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Aesthetic Facial Anatomy
Essentials for Injections
Aesthetic Facial Anatomy Essentials for Injections is the first title of a series to be published in partnership with PRIME Journal
and the World Society of Interdisciplinary Aesthetic & Anti-Aging Medicine (WOSIAM).

PRIME Journal is the leading authority on aesthetic and anti-aging medicine, providing industry news, insightful analysis, and key
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If you have not already subscribed to PRIME, visit the website today at www.prime-journal.com to guarantee each issue of the
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The WOSIAM is a nonprofit organization based in Paris, and membership is available to anyone who has participated in any
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 Aesthetic Facial Anatomy
Essentials for Injections

Edited by

Ali Pirayesh, MD, FCC (Plast)

Plastic, Reconstructive and Aesthetic Surgeon
Founder, Amsterdam Plastic Surgery Clinic, the Netherlands
Consultant, Burns and Tissue Regeneration Unit
University Hospital, Gent, Belgium
Research Consultant, University College Hospital, London, UK

Dario Bertossi, MD
Associate Professor of Maxillofacial Surgery
Specialist in Maxillofacial Surgery, Otolaryngology
Facial Plastic Surgeon
Department of Surgery, Dentistry, Pediatrics and Gynaecology
Chief of Maxillofacial Plastic Surgery Unit
University of Verona, Verona, Italy
Professor of Practice, University of London
Centre for Integrated Medical and Translational Research, London, UK

Izolda Heydenrych, MD
Dermatologist, Founder and Director, Cape Town Cosmetic Dermatology Centre
Consultant, Division of Dermatology, Faculty of Health Sciences
University of Stellenbosch, Stellenbosch, South Africa

With Forewords from Mauricio de Maio, Pierfrancesco Nocini, and Foad Nahai
CRC Press
Taylor & Francis Group
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 CONTENTS
Preface.......................................................................................................................................................... vii
Forewords..................................................................................................................................................... viii
Contributors.................................................................................................................................................... ix

A Aesthetic Regions of the Face.............................................................................................................1

Alessandro Gualdi, Michele Pascali, Heidi A. Waldorf, Rene van der Hulst,
Philippe Magistretti, and Dario Bertossi

B Facial Layers..........................................................................................................................................7
Eqram Rahman, Yves Saban, Giovanni Botti, Stan Monstrey, Shirong Li, and Ali Pirayesh

C Aging of Skin, Soft Tissue, and Bone................................................................................................13

Daria Voropai, Steven Dayan, Luis Fernando Botero, Chiara Botti, Leonard Miller,
and Ali Pirayesh

D Myomodulation....................................................................................................................................17
Mauricio de Maio and Izolda Heydenrych

E Botulinum Toxins.................................................................................................................................33
Massimo Signorini, Alastair Carruthers, Laura Bertolasi, Neil Sadick,
Wolfgang G. Philipp-Dormston, and Dario Bertossi

F Absorbable Soft Tissue Fillers: Core Characteristics.................................................................... 44

Ali Pirayesh, Colin M. Morrison, Berend van der Lei, and Ash Mosahebi

G Complications of Absorbable Fillers................................................................................................ 54

Maurizio Cavallini, Gloria Trocchi, Izolda Heydenrych, Koenraad De Boulle,
Benoit Hendrickx, and Ali Pirayesh

1 Forehead..............................................................................................................................................70
Izolda Heydenrych, Fabio Ingallina, Thierry Besins, Shannon Humphrey,
Steven R. Cohen, and Ines Verner

2 Temporal Region and Lateral Brow...................................................................................................94

Krishan Mohan Kapoor, Alberto Marchetti, Hervé Raspaldo, Shino Bay Aguilera,
Natalia Manturova, and Dario Bertossi

v
 Contents

3 Periorbital Region and Tear Trough................................................................................................. 114

Colin M. Morrison, Ruth Tevlin, Steven Liew, Vitaly Zholtikov, Haideh Hirmand,
and Steven Fagien

4 Cheek and Zygomatic Arch..............................................................................................................132

Emanuele Bartoletti, Ekaterina Gutop, Chytra V. Anand, Giorgio Giampaoli,
Sebastian Cotofana, and Ali Pirayesh

5 Nose���������������������������������������������������������������������������������������������������������������������������������������������������152
Dario Bertossi, Fazıl Apaydın, Paul van der Eerden, Enrico Robotti,
Riccardo Nocini, and Paul S. Nassif

6 Nasolabial Region.............................................................................................................................171
Berend van der Lei, Jinda Rojanamatin, Marc Nelissen, Henry Delmar,
Jianxing Song, and Izolda Heydenrych

7 Lips����������������������������������������������������������������������������������������������������������������������������������������������������183
Ali Pirayesh, Raul Banegas, Per Heden, Khalid Alawadi, Jennifer Gaona,
and Alwyn Ray D’Souza

8 Perioral Region..................................................................................................................................198
Krishan Mohan Kapoor, Philippe Kestemont, Jay Galvez, André Braz,
John J. Martin, and Dario Bertossi

9 Chin and Jawline...............................................................................................................................211

Ash Mosahebi, Anna Marie C Olsen, Mohammad Ali Jawad, Tatjana Pavicic,
Tim Papadopoulos, and Izolda Heydenrych

10 Neck and Décolletage.......................................................................................................................226

Kate Goldie, Uliana Gout, Randy B. Miller, Fernando Felice, Paraskevas Kontoes,
and Izolda Heydenrych

Video Appendix: How I Do Regional Treatments.........................................................................................236

Index............................................................................................................................................................237

vi
 PREFACE
Anatomy has long been the compass guiding who enjoy passing on their passion, tips and tricks in
clinicians through the astounding complexity of the this ever expanding field.
human body.
This book by the Aesthetic Facial Anatomy group
Many textbooks of anatomy display the vital structures is a multi-author, cross-specialty consensus on the
and their anatomical relationships in order to guide essential knowledge of clinically relevant anatomy
medical students and physicians, thus enabling them and injection guidelines mandatory for safe, effective
to learn and execute medical treatments. and aesthetically pleasing application of aesthetic
medicine, and is encouraged to be regularly updated
online by the many authors.
We encountered a void in the plethora of anatomical
scripts where both essential clinical anatomy and The men and women who allowed us to explore
an aesthetic eye for beautification and rejuvenation their anatomical structures after their passing
need to merge. Only a paucity of mostly single- in order for us to pass on this knowledge to our
author texts exist on the essential anatomy for peers are the true hero educators which we should
aesthetic medicine. honour. It has been a privilege to work on this
ongoing project.
The global conference platform of Euromedicom and
its network provided us with unparalleled access to Ali Pirayesh, Dario Bertossi, and
the greatest minds in surgical and medical aesthetics Izolda Heydenrych

vii
 FOREWORDS
“We shall not cease from exploration Fillers and toxins have proven to be affordable
And the end of all our exploring and safe treatments for the aging face. Injectables
Will be to arrive where we started continue to gain popularity and are by far the most
And know the place for the first time…” sought after cosmetic treatments worldwide. With
—from TS Eliot, “Little Gidding”, Four Quartets, this increase in demand and popularity, there arises
with permission from Faber & Faber Ltd. the need for appropriate training; a need to assure
safety as well as efficacy of results.
The ancient art of anatomy, which has long I congratulate the editors Dr Pirayesh, Dr. Bertossi
fascinated the human mind, has in recent years and Dr. Heydenrych for bringing together such an
been considerably expanded by the field of aesthetic illustrious group of thought leaders to share their
medicine. This book beautifully demonstrates knowledge and expertise in this book which is
the fascinating detail beneath the surface of our designed to improve results and enhance safety.
everyday work and should form an invaluable The most feared and devastating complication of
practical resource for those passionate about the injectables is intra-arterial injection of fillers leading
field of medicine. to tissue necrosis and vision loss. The chapters
This initiative is aimed at elevating both procedural organized by facial regions accurately describe the
safety and clinical excellence. anatomy in minute detail, with beautiful medical
illustrations and immaculately clear cadaver
I am proud to be part of it.
dissections which highlight the location and course
Mauricio de Maio, MD of blood vessels at risk. The risk to blood vessels
in each location is outlined and safe injection
During my 40 years of practice, I have trained many techniques are recommended that reduce risk.
residents, some of them who are now masters in the This book will be invaluable not only to the novice
field of facial aesthetics, where they are witnesses eager to perfect their injection technique but also to
of the impressive growth this field has undergone those of us who have had years of experience. As
during the last few decades. As a teacher, my someone with a long career as a surgical educator
role has always been to accurately evaluate the and proponent of patient safety, I plan to put this
international scientific production. As I received the book in the hands of all our trainees.
first draft of this comprehensive book, I realized
that its impact on the medical aesthetic field will be Foad Nahai, MD FACS FRCS (Hon)
great as it will provide the reader a solid scientific
knowledge and a practical tool for beginners as well
as for the advanced injectors.
I wish for all readers to understand the deepest
meaning of this work. If culture and learning are
made to light up our minds before our hands, the
result has been achieved.
Pierfrancesco Nocini, MD

viii
 CONTRIBUTORS
Shino Bay Aguilera Emanuele Bartoletti
Dermatologist Plastic Surgeon
Assistant Professor of Dermatology Studio Bartoletti-Cavalieri
Shino Bay Cosmetic Dermatology Fatebenefratelli Hospital
and Laser Institute Rome, Italy
and
Dermatology Department Laura Bertolasi
NOVA Southeastern University Department of Neurosciences
Fort Lauderdale, Florida, USA Unit of Neurology AOUI
Verona, Italy
Khalid Alawadi
Consultant Plastic and Hand Surgeon Thierry Besins
Department of Hand and Reconstructive Plastic Surgeon
Microsurgery Private Clinic
Rashid Hospital Nice, France
Dubai Health Authority
Dubai, United Arab Emirates Luis Fernando Botero
Plastic Surgeon
Clinica Quirofanos El Tesoro
Chytra V. Anand
Medellín, Colombia
Chief Cosmetic Dermatologist
Kosmoderma Clinics
Chiara Botti
Bangalore, India
Plastic Surgeon
Villa Bella Clinic
Fazıl Apaydın Salo, Italy
ENT Surgeon
Department of Otorhinolaryngology Giovanni Botti
Ege University Plastic Surgeon
Izmir, Turkey Villa Bella Clinic
Salo, Italy
Raul Banegas
Plastic Surgeon Koenraad De Boulle
Director of Centro Arenales Dermatologist
Medical Center Aalst Dermatology Clinic
Buenos Aires, Argentina Aalst, Belgium

ix
 Contributors

André Braz Wolfgang G. Philipp-Dormston

Dermatologist Dermatologist
Private Practice Medical Director, Department for Dermatology,
Rio de Janeiro and São Paulo, Brazil Dermatosurgery and Allergology
Clinic Links vom Rhein
Alastair Carruthers Cologne, Germany
Dermatologist
Clinical Professor of Dermatology Paul van der Eerden
University of British Columbia ENT/Facial Plastic Surgeon
and Lange Land Hospital
Private Practice Zoetermeer, the Netherlands
The Carruthers Clinic
Steven Fagien
Vancouver, British Columbia, Canada
Oculoplastic Surgeon
Maurizio Cavallini Aesthetic Eyelid Plastic Surgery
Plastic Surgeon Private Practice
Unit of Plastic Surgery and Dermatology Boca Raton, Florida, USA
CDI Hospital Fernando Felice
Milan, Italy Associate Professor in Anatomy
University of Buenos Aires
Steven R. Cohen
Aesthetic Plastic Surgeon, Private Practice
Plastic Surgeon
Buenos Aires, Argentina
Clinical Professor of Plastic Surgery
University of California, San Diego and Jay Galvez
Private Practice Facial Plastic Surgeon
FACES+ Galvez Clinics
La Jolla, California, USA Makati City, the Philippines
Sebastian Cotofana Jennifer Gaona
Associate Professor of Anatomy Plastic and Reconstructive Surgeon
Department of Clinical Anatomy Founder of Keraderm and INTI Foundation
Mayo Clinic Private Practice
Rochester, Minnesota, USA Bogota, Colombia
Steven Dayan Giorgio Giampaoli
Facial Plastic Surgeon Resident in Maxillofacial Surgery
Clinical Assistant Professor Maxillofacial Surgery Department
University of Illinois University of Verona
Chicago, Illinois, USA Verona, Italy

Henry Delmar Kate Goldie

Plastic Surgeon Aesthetic Physician
Clinique Del Mar Medical Director, European Medical Aesthetics Ltd
Antibes, France London, UK

x
 Contributors

Uliana Gout Fabio Ingallina

Aesthetic Physician Plastic Surgeon
London Aesthetic Medicine Clinic and Academy Private Practice
London, UK Catania, Italy
Alessandro Gualdi
Plastic Surgeon Mohammad Ali Jawad
Clinical Professor Plastic, Reconstructive and
Vita-Salute San Raffaele University Burn Surgeon
Milano, Italy R5 Aesthetic and Healthcare
Karachi, Pakistan
Ekaterina Gutop
Dermatologist Krishan Mohan Kapoor
Actual Clinic Consultant Plastic Surgeon
Yaroslavl, Russia Plastic and Cosmetic Surgery
Per Heden Fortis Hospital
Plastic Surgeon Mohali, India
Associate Professor in Plastic Surgery and
Karolinska Institute
Stockholm, Sweden Honorary Senior Clinical Lecturer
University of London
Benoit Hendrickx London, UK
Plastic Surgeon
Associate Professor Philippe Kestemont
University Hospital Brussels Facial Plastic Surgeon
Brussels, Belgium Saint George
Haideh Hirmand Aesthetic Medicine Clinic
Plastic Surgeon Nice, France
Clinical Assistant Professor of Surgery
Cornell-Weill Medical College Paraskevas Kontoes
New York-Presbyterian Hospital Plastic Surgeon
New York City, New York, USA DrK Medical Group
Athens, Greece
Rene van der Hulst
Head and Professor of Plastic Surgery
Maastricht University Medical Center Berend van der Lei
Maastricht, the Netherlands Plastic, Reconstructive and Aesthetic
Surgeon
Shannon Humphrey Professor, Aesthetic Plastic Surgery
Clinical Assistant Professor Department of Plastic Surgery
Department of Dermatology and Skin Science University Medical Centre Groningen
University of British Columbia Bey Bergman Clinics
Vancouver, Canada Groningen, the Netherlands

xi
 Contributors

Shirong Li Leonard Miller

Professor of Plastic Surgery Plastic Surgeon
Department of Plastic Surgery Founder, Boston Center for Facial Rejuvenation
Third Military Hospital Brookline, Massachusetts, USA
Chongking, China
Randy B. Miller
Steven Liew Plastic Surgeon
Plastic Surgeon Miller Plastic Surgery
Medical Director Shape Clinic Miami, Florida, USA
Darlinghurst, Australia
Stan Monstrey
Philippe Magistretti Professor in Plastic Surgery
Consultant Radiologist and Aesthetic Plastic Surgery, Burns and Tissue Regeneration Unit
Physician Gent University Hospital
The Summit Clinic Gent, Belgium
Crans Montana, Switzerland
Colin M. Morrison
Mauricio de Maio Consultant Plastic Surgeon
Plastic Surgeon St. Vincent’s University Hospital
MD Codes™ Institute Dublin, Ireland
São Paulo, Brazil
Ash Mosahebi
Natalia Manturova Professor of Plastic Surgery
Plastic Surgeon Royal Free Hospitals and University College Hospital
Head, Department of Plastic and Reconstructive London, UK
Surgery
Cosmetology and Cell Technologies Paul S. Nassif
Russian National Research Medical Facial Plastic and Reconstructive Surgery
University Assistant Clinical Professor
Moscow, Russia Department of Otolaryngology – Head and Neck
Surgery
Alberto Marchetti Division of Facial Plastic and Reconstructive Surgery
Plastic Surgeon University of Southern California Keck School of
San Francesco Clinic Medicine
Verona, Italy Los Angeles, California, USA

John J. Martin Marc Nelissen

Oculoplastic Surgeon Plastic Surgeon
Oculo-facial Plastic Surgery Global Care Clinic
Miami, Florida, USA Heusden-Zolder, Belgium

xii
 Contributors

Riccardo Nocini Hervé Raspaldo

ENT Surgery Facial Plastic Surgeon
Department of Otolaryngology Chef de Clinique des Universités
Department of Surgical Sciences, Dentistry, Face Clinic Genève
Gynecology and Pediatrics Geneva, Switzerland
University of Verona
Verona, Italy Enrico Robotti
Plastic Surgeon
Anna Marie C Olsen Chief, Department of Plastic Surgery
Dermatologist Papa Giovanni XXIII Hospital
Private Practice Bergamo, Italy
London, UK
Yves Saban
Tim Papadopoulos Facial Plastic Surgeon
Plastic Surgeon Private Practice
Private Practice Nice, France
Sydney, Australia
Neil Sadick
Michele Pascali Dermatologist
Plastic Surgeon Sadick Dermatology
Plastic Surgery Academy Roma New York City, New York, USA
Rome, Italy
Massimo Signorini
Tatjana Pavicic Plastic Surgeon
Dermatologist Studio Medico Skin House
Private Practice for Dermatology Milano, Italy
and Aesthetics
Munich, Germany Jianxing Song
Professor of Plastic and Reconstructive Surgery
Eqram Rahman Changhai Hospital, Second Military Medical
General Surgeon University
Associate Professor Shanghai, China
Division of Surgery and Interventional
Science Alwyn Ray D’Souza
University College London Plastic Surgery
London, UK London Bridge Hospital
London, UK
Jinda Rojanamatin
Dermatologist Ruth Tevlin
Head of Dermatosurgery and Laser Department Department of Surgery
Institute of Dermatology Stanford University School of Medicine
Bangkok, Thailand Stanford, California, USA

xiii
 Contributors

Gloria Trocchi Heidi A. Waldorf

Specialist in Internal Medicine Dermatologist
Aesthetic Medicine Department Waldorf Dermatology Aesthetics
Fatebenefratelli Hospital Nanuet, New York, USA
Rome, Italy
and
Ines Verner
Dermatologist Associate Clinical Professor
Department of Dermatology and Regenerative Department of Dermatology
Medicine Icahn School of Medicine of Mount Sinai
Verner Clinic New York City, New York, USA
Tel Aviv, Israel
Daria Voropai Vitaly Zholtikov
Aesthetic Physician Plastic Surgeon
AEGIS London Private Practice “Atribeaute Clinic”
London, UK Saint Petersburg, Russia

xiv
A AESTHETIC
REGIONS OF
THE FACE
Alessandro Gualdi, Michele Pascali, Heidi A. Waldorf,
Rene van der Hulst, Philippe Magistretti, and Dario Bertossi

FOREHEAD During the aging process, the forehead surface

increases due to progressive hairline recession and
widening of the orbital rims, with subsequent descent
The superior forehead margin lies at the hairline, whilst of the eyebrows. The lateral forehead aspect remains
the lateral border is formed by the temporal crest where relatively unchanged.
the frontalis and temporalis muscles fuse. The glabella,
frontonasal groove (central), and the eyebrows over- Insightful understanding of the forehead and gla-
lying the supraorbital ridges form the inferior bound- bella is of great clinical importance. The frontalis is
ary (Figure A.1). The forehead does not demonstrate a very superficial muscle which may demonstrate
overt ethnic variations, but is usually shorter in South several anatomical variants which need be taken into
American and Asian patients whilst Caucasians and account for effective treatment with neuromodulators.
Africans have a higher, yet variable forehead height. The corrugator, one of the most important targets for
neuromodulator treatment, lies at the medial orbital
rim. Its medial origin is deep on bone, after which it
courses superolaterally to insert into the skin over the
lateral brow. Here it fuses with inferior frontalis fibers.
Procerus is a vertical, medial muscle lying deep at the
radix of the nose. The supratrochlear and supraorbital
vessels are the major vessels in this area. They are
delineated by overlying creases, and knowledge of
their anatomical depth is of paramount importance
as communications between internal and external
carotid circulations pose a high risk for blindness
after inadvertent intravascular filler injection. Nerves
Figure A.1 The frontal area. and vessels generally follow an adjacent course.

1
 Aesthetic Regions of the Face

It is important to note that a deep branch of the supra- temporal vein. This is a very large vein draining retro-
orbital nerve runs approximately 1 cm medial to the gradely to the jugular vein and inadvertent injection may
temporal crest. To minimize pain or nerve damage, it cause embolism and death. The middle temporal vein
is advisable to avoid injecting this region with sharp anastomoses with the sentinel vein. Injections should
needles. be either very deep or very superficial, and done with
knowledge of the course of the middle temporal vein,
which runs 1–2 cm above the zygomatic arch.

TEMPORAL REGION
EYE AND PERIORBITAL REGION
The temporal region is a well-defined region extend-
ing from the temporal crest to the zygomatic arch
(Figure A.2). The orbital margin forms the anterior The periorbital region extends from beneath the
and hairline the posterior limit. There is little ethnic eyebrow to the zygomatico-malar ligament, and lies
variation in the extent of the temporal region, but in between the nasojugal sulcus and lateral aspect of
African skulls, the temporal bone is very thick, mak- the orbicularis retaining ligament (Figure A.3).
ing temporal hollowing uncommon. The temporal
area contributes to the aging process due to wid- The periorbital region is the area demonstrating the
ening of the lateral orbital margin and concomitant most pronounced age and ethnic variation. In African
underlying bone resorption, thus causing a hollowed, skulls, the orbits are wider and more rectangular,
aged or diseased appearance. The temporal artery and demonstrate earlier onset of bone resorption.
courses from deep to superficial through the tempo- The scant subcutaneous fat and protruded superior
ral fossa. It passes close to the ear, near the root of orbital margin causes a hollow-eyed look due to sig-
the helix, before running in the temporoparietal fascia nificant retraction of the periorbital tissues. Although
to pass approximately 2 cm lateral to the brow. It may the bone structure in Asian patients is similar to
anastomose with the supratrochlear and supraorbital Caucasians, the tendon structure differs and the
vessels, thus comprising another danger zone for upper eyelid forms an epicanthic fold.
potential blindness after inadvertent filler injection.
During the aging process, underlying bone resorp-
The temporal area contains important veins, the tion leads to progressive widening of the orbit. The
most important and dangerous of which is the middle

Figure A.2 The temporal area. Figure A.3 The periorbital area.

2
 Cheek

eyebrows descend, and eyelid skin laxity may cause The deep subcutaneous branch divides close to the
blepharochalasis and ptosis, thus impairing vision. alar nasal sulcus to form the lateral nasal and angular
The site for the neuromodulator injection is usually arteries. In Africans, short noses with large nostrils
in the lateral preseptal orbicularis oculi muscle where and tips are characteristic. The central maxilla is well
there is no vascular danger zone. The use of neuro- developed and protrudes anteriorly. The nasal dor-
modulators in the upper eyelid is not recommended, sum is usually flat and the radix is located slightly
because of the high risk of upper eyelid ptosis. The above the intercanthal line. Asian patients have a flat
upper lid is a highly dangerous zone for filler injec- nose, low radix and underrepresented dorsum. The
tions as connections between the supratrochlear, nostrils are thin, and the tip is usually very short and
medial palpebral and ophthalmic arteries may lead to rounded. With aging, the nasal cartilage enlarges and
blindness after inadvertent intravascular filler place- the nasal bone cavity widens. The cartilage becomes
ment. It is thus imperative to have insightful anatomy thinner and the tip falls downward. Although the bony
knowledge and to use a cannula when treating the dorsum does not change in older patients, it may
A-frame deformity of the upper eyelid. become thinner, with a “sharper” edge. The lateral
nasal vessels run above the alar groove to provide
vascularization to the tip of the nose, together with
an artery coming from the superior labial artery and
NOSE passing through the columella. The tip is highly vas-
cularized, especially in the superficial plane.
The nose is ethnically distinct, with variable bone
structure and cartilage development. The radix of the nose is also a dangerous area due
to the arborization of vessels. It is important to inject
It extends from the radix superiorly, to the nostrils on the periosteum to avoid embolization or compres-
and the columella inferiorly, and naso-jugal grooves sion of especially the dorsal branch of the supra-
laterally (Figure A.4). trochlear artery. Close to the radix, just below the
medial canthus, the angular and facial veins anas-
The nose represents a vascular danger area. Above tomose before draining into the cavernous sinus,
the modiolus, the facial artery superficializes and making this an important danger zone. It is advised
branches in two. that injections are placed from lateral to medial, with
massage toward the more medial location. Using a
cannula may prevent complications. The mid-third
dorsal aspect of the nose is considered the safest
injection area.

CHEEK

The cheek lies in the infraorbital region, extend-

ing laterally from the ear to the nose (above) and
mouth (below) in the medial aspect (Figure A.5).
Figure A.4 The nasal area. African patients have larger cheeks and pronounced

3
 Aesthetic Regions of the Face

the medial limbus. It is important to avoid intravascular

injection by placing injections lateral to the foramen.
Avoid embolization into the facial vein, which runs from
the mandibular angle to the medial orbital canthus.

LIPS AND PERIORAL REGION

The perioral region comprises the lips and area

­corresponding to the orbicularis oris muscle (Figures
A.6 and A.7).

Figure A.5 The cheek area. Whilst the extent of the mouth region does not vary
among ethnicities, lip proportions do. African and
Mediterranean patients generally have bigger lips,
zygomatic bones, both frontally and laterally, whilst a while Asian, North European, and North American
prominent central maxilla often prevents a flat-faced patients have thinner lips.
appearance.

Asian patients also have pronounced cheekbones,

but the flatter nose and small maxillary bones con-
tribute to the typically flatter Asian face. The cheek
fat compartment is usually well developed.

With aging, widening of the orbital and nasal cavi-

ties and thinning of bone cause soft-tissue sagging,
thus enhancing the nasolabial folds, tear troughs and
marionettes lines.

The facial nerve originates near the ear lobe, deep

to the parotid gland, after which it divides into five Figure A.6 The perioral area.
branches after emerging from the anterior parotid
border. The frontal nerve superficializes above the
zygomatic arch, where it accompanies the superficial
temporal artery. This represents a danger area.

The facial fat compartments are very well defined

and may be divided into superficial and deep groups.
Volumizing certain compartments ensures maximal
projection, whilst injecting into others may induce sag-
ging (see Cheek chapter). The infraorbital nerve enters
the face via the infraorbital foramen which lies 6–8 mm
below the infraorbital rim on a perpendicular line at Figure A.7 The lip area.

4
 Jaw

Elderly patients also present with thinner lips. In the

case of total or partial edentulism, there may be
moderate to severe alveolar crest atrophy, causing a
retraction of the lips and perioral tissue with shorten-
ing of the nose-chin length.

Several muscles insert into the modiolus to exert

an effect on smiling. Zygomaticus major is stronger
in effecting an upwards or zygomatic smile. As the
elevators weaken with age, risorius may dominate Figure A.8 The chin and jawline area.
to cause a more horizontal smile. Eventually, the
depressor anguli oris (DAO) may dominate to cause
a downwards smile. The zygomaticus minor, levator mandible. In elderly or edentulous patients, the fora-
labii superioris, and levator labii superioris aleque men is usually closer to the alveolar ridge. Injecting
nasi insert into the upper lip. the mental nerve may cause permanent dysesthesia,
paresthesia, or anesthesia of the lower lip.
After passing below the commissure, the facial artery
superficializes and divides into superior and inferior
labial branches. The superior labial artery penetrates JAW
the orbicularis oris to enter the lip, running at the junc-
tion of the dry and wet mucosae. The inferior labial
artery originates from the facial artery below the The jaw area extends from the DAO (anteriorly) to
commissure, and runs from deep to superficial close the temporomandibular joint posteriorly; inferiorly, it
to the mucosa. Inferiorly, there is more variation in is defined by the bony margin of the jawline (Figure
morphology. A.9). There are no technically specific aging changes
other than soft-tissue sagging. The facial artery
crosses the mandible approximately 1 cm anterior to
the anterior border of the masseter. The latter is the
CHIN strongest muscle in the body.

The chin lies between the DAO (laterally), inferior

margin of the orbicularis oris (superiorly) and man-
dibular margin inferiorly (Figure A.8). African patients
have a wider chin, thicker bone, and more prominent
lower maxilla.

Asians often present a retracted maxilla and smaller

chin. Apart from soft-tissue sagging, aging does not
affect the chin area directly. However, anterior protru-
sion may result due to loss of occlusion in edentulous
patients. Although the chin is a relatively safe area
to treat, it is important to note the emergence of the
mental nerve just below the two premolars of the Figure A.9 The neck.

5
 Aesthetic Regions of the Face

NECK the anterior border of the sternocleidomastoid, the

midline of the neck, and inferior border of the man-
dible. The posterior triangle is defined as the area
The neck is defined as the anatomical area o­ riginating bounded by the posterior border of the sternocleido-
anteriorly from the inferior surface of the mandible, mastoid (SCM), anterior border of the trapezius and,
running to the superior surface of the manubrium inferiorly, the lateral third of the clavicle. The visible
sterni. The posterior neck borders are bounded anterior triangle is the predominant focus of aesthetic
superiorly by the occipital bone of the skull and infe- treatments. With aging, the neck develops increased
riorly by the intervertebral disc between CVII and T1. soft tissue laxity, excess skin, fat accumulation and
The neck is further divided into anterior and poste- loss of the cervicomental angle.
rior triangles. The anterior triangle is bounded by

6
B FACIAL LAYERS
Eqram Rahman, Yves Saban, Giovanni Botti,
Stan Monstrey, Shirong Li, and Ali Pirayesh

The face, with its diverse ability to portray emotions However, Mendelson and Wong (2013) have posed
whilst communicating, is one of the most uniquely that a more global understanding is facilitated by
recognizable areas of the human body. An increasing distinguishing between functional regions and con-
interest in facial aesthetics, coupled with consider- sidering the anatomy in terms of a layered construct
able research, has extended our understanding of bound together by retaining ligaments.
the facial layers and the subtle physical variations
resulting from underlying bone structure and genetic Seven major layers may be differentiated [2] (see
factors. With progressive aging, the face undergoes Figure B.1):
asynchronous changes which may present unique
surgical challenges. Insightful understanding of facial 1. Skin
anatomy as pertaining to the aging process facilitates 2. Superficial fat
treatment planning and predictable outcomes [1]. 3. Superficial muscular aponeurotic system (SMAS)
Traditionally the face has been divided into upper, 4. Muscle
middle and lower horizontal thirds with the upper face 5. Vasculature
extending from the trichion to the glabella, the mid- 6. Deep fat
face from glabella to the subnasale, and lower face 7. Bone
extending to the menton.

Figure B.1 The schematic illustration of the facial layers.

7
 Facial Layers

SKIN The superficial and deep layers are separated by

the superficial muscular aponeurotic system (SMAS).
Superficial fat is understood to be separated into
The skin represents the superficial layer of the face unique compartments, which are divided by fascial
and is an important indicator of age. In youth, the skin septae containing vascular structures [2,5]. The
is smooth, firm, unblemished, and retains a uniform major role of the fat layers is as a gliding plane for
texture [3]. The skin may be histologically divided into the facial mimetic muscles [5].
epidermis and dermis, with the dermis consisting of
collagen, elastic fibers, and ground substance com- The superficial fat compartments comprise the
prising mucopolysaccharides, hyaluronic acid, and nasolabial, medial, middle, and lateral temporal-
chondroitin sulphate [3]. cheek, central, middle, and lateral temporal-cheek
(found within the forehead) and superior, inferior,
Cutaneous aging often escalates from the fourth and lateral orbital fat pads. The nasolabial fat,
decade under the influence of contributory genetic, located medial to the cheek fat pads, plays a pro-
hormonal, behavioural and environmental factors nounced role in sagging of the nasolabial fold. The
[3,4]. During soft tissue aging, the two distinct pro- orbicularis retaining ligament (ORL) is situated
cesses of deflation and descent manifest as excess 2–3 mm below the inferior orbital rim and forms the
skin [5]. Wrinkles start to appear in the lower eyelids superior border of both the nasolabial and medial
and lateral orbital areas, along with the development cheek fat compartments. The middle cheek fat com-
of dyschromia, textural changes, pigmentation, dry- partment, juxtaposed between the medial and lat-
ness, thinning, folds, drooping, and mimetic lines [3]. eral temporal-cheek fat compartments, contains a
The midface is particularly susceptible to UV-induced superior fascial border known as the superior cheek
aging, with the subsequent development of rough, septum [2].
wrinkled and leathery skin carrying a higher inci-
dence of telangiectasias, premalignant conditions The individual fat compartments age at different
and malignancies. Other causes of extrinsic aging tempi and vary metabolically, thus contributing to
include smoking, pollution, infrared-A radiation and segmental loss of fullness and the stigmata of aging.
also visible light [3,4]. Recent advances in the under- The periorbital, forehead, malar, temporal, mandibu-
standing of volume loss as a critical component of lar, mental, glabellar, and perioral sites are prone to
facial aging, and the subsequent integration of vol- volume loss, whilst the nasolabial and inferior jowl
ume replacement into both surgical and non-surgical compartments may hypertrophy. The infraorbital and
treatment algorithms, arguably represents one of the malar fat pads often become more prominent, with
most significant advances in the field of facial reju- anterior protrusion of the malar fat causing it to bulge
venation [6]. against the nasolabial crease, thus emphasizing the
nasal fold [6]. It is important to understand that indi-
vidual fat pads behave differently after injection with
fillers, with inferior displacement of the superficial
SUPERFICIAL FAT nasolabial, middle cheek, and jowl compartments
after injection. However, injection into the medial and
In youth, the facial fat consists of a diffuse, bal- lateral cheek and superficial temporal compartments
anced spread of superficial and deep fat which cre- lead to an increase in local projection without inferior
ate the different arcs and convexities of the face. displacement.

8
 Muscle

SUPERFICIAL MUSCULAR should be performed deep to the superficial tempo-

APONEUROTIC SYSTEM (SMAS) ral fascia in order to avoid accidental denervation-
related injuries [2].

The SMAS, which has been recognized since 1799,

is a unique subcutaneous fascia which is continu-
ous with the platysma below and galea above. It DEEP FAT
acts as an investing fascia for the facial mimetic
muscles, thus playing an important role in facial
expression [2,5]. The SMAS is firmly adherent to The deep fat comprises the medial and lateral sub-
the parotid–masseteric fascia in the lateral aspect, orbicularis oculi fat (SOOF), and the deep medial
where it is known as the immobile SMAS. The facial cheek fat. Whilst the majority of the SOOF is found
retaining ligaments, which originate from either the inferior to the lateral aspect of the infraorbital rim, it
periosteum (zygomatic and mandibular retaining is also found underneath the orbicularis oculi muscle
ligaments) or underlying muscle fascia (masseteric [7]. Other deep fat compartments include the tem-
and cervical retaining ligaments) transmit through poral fat pad and a deep addition of this pad known
the SMAS to the overlying skin and serve as barri- as Bichat’s fat pad [3]. The deep, supraperiosteal
ers between the superficial and deep facial fat com- fat layer is located beneath the SMAS. Although the
partments [12]. Neurovascular structures, or “facial SMAS is sandwiched between fat layers, there are
danger zones,” are located between these retaining bilaminar connecting membranes or fusion zones
ligaments [4]. containing neurovascular structures [7]. Compared
with the superficial fat layer, the deep fat layer is com-
Superiorly, the SMAS passes over the zygomatic posed of segmental, large white lobules containing a
arch to meet with the superficial temporal fascia [5]. scant system of thin fibrous septae [3]. With aging,
The SMAS is considerably thicker over the parotid the deep fat layers may disintegrate and descend,
gland, but thins substantially as it courses medially. resulting in a more prominent appearance of the infe-
Superior to the zygomatic arch, the SMAS is known rior border of the orbicularis oculi which may accen-
as the superficial temporal fascia where it splits to tuate the malar crescent and the nasojugal fold [6].
accommodate the temporal branch of CN VII and the Post-menopausal changes due to decreased estro-
intermediate temporal fat pad [2,7]. gen may cause increased fat deposition in combina-
tion with decreased superficial fat [3].
Degenerative changes in the viscoelastic proper-
ties and three-dimensional structure of the SMAS
result in ptosis. Researchers have hypothesized
MUSCLE
that there is earlier and more progressive aging in
the midface due to a decreased amount of SMAS
[4]. With increasing age, retaining ligaments are The facial muscles can be categorized as periocular
at risk of weakening, thus leading to further pto- and perioral and broadly organized into four layers,
sis of the masseteric SMAS and resultant jowl where CN VII runs between the deepest and third
­formation [2]. layer. The first, superficial layer consists of the orbi-
cularis oculi, the zygomaticus minor, and the depres-
Due to the proximity of the SMAS to the temporal sor anguli oris. The second layer contains the levator
branch of CN VII, any dissection in this location labii superioris alaeque nasi, the zygomaticus major,

9
 Facial Layers

the risorius, the depressor labii inferioris, and the medial to lateral at the junction of the proximal third
platysma. The third layer includes orbicularis oris after which it becomes the angular artery which anas-
and levator labii superioris. The final, deepest layer tomoses with the superficial temporal artery (STA).
consists of the buccinator, the levator anguli oris, and
the mentalis [8]. Whilst the major function of facial The ophthalmic artery is the major artery supplying
muscles relates to facial movement, they also play a the orbit. Originating from the internal carotid artery
significant role in maintaining soft-tissue support. The in the middle cranial fossa, this artery traverses
SMAS unites and advances the facial muscles, espe- the optic foramen and subdivides into numerous
cially the zygomaticus major and orbicularis oris [2,5]. branches inside the orbital cavity [7].
The mimetic muscles of the cheek are separated into
a superficial and deep layer. The superficial layer The superficial temporal artery represents the final
consists of zygomaticus major and minor, levator branch of the external carotid artery. This artery
labii superioris, risorious, depressor anguli oris, orbi- arises inside the parotid gland at the point where
cularis oculi, and the orbicularis oris. The deep layer the maxillary artery branches off the external carotid
contains the levator anguli oris, buccinator, depressor artery. Bilaterally, this artery supplies a large area of
labii inferioris, and the mentalis [5]. facial skin, including the lateral forehead, the temple,
the zygoma, and the ear. One prominent branch that
Muscular aging can cause prominent changes such stems from the superficial temporal artery includes
as declining muscle mass and strength. An example the transverse facial artery (also originating from the
of this can be seen in the midface, where the orbi- parotid gland) [7].
cularis oris thins with age while the orbicularis oculi
does not. Extensive investigations of facial MRIs at
The forehead is supplied by the supraorbital and
different ages have shown that the midface mus-
supratrochlear arteries (branches of the ophthalmic
cles start to shorten and straighten simultaneously.
artery). The nose has a particularly intricate vascu-
Researchers have hypothesized that this, in addition
lar network of tiny arteries within the alae, tip and
to a lifetime of facial contractions, may cause pro-
columella. Most of this is supplied by the lateral
lapse of the deep midfacial fat compartments [4].
nasal artery (originates from the facial artery) or
superior labial artery (also originates from the facial
artery). The upper lip is supplied primarily by the
VASCULATURE superior labial artery, while the lower lip is supplied
by three labial arteries. The chin’s main vasculature
Three major arteries originating directly from the is the mental artery (branch of the inferior alveolar
external carotid artery or subsequent branches pro- artery) [7].
vide arterial supply to the face: the facial, transverse
facial, and infraorbital arteries [7,9]. The facial artery, The majority of veins are located close to the simi-
which is the largest, crosses the inferior border of larly named arteries. After crossing the inferior man-
the mandible just anterior to the masseter, where its dibular border with the facial artery, the facial vein
pulsation may be felt, after which it travels in a coiled takes a direct path to the medial canthus. The lateral
fashion towards the pyriform fossa [9]. It runs from forehead and temporal/parietal regions usually drain
deep on the mandible, over the buccinator, beneath via the superficial temporal vein, while the middle
risorius and zygomaticus major, under or over zygo- forehead and upper eyelid drain via the angular or
maticus minor, crosses the nasolabial fold from ophthalmic veins within the cavernous sinus. Venous

10
 Bones

drainage of the midface is via the infraorbital vein and The greater auricular nerve is found approximately
pterygoid plexus; certain structures, such as the lips 5 cm inferior to the external auditory meatus, running
and cheeks drain into the facial vein [7]. deep within the superficial cervical fascia. The men-
tal nerve, a branch of the inferior alveolar nerve, exits
The location, size and origin of the major arteries may the mental foramen where it can be seen and pal-
vary between individuals and races [7,9]. With aging, pated when the oral mucosa is stretched. This nerve
random degenerative changes can occur in individual provides innervation to the lower lip and the man-
vessels, including increased diameter, decreased dible. The buccal mucosa and the skin on the cheek
elasticity, and arterial hypertension. These changes is innervated by the buccal branch of the mandibular
can result in elongation and further tortuosity of these nerve, while the anterior two-thirds of the tongue is
arteries [9]. innervated by the lingual nerve (a branch of the man-
dibular division of the trigeminal nerve) [2].
The facial artery crosses the inferior border of the
mandible just anterior to the masseter, where its pul- Face transplants have rapidly blossomed into a fea-
sation may be felt, after which it travels in a coiled sible management for patients with extreme disfig-
fashion towards the pyriform fossa [9]. It runs from urements. To help repair damaged facial expression
deep on the mandible, over the buccinator, beneath muscles and preserve their function, it is vital also
risorius and zygomaticus major, under or over zygo- to understand that these muscles do not contain
maticus minor, crosses the nasolabial fold from proprioceptive receptors, compared with mastica-
medial to lateral at the junction of the proximal third tion muscles (which are innervated by the trigeminal
after which it becomes the angular artery which anas- nerve and thus contain proprioceptors) [7].
tomoses with the superficial temporal artery (STA).

BONES
NERVES
Youthful features have been said to be optimally
present at a point in time when a specific set of skel-
Cranial nerve (CN) VII—the facial nerve—is the main
etal proportions are ideal for their soft-tissue enve-
motor innervation of the facial muscles, with damage
lope. The skeletal framework forms the basis on
to CN VII being one of the most dreaded (but rare)
which unique facial characteristics are built, render-
complications of surgery. After exiting the stylomas-
ing underlying bone vital in providing and preserving
toid foramen, an upper and lower division develops
ideal soft-­tissue relationships.
as it passes through the parotid gland before trav-
elling to the facial muscles [3]. This nerve harbors
Important facial bony constituents include the fron-
significant clinical implications during facial surgery
tal, maxillary, zygomatic, palatine, nasal, temporal,
[5]. Another significant clinical consideration during
lacrimal, ethmoidal and mandibular bones. Bone
a mandibular block (CN Vll), is potential hemifacial
provides structural support and attachment sites for
paralysis, otherwise known as Bell’s palsy [7].
the muscles of facial expression and mastication, and
also protects certain structures such as the eyes.
Other important innervations include CN V (trigemi-
nal nerve), which has three branches as well as addi- The facial skeleton undergoes both expansion and
tional branches from the cervical plexus. selective resorption throughout life, with the pyriform

11
 Facial Layers

and orbital apertures being particularly susceptible by the aging process. This layered structure provides
to age-related resorption. Maxillary recession and a an intricate canvas, adding to the functional and artis-
10° decrease in the maxillary angle have been noted tic imagery required during aesthetic treatments.
after 60 years of age [11]. Midface skeletal involution
also occurs from the sixth decade, occurring more By first breaking the anatomy down into basic layers,
frequently in women than men [4]. Skeletal regres- it is easier to visualize the integral structural an func-
sion of particularly the inferolateral orbital rim and tional components before attempting to brainstorm
alveolar ridges, contributes to loss of midfacial sup- novel aesthetic solutions.
port and also loss of overall facial height.
Age-related changes within the nasal aperture,
References
paired nasal bones, and ascending processes of
maxillae may lead to prominent changes, including 1. Kumar N et al. Plast Reconstr Surg Glob Open.
nasal lengthening, sagging of the tip, and posterior 2018;6(3):e1687.
displacement of the columella and lateral crura [11]. 2. Prendergast PM. Anatomy of the face and neck.
Selective resorption of the upper jaw may lead to a In: Cosmetic Surgery: Art and Techniques.
subsequent loss of dentition, with Bartlett et al. [13] Shiffman, MA and Di Giuseppe, A. eds. Springer:
demonstrating that decreasing height of the maxilla Belin, Heidelberg, 2013.
and mandible correlate strongly with eventual loss 3. Khazanchi R et al. Indian J Plast Surg. 2007;
of dentition. 40(2):223–9.
4. Wulc AE et al. The anatomic basis of midfacial
Loss of teeth generally affects the mandible more aging. In: Hartstein M et al., eds. Midfacial Reju-
than the maxilla, with women at a higher risk of this venation. New York, NY: Springer; 2012: 15–28.
loss [4]. 5. Barton FE. Aesthetic Surg J. 2009;29(6):449–63.
6. Coleman SR and Grover R. Aesthetic Surg J.
Individuals with prominent bony features, including a
2006;26(1S):S4–9.
supraorbital bar, strong cheekbones, and prominent
7. Von Arx T et al. Swiss Dent J. 2018;128:382–92.
jawlines have been said to age more favorably [11].
8. Freilinger G et al. Plast Reconstr Surg. 1987;
80(5):686–90.
9. Soikkonen K et al. Br J Oral Maxillofac Surg.
1991;29(6):395–8.
CONCLUSION
10. Mangalgiri A et al. Indian J Otolaryngol Head
Neck Surg. 2015;67(1):72–4.
The face is unique in its profound ability to communi- 11. Mendelson B and Wong CH. Aesthetic Plastic
cate, express emotion and masticate. As a result of Surgery. 2012;36(4):753–60.
this intricate functionality, it is imperative that medical 12. Rohrich R et al. Plast Reconstr Surg Glob Open.
practitioners have an insightful understanding of appli- 2019;7(6):2270.
cable anatomy. Each facial layer is morphologically 13. Bartlett SP et al. Plast Reconstr Surg. 1992;90(4):​
and clinically distinct and may be differentially affected 592–600.

12
C AGING OF SKIN,
SOFT TISSUE,
AND BONE
Daria Voropai, Steven Dayan, Luis Fernando Botero,
Chiara Botti, Leonard Miller, and Ali Pirayesh

Facial aging is a complex, multifactorial process of the skeletal base, it is of great importance to know
involving multiple facial layers. Changes in the skin, the relationships between the different bones, transi-
skull, and soft tissues play contributory roles. Loss tions, and landmarks.
of collagen and elastin, combined with epidermal
thinning, contributes to the appearance fine rhytides. The face may be divided into thirds (upper face, mid-
Distributional changes in the superficial and deep fat face, and lower face) in order to identifying important
pads, in addition to bone remodeling, constitute key bony and soft tissue landmarks (Figure C.1).
morphological factors and result in the characteristic
inverted heart shape of the aging face. Understanding The upper face consists of mainly the frontal bone,
these multifactorial aging pathways facilitates effec- which forms the upper third of the anterior adult skull
tive aesthetic treatments. giving the forehead an aesthetically pleasing curva-
ture. The frontal bone can be divided into three parts
The main function of the facial skeleton is to protect (see also Chapter 1, Forehead):
the brain and important sensory organs of smell,
sight, and taste, and to provide a foundation for the 1. Squamous part of the frontal bone
face. The skull is subdivided into two main parts: the 2. Glabella and nasion
cranial vault, which protects the brain and houses 3. Supraorbital ridge
the middle and inner ear structures, and the facial
bones, which form the support for the soft tissues of The important aesthetic landmark of the upper
the face, the nasal cavity, the eyeballs, and the upper third is the nasion, defined as the suture between
and lower teeth. the frontal and nasal bones in the midsagit-
tal plane. Together with the nasion, the glabellar
The adult skull comprises 22 separate bones, of which angle (the line connecting the maximal glabellar
only one, the mandible, is mobile and not fused as a prominence with the nasofrontal suture, as com-
single unit. In order to understand the aging process pared to the horizontal or nasal-sellar line) is used

13
 Aging of Skin, Soft Tissue, and Bone

Upper Third

Middle Third

Lower Third Figure C.2 Skeletonized facial features.

to the more skeletonized appearance of the face of

Figure C.1 Facial bone sutures. the older individual, hence the prominent lateral orbital
rims, temporal crest, and zygomatic arch.
as an anthropometric measurement in facial and
­cephalometric analysis. Soft tissue changes in the aging upper face are also
of note. A well-accepted theory is that of volume loss
There is no clear understanding as to which aging due to lipo- and muscle atrophy [3]. Foissac et al. [11]
changes occur in the cranium and the upper face. looked at magnetic resonance imaging scans of 85
A well-researched change is the decrease in glabel- female Caucasians (age 18 to >60 years) to analyze
lar angle [2,3]. However, Cotofana et al. [1] studied the volume and distribution of the central forehead
computed tomographic multiplanar scans of 157 and the temporal fat compartments. They concluded
Caucasian individuals between the ages of 20 and that there is an increase in fat volume in the older
98 years and found significant results, which comple- group, with an increased basal expansion of the
mented the results of Yi’s [8,9] study looking at aging compartments (central fat compartment increasing
changes of the frontal eminence and the concavity of by 155% and temporal fat compartment by 35.5%).
the forehead (however, limited to the Korean popula- Combinations of these findings result in visual aes-
tion). Yi’s study concluded that in both genders, aging thetic implications for the aging upper face, which
was associated with increasing length of the c­ oncavity include enhanced forehead concavity, brow ptosis,
(Figure C.2). Cotofana [1] documented a decrease in temporal hollowing, and a more prominent supraor-
sagittal diameter in men (−2.24%), an increase in bital ridge due to a decreased glabellar angle.
transverse diameter in both women and men (1.97%
vs 2.22%), and a decrease in calvarial volume in men The midface is a merging of the following bony
and women (5.4% vs 5.1%) (Figure C.2). Furthermore, structures: nasal, lacrimal, ethmoid, maxillary, zygo-
lateral expansion of the skull [1] could also contribute matic, and palatine bones [5]. The main function of

14
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complicated with lymphadenitis: hence the grouping of these
different morbid conditions under the heading of lymphogenic
diathesis.
Investigations have now thrown more light on the subject because
of the more perfect recognition of the varieties of white blood
corpuscles, and the above-mentioned morbid conditions may be
defined as follows:—
(1.) The first variety consists of a more or less marked adenitis or
lymphadenitis without leucæmia (aleucæmic lymphadenitis).
(2.) The second variety, consisting of leucæmic lymphadenitis, or
leucocythæmia, is a lymphatic lucæmia or lympho-cythæmia, the
anatomical characteristic of which is enlargement of lymphatic
glands, and the histological characteristic increase in number of the
large and small lymphocytes.
(3.) A third variety, formerly regarded as simple leucæmia without
lymphadenitis, is myelogenic leucæmia or myelo-cythæmia, the
anatomico-pathological characteristic of which is to be found in
myeloid hypertrophy of the bone marrow, giving to the bone marrow
on post-mortem examination a puriform appearance, and in the
myeloid condition of the spleen.
Histologically this variety is characterised by an absolute increase
in numbers of the large mono- and poly-nuclear eosinophile
leucocytes.
Symptoms. Simple lymphadenitis begins in an insidious manner,
and is characterised by weakness, anæmia, paleness of the mucous
membranes, and wasting without apparent reason, although the
appetite is preserved. It is only at a later stage that the glandular
enlargements are discovered (adenitis), and often this discovery is
not made until the veterinary surgeon is called in.
The existence of the disease is indicated by enlargement of the
superficial glands, and this enlargement, which may commence at
any point, extends along the course of the lymphatic vessels to the
neighbouring glands, until in a shorter or longer time it involves all
the lymphatic glands in the body.
The enlargement of the glands is usually symmetrical, and on
clinical examination it is sometimes easy to detect at the outset an
increase in size of the retro-pharyngeal glands, the glands of the
neck, the prescapular glands, the glands of the flank, etc.
Rectal exploration reveals hypertrophy of the glands of the pelvis
and of the sublumbar region, etc. The animals waste very rapidly,
and sometimes in a few months become incapable of standing. They
develop cachexia, and die in a state of exhaustion, with no other
lesions than those of lymphatic hypertrophy. Neither do they exhibit
any marked increase in the number of white corpuscles in the blood.
In lympho-cythæmia the beginning of the disease is often identical
with that of simple lymphadenitis, the increase in the number of
white blood corpuscles not occurring until later. In other cases, on
the contrary, leucæmia appears first, and the enlargement of the
lymphatic gland follows; but what characterises this form and allows
of it being distinguished from myelo-cythæmia is the great increase
in the number of large or small lymphocytes. The development is
identical with, and sometimes much more rapid than, that of the
preceding form. The animals waste away and become anæmic and
cachectic, dying at last in a state of absolute exhaustion.
Post-mortem examination reveals, as in the previous condition,
symmetrical hypertrophy of all the lymphatic glands; the spleen is
very often enormous, and the liver is sometimes affected, as are also,
in exceptional cases, the kidneys.
It may happen that the spleen alone appears affected, or at least
that it has been first attacked, a fact which explains the existence of
leucæmia before any enlargement of the lymphatic glands.
Causation. The causes of lymphadenitis and of lympho-cythæmia
are unknown in veterinary as in human medicine. Apparently these
diseases are more common in adults than in young animals. Some
regard them as infectious in character, but this can hardly be the
case, as all experimental attempts to transmit the diseases have
failed. It is more plausible to compare the development of these
morbid conditions with that of malignant tumours, and although
some doubt still exists, simple lymphadenitis may be described as an
aleucæmic lymphoma or lympho-cytoma, which has gradually
become generalised, spreading by way of the lymphatic channels
from the gland first affected through the surrounding glandular
system. Lympho-cythæmia, on the other hand, may be said to be a
leucæmic lympho-cytoma, which spreads both by the blood
circulation and by the lymphatic paths (spleen, hæmatopoietic
glands and organs).
This view of the development of the lesions enables us to class
lympho-sarcomata with lymphomata and lympho-cytomata. The
malignant character and extremely rapid development of lympho-
sarcomata appear due to its extending by contiguity of tissue, and
simultaneously by the lymphatic paths.
This new grouping would consequently place on one side
myelogenic leucæmia, also called myelo-cythæmia, which is perhaps
a different morbid species. This would destroy the unity implied in
Jaccoud’s theory of the lymphogenic diathesis; but for all that this
method of grouping might be justified by reference to specific
cellular characteristics. In myelo-cythæmia the disease appears to
commence as a lympho-cythæmia, i.e., it is unaccompanied by
enlargement of lymphatic glands or hypertrophy of the spleen or
liver, though the blood appears leucæmic. The condition is not a
leucæmia due to lymphocytes, but rather a leucæmia produced by
mono- and poly-nuclear eosinophile leucocytes, i.e., leucocytes
derived from the bone marrow.
The patients are carried off rapidly after persistent wasting,
decline and cachexia, whilst on post-mortem examination the
puriform aspect of the bone marrow is an extremely striking
characteristic.
Diagnosis. There is rarely much difficulty as regards the
diagnosis. The enlargement of the lymphatic glands, for instance, can
readily be detected, and the only disease with which this can possibly
be confounded is tubercular enlargement.
With the means at present available for diagnosing tuberculosis,
such as microscopic examination of the discharge, inoculation with
discharge, examination of material from the glands, injection of
tuberculin, etc., the nature of the disease can always be placed
beyond doubt.
In lympho-cythæmia and in myelo-cythæmia, the whitish-violet
lactescent appearance of the blood is of unmistakable significance,
particularly when the manifest progressive wasting of the whole
system is taken into account.
 Histological examination of the blood after fixation and staining
will in the former cases reveal the presence of very large numbers of
lymphocytes, and in the latter an absolute increase in the number of
the mono- and poly-nuclear lymphocytes. It should be easy,
therefore, to distinguish the two diseases, especially as other
symptoms vary.
In the early stages leucæmia may be mistaken for the leucocytosis
seen in infectious diseases. These forms of leucocytosis are very
common in animals of the bovine species. They occur in certain
forms of tuberculosis, in uterine infections, in cases of internal
suppuration, in tumour of the heart, the rumen, etc., and vary in so
far as one style or another of white blood corpuscle predominates.
The diagnosis, therefore, necessitates that the white blood corpuscles
should be counted, and whenever it is found that their variations in
number are no more than between 5,000 and 15,000 per cubic
millimètre, the case may be regarded as one of temporary
leucocytosis.
If, on the other hand, those corpuscles number more than from
15,000 to 20,000, or, as may sometimes happen, they attain to from
200,000 to 300,000 per cubic millimètre (one white to two or three
red blood corpuscles), the case is one of leucæmia, and, according to
the predominance of the particular type of cell, it is a lympho-
cythæmia or a myelo-cythæmia.
In leucæmic conditions the red blood corpuscles are also present
in fewer than the normal numbers. They are more irregular, assume
giant and dwarf forms (macrocytes and microcytes), sometimes
exhibit lacunæ, and are always polychromatophile, i.e., without
special affinity for any particular constituent of double or triple
stains.
Prognosis. The prognosis of diseases included in the
lymphogenic diathesis is extremely grave, and in the present state of
our knowledge it may be assumed that sooner or later death is
inevitable.
Treatment. Treatment can scarcely be considered to exist, for at
the best it can only delay the development of the disease.
Nevertheless, and with this reservation, it is certain that preparations
of iron, iodine and arsenic have a certain effect, probably by acting
on the hæmatopoiesis.
 CASEOUS LYMPHADENITIS OF THE SHEEP.

In the sheep the lymphatic glands are sometimes the seat of

peculiar changes, which do not appear to have any marked effect on
the general condition. Thus a post-mortem examination or an
examination of animals in the slaughter-house sometimes shows a
certain number of isolated or symmetrical glands, such as the
mediastinal, tracheal, inguinal, pelvic or sublumbar glands, to be
greatly enlarged and completely degenerated. The precrural,
prescapular, and popliteal glands are said to be most frequently
affected. Their contents are caseous and yellowish, enveloped in a
fibrous sheath, and show no signs of peripheral inflammation. The
other organs and viscera may either be healthy or exhibit caseous
lesions identical with those found in caseous broncho-pneumonia.
The causes of this disease are imperfectly understood, although
Cherry and Bull (1899, the Veterinarian, Vol. LXXII., No. 860, p.
523) have isolated from the lesions an organism identical with
Preisz’s bacillus and with the microbe of ulcerative lymphangitis in
the horse.
Norgaard and Mohler (Annual Report, United States Bureau of
Agriculture, 1899, p. 638) have studied the disease. In June, 1897,
Turski, at Danzig, found about 150 breeding ewes, from eight to
twelve years old, suffering from nodules or abscesses the size of a
child’s fist in the inguinal and prescapular regions. They had been
sold for slaughter, and many were in very poor condition. The
disease occurs in Europe, Western America, South America, and
Australia. Several thousand cases are annually seen in the slaughter-
houses of the United States.
The symptoms generally escape notice, and it is only by accident
that one sometimes detects marked enlargement of the lymphatic
glands of the neck or of the superficial inguinal glands. The patients,
moreover, may remain in very good bodily condition, so that the
lesions are only discovered on the meat being inspected.
Having regard to our imperfect knowledge of this disease, it is
impossible to express an opinion as to its importance or treatment.

GOITRE IN CALVES AND LAMBS.

 Although not strictly relevant to the foregoing matter, a few
remarks may here be made on the subject of goitre.
True goitre consists in hyperplasia of the follicles of the thyroid
gland, with colloid change of their contents, which are chiefly
albuminous. The swelling is mainly due to enlargement of the
follicles, and is termed struma follicularis. It may attack the entire
organ or only one-half; less frequently it is confined to certain
sections. Other varieties of goitre are recognised, such as fibrous,
varicose and cystic goitre. (For fuller details see Möller and Dollar’s
“Regional Surgery,” p. 149.)

Fig. 213.—Calf showing swelling due to goitre.

Treatment by injection of thyroid juice or by feeding on thyroid

extract has given better results than drugs.
The following account of an outbreak in New Zealand is
summarised from the Annual Report of the Chief Veterinarian of
New Zealand, 1901:—
The calves affected were born with enlarged thyroids. The farm is
of rich alluvial deposit, and rather below the level of the river, which
it borders. The land has been in occupation, however, for many
years, and no similar condition had been previously noted. At first,
as calves only were affected, it was thought possibly to be due to the
bull, a two-year-old animal, but when a foal was born suffering from
a similar malformation this theory naturally fell to the ground.
The land had been ploughed with a special plough 20 inches deep,
but this is no uncommon practice in the island.
About the same time, a similar disease was discovered affecting
lambs at a farm near Outram. From 450 ewes, 150 lambs had been
lost, the glands being enlarged to the size of a cricket ball. A few had
been born dead, many only lived a few hours, others lived several
days, and a considerable number recovered. There was no
connection, directly or indirectly, between the two farms, they being
at least fifty miles apart. A few of the calves died or were killed, the
remainder recovered, and the foal grew rapidly better. The land on
both farms is very similar in composition.
Mr. Wilkie states, from observation of previous cases in lambs,
that “it appears to be always associated with malnutrition and a
condition of anæmia in the parent, induced in most cases by feeding
with watery, innutritious foods.”
Specimens were forwarded, from a calf and from a lamb, of
enlarged glands. The gland of the calf was enormously enlarged,
being at least twice the size of an orange, dark in colour, flabby in
consistency, and on section a mucous material exuded copiously
from the cut surface. Micro-examination showed the acini to be
larger than normal, filled with the usual mucous material, and lined
with cubical epithelium. The connective tissue surrounding the
alveoli was, however, crowded with round-cells, so much so that the
whole parenchyma seemed to be practically composed of these cells.
A specimen of an enlarged thyroid from the lamb was about the
size of a sheep’s kidney, and very much the same shape and colour.
Sections microscopically examined showed a different condition to
that of the calf’s thyroid. Here the acini were filled with epithelial
cells loosely arranged as if the lining epithelium had been
proliferating rapidly, while the connective tissue surrounding the
acini was fairly normal. The section had a somewhat adenomatous
appearance.
 SECTION V.
NERVOUS SYSTEM.

CEREBRAL CONGESTION.
According to Cruzel, cerebral congestion is somewhat frequent in
working oxen subject to continued concussion from the yoke,
especially among animals working on a rocky soil. The condition may
also be produced by prolonged exposure to the sun, as well as by
sudden and intense cold.
Passive cerebral congestion by stasis may be produced by any
cause markedly interfering with the return circulation (pericarditis
due to foreign bodies). Clinically it is of no importance.
The animals, previously in good health, suddenly appear
comatose. They are insensible to stimulation of any kind, the head is
rested on any convenient object or is held stationary, the animal
looks drowsy, the gait is hesitating or vacillating, the respiration slow
or irregular. Left at liberty, the animal does not seem to know where
it is going; indeed, sometimes it is absolutely blind and strikes
against any obstacle in its path, or falls and suffers from epileptiform
convulsions. The cranial region is abnormally warm. The course of
the attack is rapid, and the animal either dies in a state of coma or
convulsions or else recovers rapidly.
Diagnosis. The diagnosis is decidedly difficult; and the
prognosis should be reserved.
Treatment commences with free bleeding, the amount of blood
drawn being proportioned to the animal’s size. The sides of the body
may then be stimulated and a purgative administered.
 MENINGITIS.
The generic term “meningitis” includes all inflammations of the
arachnoid, pia mater and internal surface of the dura mater.
These forms of inflammation occur in diseases such as
tuberculosis and in parasitic diseases of the brain. Under other
circumstances, they are rare, and may be produced by very varying
causes.
An epizootic cerebro-spinal meningitis of the bovine species has
also been described, principally in Germany. It seems almost
unknown in France, and French literature contains no well-
authenticated case.
Furthermore, an epizootic cerebro-spinal meningitis of sheep, or
rather of lambs, has been described in Germany, in Italy, and in
France. These descriptions are all open to many objections. It seems
that under the term “cerebro-spinal meningitis” have been grouped
cases of enzootic tetanus, doubtful cases of poisoning, and
particularly cases of cœnurosis in the first stage of development. We
therefore discard these descriptions, which differ too much among
themselves to be of any value.
Causation. Meningitis occurs in the ox and sheep as a
complication of wounds in the cranial region, accompanied by
fissuring of the bone, periostitis, abscess formation, etc.
It is also seen as a complication of fractures of the horns, and old-
standing catarrh of the facial sinuses. In the sheep it follows parasitic
catarrh due to the larvæ of œstridæ.
The meningitis appears, according to circumstances, in the forms
of local meningitis, anterior frontal meningitis, basilar meningitis,
etc. Finally, it may develop as a complication of different diseases,
such as gangrenous coryza, purulent infection, subparotid abscess,
suppurative phlebitis, suppuration of the eye or of the orbit, etc.
Symptoms. It is difficult to detect and interpret the first
symptoms shown, because these chiefly consist in dulness, want of
appetite and constipation, without any particular fever. At a later
stage, excessive excitability is produced by noises, by changes of
light, or by handling. Careful examination of the patients shows a
change in their expression, rapidly followed by contraction and
inequality of the pupils or deviation of the visual axis (strabismus,
squinting). The pulse becomes irregular, as also the respiration. The
appetite is entirely lost, and it is not uncommon to note a contraction
of the muscles of the neck and jaws, as well as inability to move
about and symptoms similar to those of dropsy of the cerebral
ventricles.
The chronic form is rare.
Lesions. The lesions comprise local or general hyperæmia and
exudative inflammation of the pia mater and arachnoid, together
with the formation of false membranes or of pus in the subdural
space. The meninges are partially adherent, and the superficial layers
of the brain are also inflamed by contiguity of tissue.
Diagnosis. The diagnosis must be based on the disturbance of
vision, movement, and appetite, and on the course of the symptoms,
as well as on the external signs in the case of such diseases as are
prone to become complicated with meningitis.
Prognosis. Sooner or later the case is likely to end fatally, and
there is no practical use in treating the patient.
Treatment. If in exceptional cases slaughter is objected to, setons
and blisters may be applied to the poll or the parotid region, or the
parts may be enveloped in ice bags or compresses of iced water
frequently renewed.
 ENCEPHALITIS.
Encephalitis, i.e., inflammation of the cerebral substance, is very
closely allied to meningitis; in a great number of cases meningitis
and encephalitis co-exist. In other cases encephalitis may be found
apart from meningitis, and vice versâ. Moreover, many of the
symptoms of meningitis are to be found in cases of encephalitis.
Encephalitis may develop as a complication of meningitis.
Encephalitis may also follow abundant parasitic infestation, as in
cœnurosis (which will be particularly studied as it affects sheep), or
microbic infection, the commonest form of which in the ox is
tuberculosis. The encephalitis may be diffuse or circumscribed,
according to the cause, while the symptoms are varied and
numerous. Very frequently, particularly in cases of tuberculosis,
encephalitis assumes a chronic form.
Symptoms. The earliest symptoms are extremely difficult to
detect, because they are scarcely characteristic and because it is
impossible to ascertain the sensations of the animal.
It is only when the disturbances in walking, in the eyesight, in
swallowing, etc., are noted that suspicion is aroused.
The symptoms may appear suddenly. Nevertheless it is beyond
doubt that there are certain slightly marked prodromata, indicated
by diminution of appetite, wasting, and changes in vision. Soon
afterwards occur other forms of disturbance, which may be classified
under the heading of “motor, visual, nervous, and impulsive.” The
patients appear stunned, their movements are slow and hesitating,
they partially lose control over their limbs and display lameness,
with spasmodic movements of one or two limbs. Examination of the
joints shows no injury. The lameness may simultaneously affect two
diagonal limbs or two fore and two hind limbs, or even three limbs.
This lameness is of central origin.
The ocular disturbance is marked by diminution or loss of vision,
by strabismus, or by frequent unconscious movements of the eyes
and eyelids, and also more particularly by inequality, contraction or
dilatation of the pupils.
 Nervous, impulsive disturbance is most readily noted when the
animals are at liberty. Even when the sight remains, they seem quite
incapable of avoiding obstacles or as though absolutely forced to
move to the right or left, etc.
Attacks of giddiness, moreover, are not unusual under the
influence of the slightest excitement. During such attacks the
animals thrust the head against a wall, or they involuntarily recoil or
make lateral movements. In many cases these vertiginous attacks
end by the animal falling and showing epileptiform convulsions,
during which it may die.
The symptoms are never the same in two different animals, but
they may easily be classed according to the above indications. The
indications furnished by the condition of the eyes and by the peculiar
impulsive movements are particularly significant.
On the other hand, there are modifications in breathing without
apparent local cause, and difficulty or even impossibility of
swallowing, etc., although there exists no material obstacle.
Diagnosis. The condition is often confused with meningitis, and
the mistake is not serious, because meningitis and encephalitis
frequently accompany one another.
Prognosis. The prognosis must be regarded as fatal. The patients
very seldom recover, and there is no reason for keeping them alive.
Treatment. Here, again, blisters may be applied to the upper
extremity of the neck, or setons may be passed. Cooling applications
to the cranial region have also been suggested. None of these
methods produces more than a temporary palliative effect.
 CEREBRAL TUMOURS.
The brain may be injured and compressed by various tumours of
other than parasitic origin. Such tumours may originate in the bones,
the meninges or the choroid plexus, or they may simply be due to
generalisation of a previously existing tumour. Whilst of very varied
origin and nature, all tumours of the cranial cavity have one common
effect, viz., to compress the brain. This continuous compression
causes progressive atrophy of the brain, but its existence is not
always suspected, because the lesions may not give rise to any
marked symptoms.
The hind portions of the hemispheres and the white substance are
generally very tolerant. The front portions, on the other hand—the
frontal lobes and the grey substance—resent compression, which
provokes various symptoms in consequence.
The symptoms of compression and atrophy of the brain differ
greatly, a fact which is easily understood, inasmuch as the seat of the
change may vary, and therefore it is possible only to trace the chief
manifestations, which suggest the existence of a cerebral tumour.
The general changes are indicated by signs precisely similar to
those so common in horses with dropsy of the ventricles (general
depression, inability to back, long intervals between the prehension
of successive mouthfuls of food, sudden cessation of mastication,
etc.), by an impulsive or automatic gait, and by the assumption of
strange attitudes (kneeling down in front, etc.). When at rest the
animals appear to be in a state of continual torpor.
Special symptoms sometimes occur, which enable the seat of the
injury to be localised in more or less exact fashion. These symptoms
affect the vision (amblyopia, amaurosis, strabismus, nystagmus),
general sensibility (hyperæsthesia, anæsthesia, etc.), and the power
of movement (total, partial or crossed hemiplegia, want of co-
ordination of movements, etc.).
Trifling stimuli almost always lead to marked and even
epileptiform attacks.
 The diagnosis of cerebral tumours is very difficult, particularly
when attempts are made to indicate their exact seat, but that of other
cerebral lesions is somewhat easier.
The prognosis is very grave, and in the case of domestic animals
nothing can be done. In the ox intra-cranial operations are difficult,
by reason of the presence of the sinuses which obstruct the approach
to the brain cavity; economically surgical treatment is seldom
advisable.
 INSOLATION.
Insolation is an exceptional accident in animals of the bovine,
ovine, or porcine species. If at liberty these animals move about, and
always seek shelter when the sun is fierce. If, on the contrary, they
are harnessed and kept standing for long, exposed to the full midday
sun during June, July or August, they may suffer from insolation.
During the International Cattle Show attached to the Exhibition of
1900 in Paris, a considerable number of cases of insolation occurred
in animals of one class, exposed to the full midday sun, in an ill-
ventilated spot. The other classes only received sunlight from the
sides, and in them not a single case occurred.
Death may follow in a few hours; it is difficult to say precisely how
it is brought about, but it is always accompanied by congestion of the
cerebro-spinal centres and general blood stasis.
The symptoms of the development of insolation occur very
rapidly. In animals of the bovine species there is accelerated
respiration, which soon amounts to dyspnœa. The mucous
membranes then become cyanotic. The animals attacked seem
anxious, although not agitated, and soon afterwards the eyes water,
the mucous membrane and the lips of the vulva display œdematus
infiltration and congestion, and areas of cutaneous congestion,
closely resembling mud fever in the horse, appear over the mammæ.
At this stage the animals move with difficulty, and show all the
symptoms seen at the outset of gangrenous coryza.
All these symptoms develop in one, two, or three hours, and death
may follow if nothing is done. They disappear, however, as rapidly as
they appear. In an hour or less we have seen in some cases a
complete return to the normal condition. Given the facts, the
diagnosis is extremely easy.
Treatment. Treatment should be commenced by immediately
removing the animal to a cool, airy, shady place. It may then be bled,
and the head and neck should be freely drenched with cold water.
The symptoms generally disappear as though by magic.
 POST-PARTUM PARALYSIS—MILK FEVER—
MAMMARY TOXÆMIA—PARTURIENT APOPLEXY
—DROPPING AFTER CALVING.
For a great part of the following short account we are indebted to
an excellent report by J. J. Repp, V.M.D., in the Journal of Comp.
Medicine and Veterinary Archives, September, 1901:—
The word “fever” in connection with the terminology of this
disease is not very appropriate, because in the majority of cases fever
is not present, but the animal has a subnormal temperature. The
term milk fever is very misleading and indefinite, as it is also used by
the laity to designate other diseases, such as parturient septicæmia
and the various forms of mammitis. Parturient paralysis must be
clearly differentiated from parturient septicæmia, which is a disease
of an entirely different character and which may occur in any of the
domestic species, whereas parturient paralysis occurs only in the
cow.
Distribution. Parturient paralysis occurs wherever milch cows
are kept. It is more prevalent in dairy districts, because it is the heavy
milking strains of cows that are most subject to the disease.
Cause. No definite cause can be assigned for this disease.
Schmidt’s theory is that parturient paralysis is caused by the
evolution in the mammary gland of a poisonous substance through
the over-activity of the epithelial cells of this gland excited by the
determination to the udder after birth of large quantities of blood
which was supplied to the uterus and the fœtus before birth, but
which now goes to the udder because of the natural demand for milk
secretion. This poisonous substance being carried in the circulation
to various parts of the body, brings on the symptoms which
characterise the disease. It is well recognised that living cells may,
under certain circumstances, produce poisonous substances.
Schmidt’s theory, therefore, is in accord with an established
principle.
 Pathogenesis, or generation, of the disease. Parturient
paralysis, as a rule, occurs in cows which give a heavy flow of milk
and which are in a high state of nutrition. It may develop at any age,
but is extremely rare in cows before they have reached adult age and
have given birth to several calves. It is also rare in old cows. It occurs,
then, in cows which are of middle age and in the full height of their
activity as milk producers. The disease attacks the cow after she has
given birth to a calf, usually within twenty-four hours thereafter, but
in some cases not until a week or even a month after parturition. In a
few cases the disease has its inception a short time before
parturition. Cows which are stabled and deprived of exercise are said
to be more prone to the disease than those which are permitted to
exercise at will. There are many exceptions to this statement,
although it is the usual teaching. Further observation may show that
it is not correct. In Iowa more cows take this disease while at pasture
than in any other circumstance. This doubtless arises from the fact
that in Iowa cows are given more freedom than is customary in older
dairy States. The disease may arise at any time in the year, but, on
account of the fact that spring-time is pre-eminently the calving
season, most cases originate at this season.
Morbid anatomy. The morbid alterations are limited and
variable, and offer nothing characteristic. The blood is irregularly
distributed, a condition which probably indicates marked vaso-
motor disturbance resulting from the profound interference with the
nervous functions which accompanies the disease. The abdominal
organs are usually filled with blood. The brain may be anæmic,
œdematous, easily torn, and yellowish in colour. In other cases it
shows hyperæmia of the meninges and of the brain substance.
Symptoms. The disease usually appears within twenty-four to
forty-eight hours after parturition. In extreme cases it may not occur
until two months or even six months after parturition. It may rarely
occur before birth. It usually follows an easy birth. At the onset of the
disease the cow manifests some uneasiness; it moves about in a
restless manner, stamps, strikes the abdomen with its hind legs,
perhaps bellows, grinds the teeth, and may have spasms of groups of
muscles or even a general convulsion. After this period, which may
be unnoticed, the symptoms of paralysis come on. The cow shows
weakness, staggers, and at last falls. As the paralysis advances it
stretches on the ground, lying on its side usually with the neck bent
to one side so as to bring the nose into the flank or the costal region.
This is the characteristic position in parturient paralysis. If the head
is brought into the normal position, it at once returns to the
unnatural position in which it was found. The animal is in a state of
partial or complete unconsciousness, does not respond to blows or
calls, and takes no note of its surroundings. The eye is dull and not
sensitive to the finger touch, sunken, pupil dilated, and the upper lid
is drooping; the tongue is paralysed, saliva runs from the mouth, the
pharynx and œsophagus have lost the power of motion, so that the
animal is unable to swallow; the peristalsis of the stomachs and
intestines is in abeyance, and as a result digestion is arrested,
fermentation sets in, and the animal becomes tympanitic; the
contents of the rectum and colon are hard and dry, and may be
covered with mucus or blood, urination is suspended; the os uteri is
almost invariably dilated if the disease occurs within a day of
parturition; pulse small, often imperceptible, 60 to 120 per minute;
temperature, usually normal or below normal, may be as low as 95°
Fahr., in some cases may be as high as 105° Fahr. Such a high
temperature probably does not occur in a case of pure parturient
paralysis, but only when there is a complication of parturient
septicæmia. The extremities are cold. The after-birth is sometimes
retained. There may be accompanying prolapse of the uterus.
Course. Without treatment, and, indeed, with most kinds of
treatment which have been applied in the past, the disease usually
runs rapidly to a fatal issue. It lasts two to three days, and in some
cases longer, the condition gradually becoming more and more
aggravated. Death results from sudden failure of the heart or brain,
and is often preceded by profuse diarrhœa. In milder cases the cow
may linger as long as two to four weeks and then die of pneumonia,
which results from the inhalation, or introduction through attempts
at medication, of foreign substances into the lungs during the period
of paralysis of the pharynx and œsophagus. If recovery occurs, the
animal is entirely well in two to five days. In rare cases paralysis of
the hind parts may persist for a long while.
Diagnosis. This is made by a study of the history and symptoms.
It is comparatively easy.
 Differential diagnosis. It must be distinguished from ante-
partum paralysis, broken-back, parturient septicæmia; but one
familiar with the character of these diseases will find no difficulty in
making this differentiation.
Treatment. This may be considered under two distinct
subdivisions, viz., preventive treatment and curative treatment.
(a) Preventive treatment.—By considering what has been said
under the head of “generation of the disease,” one can easily infer
what measures should be adopted to prevent the disease. Cows in the
later stage of gestation should be fed moderately, grain especially
being given sparingly or entirely withheld; the animals should be
given an opportunity to take plenty of exercise; the bowels should be
kept in good condition by the administration of such salines as
magnesium sulphate, sodium chloride, and sodium bicarbonate. The
after-birth should be removed soon after parturition and several
uterine douches administered.
(b) Curative treatment.—The older methods of treatment
comprised: warmth and friction to the mammary gland; the
administration of sedatives, such as opium, chloral and bromide of
potassium; stimulants, including ammonia, ether, turpentine and
alcohol; washing out the uterus with water or disinfectant solutions;
the relief of tympany by the use of the trocar and canula (by which
instrument medicines may also be injected directly into the rumen);
the removal of fæces from the rectum; warm clothing of the body and
general attention to the animal’s comfort, and to the teachings of
hygiene. For all these widely diversified methods good results have
been claimed, and, we may add, bad ones at times recorded. F. T.
Harvey (Cornwall) estimates the average mortality at from 40 to 66
per cent., though he claims for his more recent practice a lessened
mortality of only 20 per cent.
Schmidt does not claim that his method of treatment disposes
bodily of the morbid condition, but that it does measurably assist
Nature in her efforts to restore the animal to the normal
physiological state. It is well known that after the beginning of the
attack the animal, if left to itself, rapidly grows worse until the crisis
of the disease is reached, at which time death occurs or
convalescence begins, usually the former. It has been observed,
however, that if the treatment is applied within a few hours after the
inception of the disease its progress is modified in such a way that
convalescence at once begins, as a rule, and the animal hastily
recovers its health, usually within twelve hours, although in extreme
cases it may be as late as forty-eight hours. The following is an
outline of the plan of treatment of parturient paralysis suggested by
Schmidt. The operator should disinfect his hands and the udder and
teats of the cow by washing with a 5 per cent. solution of carbolic
acid or creolin, or a 1½ per cent. solution of lysol or trikresol. The
apparatus needed for the treatment consists of a small glass funnel, a
rubber hose three feet long and one-eighth inch in calibre into which
the funnel fits, and an ordinary milking tube over which the rubber
hose fits. This apparatus should be sterilised immediately before it is
used by boiling or soaking in such a solution as recommended for
washing the udder. Dissolve from 2 to 2½ drachms of potassium
iodide—the size of the dose depending upon the size of the cow and
the character of the attack—in about one quart of clean water
previously boiled to sterilise it, and allow the solution to cool to a
little above body temperature, or 40° C. or 104° Fahr. The
temperature may be determined with the clinical thermometer.
Withdraw all the colostrum or milk from the udder. Then insert the
milking tube, with hose and funnel attached, into one of the teats,
elevate the funnel about two feet above the teat and slowly pour in
one-fourth of the solution, allowing the funnel and hose to become
empty several times during the process in order to permit the
entrance of a liberal quantity of air. Repeat this infusion with the
other three quarters of the udder. After all is introduced, knead the
udder carefully so as to cause the solution to permeate the ducts and
acini as much as possible.
As the condition of the cow is usually such as to call for additional
treatment, the veterinarian should not be content with injecting the
potassium iodide solution, but should resort to any and all other
measures which promise assistance.
As the cow is usually unable to urinate, the bladder will be found
filled with urine. This should be removed with the catheter, and its
removal accomplished at intervals until the recovery of the cow
renders this procedure no longer needful.
It may be advisable that catharsis be brought about. As the cow is
usually unable to swallow, it is dangerous to attempt to give
medicines by the mouth. This may be done if assurance that the cow
can swallow is obtained. Some have given medicines successfully
through a probang inserted into the stomach. The plan is feasible.
Schmidt says that he usually resorted to an aloe powder. If this is
done 1 ounce to 1½ ounces of aloes may be given. It would seem
preferable to give the aloes in a bolus, capsule, or drench. Some have
given linseed oil or Epsom salts. If the animal cannot swallow and a
probang is not at hand, one may administer 1½ to 2 grains of
physostigmine salicylate subcutaneously, repeating the dose in about
three hours if purgation is not produced. Rectal injections should be
given at short intervals in order to get rid of the accumulation of
hard, dry fæces in the rectum. These injections may be of linseed oil,
cotton-seed oil, or warm soap solution. Schmidt recommends, also,
enemata of sodium chloride solution. Meanwhile the cow should be
kept propped up on the sternum by means of bags of straw or pieces
of wood. If the temperature is below normal, as it usually is, the cow
should be thickly clothed with blankets and straw heaped up about it.
Schmidt used powdered digitalis given by the mouth when the heart
was rapid and weak. It would seem much better in every way to give
the tincture of digitalis subcutaneously. He has also resorted to
subcutaneous injections of camphor and caffeine. This is good
treatment. If the cow does not show marked improvement within
eight hours the potassium iodide infusion may be repeated. Schmidt
has found that as much as 6 drachms may be injected into the udder
without harm to the cow. Schmidt, in his first report, made in 1898,
recorded 50 cases treated for parturient paralysis by this method
with but two deaths from the disease. There were, however, only 46
recoveries, as two cows were slaughtered for beef during the first day
of convalescence. A short time later a report was made by Jensen
showing that in Denmark up to that time sixty-five veterinarians of
that country had treated 412 cases by the Schmidt method, 90 per
cent. of which recovered. Such results seem to indicate this as the
treatment par excellence for parturient paralysis. It still remained to
secure the introduction of this treatment into the United States and
to determine what results could be obtained. In all 166 cases were
reported; of these 166, 119 resulted in recovery, while 47 were fatal.
Of the fatal cases, in eight of the cows death may be traced to some
complication, such as prolapse of the uterus, foreign-body
pneumonia, etc. In these cases the Schmidt treatment cannot be said
to have failed, for it is not in any way intended that it shall be able to
overcome such accidental conditions. If the cow has recovered from
its condition of paralysis as a result of the Schmidt treatment far
enough to be out of danger from that source and to promise recovery,
but later falls a victim to some complication that is in no measure a
part of parturient paralysis, but only a result of that disease, it may
with justice be said that the Schmidt treatment was a success so far
as the malady against which it was directed is concerned. Looking at
the reports from this generous point of view, in 127 cases out of 166,
or 76·5 per cent., the Schmidt treatment was successful so far as the
parturient paralysis was concerned.
In a paper published in the Berliner Thierärztliche Wochenschrift
in August, 1902, Schmidt reviews the results of his treatment as
evinced by 914 patients treated by thirty-one different practitioners:
884, or 96·7 per cent., recovered, twelve died and six were
slaughtered during the course of the disease. Twelve others were
slaughtered at a later period in consequence of complications.
Jensen reported the results of 1,744 cases.
Schmidt also found that the simple injection of air was in many
cases sufficient to produce recovery, and subsequent observation
tends to show that the fluid injected is of less importance than was
first anticipated. A large number of unirritating solutions may be
employed. Schmidt, however, still counsels the use of a quart of 1 per
cent. solution of iodide of potassium, in which can be dissolved 5
grammes of caffein sodio-salicylate if the heart’s action is weak.
About 10 ounces of this solution are injected into each quarter, and
are followed by a liberal injection of air. The parts should afterwards
be freely massaged.
 CŒNUROSIS (GID, STURDY, TURN-SICK).
Cœnurosis is a disease due to invasion of the animal body by
embryos of larvæ of the Tænia cœnurus of dogs and wolves. These
embryos only develop freely in the brain substance (Cœnurus
cerebralis) and medulla oblongata. The hosts of the larvæ include
the calf, sheep, goat, roedeer, reindeer and horse.
The disease was formerly erroneously called “turn-sick,” for the
turning is only a manifestation, and even a tardy manifestation, of
the disease, while in addition it is not invariably present.
Cœnurosis principally attacks lambs of from three to six months,
although it occurs up to eighteen months, and sometimes even two
years. It is exceptional, however, in adults. Similarly in the bovine
species it usually affects young animals up to the fourth or fifth year.
Cœnurosis with diffuse parasitic encephalitis often remains
unrecognised, the animals being regarded as affected with epizootic
meningitis of unknown cause or septic intoxication, and when they
die the owners are ignorant as to the cause of death. The stage
corresponding to turn-sick, which is an advanced phase of the
disease, is only seen in animals which have been infested to a slight
extent, and in which three or four parasites only, sometimes only
one, have attained the brain and developed there. Such cases exhibit
all the classic symptoms of turn-sick, viz., turning movements,
heaviness, vertigo, etc.
Causation. Cœnurosis is due solely to one cause, viz., the
ingestion of eggs or embryos in feeding or drinking.
The Tænia cœnurus lives in the dog, and fertilised segments are
passed with the fæces in yards, pastures and fields, and on the
margins of roads, ditches and ponds. Amongst damp grass or in
water the eggs, which contain more or less well-developed embryos,
may retain their vitality for several weeks, and when swallowed the
embryos are set at liberty in the intestine.
The six-hooked embryos perforate the walls of the intestine, pass
into the blood stream or chyle ducts, and from these points are
carried in all directions. Those which gain the nervous centres, the
brain or spinal cord, continue to develop; the others, dispersed
through different tissues, degenerate and disappear.
Experimental infection with these parasites shows that the brain is
invaded after about a week’s time. From the twentieth day the
presence of embryos can easily be detected in the superficial layers of
the convolutions. They make their way through the grey substance,
leaving behind them greenish-yellow sinuous tracts with caseous
contents.
The cyst or finn undergoing development can be found at the end
of one of these tracts in the form of a little transparent bladder, of a
size varying between that of a pin’s head and that of a lentil or a
small hazel-nut.
Later the tracts, with their caseous contents, disappear, and the
development of many of the vesicles proves abortive. At the end of a
month the vesicles, continuing to develop regularly, attain to about
the size of a pea. Between the fiftieth and sixtieth days heads or
scolices appear in the interior of the vesicle, which then reaches the
dimensions of a hazel-nut. From this time the vesicles continue to
increase in size until the death of the patient. Usually they become as
large as a walnut, or even larger, and the interior contains hundreds
of scolices, each showing a head.
 Fig. 214.—Brain of sheep. Cœnurosis of the left
hemisphere. Œstrus larvæ exposed by trepanation.

The cystic phase only develops completely in animals whose brains

contain a limited number of cysts, and in such the signs of turn-sick
are well developed. In others, where the numbers are large (ten to
fifteen embryos or more), death occurs during the primary stage,
usually towards the end of the first month, in consequence of acute
encephalitis and without any of the symptoms of turn-sick.
 Fig. 215.—Skull of a sheep showing the
brain infested with a gid bladder-worm
(Cœnurus cerebralis). Two-thirds natural
size.

The number of animals attacked is sometimes enormous. Moussu

has recorded cases where fifty, one hundred, and even four hundred
lambs of one flock were affected. The enormous mortality in such
cases is very apt to cause errors in diagnosis. Cœnurosis occurs most
frequently during rainy seasons, moisture favouring the preservation
of the eggs. Young animals become infected, particularly during the
spring and autumn, more rarely in the summer, as prolonged
desiccation, say for a period of twelve to fifteen days, destroys the
vitality of the eggs, but animals may become infested at any time
through drinking contaminated water. Moussu has seen cœnurosis
(acute encephalitis) from the last-named cause in the middle of
January.
 Symptoms. First phase.—Disseminated encephalitis.—The
symptoms vary with the phases of evolution of the parasite and of the
disease which it causes. After the six-hooked embryos have
penetrated to the brain, the animals affected lose appetite and show
a certain degree of dulness, which is all the more marked inasmuch
as the animals usually affected are young, and therefore should
appear bright and alert. Then follow wasting and depression; the
animals remain stationary for whole hours together, the head being
carried low or inclined to one side. At this stage disturbance in vision
and irregularities in movement may appear.
The eyesight is almost always
affected, but the symptoms may vary
widely. In some cases the patients seem
to be absolutely blind, and strike
against any obstacle in their way; in
others the power of vision seems to be
lost only on one side. All that can be
discerned objectively is an inequality in
the pupils, together with retraction or
dilatation, convergent or divergent
strabismus, nystagmus, etc. The
humours of the eye appear infected, but
examination with the ophthalmoscope
reveals lesions of more or less extensive
neuro-retinitis.
The visual disturbance is of central
origin. The powers of movement may
be affected in numerous ways, which at
times are extremely difficult to estimate
with accuracy. Sometimes the gait is
uncertain, inco-ordinated, and
hesitant; at others the animal shows
Fig. 216.—An adult gid lameness or loss of control over a front
tapeworm (Tænia or hind limb, or over two limbs
cœnurus). Natural size. simultaneously (either the two front or
(After Railliet.) hind limbs or the diagonal limbs), or it
may be absolutely unable to stand.
 It walks obliquely, or
the front or hind limbs
collapse; or again, it
may persistently lie
down, a fact which
makes the shepherd
think it is suffering
from paralysis. On
examination, however,
no true indications of
paralysis can be found;
sensation and motor
power are both
preserved in a modified
form.
Death is very
frequent at this stage of
the disease; the animals
eat little or nothing,
refuse drink, and die of
exhaustion.
All this general Fig. 217.—Sexually mature segment of the
disturbance is of gid tapeworm (Tænia cœnurus). cp, Cirrus
central origin, and is pouch; gp, genital pore; n, nerve; ov,
due to disseminated ovary; sg, shell gland; t, testicles; tc,
parasitic encephalitis, transverse canal; ut, uterus; v, vagina; vc,
but up to this point the ventral canal; vd, vas deferens; vg,
seat of the disease is vitellogene gland. × 20. (After Deffke.)
not yet clearly
apparent.
Second phase.—Turn-sick.—The central symptoms are slow of
development, and are due to the progressive growth of one or two,
more rarely three or four, fertile vesicles. These are the true
symptoms of turn-sick, and it is only after this phase of the disease
has developed that the term becomes appropriate.
Left at liberty, the patient usually walks in a circle towards the
right or left in an impulsive and irresponsible fashion. Sometimes it
describes a circle, always of the same size. In other cases, on the
 Fig. 218.—Brain of a lamb infested with young gid bladderworms
(Cœnurus cerebralis). Natural size. (After Leuckart.)

contrary, it travels along a spiral track, getting further from or nearer

to the centre as the case may be. The turning movement may become
so accentuated that the animal appears to revolve as on a pivot, and
if it is confined in a field or straw-yard its legs become caught in the
litter and it falls to the ground.
Attempts have been made under these circumstances to discover
the exact point of compression, i.e., the point at which the cyst exists,
by noting the direction of the turning movement. The diagnosis,
however arrived at in this way is frequently illusory, because it is not
uncommon to find two or three vesicles, and in any case the most
important information in regard to diagnosis is to be derived from
the ocular symptoms.
When only one vesicle exists, the turning movement usually occurs
towards the side on which it is situated, and the eye of the opposite
side is affected with amaurosis.
 Fig. 219.—Sheep’s skull, the hind portion thin and
perforated, due to the presence of gid bladderworms
(Cœnurus cerebralis). (After Dewitz.)

If the cyst is situated near the olfactory lobes, the animal marches
with a high-stepping movement and the head drawn back towards
the body. If the cyst is in the cerebellum the animal is incapable of
moving, because it can no longer co-ordinate its movements. Finally,
if the cyst develops in the occipital region, animals turn towards the
wind, with the neck raised and the head extended.
At the moment when they fall to the ground they sometimes have
epileptiform convulsions, grind their teeth, and salivate profusely. In
a severe attack even death may supervene at this point.
Cœnurosis of the Medulla. The embryos may develop in the
medulla oblongata as well as on the brain itself. Compression and
atrophy of the medulla then give rise to true paralysis.
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