae, 102, 102f
neuromuscular adaptations, 303–304 147f Vertebral column, 101–102, 101f
training principles of, 303 contracted muscle, 146 Vertebral end-plate lesions, 131
resistance, 304–306 elastography and, 149–150 Vertical equilibrium, 188
clinical prescription of, 305–306 of elbow, 587, 587f Vertical ground reaction forces (VGRF),
duration of, 305 for lateral ligament or syndesmosis injury, 523
frequency of, 305 548 Vestibular feedback, in lumbar spine, 316
intensity of, 304–305 measuring tissue motion and mechanical Vestibular organs, in postural control, 31
volume of, 305 properties of muscle-tendon unit, Vibration thresholds, 195–196, 195t, 196f
strength, 304 146–148, 148f Visceral pain, referral, sites of, 343, 344f
Transcranial direct current stimulation, motion tracking using tissue Doppler and Vision, in postural balance, 30–31
184 B-mode speckle tracking, 148–149, Visual feedback, in lumbar spine, 316
Transcranial magnetic stimulation (TMS) 149f Vital sign, measurement of, in
cortical silent period, 183 perimuscular connective tissue thickness, physiotherapy, 365
mapping of motor cortex using, 146 Volar plate injury, at proximal
181f in physiotherapy practice and research, interphalangeal joint, 599–600
paired-pulse, 183 144–152 Voltage, 19–20
repetitive, 183–184 relationship between muscle size and Voltage clamp method, 21, 21f
of rotator cuff tendinopathy, 564 strength, 146
single-pulse, 179–183 reliability and, 146
Transcutaneous electrical nerve stimulation types of, 145t W
(TENS), 165, 270–272, 334 technical considerations and, 144 ‘Wait and see’ user, of self-management
clinical studies of, 270–271 validity of, against imaging techniques and website, 360
development of, 336–337 electromyography, 146 Walking cane, use of, 543
dosing of, 271 Uncinate processes, 97 Warm detection threshold, 195t
high-frequency, 271 Uncovertebral joints, 97 Water separation, 154–155
low-frequency, 271–272 Unloader braces, for knee osteoarthritis, Wear-and-tear, theory of ageing, 127t
science mechanisms of, 271–272 541–542 ‘Wear-and-tear’ joint disease, 537
Transient ischaemia, entrapment Unloading, of painful structures, 340 Weight
neuropathies and, 82–83 Unmyelinated nerve fibres, 78, 79t healthy, optimizing, 376t
Transient ischaemic attack, manual Unstable rocker-soled shoes, for knee loss, behaviour modification for, 371
therapy-induced, 350b osteoarthritis, 542–543 Whiplash-associated disorders, 423–432
Translational research, 3 Unstable shoulder, 568–575 acute, 428–429
Transmembrane antiporter molecule, assessment of, 569–570 beliefs and expectations about recovery
21–22 interview, 569 and, 425–426
Transverse ligament, 94, 95f orthopaedic instability tests, 570 chronic, 429–430
integrity of, tests for, 353–354 physical examination, 569–570, compensation and social systems and, 425
Treatment-based classification system, 570f–571f as culturally-dependent condition,
470–474 generalized joint hypermobility and, 425–426
classification categories of, 470–473 573 future directions of, 430
conclusion in, 473 joint hypermobility syndrome and, 573 injustice to, 425
intervention procedures originally management of, 570–573 introduction, 423
proposed in, 471t anterior dislocation, 570–571 medication for, 429
manipulation classification in, 470–472 anterior or posterior subluxation and pain perception and, cultural differences
signs and symptoms originally proposed multidirectional instability, 571 in, 425
in, 471t conservative rehabilitation principles, and post-traumatic stress disorder, 425
specific exercise classification in, 472 571–573, 572t recovery from, expectations in, of
stabilization classification in, 472 posterior dislocation, 571 non-injured laypersons, 426
traction classification in, 472–473 shoulder instability and, 573 role of tissue damage in, 423–425
Treatment effect modification research, 246, Upper motor neurons, 36–37 and clinical presentation of, 424
246t, 247b Upper quarter screen (UQS), 558–559 evidence supporting, 423–424
626 Index

social-cognitive model of, 425–426 Wrist/hand, 595–605 instabilities, 600–602

summary for, 424–425 assessment of, principles of, 595–596 joint injury, 599–600
sympathetic reactivity to pain and, clinical context, 595 osteoarthritis, 602–603
15–16 examination, 595 soft tissue conditions, 603
treatment of, 428–430 history, 595 tendon injury, 599
Wind-up, 9, 10b, 10f, 195t inspection, 595
ratio, 197 investigations, 596
Withdrawal N-of-1 design, 218, 218f mechanism of injury, 595 X
Work disability, prevention of, 380, 382–385 palpation and provocative tests, 596 X-ray, for cam lesions, 508
beyond physical symptoms, 384–385 previous injuries, 595
promotion of ability in, 385 range of motion, 595–596
systems approach to, 382–384, 383f sensation, 595 Y
Work-related musculoskeletal disorders, strength, 596 Y Balance Tests, 396
380 instabilities of, 600–602 ‘You tell me first’ sequences, 253
body regions involved in, 380 management of, principles of, 596–597
clinical syndromes in, 380 exercises, 597, 598f
hazards for, 381 immobilization, 597 Z
physical, 381 oedema control, 597 Z-score quantitative sensory testing, 198f
psychosocial, 381 scar and wound care, 597 Zygapophysial joint disorder, 410
risk control in, 382 therapy, 596–597
Worker health, factors threatening, 379–380 managing common conditions of,
World Health Organization (WHO), 609 597–603
World Health Professions Alliance, 371 complex regional pain syndrome, 603
Wound, care of, 597 fractures, 597–599