2 5262846139022968480

MANAGEMENT OF VERTIGO
Made Easy ®
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MANAGEMENT OF VERTIGO
Made Easy ®
Santosh Kumar Swain

MS (ENT) DNB (ENT) MNAMS Fellowship in Neuro-otology
Associate Professor
Department of Otorhinolaryngology
Institute of Medical Sciences and SUM Hospital
Siksha O Anusandhan University
Bhubaneswar, Odisha, India
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Management of Vertigo Made Easy ®

First Edition: 2016
ISBN: 978-93-5250-029-1
Printed at
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Dedicated to
My parents who gave me life and a value
My teachers who gave me knowledge and a profession, and
My patients who gave me appreciation and encouragement.
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Preface
For the most medical practitioners, a heart-sinking moment is

inevitable when confronted by a patient presenting with vertigo.
The diagnosis and management of vertigo have always been an
enigma because of the complexity of the balance system and
inherent compensatory mechanisms as well as redundancy of
functions render the system immune to most diagnostic tests.
Management of Vertigo Made Easy ® is written for everybody who
wants to learn vertigo and treat dizzy patients. Medical students,
interns, residents, primary care physicians, and consultants can
use this book for proper management of vertigo patients. The
most important point in managing vertigo patient is always to
take good history. This is followed by appropriate examinations
and investigations. Basic concepts in assessing, diagnosing and
managing common peripheral vestibular disorders are briefly
described, and special emphasis is given on how to rule out
central vertigo. The book is a reader’s delight and is sure to spark
an interest in managing vertigo patients.
Santosh Kumar Swain
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Acknowledgments
I am deeply indebted to my teacher and mentor Professors

(Drs) Abhoy Kar, GC Sahoo, SN Panda, RN Samal, S Behera, RK
Pattnaik, and KC Mallick, Souvagini Acharya, and Satyajit Mishra
for their great moral support in writing this book.
I sincerely thank President Manoj Ranjan Nayak and
Management Member Er GB Kar, Siksha ‘O’ Anusandhan University,
Bhubaneswar, Odisha, for their great support behind this work.
I heartily thank Shri Jitendar P Vij (Group Chairman), Mr Ankit
Vij (Group President) and Mr Tarun Duneja (Director-Publishing) of
M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India,
for strong belief in the book for benefiting the medical fraternity.
I can never forget people, who came in my professional training
to teach, appreciate and encourage my hard work, Professors
Anand Job, Rita Ruby Albert, Achma Balraj, Rupa Vedanta, Christian
Medical College, Vellore, Tamil Nadu, India.
I am very much thankful to Mahesh Ch Sahu, Somadatta Das
of Central Research Laboratory, and Manoj Mishra and Susanta
Kumar Khuntia of Central Library, for their help in editing the
manuscript.
My patients are the another source of inspiration for attempting
to write vertigo in simple and lucid manner.
Last but not least, I am grateful to my parents, wife (Swagatika)
and son (Ishan), without their encouragement and cooperation,
the book could never have been written.
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Contents
1. Introduction 1
Definition of Vertigo 2
Classification 2
Vertigo Pearls 3
Quality of Life in Vertigo Patient 4
2. Physiology of Vertigo 5
Functional Anatomy 5
Basic Physiology of Balance Disorder 8
3. Causes of Vertigo 11
Peripheral Causes 11
Central Causes 13
Peripheral Vestibular Disorders 13
Labyrinthine Vertigo 16
Central Vestibular Disorders 17
Basics of Peripheral Vertigo 21
Epidemiology of Peripheral Vertigo 21
Basics of Central Vertigo 21
Epidemiology of Central Vertigo 21
Physiological Vertigo 22
Drugs Causing Dizziness 23
Ototoxicity and Dizziness 23
Old Age and Dizziness 24
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xii Management of Vertigo Made Easy
Dizziness in Children 24
Dizziness in Pregnancy 25
Post-Traumatic Vertigo 25
4. Diagnosis of Vertigo from History 28

Things about Dizzy Spells 28
Assess the Problem 29
History Tells Diagnosis 29
Vertigo Diagnosis 35
5. Clinical Tests for Vertigo 37

Routine Examinations for Vertigo Patients 37
Special Vestibular Tests 50
Oculomotor Tests 52
Cerebellar Tests 53
Tests for Utricular/Otolithic Dysfunction 53
6. Investigations for Vertigo 55

Hematological Tests 55
Audiological Test 55
Radiological Tests 55
Glycerol Test 56
Special Vestibular Investigations 57
Conditions Requiring Urgent
Neuroimaging (CT/MRI) 61
7. Treatment of Vertigo 62
Objective of Treatment 62
Principles of Management of Vertigo 62
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Contents xiii
Rotatory Vertigo 66
Episodic for Hours 67
Prolonged Rotatory 68
Unsteadiness 69
Medications in Central Vertigo 75
Particle Repositioning and Exercises for BPPV 76
8. Vestibular Rehabilitation Exercises 85

Mechanisms 85
Cawthrone-Cooksey Exercises 86
Eye Exercises 86
Head and Neck Exercises 86
9. Important Clinical Conditions of Vertigo 96

Ménière’s Disease 96
Benign Paroxysmal Positional Vertigo 99
Vestibular Neuronitis 99
Perilymph Fistula 100
Superior Semicircular Canal Dehiscence 101
Labyrinthitis 102
Acoustic Neuroma 102
Bilateral Vestibulopathy 103
Autoimmune Labyrinthitis 104
Central Causes of Vertigo 104
Motion Sickness 107
10. Approach to Vertigo by General Practitioner 110

Diagnosis of Otologic Vertigo 111
Conditions Requiring Urgent
Referral to Balance Specialist 111
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xiv Management of Vertigo Made Easy
Simplified Approach to Get a Diagnosis 111

Guiding for Evaluation of Dizzy Patients 115
11. Interesting Case Series 119

Case 1: Vestibular Neuronitis 119
Case 2: Ménière’s Disease 120
Case 3: Benign Paroxysmal Positional Vertigo 122
Case 4: Ménière’s Disease 123
Case 5: Migraine-related Vertigo 123
Case 6: Perilymph Fistula 126
Case 7 127
Case 8 128
Case 9 129
Case 10 130
12. Vertigo Clinic Evaluation Format 131

History 131
Examinations 134
Investigations 136
Management 136
Points to Remember 137

Bibliography 149
Index 151
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CHAPTER 1
Introduction
Vertigo and dizziness are extremely common problem, but are

often misdiagnosed. The problem occurs because patients use the
term very loosely to describe a broad variety of unpleasant and
unfamiliar sensations, including spinning, faintness, unsteadiness
and numbness or lightheadedness. The only common feature is a
feeling of uncertainty of position or motion.
Vertigo is a feeling in which the external world seems to
revolve around the individual or in which the individual seems to
revolve in space. Vertigo is not a disease but is a symptom. Vertigo
is a very distressing symptom not only for patients but also for
the treating doctors. It is a challenging problem for diagnosis and
treatment. It is prevalent amongst 10% of the patients visited by an
ENT specialist. It is 5% of patients visiting the general practitioner
are suffering from the vertigo. For treatment of vertigo, most
of the patients run among neurologists, ophthalmologists,
otolaryngologists, orthopedicians and general physicians and
finally frustrated and seek advice from psychiatrists. This book is a
honest trial for making simplification of vertigo approach and give
justice to dizzy patient.
The basic aim of this book is to answer:
zz Does the subject really have a balance disorder?
zz If so, whether it is a central or peripheral disorder?
zz What is the probable etiology?
zz What is the best possible treatment?
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2 Management of Vertigo Made Easy
DEFINITION OF VERTIGO
zz Vertigo is defined as a subjective sense of imbalance.
zz Vertigo is defined by Cawthorne (1957) as a Hallucination of
movement and can be applied to any movement provided that it
does not exist outside the sense of sufferer.
zz True vertigo is a sense of rotation of one’s body or head
(subjective), or of the environment (objective), or sense of

falling.
zz Vertigo may be defined as a hallucination of movement, that
is the patients feel that they or their environments are moving.

zz Vertigo could be defined as a false sense of orientation of the
patient with respect to his environment. The patient feels that

he is moving or that the surroundings are moving.
zz A balance disorder/vertigo is a medical condition that causes
an individual to feel unsteady when standing or walking and

may be accompanied by feelings of giddiness or woozings or
having a sensation of movement, spinning or floating.
Vertigo is often thought to be synonymous with dizziness.
Vertigo is a sensation of disorientation in space along with a
sensation of motion. Dizziness is an imbalance usually associated
with cardiovascular, neurosensory and psychiatric conditions and
few medications.
Visual, proprioception and vestibular systems coordinate with
the central nervous system (CNS) to maintain equilibrium and
provide a sense of spatial orientation. Any disease that disrupts
this system leads to vertigo and disequilibrium.
CLASSIFICATION
All dizzy patients can be divided into those who are spinning and
those who have a sense of unsteadiness.
Sensation of rotation is subdivided further into those in whom
it lasts for hours. We almost never get a patient coming and
complaining of two minutes of dizziness. It is usually significantly
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Introduction 3
less or significantly longer. And of course the prolonged can last

for weeks or months or even forever.
zz Sensation of rotation:
—— Episodic—seconds/hours
—— Prolonged—weeks.
zz Sensation of unsteadiness:
—— Episodic—seconds/hours to days
—— Prolonged—weeks to months or forever.
The sensation of rotation most commonly arises from a problem

within the labyrinth whereas the sensation of unsteadiness is
more a problem within the whole system rather than especially
localized to the labyrinth.
Remember during Managing the Vertigo Patients

zz Advice patient not to be panic.
zz Underlying causes of the most of vertigo are simple.
zz Most of them do not require admission in intensive care.
zz Do not advice costly investigations such as computed
tomography (CT), magnetic resonance imaging (MRI), etc.
until really indicated.
zz Learn the art of the history taking for diagnosis of vertigo.
zz Think about common causes first.
VERTIGO PEARLS
zz Vertigo: It is a symptom, not disease.
zz History gives the diagnosis in 90% cases.
zz Majority of the cases are peripheral.
zz Have low threshold for suspecting TIA/stroke.
zz Do not be reassured with a normal CT/MRI.
zz Use vestibular suppressants judiciously and only for few days,
if there is disabling rotatory vertigo. Never prescribe vestibular
suppressants for imbalance/ataxia as it worsens the situation.
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zz Judicious use of newer technology: Videonystagmography

(VNG), MRI and special chairs.
Prevalence of Vertigo in Community

zz Vertigo is being reported to occur in 25% of middle-aged
population and about 40% in elderly.
zz By the age of 75 years, dizziness is the most common cause for
seeking medical advice.
zz It is the ninth most common cause for primary care physician
visits.
zz As per American Institute of Health Statistics data, 50% of all
accidental death from fall above 65 years is due to balance
disorder.
QUALITY OF LIFE IN VERTIGO PATIENT

Quality of life is hampered in vertigo patients. Factors that affect
quality of life in patients with vertigo are:
zz Agoraphobia.
zz Social impairment.
zz Depression.
zz Anxiety neurosis.
zz Drug side effects.
zz 3Fs syndrome (Fear of frequent falling).
There is always a need to develop a systematic, efficient and

formal assessment strategy for the diagnosis of the symptom
complex of dizziness or vertigo and disequilibrium is paramount
in order to provide appropriate management and rehabilitation.
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CHAPTER 2
Physiology of Vertigo
The ability to maintain balance is essential to nearly all activities

associated with daily livings. Maintenance of balance is a dynamic
process involving the vestibular system, the visual system,
the proprioceptive system and the central nervous system.
Considering the complexity of these mechanisms of postural
control, it is indeed amazing that the sense of maintaining balance
does not surface to our awareness in daily life. We become aware
of posture and balance only when there is a malfunction of any or
all the components involved.
FUNCTIONAL ANATOMY
Vestibular system has two components—peripheral and central.
Central vestibular system consists of vestibular nuclei, connections
of vestibular nuclei to cerebellum, spinal cord and extraocular
motor nuclei. Peripheral vestibular system consists of labyrinth.
The labyrinth (Figs 2.1A and B) consists of vestibule, semicircular
canals and vestibular nerves. Utricle and saccule constitutes the
vestibule. The labyrinth has bony and membranous part. The
membranous labyrinth contains hair cells that sense the motion
of head. The hair cells are located in the ampulla of the three
semicircular canals and in the macula of the utricle and saccule.
The hair cells of the semicircular canals are stimulated only
when there is an angular acceleration. The hair cells of the utricle
are stimulated, when the head moves forward or backward,
and the hair cells of the saccule are stimulated when the head
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Figs 2.1A and B Inner ear and its parts
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Physiology of Vertigo 7
Fig. 2.2 Vestibular nuclei and their connections (Vestibular pathway)
moves sideways. The utricle and saccule sense gravitational

orientation and linear acceleration.
The sensory impulses from the labyrinth travel through the
vestibular nerve to reach the Scarpa’s ganglion. From Scarpa’s
ganglion, the impulses are relayed to vestibular nuclei. There are
four vestibular nuclei (Fig. 2.2): Superior (Bechterew’s nucleus),
inferior (spinal nucleus), medial (Schwalbe’s nucleus) and lateral
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(nucleus of Deiters). Superior nucleus is situated at pons. Inferior

nucleus is at lower medulla, medial nucleus is at floor of fourth
ventricle (medulla) and lateral nucleus is at upper medulla. The
superior vestibular nuclei transmit impulses to medial longitudinal
fasciculus (MLF), and hence to the 3rd, 4th and 6th cranial nerve
nuclei. From lateral vestibular nuclei, impulses are transmitted to
brainstem from where it reaches spinal cords to control muscles of
extremities. Medial and inferior vestibular nuclei relay impulses to
medial longitudinal fasciculus and then to reticular formation and
11th cranial nerve nucleus respectively.
CLINICAL TIPS
Labyrinth contains two main sensory end organs which help in maintaining
balance, i.e. utricle and semicircular canals. Utricle by gravitational pull of its
chalk particles give information about position of head in space. Semicircular
canals give information about the change of position of head in space.
BASIC PHYSIOLOGY OF BALANCE DISORDER

The balance system is a complex multiorgan and multisystem
mechanism. The central nervous system, the peripheral nervous
system, the musculoskeletal system, the visual system and of
course, the vestibular system, all work in tandem to maintain the
body’s balance (Fig. 2.3).
The information about the spatial orientation (i.e. position of
the body in relation to the ground and surroundings) is provided
to the central nervous system from three sources the vestibular
labyrinths of the two sides, the two eyes and the sensory receptors
called proprioceptors in the muscles of the limbs (mainly the lower
limbs)—the neck and trunk. The central nervous system integrates
the information from these three sources and in response to it,
generates a motor reaction. Motor reaction or response means a
contraction of the requisite muscles in the body so that the subject
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Physiology of Vertigo 9
Fig. 2.3 Components responsible for maintaining balance
can effectively maintain his posture without falling, despite

sudden changes in the subject’s position or in his environment.
The accuracy of timing, preciseness and perfect coordination of
the muscular contraction of the extraocular and skeletal muscles
is maintained by the cerebellum.
The vestibular labyrinth has a basic resting activity which
discharges impulses at a steady rate even in the absence of an
external stimulus and is responsible for maintaining muscle tone.
The resting activity from each labyrinth tends to deviate the eyes
and the body to the opposite sides being normally equal, a state
of balance is maintained. For example, the resting activity of the
right vestibular labyrinth tries to move the eyes to the left, while
that of the left vestibular labyrinth tries to move them to right.
The two forces or actions being equal, balance each other and
hence no eye movement occurs. The same is true for the muscles
of the neck and the trunk. Physiological or pathological stimuli
that upset this balance between the two sides will produce a state
of disequilibrium, leading to nystagmus and body deviation.
Two key pathways from the vestibular apparatus are involved
in the maintenance of gaze and posture, i.e. the vestibulo-ocular
reflex (VOR) and the vestibulospinal reflex (VSR). Vestibular
pathways and their cardinal features are given in Table 2.1.
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Table 2.1 Vestibular pathways and their cardinal features

Pathways Cardinal features
Vestibulo-ocular reflex (VOR) Nystagmus
Vestibulospinal tracts (VSTs) Falling to side
Vestibulocerebellar tracts (VCTs) Ataxia, past pointing
Emetic pathways Nausea, vomiting
Parietotemporal cortex Vertigo
Any disturbance in labyrinth or vision or proprioception leads

to balance disorder.
Vertigo is usually considered as a difficult problem to manage

as a vast variety of causes may be involved in causing imbalance
such as:
zz Otological problems.
zz Visual problems.
zz Locomotive system disturbances (Proprioceptive system).
zz Central nervous system.
zz Cardiovascular system.
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CHAPTER 3
Causes of Vertigo
Disorders of the vestibular system can be divided into: (A) Peripheral

vestibular origin, and (B) Central origin.
Peripheral causes: It involves vestibular end organs and their first
order neurons (vestibular nerve) . The cause lies in the inner ear or
the 8th nerve.
Central causes: It involves the central nervous system after the
entrance of vestibular nerve in the brainstem and involves
vestibule-ocular, vestibule-spinal and other central nervous
system pathways.
Common causes of dizziness are provided in Box 3.1.
PERIPHERAL CAUSES
Lesions of end organs and vestibular nerve
zz Ménière’s disease.
zz Benign paroxysmal positional vertigo (BPPV).
zz Vestibular neuronitis.
zz Labyrinthitis.
zz Perilymph fistula.
zz Vestibulotoxic drugs.
zz Syphilis.
zz Acoustic neuroma.
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Box 3.1 Common causes of dizziness

Peripheral vestibular disorders
• Benign paroxysmal positional vertigo
• Ménière’s disease
• Vestibular neuritis
• Labyrinthitis
• Perilymph fistula
• Bilateral vestibulopathy
Central disorders
• Cervical vertigo
• Traumatic head injury
• Migraine
• Multiple sclerosis
• Anterior or posterior inferior cerebellar stroke
• Transient ischemic attacks
• Post-traumatic anxiety symptoms
• Vestibular ocular dysfunction
Psychiatric disorders
• Panic disorders
• Agoraphobia
• Hyperventilation syndrome
Other causes
• Presyncope
• Low blood pressure
• Arrhythmias
• Vertebral artery trauma
• Alternobaric vertigo
• Diabetes mellitus
• Thyroid dysfunction
• Human immune deficiency virus
• Syphilitic labyrinthitis
• Epstein-Barr virus
• Brainstem hemorrhage
• Friedreich’s ataxia
• Recent diplopia
• Medications
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Causes of Vertigo 13
Vertigo with Deafness

zz Labyrinthitis.
zz Acoustic neuroma.
zz Labyrinthine trauma.
zz Ototoxic vertigo.
Vertigo without Deafness

zz Benign paroxysmal positional vertigo.
CENTRAL CAUSES
zz Lesions of brainstem and central connections.
zz Posterior-inferior cerebellar artery syndrome.
zz Vertebrobasilar insufficiency.
zz Basilar migraine.
zz Multiple sclerosis.
zz Tumors of the brainstem and fourth ventricle.
zz Epilepsy.
zz Cervical vertigo.
PERIPHERAL VESTIBULAR DISORDERS

Ménière’s Disease
zz It is also called as endolymphatic hydrops (Fig. 3.1).
zz It is characterized by vertigo, fluctuating sensorineural hearing
loss, tinnitus and sense of fullness in the involved ear.
zz Vertigo is of sudden onset.
zz Vertigo lasts for a few minutes to 24 hours or so.
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Fig. 3.1 Inner ear hydrops
Benign Paroxysmal Positional Vertigo (BPPV)

zz It is characterized by the vertiginous episodes with the
positional changes of head, usually in supine position with
involved ear downwards.
zz It is due to displacement of the otoconia, which tend to reach
the posterior semicircular canal.
zz The attack usually starts within 5 seconds and lasts for about
one minute.
zz There is rotatory nystagmus with quick component towards
the involved ear.
Vestibular Neuronitis
zz It is characterized by severe vertigo of sudden onset with no
cochlear symptoms.
zz Attack lasts for few days to 2 or 3 weeks.
zz It is thought to occur due to a virus that attacks vestibular
ganglion.
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Labyrinthitis
zz There is severe vertigo and sensorineural hearing loss.
zz There is severe nausea and vomiting.
zz Nystagmus is seen to the opposite side due to destruction of
the affected labyrinth.
zz Labyrinthitis is seen in unsafe type of chronic suppurative
otitis media (CSOM).
Vestibulotoxic Drugs
zz Aminoglycoside antibiotics, particularly streptomycin,
gentamycin, kanamycin have shown to affect hair cells of the
crista ampullaris and to some extent those of the maculae.
zz Certain drugs which cause dizziness or unsteadiness
are antihypertensive, labyrinthine sedatives, estrogen
preparations, diuretics, antimicrobials (nalidixic acid,
metronidazole) and antimalarials.
Head Injury
zz Head injury may cause concussion of the labyrinth, completely
disrupt the bony labyrinth or the 8th nerve or cause perilymph
fistula.
zz Severe acoustic trauma such as that caused by an explosion
can also disrupt the vestibular end organ (otoliths) and result
in vertigo.
Perilymph Fistula
zz A perilymph fistula causes intermittent vertigo and fluctuating
sensorineural hearing loss, sometimes with tinnitus and sense
of fullness in the ear.
zz In this condition, perilymph leaks into the middle ear through
the oval or round window.
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zz It can follow as a complication of stapedectomy or ear surgery

when stapes is accidently dislocated.
zz It can also result from sudden pressure changes in the middle
ear (e.g. barotraumas, diving, forceful Valsalva) or raised
intracranial pressure (weightlifting or vigorous coughing).
Syphilis
zz Syphilis of inner ear, both acquired and congenital causes
dizziness in addition to sensorineural hearing loss.
zz Late congenital syphilis usually manifests between 8 and 20
years, mimics Ménière’s disease.
zz Hennebert’s sign, i.e. a positive fistula test in the presence of
an intact tympanic membrane is present in congenital syphilis.
zz Neurosyphilis (tertiary acquired) can cause central type of
vestibular dysfunction.
Acoustic Neuroma
zz It is a peripheral vestibular disorder as it arises from 8th cranial
nerve within internal acoustic meatus.
zz It causes only unsteadiness or vague sensation of motion.
LABYRINTHINE VERTIGO
Labyrinthine vertigo is classified into groups, i.e. due to
zz Labyrinthine stimulation.
zz Labyrinthine depression.
Both the types may be unilateral and bilateral.
Unilateral Labyrinthine Stimulation

Ear surgery: This can be a short period of postoperative dizziness
due to stimulation of labyrinth for which all postoperative
ontological cases should be assessed.
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Caloric stimulation: This is usually seen in caloric test but may also
occur in syringing the ear with water used at temperature above
or below the normal body temperature, i.e. 37°C. So, proper care
should be taken to assess the temperature of water used for
syringing.
Benign paroxysmal positional vertigo (BPPV): It is the most common
cause of vertigo encountered in day-to-day ENT practice.
Bilateral Labyrinthine Stimulation

It usually occurs in pseudophysiological condition in everyday life
such as head spins, swings, travel sickness, etc.
Unilateral Incomplete Depression of Labyrinth

Unilateral Complete Depression of Labyrinth

Trauma: This may due to head injury with transverse fracture of
temporal bone or surgery with deliberate labyrinthectomy or
accidental destruction of inner ear function in tympanoplasty or
stapedotomy, etc.
Infections: Bacterial and viral labyrinthitis can cause sudden and
complete destructive episode producing vertigo which behaves
clinically in the same way.
Vascular: Vascular catastrophe affecting the inner ear can result in
severe loss of labyrinthine function with/without loss of hearing.
Various factors have to be taken into account such as atresia
of vertebral artery, arteriosclerosis that may cause stenosis or
occlusion of arteries and embolism occurring in both the arterial
wall and heart.
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Bilateral Complete Depression of Labyrinth

It may occur suddenly in vertebrobasilar disease and gradually
with ototoxic drugs.
CENTRAL VESTIBULAR DISORDERS

Posterior Inferior Cerebellar Artery Syndrome
(Wallenberg’s Syndrome)
zz There is thrombosis of the posteroinferior cerebellar artery
cuts-off blood supply to lateral medullary area.
zz There is violent vertigo along with diplopia, dysphagia,
hoarseness of voice, Horner’s syndrome, sensory loss on
ipsilateral side of face and contralateral side of the body and
ataxia.
zz There may be horizontal or rotatory nystagmus to the side of
the lesion.
Vertebrobasilar Insufficiency
zz It is a common cause of central vertigo in patients above the
age of 50 years.
zz There is transient decrease in cerebral blood flow.
zz Common cause is atherosclerosis.
zz It may be precipitated by hypotension or neck movements,
when cervical osteophytes press on the vertebral arteries
during rotation and extension of the head.
zz Vertigo is sudden in onset, lasts for several minutes and is
associated with nausea and vomiting.
zz Neurological symptoms such as visual disturbances, drop
attacks, diplopia, hemianopia, dysphagia, hemiparesis due to
ischemia of the other areas of the brain.
zz Some may only complain intermittent attacks of dizziness or
vertigo on lateral rotation and extension of the head.
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Basilar Artery Migraine

zz Basilar artery migraine produces occipital headache, visual
disturbances, diplopia and severe vertigo which is abrupt and
may last for 5–60 minutes.
zz It is common in adolescent girls with strong menstrual
relationship and positive family history.
Cerebellar Disease
zz Acute cerebellar disease may cause severe vertigo, vomiting
and ataxia simulating an acute peripheral labyrinthine disorder.
zz Tumors in cerebellum are slow growing and produce classical
features of cerebellar disease, i.e. incoordination, past-
pointing, adiadochokinesia, rebound phenomenon and wide
base gait.
Multiple Sclerosis
zz It is a demyelinating disease affecting young adults.
zz Vertigo and dizziness are common symptoms.
zz Multiple neurological signs and symptoms like blurring or loss
of vision, diplopia, dysarthria, paresthesia and ataxia.
zz Spontaneous nystagmus may be seen.
zz Acquired pendular nystagmus, dissociated nystagmus and
vertical upbeat nystagmus are important features in diagnosis.
Tumors of Brainstem and Floor of Fourth Ventricle

zz There are neurological signs and symptoms in addition to
vertigo and dizziness.
zz Positional vertigo and nystagmus may also be the presenting
features.
zz CT scan and MRI are useful in their diagnosis.
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Temporal Lobe Epilepsy

zz Vertigo may occur as an aura in temporal lobe epilepsy.
zz History of seizure and /or unconsciousness following the aura
may help in the diagnosis.
zz Sometimes vertigo is the only symptom of epilepsy and that
may create a difficult diagnostic problem. EEG may show
abnormalities during the attack.
Cervical Vertigo
zz It is a controversial diagnosis. At this point, it has not been
established as a clear physiologically proven clinical entity.
zz It may follow injuries of the neck.
zz It is aggravated with movements of the neck to the side of the
injury.
zz X-ray shows cervical lordosis. On examination shows
tenderness of the neck and spasm of the neck muscles and
limited neck movement.
zz Exact mechanism of vertigo is not known. It may be due
to disturbed vertebrobasilar circulation, involvement of
sympathetic vertebral plexus or alteration of tonic neck reflexes
or inflammation of the deep cervical muscles or intervertebral
ligaments.
Other Causes of Vertigo

zz Ocular vertigo: Balance is maintained by the eyes, labyrinth
and somatosensory system. A mismatch of information from
any of these organs causes vertigo. Ocular vertigo may occur
in case of sudden extraocular muscle paralysis or high errors
of refraction.
zz Psychogenic vertigo
—— This diagnosis is suspected when patients suffering from
emotional tension and anxiety.
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—— Most of the times symptoms of neurosis, e.g. palpitation,

breathlessness, fatigue, insomnia, profuse sweating and
tremors are also present.
—— Symptoms of vertigo are often vague in the form of floating
or swimming sensation or light-headedness.

—— There is no hearing loss or no nystagmus. Caloric test shows
an exaggerated response.
zz Anemia.
zz Hypoglycemia.
zz Orthostatic hypotension.
BASICS OF PERIPHERAL VERTIGO

False sensation of movement when no movement is actually
occurring; results from peripheral causes such as inflammation,
infection or other disorders of the ear or vestibular nerve.
EPIDEMIOLOGY OF PERIPHERAL VERTIGO

zz It accounts for 54% of cases of dizziness reported in primary
care.
zz More than 90% of these patients are diagnosed with peripheral
causes, such as BPPV.
BASICS OF CENTRAL VERTIGO

False sensation (hallucination) of movement originating from
the central nervous system (CNS); results from hemorrhagic or
ischemic injuries to the cerebellum, the vestibular nuclei and their
connections within the brain stem, lesions of cranial nerve VII,
intracranial neoplasms, infection, trauma and multiple sclerosis.
EPIDEMIOLOGY OF CENTRAL VERTIGO

zz About 7–17% cases of vertigo are central in origin.
zz Incidence of ischemic strokes primarily affecting the
cerebellum is 1.5%.
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zz About 10% of patients with an isolated cerebellar infarction

presents with only isolated vertigo and imbalance.
zz Incidence of cerebrovascular disease (cerebellar infarction) is
slightly higher in men than in women.
zz Elderly patients have a higher incidence of central vertigo
owing to increased incidence of cerebrovascular disease. The
mean age of patients with cerebellar infarction is 60–80 years.
PHYSIOLOGICAL VERTIGO
zz It includes motion sickness and height vertigo.
zz It occurs when there is a mismatch between the vestibular,
ocular and proprioceptive inputs due to an external stimulus
(Unlike pathological vertigo which is due to a lesion in the
vestibular pathway) .
Motion Sickness
zz It includes car sickness, sea sickness, flight sickness and space
sickness.
zz It is an acute disorder with symptoms appearing within
minutes to hours of the stimulus and disappearing within
hours after the stimuli.
zz Reading in a moving or accelerating vehicle can cause this
condition.
zz Continuous exposure, as in sea travel leads to centrally
mediated adaptation in about 3 days.
zz Prevention by adaptation exercises with intermittent exposure
to the stimulus.
zz Pharmacotherapy for motion sickness: Meclizine, dimen
hydrinate or scopolamine may benefit by inhibiting neuronal
activity.
zz Specific measures such as sitting in the front seat of the car,
reducing accelerating movements may be of benefit.
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Height Vertigo
Dizziness occurs when looking down from a great height or
looking up a tall building or cliff.
DRUGS CAUSING DIZZINESS

zz Aminoglycosides, cisplatin–damage vestibular hair cells →
cause vertigo, disequilibrium.
zz Antiepileptics (carbamazepine, phenytoin)–cause cerebellar
toxicity → cause disequilibrium.
zz Alcohol → CNS depression, cerebellar toxicity, changes
in cupula specific gravity → cause disequilibrium and
intoxication.
zz Anticoagulants → cause hemorrhage into inner ear or brain
→ vertigo.
zz Antihypertensives and diuretics → cause postural hypotension
→ faint like dizziness.
zz Methotrexate → cause brainstem and cerebellar toxicity →
cause disequilibrium.
zz Parkinsonian drugs, e.g. bromocriptine, levodopa/carbidopa;
muscle relaxants like baclofen → cause postural hypotension
→ leads to faint like sensation.
zz Urologic drugs like sildenafil, oxybutynin → cause postural
hypotension → faint like sensation.
OTOTOXICITY AND DIZZINESS

zz Ototoxicity can cause vestibulotoxicity (damage to the
vestibular apparatus) or cochleotoxicity (damage to the
cochlea).
zz Vestibulotoxicity causes vertigo while cochleotoxicity causes
tinnitus and hearing loss.
zz Topical ototoxicity occurs with antibiotic eardrops used for the
treatment of chronic suppurative otitis media, where there is a
perforated eardrum.
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zz Bilateral vestibular loss can occur with the use of systemic

ototoxic agents, such as aminoglycoside antibiotics. This
results in oscillopsia.
OLD AGE AND DIZZINESS

Dizziness is a common problem in the elderly and can lead to
problems with balance, which in turns, results in falls with head
injuries or long bone fractures. Different terms are used to describe
dizziness among the elderly including multisensory dizziness,
disequilibrium of aging or presbyastasis.
The cause is usually multifactorial and contributed by the
following:
zz From fifth decade onwards, degenerative changes occur
throughout the vestibular apparatus; loss of hair cells,

otoconia, nerve fibers and Purkinje cells (cerebellum) .
zz Degenerative changes also affect the visual and proprioceptive
inputs.
zz Degenerative changes of the CNS, such as brainstem and
cerebellar atrophy and white matter changes.

zz Coexiting medical conditions, such as Parkinson’s disease or
diabetes mellitus with peripheral neuropathy.

zz Medications used for comorbid conditions may also cause
dizziness.
Management Old Age Dizziness

zz Identifying and managing individual contributory factors like
changing antihypertensive drugs and cataract surgery, etc.
zz Physiotherapy: Stimulate central compensation, strengthen
sensory inputs and strategies to improve balance and prevent
falls.
zz Pharmacotherapy.
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DIZZINESS IN CHILDREN
zz It is less common complaint in children than adults.
zz Assessment of a dizzy child is challenging because child is
unable to communicate properly.
zz The child’s symptoms may be attributed to behavioral
problems or clumsiness.
zz Many of the causes of vertigo in adults can also affect children.
These include BPPV, vestibular neuronitis, perilymph fistulas,

traumatic labyrinthine injuries and migraine.
zz Bilateral vestibulopathy can occurs secondary to ototoxicity or
bacterial meningitis.
zz Motion sickness, however, does not affect children below the
age of two.
zz The diagnosis and management of a dizzy child will frequently
need the expertise of a pediatrician.

Diagnoses of vertigo from clinical presentation are given in
Table 3.1.
DIZZINESS IN PREGNANCY
zz It is often due to hyperemesis gravidarum, which occurs mainly
in the first trimester.
zz Auditory or vestibular complaints in pregnancy can be
obstetric (antiphospholipid syndrome) or otologic (Ménière’s
disease, acoustic neuroma).
zz If vestibular cause is suspected, then further assessment by an
otologist is required.
zz Administration of any drugs during this period should be done
with caution due to fetal risk of teratogenicity.
POST-TRAUMATIC VERTIGO
Vertigo or dizziness following trauma can be due to a number of
causes secondary to head injury or a whiplash injury to the neck.
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Table 3.1 Determining the causes of vertigo from clinical presentations

Clinical features Possible causes
• Episode of vertigo lasting for hours, fluctuating and Ménière’s disease
progressive sensorineural hearing loss and tinnitus
• Episodes of vertigo lasting less than 1 minute that Benign positional
are brought by rapid head movement in a nonaxial vertigo
plane
• Vertigo and hearing loss following bacterial or viral Labyrinthitis
infection
• Hearing loss and vertigo following injury to the ear Perilymph fistula
or barotraumas (such as from recent air travel or
diving)
• Acute onset of vertigo that lasts days to weeks, Vestibular
nausea and vomiting neuronitis
• V ertigo accompanied by diplopia, dysarthria, Brainstem ischemic
dysphagia, drop attacks, paresthesia and loss of or infarction
motor function
• Vertigo and dysdiadochokinesia Cerebellar stroke
• Vertigo and other neurological symptoms that Multiple sclerosis
suggest multiple sclerosis
• Asymmetric sensorineural hearing loss, imbalance Acoustic neuroma
particularly in the dark, vertigo (rare), hypoesthesia,
facial paralysis (rare)
• Vertigo episodes lasting for hours with no significant Migrainous vertigo
auditory symptoms; personal or strong family
history of migraine
zz Benign paroxysmal positional vertigo: It is usually by

canalolithiasis of the posterior semicircular canal. It can be
bilateral, with one ear more severely affected compared to the
other.
zz Acute labyrinthine failure: It occurs from transverse fracture of
otic capsule which results in hearing loss and severe vertigo.
Clinical features are similar to that of vestibular neuritis.
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zz Perilymph fistula: Leakage of perilymph from the round

window or oval window. It usually is due to subluxation of the
stapes into the inner ear.
zz Acute labyrinthine or brainstem concussion: Features are similar
to acute labyrinthine fracture except that there is no evidence
of fracture clinically or radiologically and symptoms are
transient.
zz Whiplash injury: It is due to hyperextension of the neck
following road traffic accident. It results in injury of the anterior
spinal ligaments and deep cervical muscles, which contain
proprioceptive nerve endings. In addition, the vertebral
arteries can be injured resulting in vertebrobasilar ischemia.
zz Postconcussion syndrome: A mild form of brain injury, which can
present with a variety of symptoms, which include dizziness,
headache, cognitive and behavioral changes. A diagnosis is
made when the symptoms persists for more than 3 months
after the injury or start within a week of the trauma.
zz Malingering: It should be considered in patients with delayed,
exaggerated or chronic symptoms without objective findings
and when monetary gain or compensation is sought.
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CHAPTER 4
Diagnosis of Vertigo
from History
The reasons for good history taking are:

zz To get a diagnosis.
zz Taking a good history is a part of treatment.
zz The patient feels you are interested for the problem solving.
zz When we give reassurance, which hopefully we will be able to
give at the end, patients are able to accept the reassurance and
take comfort from it.
zz To be a proper doctor.
Two important causes of failure to manage the vertigo patients:

1. Reluctance to take a good history.
2. Failure to think about pathology.
When you are taking a history you begin at the beginning.
THINGS ABOUT DIZZY SPELLS

zz Are they spells or is it just one attack?
zz Are they of sudden onset when they come?
zz Are they associated with other symptoms such as nausea,
vomiting, deafness or tinnitus?
zz Do they stop suddenly or gradually?
zz How is the patient between attacks?
zz Ask the patient when was the last time, they were perfectly
stable and free from dizziness.
zz Try to get a clear, coherent and chronological history to get a
right diagnosis.
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Diagnosis of Vertigo from History 29
ASSESS THE PROBLEM

zz Find out the details of the inconvenience that the patient
experiences from the dizziness.
zz Start assessing the problem when the patient is coming into
your consulting chamber.

zz Did he walk in unaided or did he stagger in or did somebody
help him in?

zz How much problems interferes with his everyday life.
If we are reluctant to take the history, then there is failure to

think about the pathology.
Investigations are no substitute for a good history.
Key Points Behind Good History Taking

zz Begin at the beginning.
zz Stay in control.
zz Assess the extent of the problem.
zz Investigations are no substitute.
zz A good history is a part of the treatment.
HISTORY TELLS DIAGNOSIS

zz History of vertigo, vomiting, tinnitus and deafness refers to
Ménière’s disease.
zz History of vertigo during changing head position refers to
BPPV.
zz History of cough, cold, fever followed by vertigo and deafness
refers to viral labyrinthitis.
zz History of cough, cold, fever followed by vertigo but no
deafness refers to vestibular neuronitis.
Onset of Vertigo
Ask is this the first attack or recurrent?
zz If recurrent vertigo
—— Ménière’s disease.
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—— Migraine.
—— Hypoglycemia.
zz If non-recurrent vertigo
—— Vestibular neuronitis.
—— Drug-induced.
—— Labyrinthitis.
zz In case of chronic vertigo suspect

—— Brain tumor.
—— Hypertension.
—— Diabetes.
—— Head injury, etc.
Drug History
Drugs causing vertigo are
zz Antiepileptic.
zz Antirheumatic.
zz Antihypertensive.
zz Antidiabetic.
zz Aminoglycosides.
zz Barbiturates, etc.
Past history of head injury, surgery and fever must be asked.
Personal History
Personal history of
zz Blood pressure (High or low).
zz Diabetes.
zz Alcohol.
zz Tobacco.
zz Otorrhea.
zz Cervical spondylosis.
zz Heart disease.
zz Arthritis, etc.
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The simplified approach to dizzy patients was first described

by Drachmann in 1972. The dizziness can be described in four
forms:
1. Dizziness type-1 or true vertigo:
zz It is a vestibular problem, either peripheral or central
connections.
zz The patient describes spinning or a definite rotatory
feeling, typically precipitated by fast head movement,

getting up or lying down and even turning in bed.
2. Dizziness type-2 or presyncope:
It is essentially cardiovascular and the patient feels faintness or
darkness before his eyes, when upright or on getting up.
Causes are:
zz Postural hypotension (Confirmed by checking BP in supine
and standing position).

zz Vasovagal attacks.
zz Hyperventilation.
zz Low cardiac output states.
3. Dizziness type-3:
zz It is basically unsteadiness or incoordinates of gait or
feeling of loss of balance.

zz It typically occurs when the patients stands up or walks
and is worsened by uneven ground or turning.

zz It never occurs when sitting or lying in bed.
Causes: Mostly neurological. These are:

zz Gait ataxia.
zz Parkinsonism and other extrapyramidal disorders.
zz Cerebellar ataxia.
zz Myelopathy (e.g. cervical spondylotic myelopathy).
zz Neuropathy.
zz In the elderly, it can be due to impairment of multiple
sensory organs, including vision, vestibular and peripheral

neuropathy as well as chronic cerebral ischemia.
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4. Dizziness type-4:
zz It is predominantly psychogenic.
zz The patient may be vague or describe numbness or
heaviness or light feeling in the head.

zz It is actually an abnormal sensation in head, not fitting into
the earlier three types.
Traditional Symptomatic Approach

zz True Vertigo-Vestibular—Ear problem.
zz Presyncope-Cardiovascular—Medical/Cardiological problem.
zz Disequilibrium-Neurological-Neuro problem.
zz Nonspecific dizziness—Psychiatric–No problem.
Certain aggravating factors trigger the vertigo and are helpful

for the diagnosis of specific type of vertigo (Table 4.1).
Associated Features Suggesting a

Central Cause of Vertigo (Box 4.1)
Ds
zz Diplopia.
zz Dysarthria.
zz Dysphagia.
zz Dysphonia.
zz Dysmetria.
zz Dysesthesia.
zz Drop attacks.
zz Down-is-up distortions (room tilt illusions).
Table 4.1 Triggers often give important clue for diagnosis

Trigger Possible diagnosis
When turning in bed True vertigo, e.g. BPPV
When getting up suddenly Postural hypotension
When walking or turning Type-3 or balance disorder
When tired or stressed out Type-4 or presyncope
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Box 4.1 Indicators of central causes of vertigo

• Focal neurological symptoms/signs (Deadly Ds—diplopia, dysarthria,
dysphagia)
• Ataxia out of proportion to vertigo
• Nystagmus-Pure vertical (upbeating or downbeating), direction changing
or gaze evoked and other eye movement abnormalities, e.g. gaze palsy,
skew deviation (vertical misalignment of the eyes)
• Sudden, severe or sustained head or neck pain
Table 4.2 Duration of the vertiginous event

Acute long duration (Peripheral) Vestibular neuritis, labyrinthitis,
labyrinthine ischemia, labyrinthine
concussion
Acute long duration (Central) Cerebellar infarct, cerebellar hemorrhage,
brainstem infarct, multiple sclerosis
Recurrent long duration Autoimmune inner ear disease, Ménière’s
(Peripheral) disease, vestibular neuritis (recurrent)
Recurrent long duration Vertebrobasilar ischemia, multiple
(Pentral) sclerosis, migraine
Recurrent brief duration BPPV, superior canal dehiscence
(Peripheral)
Recurrent brief duration Cerebellar tumor, cerebellar atrophy,
(Central) multiple sclerosis
Diagnosis from Duration of Vertigo (Table 4.2)

zz If it is less than a second: This is typically motion sensitivity or a
feeling of transient dizziness on sudden movement, often only
in one direction. The cause is typically old unilateral vestibular
deficit, migraine or psychogenic. The patient may feel the need
to hold on for support suddenly.
zz Transient vertigo lasting a few second: It is typically positional
and the most common cause is BPPV. There are also central
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Table 4.3 Characteristic of peripheral and central vertigo

Characteristics Peripheral Central
• Overall illness Looks worse Milder illness
• Vertigo More Less
• Ataxia Less More
• Tinnitus/deafness/ear pain Often present Usually absent
• Diplopia/dysarthria/ Not present Usually present
sensory or motor
symptoms, Horner’s
syndrome
• Nystagmus pattern Unidirectional, Direction changing
horizontal, rotatory
• Nausea, vomiting May be severe Varies
causes of which migraine is quite common, but there are some

rare causes like TIA, posterior fossa tumor and demyelination.
zz Transient vertigo lasting a few minutes: It is uncommon, but we
need to consider a vertebrobasilar transient ischemic attack

(TIA) or migraine or psychogenic. Even if the patient does not
have diplopia or dysartheria or other neurological symptom
and has vertigo or vertigo with tinnitus or deafness lasting for
a few minutes, we need to keep in mind the possibility of a TIA,
and therefore the possibility of a dangerous stroke occurring
later.
zz Short attacks of vertigo lasting minutes to hours: It may occur in
Ménière’s disease, migraine, stroke or psychogenic.

zz Vertigo for days to weeks: Seen in acute peripheral
vestibulopathy, migraine, psychogenic.

zz Continuous vertigo for weeks is usually psychogenic.
Peripheral vertigo and central vertigo are differentiated from

certain clinical features and history (Tables 4.3 and 4.4).
CLINICAL TIPS
The three most important things in the management of vertigo are History,
History and History only must be for the management of vertigo.
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Table 4.4 Vertigo of peripheral and central origin from patient history
Peripheral Central
• A definitive sensation of • The vertigo is mild and more like
movement is present unsteadiness
• Vertigo is severe and paroxysmal • Vague, no specific onset or
termination
• The attacks last from minutes to • The attacks of vertigo lasts for
days weeks
• Nystagmus and associated • Often no apparent nystagmus
vestibular symptoms are common
• Presentation: Severe rotating or • Imbalance, lightheadedness,
spinning sensation usually with disorientation
nausea and vomiting
• Consciousness maintained • Consciousness may be lost
• Presence of systemic disorders: • Often diabetes, hypertension,
Usually absent atherosclerosis present
• Progress of disease: Improves as • Patient usually goes downhill and
peripheral lesions are self-limiting symptoms increase
and central compensation takes
place
• Associated features: Aural • Neurological features such as
symptoms such as deafness, diplopia, headache, motor/sensory
tinnitus, nausea and vomiting are loss present
often present
VERTIGO DIAGNOSIS
zz Vertigo → History and physical examination → Blood pressure
(Lying and supine) → Orthostatic → Diagnosis of orthostatic
hypotension.
zz Vertigo → Irregular pulse → Diagnosis of cardiac arrthythmia.
zz Vertigo → Abnormal neurological examination → Differential
diagnosis of CVA, CNS drugs, multiple sclerosis.
zz Vertigo → History of cervical spine trauma → Yes → Vertigo-
induced by position change → Yes → Diagnosis: BPPV.
zz Vertigo → History of recent viral illness → Yes → Diagnosis:
Viral labyrinthitis.
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Box 4.2 Vertigo with deafness

Differential diagnosis
• Ménière’s disease
• Labyrinthitis
• Acoustic neuroma
• Labyrinthine trauma
• Perilymph fistula
• Ototoxicity
Box 4.3 Vertigo without deafness

• Vestibular neuronitis
• Benign paroxysmal vertigo
• Ototoxicity to the vestibule
• Motion sickness
zz Vertigo → Drug history: antibiotics, diuretics or chemotherapy

→ Yes → Diagnosis: Toxic labyrinthitis.
zz Vertigo → History of trauma → Yes → Barotrauma/Head
trauma → Diagnosis: Round window rupture (In case of
Barotrauma); temporal bone trauma (In head trauma).
zz Vertigo → History of hearing loss → Differential diagnosis:
Ménière’s disease, acoustic neuroma, toxic labyrinthitis,
neurosyphilis (Boxes 4.2 and 4.3).
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CHAPTER 5
Clinical Tests for Vertigo
Before assessing a dizzy patient, it should be born in mind that

the results of these tests may be affected by prior medication like
vestibular suppressants, antidepressants or sedatives. It is prudent
to ask the patient to stop taking any of these medications 24–48
hours prior to vestibular assessment.
Also, if the patient demonstrates any sign of neurological
emergency such as brainstem stroke, then it is imperative that the
whole test battery is bypassed to carry out a thorough radiological
assessment and neurological consult for the same.
ROUTINE EXAMINATIONS FOR VERTIGO PATIENTS

zz General examinations.
zz Examine the ears.
zz Examine the cranial nerves (III–XII).
zz Look for the nystagmus.
zz Do balance tests.
zz Do positional test.
zz Tests for cerebellum.
General Examination
zz Blood pressure.
zz Pulse rate.
zz Temperature.
zz Pallor.
zz Postural hypotension.
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CLINICAL TIPS
Blood pressure measured in supine position and again 1 min after the
patient stands. A systolic blood pressure drop of 20 mm Hg, diastolic blood
pressure decrease of 10 mm Hg, or pulse increase of 30 beats per minute is
indicative of orthostatic hypotension.
Examination of the Pinna and External Auditory Canal

The pinna and external auditory canal should be thoroughly
examined for any vesicles which may indicate Ramsay Hunt
syndrome (it causes vertigo, deafness and facial palsy). The post-
auricular area and space between the tragus and helix should
be searched for any scar marks of surgical incision which may be
suggestive of previous ear surgery.
Otoscopic Examination (Fig. 5.1)

It can help to identify any perforation in tympanic membrane or
glomus tumor or otitis media. It is always important to rule out
bacterial labyrinthitis and perilymph fistula during otoscopic
examination.
Fig. 5.1 Otoscopic examination of the ear
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Clinical Tests for Vertigo 39
Tuning Fork Test

Hearing tests are must in any neuro-otological evaluation. A high-
frequency hearing loss indicates a lesion in the basal turn of the
cochlea, i.e. in the portion of the inner ear adjacent to the vestibular
labyrinth. So, suspicion of high frequency deafness is of significant
clinical relevance in balance disorder patients. Tuning fork
(Fig. 5.2) test is used for hearing assessment at out-patient
department.
Rinne’s Test
zz Rinne positive in normal or sensorineural hearing loss.
zz Rinne negative in conductive deafness of the tested ear.
zz False Rinne negative occurs in unilateral severe sensorineural
deafness.
Weber’s Test
zz Center or equal bilaterally in normal case.
zz Lateralized to one side in conductive deafness in that side and
sensorineural deafness of the opposite side.
Fig. 5.2 Tuning fork
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ABC Test
ABC is reduced in sensorineural deafness.
Neurological Examination
zz Examination of cranial nerves at least 3rd, 4th, 5th, 6th, 7th and
9th should be done.
zz Babinski’s test should be done.
zz Deep tendon reflexes should be checked.
zz Evaluation of motor and sensory loss.
zz Cerebellar function tests.
Spontaneous Nystagmus
Nystagmus is assessed by asking the patient to sit in front of the
examiner. The examiner keeps moving the fingers 45 cm from the
patient’s eyes and moves it right, left up and down taking care not
to move more than 30° from the central position to avoid gaze
nystagmus.
Presence of spontaneous nystagmus indicates an organic
lesion which may be peripheral (Lesion at labyrinth or 8th nerve)
or central (Lesion at vestibular nuclei, brainstem or cerebellum).
Peripheral vestibular nystagmus is horizontal rotatory and have
both fast and slow components. Peripheral nystagmus is fatiguable
but reproducible.
The following types of nystagmus may be considered to be of
central nervous system origin:
zz Pure vertical nystagmus.
zz Direction changing/unipositional nystagmus.
zz Active nystagmus without vertigo.
zz Failure of fixation: A nystagmus generated by a central
vestibular pathology often (but not always) increases in

intensity when the eyes are open (i.e. optic fixation) and
decreases when the eyes are closed. This is just the opposite of
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Fig. 5.3 Frenzel’s glass
a peripheral vestibular lesion. Removal of optic fixation with a

Frenzel’s glasses (Fig. 5.3) may help unmask latent nystagmus.
zz Dysconjugate eye movement in nystagmus, and gaze
nystagmus (the patient cannot maintain conjugate eye

deviation away from the midline).
Rotatory nystagmus, however is commonly associated with
peripheral vestibular system disorders. Spontaneous nystagmus in
peripheral vestibular disease, is an oscillating motion of both eyes
that has two phases, a slow one that moves toward the side of the
lesion and a quick phase that moves towards the opposite side.
Therefore, this means that the slow phase indicates the side of the
peripheral lesion (Fig. 5.4).
Central and peripheral nystagmus are differentiated by certain
features are given (Table 5.1).
Alexander’s Law
Horizontal nystagmus of peripheral origin (labyrinth or VIII nerve)
obeys Alexander’s law, which states the nystagmus:
zz It is always in one direction irrespective of the direction of gaze.
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Fig. 5.4 Spontaneous nystagmus in left peripheral vestibulopathy
Table 5.1 Difference between central and peripheral nystagmus

Central nystagmus Peripheral nystagmus
Type Rotatory, mixed Horizontal/vertical
Fatiguability Not fatiguable Fatiguable
Induction Not possible Possible
Latency No latency Present (2–20 sec)
Duration No fixed duration Less than 1 minute
Accompanying symptoms CNS features Vertigo
zz Intensity of the nystagmus is greatest when looking in the

direction of the fast phase.
Opsoclonus: Here the eye movements are non-rhythmic and very
bizarre—the eyes moving rapidly but irregularly in all directions—
horizontal, vertical, oblique or rotator. It occurs in lesions of the
brainstem and cerebellum.
Ocular myoclonus: This is a pendular oscillatory movement of
the eyes which occur synchronously with similar rhythmical
movements of the soft palate, tongue and larynx. The cause is
believed to be an advanced lesion in the dentate nucleus or its
central connections with possibly a pseudohypertrophy of the
inferior olivary nucleus.
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Ocular bobbing: The eye shows irregular downward jerks occurring

abruptly. Each downward jerk is followed by a slow return of the
eyes to the mid-position. This erratic eye movement is usually
binocular but may rarely be uniocular. Ocular bobbing suggests
a CNS lesion.
Ocular flutter: This is a mild form of opsoclonus and consists of
sudden rapid oscillatory movement of the eyes lasting for very few
seconds. The patient usually complains of a sudden momentary
spell of blurring of vision but it is not accompanied by a definite
vertiginous sensation.
Corneal Reflex
Small cotton wool is taken and the patient is asked to look
straight-forward when the examiner will touch the sclera first
and then cornea. In normal condition, patient’s eyes should blink
on both sides on touching the cornea by cotton wool. Blinking
will be absent in cerebellopontine angle pathology, e.g. acoustic
neuroma. In corneal reflex, an afferent pathway (the nasociliary
branch of the ophthalmic nerve, which is a branch of the trigeminal
nerve), the spinal root of the trigeminal nerve which is the first
synapse, the second synapse which is the nucleus of facial nerve
of both sides, the efferent neural pathway (temporal branch of the
facial nerve of both sides) and the effector motor organ which is
the orbicularis oculi muscle of both sides (supplied by facial nerve).
In this, afferent is unilateral and the efferent is bilateral pathway.
Fistula Test
It is elicited by pressing the tragus or by using siegle pneumatic
speculum. Positive fistula test means that patient will complain of
vertigo while performing the test and nystagmus will be directed
towards opposite side.
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CLINICAL TIPS
Positive fistula test implies that there is a fistula communicating middle
ear and inner ear. The most common site of fistula formation is lateral
semicircular canal.
False negative fistula sign: There is fistula but the labyrinth is dead or the
fistula is covered by granulation tissue or cholesteatoma mass.
False positive fistula sign: There is no fistula but the test is positive. It is
seen in early congenital syphilis where annular ligament is lax and mobile
known as Hennebert’s sign. It is also seen in Ménière’s disease and following
fenestration surgery. Tullio phenomenon is seen in labyrinthine fistula and
following fenestration surgery where giddiness is produced more by loud
noise rather than pressure.
Valsalva Maneuver
zz Forced exhalation with closed nostril and mouth increases
pressure in the middle ear through eustachian tube. It causes
vertigo in some cases of perilymphatic fistulae.
zz Forced exhalation with closed glottis raises intracranial
pressure, which can cause dizziness in cases of superior
semicircular canal dehiscence and Chiari malformations.
Standing Test
The patient will stand with eyes open, feet close together, then eyes
closed and finally stand on one leg with eye closed. The patient
stands for about 15–20 seconds on the left leg, followed by 15–20
seconds on the right leg. Any swaying of the body is looked for.
In acute peripheral vestibular lesion, body is twisted to the side of
lesion, deviation of both arms to the side of the lesion with raising
of the hand on the healthy side with a tendency of falling to the
side of the lesion. This typical position is called discus-thrower’s
position.
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Tesrs for Vestibulospinal tract
Walking Test
zz The patient is asked to walk with feet tandem. He is also
allowed to walk with the toe of the backfoot touching the heel
of the frontfoot in a straight line with closed eye and eye open.
zz Falling or deviation or tendency to fall is noted.
zz Falling or deviating repeatedly in the same direction suggests
an unilateral vestibular lesion on the side of the fall.
zz A broad and wide-based gait with tendency to fall, suggests
the possibility of a cerebellar pathology.
zz If the patient walk backwards with feet tandem, there should
be no reason to suspect any organic balance disorder.
Romberg Test
The patient will stand with feet together and arms by the side
with eyes open first and then closed. If eyes open, patient can
still compensate the imbalance but with eyes closed, vestibular
system is at more disadvantages. In peripheral vestibular lesions,
the patient sways to the side of lesion. In central vestibular lesion,
patient shows instability. If patient performs this test without sway,
sharpened Romberg test can be performed. In this test, patient
stands with one heel in front of toes and arms folded across the
chest. Inability to perform the sharpened Romberg test indicates
vestibular impairment.
Unterburger’s Test
The blind-folded patient is asked to extend his arms and step on
the same spot alternately with each foot for 90 times in 1 min
(Fig. 5.5). In peripheral vestibular lesions, the patient rotates/
deviates to the side of the lesion. In central vestibular lesion, the
sway (i.e. the side-to-side movement while stepping) is abnormally
high.
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Fig. 5.5 Unterberger’s test
Head Shaking Test (Fig. 5.6)

The head of the patient is grasped by the clinician and shaken
rapidly and vigorously side to side for 20 times and any nystagmus
is looked for. Presence of nystagmus suggests a disorder in the
vestibular system, usually peripheral in nature. No nystagmus
is obtained on head shaking in normal subjects. Usually, a left
beating nystagmus suggests a right peripheral lesion and vice
versa. Vertical nystagmus is sometimes found in lesions of the
central vestibular system.
Rotation Test
The patient sits on a special chair (Fig. 5.7) and rotates with eyes
closed 10 times in 20 seconds. The after nystagmus is measured
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A B
Figs 5.6A and B Head shaking test
Fig. 5.7 Special chair used for rotation test
with a stopwatch, which varies from 15 to 30 seconds in a normal

individual. In active labyrinth, the nystagmus will be on the
opposite side of the rotation.
Positional Test (Dix-Hallpike Test)

It is done when patient complains of vertigo during change of
head position.
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Fig. 5.8A Steps of Dix-Hallpike test
Patient sits on a couch. Examiner hold the patient’s head,

turn it 45° to the right and then places the patient in a supine
position so that his head hangs 30° below the horizontal (Figs
5.8A and B). Patient’s eyes are observed for nystagmus. The test is
repeated with head turned to left and then again in straight head-
hanging position. Four parameters of the nystagmus are observed:
Latency, duration, direction and fatiguability. In BPPV, nystagmus
appears after a latent period of 2–20 seconds, lasts for less than
a minute and is always in one direction, i.e. towards the ear that
is undermost. On repetition of the test, nystagmus may still be
elicited but lasts for a shorter period. On subsequent repetitions,
it disappears altogether, i.e. nystagmus is fatiguable. Patient also
complains of vertigo when the head is in critical position.
In central lesions (e.g. tumors of 4th ventricle, cerebellum,
temporal lobe, multiple sclerosis, vertebrobasilar insufficiency or
raised intracranial tension), nystagmus is produced immediately, as
soon as the head is in critical position without any latency and lasts
as long as head is in that critical position. Direction of nystagmus
also varies in different test positions (direction changing) and is
non-fatiguable on repetition of test (Table 5.2).
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Fig. 5.8B Dix-Hallpike test
Table 5.2 Differences between peripheral and central causes of

positional nystagmus
Peripheral nystagmus Central nystagmus
Onset Delayed (2–20 seconds) Immediate
Distress Severe vertigo during nystagmus None
with distress
Fatiguability Fatigues on repetition of the test Does not fatigue
Duration Less than 1 minute More than 1 minute
Direction Direction fixed, towards the Direction changing
undermost ear
Minimal Physical Examination in Dizzy Patients

zz Check BP in supine and standing.
zz Check for spontaneous nystagmus fixating a target and with
fixation blocked.
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Table 5.3 How to differentiate acute posterior fossa stroke from acute
peripheral vestibulopathy?
1. Walk the patient: Stroke patient often cannot stand or walk unsupported
2. Turns the light down: Constricted pupil due to Horner’s syndrome may
appear ipsilateral to the stroke
3. Check the sensation too cold on the face and extremities: Stroke may show
sensory loss for temperature on the ipsilateral face and contralateral
extremities
4. Test for dysdiadochokinesia: It will affects the ipsilateral hand after a
cerebellar stroke
5. Unilateral hearing loss can occur ipsilateral stroke and does not prove the
origin of vertigo is peripheral
zz Check smooth pursuit and saccadic eye movements.

zz Head impulse test.
zz Hallpike test.
zz Check standing balance (Romberg) and check gait.
zz Dynamic visual quality.
Orthostatic Hypotension
Blood pressure measured in supine position and again 1 minute
after the patient stands. A systolic blood pressure drop of 20 mm
Hg, diastolic blood pressure decrease of 10 mm Hg or pulse increase
of 10 beats per minute is indicative of orthostatic hypotension. It is
seen in cases of dehydration or autonomic dysfunction.
Clinical tips differentiating central vertigo (Posterior fossa
stroke) from acute peripheral vestibulopathy are provided in
Table 5.3.
SPECIAL VESTIBULAR TESTS

Oscillopsia Test
zz This test assesses for bilateral vestibular loss as in bilateral
ototoxicity.
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zz The patient complains of his surrounding bobbles or shakes,

whenever he is in motion.
zz In this test, patient is asked to read the lowest possible on a
standard Snellen’s chart. Then with repetitive shaking of the
head in the horizontal plane, the patient is asked to read the
lowest line possible for comparison. A loss of more than four
lines during active head shaking is considered significant for
bilateral loss.
Vestibulo-ocular Reflex Suppression

zz The peripheral vestibular systems are stimulated by head
movement, while the patient is asked to fix on a certain object
during these movements to suppress the vestibulo-ocular
reflex (VOR) thus inhibiting nystagmus. This ability to suppress
the VOR is through centrally mediated smooth pursuit
pathways.
zz This is in essence optic fixation and implies the ability of the
visual system to override labyrinthine information provided
the central pathways are normal.
zz Therefore, failure of VOR suppression is indicative of central
pathology.
Head Impulse/Halmagyi Test (thrust)

zz It tests the horizontal semicircular canal.
zz In this test, quick or rapid movement of head in the horizontal
plane with gaze fixed in midpoint (examiners nose).
A peripheral disorder will result in a corrective saccade. A right
sided lesion will result in corrective saccades to the left, when
the head is turned to the right.
zz A normal test helps to differentiate vestibular neuritis from
pseudoneuritis (stroke).
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OCULOMOTOR TESTS
These tests usually assess the oculomotor nerves and their
central pathologies. Abnormalities in these tests indicate a central
pathology or pathology of the oculomotor nerves (III, IV and VI).
Fixation (Table 5.4)

The patient is asked to fixate on an object held straight ahead.
Smooth Pursuit (Table 5.5)

Patient is asked to follow moving target horizontally and vertically.
Saccade (Table 5.6)

Patient is asked to fix on target 20 to 30° from midpoint and quickly
change between right and left or up and down. Both horizontal
and vertical saccades are tested.
Table 5.4 Testing the fixation

Findings Interpretation
Able to fixate Normal
Pendular nystagmus Central cause
Jerk nystagmus Central/peripheral vestibular disorder
Table 5.5 Testing the smooth pursuit

Impaired asymmetrical Central pathology
Impaired symmetrical Central pathology/drugs/
(slow or reduced) old age/fatigue
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Table 5.6 Saccades findings

Overhooting (hypermetric)
Undershooting (hypometric)
Prolonged latency
Central disorders
Slow latency
Inaccuracy
Inability to generate
Convergence
Patient is asked to fixate at an object in front of him the object is
slowly brought to the tip of his nose. Abnormality indicative of a
central pathology.
CEREBELLAR TESTS
Past-pointing
zz The patient is asked to touch the examiner’s finger with his
index finger at different positions.
zz Intention tremor and past-pointing are indicative of a
cerebellar lesion on the affected side.
Rapid Alternating Movement

zz Pat the palm of one hand with the palm and dorsum of the
other hand alternately.
zz There will be slowness of the limb on the affected side to
perform the movement (Dysdiadochokinesia).
TESTS FOR UTRICULAR/OTOLITHIC DYSFUNCTION

Eye Cover Test (For Skew Deviation)
zz With the patient gazing forward one eye is covered followed
by the other.
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zz Vertical deviation of the uncovered eye with the other eye

covered usually indicates a central pathology.
Ocular Tilt Reaction

zz The ocular tilt reaction consists of a triad of skew deviation,
ocular torsion and head tilt.
zz The causes are Ménière’s disease, vestibular neuritis, acoustic
neuromas and strokes.
zz In one side labyrinthine hypofunction, it consists of head tilt
towards the lesioned labyrinth, skew deviation with the lower
eye on the side of the lesion and ocular counter roll (torsional
deviation of the superior poles of the eyes toward the side of
the lesion).
zz In normal patients, ocular torsion of the upper poles of the
eyes rotates toward the higher ear.
Subjective Visual Vertical

zz Injury to the otoliths or to the nerve that transmits impulses
from the otoliths and other parts of the ear to the brain,
judgment of vertical may be altered.
zz Patients with peripheral vestibular and brainstem lesions,
there is deviation of the subjective vertical.
zz However, in cerebellar lesions, there is good accuracy of the
subjective vertical.
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CHAPTER 6
Investigations for Vertigo
• ECG
HEMATOLOGICAL TESTS
zz Full blood count.
zz A raised erythrocyte sedimentation rate (ESR) may raise the
suspicion of an infecting or autoimmune pathology.
zz Fasting blood sugar.
zz Lipid profile.
zz Blood urea and serum electrolytes.
zz Cardiac enzymes.
zz Thyroid function test.
zz Fluorescent treponemal antibody-absorption (FTA-ABS) or
venereal disease research laboratory (VDRL) should be done
for detecting a syphilitic infection.
zz Test for rheumatoid factor, urine analysis, antinuclear antibody
checks for a possible autoimmune pathology.
AUDIOLOGICAL TEST
Pure tone audiometry (PTA).
RADIOLOGICAL TESTS
zz CT scan.
zz MRI.
zz Functional MRI (f-MRI).
zz Positron emission tomography (PET).
zz Single photon emission computerized tomography (SPECT).
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High Resolution CT Scan and MRI Scan Help to

Rule Out Retrocochlear Pathology
zz A unilateral or asymmetrical sensorineural hearing loss is an
indication for imaging to exclude a tumor of the VII cranial
nerve. Gadolinium MRI is the imaging of choice.
zz Consider MRI for suspecting cerebrovascular disease.
zz MRI or conventional angiography of the posterior fossa
vasculature may be useful in diagnosing vasculature causes

of vertigo such as vertebrobasilar insufficiency, thrombosis of
the labyrinthine artery, anterior or posterior inferior cerebellar
artery insufficiency and subclavial steal syndrome.
zz CT scans can be used, if MRI is contraindicated or in suspected
cases of cholesteatoma.
The structural imaging like CT scans or MRIs show abnormalities,
only when there is any structural defect of any of constituents of
the balance system, viz any tumor or bleeding/infarction of the
tissues, etc. But the balance problems are rarely caused by such
structural changes, they are usually a result of subtle functional
disorders, and hence it is functional imaging such as f-MRI, PET and
SPECT that are more relevant and more informative in disorders
of the balance system. A normal CT scan/MRI does not rule out a
balance disorder.
GLYCEROL TEST
zz It is an useful test for Ménière’s disease.
zz Glycerol is a dehydrating agent. When it is given orally,
it reduces endolymphatic pressure and thus causes an
improvement of hearing.
zz Glycerol (1. 5 mL/kg) is given to patient with an equal amount
of water and a little flavoring agent or lemon juice.
zz Audiogram and speech discrimination scores are recorded
before and 1–2 hours after ingestion of glycerol.
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Investigations for Vertigo 57
zz An improvement of 10 decibel in two or more adjacent

octaves or gain of 10% in discrimination score makes the test
positive. There is also improvement in tinnitus and in the sense
of fullness in the ear.
zz This test has a diagnostic and prognostic value. Presently, this
test is combined with electrocochleography.
SPECIAL VESTIBULAR INVESTIGATIONS

Assessment of Vestibulo-ocular Reflex
zz Electronystagmography (ENG).
zz Videonystagmography (VNG).
Assessment of Vestibulospinal Reflex

zz Craniocorpography (CCG).
zz Computerized dynamic posturography (CDP).
Electronystagmography (ENG)
zz It is the most popular vestibular function test.
zz It is a test for assessing the integrity of the vestibule-ocular
and allied reflex systems like the smooth pursuit system, the
optokinetic system and saccadic systems.
zz ENG is expressed in butterfly chart (Fig. 6.1).
Normal = 0, Hypoactivity = 1 and Hyperactivity = 2.
Videonystagmography (VNG)
zz It is a computerized process of the electronically scanning
the eye movements through small high resolution charged
coupled device (CCD) sensor cameras and then processing
the video images digitally to record and document the eye
movement and compute them for analyzing the different
parameters like speed of slow phase, culmination frequency,
etc.
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Fig. 6.1 Claussen butterfly chart
zz One of the major advantages of VNG over ENG is that VNG can
record rotatory eye movement (in BPPV) that is not possible
by ENG.
Craniocorpography
zz It tests the vestibule-spinal system.
zz It consists of photographically recording the patient’s head
and body movements as he or she performs the Unterburger’s
stepping test and the Romberg’s test.
Computerized Dynamic Posturography (CDP)

zz It is a series of vestibule-spinal tests for quantitatively
assessing balance function in different set-ups which simulate
conditions encountered in our day-to-day life.
zz The tests of CDP help us in identifying the system at fault and in
analyzing the integrity of the CNS for the proper maintenance
of balance.
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Vestibular Evoked Myogenic Potentials (VEMP)

zz Saccule is the source of VEMP.
zz If saccule is damaged, then VEMP is absent.
zz This investigation evaluates the inferior vestibular nerve which
innervates the saccule and posterior semicircular canal.
zz The saccule is sensitive to sound stimulation results in a reflex
mechanism which relaxes the sternocleidomastoid muscle.
zz In this test, clicks or tonal stimuli (sound) is introduced into one
ear and sternocleidomastoid electromyography is recorded
with electrodes.
zz It is useful in the diagnosis of superior semicircular canal
dehiscence, vestibular neuritis (when there is inferior vestibular
nerve involvement), bilateral vestibular loss and monitoring
intratympanic gentamycin therapy for Ménière’s disease.
Caloric Test
If water at 30°C and 44°C (i.e. 7°C below and above normal body
temperature) is run into the ear canal (Fig. 6.2), nystagmus is
produced in the normal persons with a healthy labyrinth. The
nystagmus lasts for about 2 minutes from beginning of stimulation.
If the time of nystagmus lasts for less than average, it is called as
canal paresis. Directional preponderance of nystagmus either to
right or to left is also a finding. Both canal paresis and directional
preponderance may occur either singly or in combination. Canal
paresis will be present in majority of patients with Ménière’s
disease, vestibular neuronitis and acoustic neuroma. In the lesion
of posterior part of the temporal lobe, directional preponderance
will be seen towards the side of the lesion.
Optokinetic Test
Patient is asked to follow a series of vertical stripes on a drum
moving first from right to left and then from left to right.
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Fig. 6.2 Caloric test
Normally, it produces nystagmus with slow component in the

direction of moving stripes and fast component in the opposite
direction. Optokinetic abnormalities are seen in brainstem and
cerebellar hemisphere lesions. Thus, this test is useful to diagnose
a central lesion.
Electrocochleography
zz Electrocochleography (ECochG) is a variant of brainstem audio-
evoked response (ABR) where sound stimulation is provided
but the recording electrode is placed as close to the cochlea,
near the tympanic membrane or transtympanic.
zz Action potential (AP) is the compound action potential of the
auditory nerve.
zz Summating potential (SP) is the response of the cochlea to
sound stimulation.
zz It is used for diagnosis of Ménière’s disease where SP/AP ratio
is more than 0.5.
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Rotatory Chair
zz This assesses both horizontal semicircular canals bilaterally
and it is considered the gold standard for bilateral peripheral
vestibular loss.
zz It is somewhat similar to the caloric test which assesses the
function of the horizontal semicircular canal.
zz The rotational chair testing has a sensitivity of 71% for
diagnosis peripheral vestibulopathies, as opposed to only 31%
sensitivity for caloric testing/ENG.
zz Used for the diagnosis of peripheral vestibular disorders,
bilateral vestibular loss, monitoring patients undergoing
pharmacologic vestibular ablation for Ménière’s disease/
syndrome and for medicolegal purposes.
CONDITIONS REQUIRING URGENT

NEUROIMAGING (CT/MRI)
zz Sudden onset of vertigo (seconds) that persists and not
provoked by position.
zz Association with deafness but no typical Ménière’s history.
zz Association with new onset (occipital) headache.
zz Acute vertigo with normal head impulse test.
zz Associated with central neurological signs such as severe gait
and truncal ataxia.
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CHAPTER 7
Treatment of Vertigo
OBJECTIVE OF TREATMENT
zz Correct the cause (Not merely suppress the symptom).
zz Promote vestibular compensation.
zz Drugs that depress the CNS jeopardize the central compen
satory mechanism and inhibit vestibular compensation.
zz Peripheral vestibular disorders are usually self-limiting.
zz Vertigo/imbalance and psychogenic disorders are
comorbid conditions; the psychogenic part needs effective
management.
zz Cognitive disorders are very common in balance disorder
patients; correction of the concomitant cognitive deficit yields
better treatment outcomes.
zz Neurotropic agents/antioxidants/cognition-enhancing drugs
have a positive role in the management of balance disorders.
PRINCIPLES OF MANAGEMENT OF VERTIGO

zz Treat the cause.
zz Suppress the vestibular system.
zz Suppress the emotional reaction.
zz Encourage the compensation.
zz Surgery.
zz Accept the problem.
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Treatment of Vertigo 63
Treat the Cause

zz Perform Epley maneuver in case of benign paroxysmal
positional vertigo (BPPV).
zz Some give steroids in acute vertigo.
zz In Ménière’s disease, treat the cause. But the sad thing is that
the cause of Ménière’s disease is not known.
Suppress the Vestibular System

This is done by giving vestibular sedatives.
Suppress the Emotional Reaction

zz Many patients feel miserable.
zz Many patients feel it is the end of the world.
zz Even some think there may be the brain tumor.
zz Some think there may occur stroke.
zz So we should reassure these patients that they are not having
a stroke, that it will settle down, that it is not going to go on
forever and that they are not going to die.
Encourage Compensation
zz We need to encourage compensation.
zz If we do nothing in a young person following a destructive
lesion, they will get better.
zz If patient is older, they need active support and instruction in
vestibular rehabilitation.
Three Simple Exercises for Compensation

1. The first, move the head from side-to-side and up-and-down.
We should explain the patient that initially these exercises will
make them feel worse for few days.
2. The second exercise is to get the patient to put his arms out in
front, to fix his eyes on his thumb nails and just move the head
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from side to side, keeping the eyes fixed on to his thumb nails.
And then do the same, up and down.
3. The third exercise is rather similar. With outstretched arms,
look at the thumb nails and just swing around from side to
side.
Generally, we advise these exercises for just 5 minutes, 4 times
a day. Initially, this makes them dizzy, but if they keep doing them,
the exercises stop making them feeling dizzy. And when that has
happened, the central compensation has occurred.
The Cowthorne-Cooksey exercises are also excellent.
Surgery
This is indicated very rarely in vertigo.
Disturbances in Labyrinth
Stimulation:
zz Benign positional vertigo rarely requires surgery.
zz Labyrinthine fistula, usually due to cholesteatoma requires
surgery.
zz Dehiscent superior semicircular canal, most of these patients
once they have this situation explained to them, feel much

better about it and usually do not require surgery.
Incomplete Destruction
Causes
zz Trauma.
zz Inflammatory diseases.
zz Vascular diseases.
Since, we have got a better understanding of vestibular

rehabilitation, surgery is almost never required in incomplete
destruction of labyrinth.
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Irritation of labyrinth
Causes
zz Chronic suppurative otitis media (CSOM).
zz Perilymph fistula.
Intermittent Failure of Labyrinth

Causes
zz Delayed hydrops.
Surgery is only very rarely indicated in intermittent failure of

the labyrinth in delayed hydrops and Ménière’s disease.
Accepting the Problem

The 6th principle of management is accepting the problem. For
example, if we got somebody particularly an elderly person with
vestibular inadequacy, there is no point in keeping on doing
investigations and keeping on trying other drugs. Sometimes,
drugs will make them worse. Here, we should reassure them that
there is no serious underlying problem, give them advice on living
with their problem, with their unsteadiness, encourage them to
use a walking stick and discharge them. Do not keep bringing
them back.
About 90% of the vertigo patients will get good result by
above six principles.
We will discuss treatment of different causes of vertigo step
by step.
We already classified the vertigo
zz Sensation of rotation
1. Episodic (seconds/hours).
2. Prolonged (weeks).
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zz Sensation of unsteadiness
1. Episodic (seconds/hours to days).
2. Prolonged (weeks to months/forever).
ROTATORY VERTIGO
Short-lived Spinning
zz The underlying pathology for the episodic spinning dizziness,
which lasts for seconds is largely labyrinthine stimulation.
zz Occasionally, it is depression but usually stimulation.
Causes of Short-lived Spinning/Episodic

Rotatory Vertigo (seconds)
zz Benign positional vertigo.
zz Labyrinthine fistula.
zz Caloric effect.
zz Alternobaric vertigo.
zz Dehiscent superior semicircular canal.
Benign positional vertigo:
zz Most common example of short-lived spinning.
zz Treatment is the Epley maneuver.
zz Drugs have no part to play in benign positional vertigo.
zz Explain to them that every time they experience dizziness they
are one step nearer to the end of dizziness.

Labyrinthine fistula:
zz If we exert the pressure in the external auditory canal or middle
ear, this conveys pressure through the vestibular system and

this moves to the ampullary cupula. Patient experiences short-
lived but very severe spinning dizziness.
zz The most common cause is the cholesteatoma.
zz The treatment is surgery.
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Caloric effect:
zz Caloric stimulation gives short-lived spinning dizziness.
zz The dizziness wears off once the caloric effect is worn-off.
Alternobaric vertigo:
zz It is a rare condition.
zz It occurs in the jet fighter pilot or in the diver.
zz There is sudden pressure change within the middle ear, which
will be transmitted into the inner ear and cause sudden short-
spinning dizziness which lasts only seconds.
Vertebrobasilar insufficiency:
zz Do not diagnose vertebrobasilar insufficiency on the evidence
of vertigo alone.
zz You need some other symptoms for diagnosis such as double
vision, blurring of vision, dysarthria and numbness.

Dehiscent superior semicircular canal:
zz Tullio phenomenon is present.
zz There is siphoning-off of the sound energy which should be
going into the cochlea.

zz Very rarely does this require surgery but sometimes it does.
EPISODIC FOR HOURS

Ménière’s Disease
zz The most common example is Ménière’s disease. The hearing
loss and tinnitus should be fluctuating in association with
the vertigo which should be rotatory, episodic, usually
incapacitating. It is usually associated with nausea and
sometimes vomiting, of sudden onset and relatively sudden
cessation with, at least in the early stages, the patient perfectly
well between attacks.
zz If there is no hearing loss, tinnitus and nausea or vomiting, only
dizziness for more than 24 hours, do not diagnose Ménière’s
disease.
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zz We cannot influence the course of Ménière’s disease. We can

treat the acute attack by labyrinthine sedatives. We cannot
influence the next attack though we can reassure the patient
that it is nothing serious.
zz Surgery for Ménière’s disease is very rarely indicated.
zz Endolymphatic sac surgery has not much helpful in disease
process.
zz Gentamycin injection is a treatment.
zz Labyrinthectomy can be done, but it destroys all the inner ear.
zz Vestibular nerve section is an useful procedure.
Syphilitic Labyrinthitis
zz Routine test is fluorescent treponemal antibody (FTA).
zz The big difference between syphilitic labyrinthitis and
Ménière’s disease is that the disease course tends to be more
rapidly progressive, and secondly that the other ear tends to
be involved much earlier than one would expect in Ménière’s
disease.
PROLONGED ROTATORY
zz The dizziness lasts for weeks and rotatory vertigo never lasts
for longer than three weeks.
zz This is due to some destruction of the labyrinth or the
vestibular nerve.
zz They have incapacitating vertigo with vomiting.
zz Spinning dizziness gradually improves but is followed by
unsteadiness which will improve.
zz The best way to make them normal is rehabilitation exercises.
zz Vestibular neuronitis is the most obvious and most common
example.
zz Trauma during ear surgery or labyrinthectomy or vestibular
nerve section can also produce prolonged rotatory vertigo.
zz Vascular lesions will also cause prolonged rotatory vertigo.
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zz Metastatic deposits in the cerebellum pontine angle can also

cause for prolonged vertigo. This is secondary from a breast
cancer. These type patients are terminally ill and very often die
undiagnosed.
UNSTEADINESS
Short-lived
zz The unsteadiness is usually a problem somewhere within the
system and so exclusively in the ear.
zz This is due to a physiological overload of the central processing.
zz It can occur when there is abnormal input which may be visual
and this includes looking down from a height where the input
is abnormal and the central processor has difficulty dealing
with it, causing a feeling of unsteadiness. Abnormal inputs can
also from the cervical spine doing the same thing.
Unsteadiness for Hours

zz The most common cause is the self-inflicted drug alcohol. But
it can also occur from other drugs.
zz Motion sickness is an another cause.
zz Perilymph fistula is also a cause.
zz Active chronic otitis media is also a cause unsteadiness which
will settle down, if we treat the otitis media.
zz Hyperventilation is another cause of this unsteadiness which
lasts for a variable period of time.
zz Psychogenic cause may be due to nervous tension or may be
due to malingering.
Prolonged Unsteadiness
zz Unsteadiness lasts for weeks to months.
zz This is due to vestibular inadequacy.
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zz The most common cause is aging.

zz The prolonged unsteadiness can again occur from drugs, the
metabolic effect for example of anticonvulsants and when we
stop the drug they get back to normal.
zz The ototoxic drug is also a cause where the damage is
permanent. They have lost their vestibular function and
patient will improve by labyrinthine exercises. Labyrinthine
sedative drugs will often make them worse. Labyrinthine
exercises will help them but remain always with a certain
degree of unsteadiness.
zz Central nervous system lesions can also cause unsteadiness.
zz Floating patients: These are patients who frequently describe
the floating sensation and they can go on for years. They never
have to cancel any social event, they can always do what they
plan to do but they just feel that they are floating. All tests are
normal. The treatment is to reassure them and there are many
instances when they will eventually settle down.
zz In case of infected mastoid cavity, patient go on for a long
period of time feeling unsteady. They settle down with the
cavity infection and then feel better.
Treatment of Peripheral Vertigo

zz Pharmacotherapy.
zz Adoptive exercise.
zz Surgery.
Pharmacotherapy
Drug therapy for vertigo is used for symptomatic treatment and to
treat the underlying disorder.
The common specific peripheral vestibular disorders amenable
to pharmacotherapy are:
zz Vestibular neuritis.
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zz Autoimmune inner disorder.

zz Infective labyrinthitis.
The common specific central vestibular disorders amenable to
pharmacotherapy are:
zz Migraine-related vertigo.
zz Epileptic vertigo.
zz Multiple sclerosis.
The causative factors for the balance disorder in the non-

specific central/peripheral vestibular disorder patients are usually
one or more of the followings:
zz Hypoxia in the brain and/or inner ear.
zz Metaboilc disorders.
zz Degenerative changes in the sensory epithelium of the inner
ear and in the neuronal tissues of the brain.

zz Neurotransmitter dysfunction (hyperactivity/hypoactivity of
neurotransmitter).
zz Psychophysiologic disorders.
CLINICAL TIPS
The aim of drug therapy in nonspecific balance disorders should be directed
to correct the possible etiologies and care being taken to ensure that the
patient gets symptomatic relief from the vertigo/vomiting and lastly the
vestibular compensatory mechanism is not inhibited in any way.
An ideal anti-vertigo drug should

zz Control vertigo/instability and nausea/vomiting.
zz Enhance cerebral and inner-ear blood flow.
zz Free from side effects such as drowsiness, central nervous
system (CNS) depression, extrapyramidal symptoms.

zz Not depress vestibular compensatory mechanism.
Treatment of Acute Vertigo Attack (Table 7.1)

zz Patients with acute severe vertigo appear ill due to the vertigo
and accompanying nausea and vomiting. It is considered as an
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Table 7.1 Drugs for acute attack/symptomatic treatment

Vestibular sedatives Benzodiazepines Diazepam, Lorazepam
Antihistamines, Meclizine, dimenhydrinate,
anticholinergics scopalamine
Antiemetics Metoclopramide, Prochlorperazine (stemetil)
phenothiazines
emergency and medical care is urgently required. If the vertigo

does not subside rapidly, it may results in hospitalization of the
patient.
zz An acute and severe episode of vertigo, regardless of the
underlying cause, will usually settle by itself within 24–48
hours due to the effect of brainstem compensation.
zz During the acute phase, supportive measures, bed rest,
vestibular suppressants (Box 7.1) and antiemetics (Box 7.2)
should be used to provide symptomatic relief.
zz Genenrally, a combination of vestibular suppressants and an
antiemetic is used. The major classes of vestibular suppressants
include antihistamines, benzodiazepines and anticholinergics.
zz There is evidence to show that use of vestibular suppressants
can delay the compensatory mechanism of brainstem
and prolong the symptoms of vertigo. In addition, these
medications carry risks of side effects. Therefore, prolonged
use of symptomatic medications for acute vertigo is best
avoided, especially if a specific treatable cause is identified.
zz When acute attack subsided, then specific treatment is done
for specific diagnosis (Table 7.2).
zz Adjunctive treatment are also useful for controlling associated
symptoms (Table 7.3).
Commonly used drugs in vertigo
zz Cinnarizine (Calcium-channel blocker).
zz Beta-histine (Vasodilator).
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Box 7.1 Drugs for controlling vertigo

• Prochlorperazine
• Dimenhydrinate
• Meclizine
• Cinnarizine
• Beta-histine
Box 7.2 Drugs for controlling nausea/vomiting

• Domperidone
• Trifluopromazine
• Metoclopramide
• Promethazine
• Ondansetron
Table 7.2 Disease specific drugs

Vestibular neuritis Steroids Prednisolone
Ménière’s disease Diuretics, beta-histine, Hydrochlorothiazide
calcium channel blocker Flunarizine, cinnarezine
Chronic vestibulopathy Piracetam
in elderly
Table 7.3 Adjunctive treatment

Psychiatric SSRI (Selective serotonin Fluoxetine
reuptake inhibitor) Amitryptilline
Tricyclic antidepressants
Complementary Ginkobiloba
zz Prochlorperazine for acute vertigo (It might precipitate

extrapyramidal symptoms).
Most of the vertigo patients always remain tense and anxious.
Hence, drugs like diazepam or alprazolam are preferred as adjuvant
therapy.
When diagnosis is viral or bacterial labyrinthitis antiviral and
broad-spectrum antibiotics must be administered.
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Anticoagulants are given when it is suspected to be of

thrombotic nature.
Intratympanic injection of gentamycin is preferred for advance
Ménière’s disease when hearing is lost but vertigo persisting.
Circulatory Mechanism of Vertigo

Increased circulatory resistance and increased blood viscosity leads
to reduced microcirculation and reduced blood supply of brain
and labyrinth leading to vestibular function and vertigo. Increased
circulatory resistance takes place as red blood cells (RBCs) loss
their flexibility due to entry of calcium ion into them. Dimension
of blood vessels through which RBCs run is 3 micron while the
size of RBC is 8 micron. Bigger size RBCs can run freely through
small size blood vessels because they are highly flexible. If calcium
ion entry into RBC, it makes them rigid. Drugs like cinnarizine
(calcium-channel blocker) and beta-histine (vasodilator) are
mostly useful for peripheral vertigo control as they both increase
the labyrinthine circulation effectively.
Another possible cause of peripheral vertigo is abnormal firing
of vestibular nuclei. Beta-histine regulates this firing activity by
blocking the H3 receptors.
Contraindications of Beta-histine
zz Bronchial asthma.
zz Peptic ulcer.
zz Pheochromocytoma.
zz Concurrent use of antihistamines.
Side effect: Cinnarizine is mildly sedating drug and not liked by

many ambulatory patients.
Dosage:
zz Cinnarizine—25 mg tid or 75 mg OD.
zz Beta-histine—8 mg tid for mild vertigo. 16 mg tid or 24 mg BD
for moderate-to-severe vertigo.
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MEDICATIONS IN CENTRAL VERTIGO

zz Migraine-related vertigo/migraine associated vertigo
—— Migraine associated vertigo is the second most common
cause of vertigo and affects almost 1% of the entire

population.
—— Along with vertigo, patient presents with episodic
throbbing headaches, usually unilateral accompanied

by other symptoms (nausea, vomiting, photophobia or
phonophobia and may be preceded by aura).
—— The duration of vertigo is usually minutes to hours, and
vertigo often occurs independently of headaches.

Treatment
—— Migraine prophylaxis, migraine-abortive medications and
vestibular exercises for vertiginous migraines.

—— Prophylaxis for migraine mainly include beta-
blockers, calcium channel-blockers (CCB) and tricyclic
antidepressants (TCA).
—— Beta-blockers act as first line therapy in the management
of migraine. They might act by decreasing prostaglandin

production.
—— CCBs such as flunarizine may reduce migraine prodromes,
the frequency of migraine attacks and also decrease the

severity and possibility the duration of these attacks.
—— TCAs such as nortriptyline prevent migraine headaches
by altering the neurotransmitters, norepinephrine and

serotonin that the nerves of the brain use to communicate
with one another.
—— Migraine diet: Avoid excessive caffeine (>2 cups of coffee/
day), monosodium glutamate, chocolate, red wine and

aged cheese.
zz Acute vertigo caused by a cerebellar or brainstem stroke is
treated with vestibular suppressants medication and minimal
head movement for first few days. As soon as tolerated,
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medication should be tapered and vestibular rehabilitation

exercises should be initiated.
zz Consider thrombolytic therapy for acute ischemic stroke only
after thorough evaluation and consultation with neurologists.
zz Lethargic patients or those with altered level of consciousness
require vigilance and close supervision, including direct visual,
ECG and pulse oximetry monitoring.
zz Consider emergent interventions to minimize edema and
brainstem compression in patients with altered consciousness
and a deteriorating course in the emergency department.
Hemorrhage or edema of posterior fossa can lead to rapid
compression and compromise of vital medullary functions,
obstructive hydrocephalus or herniations of the medullary
tonsils.
zz Do not administer anticoagulant medicine including aspirin
until intracranial hemorrhage has been ruled out by imaging.
zz Invasive actions may include endotracheal intubation to
protect the airway, control breathing and allow therapeutic
hyperventilation.
zz Consider elevating the head of the bed, performing
diuresis with mannitol or furosemide and administering
dexamethasone.
PARTICLE REPOSITIONING AND EXERCISES FOR BPPV

Epley Maneuver (Fig. 7.1)
Patient with right posterior canal BPPV.
Step 1: Make the patient sit on the examination table with eyes
open and head turned 45° to the right. Support the patient’s head
as the patient lies back quickly from a sitting to supine position,
ending with the head hanging 20° off the end of the examination
table.
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Fig. 7.1 Steps in Epley maneuver
Step 2: Turn the patient’s head 90° to the left side and let the
patient remains in this position for 30 sec. Turn the patient’s head
an additional 90° to the left while the patient rotates his or her
body 90° in the same direction. Let the patient remains in this
position for 30 sec.
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Step 3: The patient is then made to sit up slowly with the neck
flexed.
The procedure may be repeated on either side until the patient
experiences relief of symptoms.
Brandt-Daroff Exercise (Fig. 7.2)

Patient with right posterior canal BPPV
Step 1: Sit upright on the side of the bed and turns the head 45°
towards the healthy side.
Step 2: Patient tilts the body on the side of the affected side (right),
so that the head touches the bed but the nose is pointed 45°
towards the roof. Patient stays in this position for 30 sec.
Step 3: Patient sits up head straight and maintains that position
for 30 sec.
Fig. 7.2 Brandt-Daroff exercise
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Step 4: The patient then lies down on the other side with the head
touching the bed and nose turned 45° towards the roof.
Semont (Liberatory) Maneuver

Patient with left posterior canal BPPV.
Step 1: Patient sits at the side of the examination table and the
head is turned 45° towards the healthy side (right side).
Step 2: The patient is then made to lie down very rapidly towards
the side of the diseased ear such that the head hangs about 15°
below the horizontal, i.e. the head is moved by 105° from the sitting
position. The patient’s head is kept in this position for 30 sec.
Step 3: The patient is swung by 195° to the other side, i.e. towards
the side of unaffected ear and placed in such a way that the nose
points downwards. The head is maintained in this position for
30 sec.
Vestibular Rehabilitation Therapy (VRT)

The head/body/eye movement exercises induce compensation
by 3 mechanism, viz. adaptation, habituation and compensation.
So, the exercises can be broadly divided into three groups viz.
The Adaptation exercises, the Habituation exercises and the
Compensation exercises according to their mechanism of action.
1. Adaptation is achieved by some exercises in the schedule of the
Cawthrone-Cooksey exercises, e.g. gaze stabilization exercise.
It helps the patient with peripheral vestibular disorder to adapt
to the changed vestibular scenario by retaining the vestibulo-
ocular reflex to stabilize images of moving objects in the fovea.
In the gaze stabilization exercise, the patient is asked to follow
with the eyes (without moving the head), the movement of a
small rubber ball that the patient throws from one hand to the
other repeatedly over the head.
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Other gaze stabilization exercises are for example throwing

a ball to the wall repeatedly and catching it and at the same
time, following the movement of the ball with the eyes. The
gaze stabilization exercises retain the extraocular muscles and
re-caliberates the vestibulo-ocular reflex such that in spite of a
vestibular malfunction, images of moving objects can be kept
fixed in the fovea by an accurate and coordinated movement
of the eyes.
2. Habituation exercises help patients of peripheral vestibular
disorder by conditioning the brain through repeatedly
exposure of the balance system to erroneous or mismatched
sensory input. These mismatched sensory inputs induce small
tolerable spells of vertigo to which the brain gets used to, so
that minor vertiginous sensations are not bothersome to the
patient.
Repeatedly moving the head in the Y-axis, i.e. in the
pitch plane or in the X-axis, i.e. the yaw plane stimulates the
semicircular canals which inform the CNS that the subject
is moving. The patient does this exercise sitting securely on
the stool. So the proprioceptors inform the brain that there is
no movement. When these conflicting informations (sensory
mismatch/conflict) reach the CNS, the CNS is confused and it
cannot reflexly generate the requisite motor output resulting
in vertigo. These minor spells of vertigo, induced by erroneous
or mismatched sensory input, help in habituating the balance
disorder patient by conditioning the brain.
3. The compensation or substitution exercises help the patient
to enhance the visual and proprioceptive inputs so that the
deficit of vestibular input is counter-balanced. If one of the
input systems is deficient or abnormal, the balance system
can be trained to rely more on the other input system, e.g. the
visual and proprioceptive systems to maintain balance. The
visual and proprioceptive systems substitute for the deficient
vestibular input.
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Walking up and down a flight of stairs and some of the eye

movement exercises are meant to sensitize the proprioceptive
and visual input systems and retain the balance system to
rely more on proprioceptive and visual inputs rather than on
the defective vestibular input. The back movement and neck
movement exercises are believed to increase spinal input to
the balance system. The spinal afferent input to the vestibular
nucleus is believed to increase after a peripheral vestibular
damage.
Exercises in Bed
Eye movements:
zz Looking up and then down.
zz Looking alternatively left and right.
zz Convergence exercises.
Head movements:
zz Bending alternatively forward and backward.
zz Turning alternatively to left and then right.
Exercises in Sitting Position

zz Shrugging and rotating shoulders.
zz Bending forward and picking up objects.
zz Turning head and trunk alternately to the left and right.
Exercises in Standing Position

zz Changing from sitting to standing, initially with eyes open and
then with the eyes shut.
zz Throwing a small ping-pong ball in an arc from hand to hand
and following it with the eyes.
zz Throwing a small ball from hand to hand under the knee.
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Exercises while Walking

zz Throwing and catching the ball while walking.
zz Walking up and down a flight of stairs.
zz Walking around in the room with eyes open and closed.
zz Playing any game involving bending, stretching and aiming
with the ball.
Surgical Treatment
There are specific conditions where surgical intervention may be
needed such as a perilymph fistula or a superior semicircular canal
dehiscence. Surgery can be considered for Ménière’s disease and
BPPV if medical or conventional management fails.
Surgical Options in Ménière’s Disease

zz Endolymphatic sac surgery: It has a 70–90% success rate and
preserves hearing. It is reserved for patients who fail medical
and aminoglycoside therapy.
zz Vestibular nerve section: It has about 90% success rate. The
vestibular nerve can be approached via the retrosigmoid or
middle fossa route. It has risk of cerebrospinal fluid leak, facial
palsy and hearing loss.
zz Labyrinthectomy: It has a success rate around 95%. It can be
done via a transcanal or transmastoid route. The aim of this
procedure is to remove the membranous neuroepithelium
from the vestibule and semicircular canals.
zz Intratympanic gentamycin: It is a favored treatment in medically
refractory patients. Success rate is around 90%. There is risk of
hearing loss.
zz Intratympanic steroids: Success rate is 50%. Intratympanic
dexamethasone avoids the systemic complications of steroids.
It may be considered for those with severe Ménière’s disease
in pregnancy.
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Surgical Options in BPPV

Surgery for BPPV is done for intractable cases not responding to
particle repositioning procedures or vestibular rehabilitation.
zz Singular neurectomy (Posterior ampullary nerve section): Success
rate is about 97%. There is risk of hearing loss.

zz Posterior semicircular canal occlusion: Complete resolutions of
symptoms in all patients have been reported. There is a risk of

transient mild hearing loss.
SUMMARY
zz The treatment of balance disorders must be definite and
oriented to the etiology and pathogenesis of the condition.
zz Pharmacotherapy, physiotherapy, psychotherapy or rarely
surgery can be used for the management of balance disorders.
zz The important medications useful in the treatment of
balance disorders include anticholinergics, antihistamines,
benzodiazepines, calcium-channel antagonists and dopamine-
receptor antagonists.
zz Symptomatic therapy must be reserved for acute episodes.
zz In both Ménière’s disease and vestibular neuronitis, vestibular
suppressants such as anticholinergics and benzodiazepines
are useful.
zz In Ménière’s disease, salt restriction and diuretics are used as a
prophylaxis for flare-ups.
zz Drug treatments are not recommended for benign paroxysmal
positional vertigo and bilateral vestibular paresis, but physical
therapy can be very useful in both.
zz Prophylactic agents such as calcium-channel antagonists,
tricyclic antidepressants and b-blockers are the mainstay of
treatment for migraine-associated vertigo.
zz Benzodiazepines are the most useful agents when psychogenic
vertigo occurs in association with anxiety or agoraphobia.
zz Vestibular rehabilitation therapy is generally recommended to
improve quality of life.
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Tips to Prevents Fall of Vertigo Patients in Old Age

zz Always grab on to the hand-railing while climbing staircase.
zz Install grab bar in bathrooms.
zz Remember to mop-up wet and slippery areas.
zz Ensure light switch and water are in easy reach during night.
zz Preferable use of a three pronged walking stick for support.
zz Avoid clutter on the floor, remember to tuck the edge of the
carpet with a tape.
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CHAPTER 8
Vestibular
Rehabilitation Exercises
Vestibular compensation occurs naturally in most patients, but

not in all patients. In some patients, an incomplete compensation
occurs. Incomplete or total failure of vestibular compensation
is very distressing for the patient, since it leads to persistent
instability and severely incapacitates the patient. These patients
are very challenging. They can be rehabilitated properly.
Vestibular rehabilitation refers to a structured program
of treatment aimed at expediting and enhancing vestibular
compensation and rendering the dizzy patient asymptomatic. This
is usually helpful for chronic vestibular symptoms due to unilateral
labyrinthine pathology.
Usually, vestibular rehabilitation exercises are used for chronic
or uncompensated vestibular disorders. However, its early use
and benefit in managing acute peripheral vestibular disorders is
increasingly recognized.
MECHANISMS
zz Habituation/adaptive responses: It allow central nervous
system to adjust changes in labyrinthine signals, e.g. ballet
dancers and acrobats.
zz Sensory substitution: It rely more on visual or proprioceptive
input.
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CAWTHRONE-COOKSEY EXERCISES
These exercises are a set of head, body and eye movement
exercises for enhancing vestibular compensation in a patient
of peripheral vestibular lesion. Patients recovered more rapidly
using these techniques. These exercises can be broadly divided
into three groups: Adaptation exercises, habituation exercises and
compensation exercises.
zz Adaptation exercises: Gaze stabilization exercises. It helps
the patient with peripheral vestibular disorder to adopt the

changed vestibular scenario by retraining the vestibulo-ocular
reflex to stabilize images of moving objects in the fovea.
zz Habituation exercises: It helps patients of peripheral vestibular
disorder by conditioning the brain through repeated exposure

of the balance system to erroneous or mismatched sensory
input. For example, head (up and down), head (side to side),
etc.
zz Compensation exercises: The compensation or substitution
exercises help the patient to enhance the visual and

proprioceptive inputs so that the deficit of vestibular input is
counterbalanced.
EYE EXERCISES
The eye movements as seen below enhance the adaptation as
well as compensation. It helps the patient to enhance the visual
and proprioceptive inputs so that the deficit of vestibular input is
counterbalanced.
zz Looking up and down (Fig. 8.1).
zz Looking alternatively left and right (Fig. 8.2).
zz Convergence exercises (Fig. 8.3).
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Vestibular Rehabilitation Exercises 87
Fig. 8.1 Looking up and down
Fig. 8.2 Looking alternatively left and right
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Fig. 8.3 Convergence exercises
HEAD AND NECK EXERCISES

This is habituation exercises. It helps the patients of peripheral
vestibular disorder by conditioning the brain through repeated
exposure of the balance system to erroneous or mismatched
sensory inputs. These mismatched sensory inputs induce small
tolerable spells of vertigo to which brain gets used to, so that
minor vertiginous sensations are not bothersome to the patient.
The patient carries out these exercises sitting up on the bed, or if
one is stable enough, then sitting on a stool.
zz Bending alternatively forward and backward (Fig. 8.4).
zz Turning alternatively to left and then right (Fig. 8.5).
Exercises in Sitting Position

zz Shrugging and rotating shoulders (Fig. 8.6).
zz Bending forward and picking up objects from the floor
(Fig. 8.7).
zz Turning head and trunk alternatively to left and right (Fig. 8.8).
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Fig. 8.4 Bending head forward and backward
Fig. 8.5 Turning head to left and then right
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Fig. 8.6 Shrugging and rotating shoulders
Fig. 8.7 Bending forward and picking up objects from the floor
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Fig. 8.8 Turning the head alternatively to left and right
Exercises in Standing Position

zz Changing from sitting to standing, initially with eyes open and
then with eyes shut repeatedly for 15 minutes (Fig. 8.9).
zz Throwing a small ball is an arc from hand to hand and following
the moving ball with eyes (Fig. 8.10).
This is a gaze stabilization exercises which expedite adaptation.
It helps the patient with peripheral vestibular disorder to adapt
the changed vestibular scenario by retaining the vestibulo-
ocular reflex to stabilize images of moving objects in the fovea.
In this exercises, the movement of small rubber ball that the
patient throws from one hand to the other repeatedly over the
head. By this exercises, the extra-ocular muscles are retained
to move the eyes in such a fashion that the eyes remain
focused on the moving ball. In vestibular malfunction, images
of moving objects can be kept fixed in the fovea by accurate
and coordinated movements of the eyes.
zz Throwing a small ball from hand to hand under the knee
(Fig. 8.11).
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Fig. 8.9 Changing from sitting to standing position
Fig. 8.10 Throwing a ball in an arc from hand to hand
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Fig. 8.11 Throwing a ball under the knee
Fig. 8.12 Throwing and catching the ball
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Fig. 8.13 Walking over stairs
Fig. 8.14 Walking around inside the room with eye closed and open
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Fig. 8.15 Game for bending and stretching
Exercises while Walking

zz Throwing and catching the ball while walking (Fig. 8.12).
zz Walking up and down a flight of stairs (Fig. 8.13).
Walking up and down a flight of stairs sensitizes the
proprioceptive system and retains the balance system to rely
more on proprioceptive rather than defective vestibular input.
zz Walking around in the room with eyes closed and open
(Fig. 8.14).
zz Playing any game involving bending, stretching and aiming
with the ball (Fig. 8.15).
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CHAPTER 10
Approach to Vertigo by
General Practitioner
General practitioners (GP) are the first line physicians in the vertigo
management. Patients with giddiness or imbalance always seek
immediate medical help from his/her nearest doctor (GP). General
practitioner should have basic knowledge in the diagnosis and
management of vertigo so that patients will immediate relief. They
should also know which patients should be referred immediately
to the consultants.
Basic information regarding vertigo should be known to GP.
zz Episodic dizziness
—— Benign paroxysmal positional vertigo (BPPV): Manage at
Primary care by doing Epley’s maneuver. If fails—refer to

ENT specialist.
—— Postural hypotension or migraine—refer to physician.
—— Associated otologic symptoms/signs—ENT referral.
zz Acute dizziness
—— Suspected myocardial infarction/neurological findings/
Unsure—Refer to tertiary center.

—— Unstable patient or dehydrated patient—hospital
admission.
—— Stable patient or gastrointestinal infection—manage at
primary care.
zz Chronic/persistent dizziness
—— Drugs/anemia—manage at primary care.
—— Associated ear findings—refer to ENT.
—— Neurological findings/unsure—physician referral.
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Approach to Vertigo by General Practitioner 111
DIAGNOSIS OF OTOLOGIC VERTIGO

zz Vertigo (Minutes to hours)
—— Hearing loss, tinnitus, ear pressure, usually spontaneous,
horizontal nystagmus—Ménière’s disease.

zz Vertigo (Seconds)
—— No auditory symptoms, triggered by head position, crystals
in the posterior semicircular canal, rotatory nystagmus—

benign paroxysmal positional vertigo.
zz Vertigo (Days to weeks)
—— No auditory symptoms, commonly after upper respiratory
infection, viral infection of vestibular nerve, horizontal

nystagmus—vestibular neuronitis/viral labyrinthitis.
zz Vertigo (Minutes to hours)
—— No auditory symptoms, usually spontaneous, recurrent
deafferentation of vestibular nerve, horizontal nystagmus—

recurrent vestibulopathy.
CONDITIONS REQUIRING URGENT

REFERRAL TO BALANCE SPECIALIST
zz Presence of auditory symptoms (hearing loss, tinnitus, pressure
or aural fullness, particularly, if asymmetrical).
zz Nystagmus has central features.
zz Spontaneous and persists after 48 hours.
zz Signs of suppurative otitis media.
zz Auditory or vestibular symptoms are triggered by pressure
changes (barotraumas or Valsalva maneuver), suggestive of
perilymph fistula.
zz Progressive unsteadiness or falls.
zz Cardiovascular symptoms (chest pain, dyspnea, syncope, etc.).
SIMPLIFIED APPROACH TO GET A DIAGNOSIS

If patient complaints with vertigo or dizziness.
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True Vertigo (Hallucination of Rotation or

Imbalance Felt within the Head)
If there are features of true vertigo: Consider following:
zz Is there evidence of middle ear disease (discharge, perforation,
cholesteatoma, mastoiditis)?
—— Infection may spread to affect labyrinth. Requires full
otological assessment.
—— Refer to otologist.
zz Is patient receiving any vestibulotoxic drugs (amino
glycosides, anticonvulsants, furosemide, ethacrynic acid, anti-

inflammatories, salicylates, quinine)?
—— Damage may be transient (e.g. phenytoin) or permanent
(e.g. gentamicin).
—— Stop or reduce.
zz Are there any focal neurological signs?
—— Yes.
—— Cranial nerve palsies, cerebellar or long tract damage,
visual disturbance.
—— Consider: In young patients multiple sclerosis, migraine,
vasculitis; in older patients vertebrobasilar disease,

neoplasia.
—— Refer for neurological assessment.
zz Do patients have tinnitus or constitutional upset, e.g. nausea,
vomiting, sweating?
—— Yes.
—— Is hearing impaired.
Yes.
Sensorineural deafness.
—— Are symptoms recurrent?
—— Ménière’s disease.
—— Treatment: Bed rest and give drugs such as cinnarizine,
prochlorperazine and surgery for severe Ménière’s disease.
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zz Are there focal neurological signs? With tinnitus and unilateral

sensorineural hearing loss
—— Yes.
—— Progressive.
—— Yes.
—— Consider cerebellopontine angle tumor, especially acoustic
neuroma.
—— Refer to neurosurgeon for further management.
zz Is vertigo associated with a particular head position?

—— Yes.
—— Benign positional vertigo confirmed by positional test.
—— Reassure of benign nature and limited duration. Avoidance
or provocative positions and do Epley maneuver.

zz Is there a history of head injury?
—— Yes.
—— Vertigo may be associated with closed injury, with or
without skull fracture, and out of proportion with severity

of trauma.
—— Prognosis good but recovery may be protracted.
—— Supportive treatment.
zz Is vertigo associated with motion, e.g. driving, sea travel?

—— Yes.
—— Motion sickness.
—— Treatment: Avoidance of motion, antihistamines.
Dizziness (Not True vertigo)

zz Symptoms of imbalance felt in the legs: Look for evidence of
cerebellar disease, proprioceptive damage, muscular weakness
—— Consult neurologist.
zz Do symptoms suggest postural hypotension: Measure erect and

supine blood pressure?
—— Postural hypotension.
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—— Consider drugs, alcohol, diabetes, anemia, Addison’s

disease, autonomic neuropathy.
zz If BP is raised
—— Investigate and treat as appropriate.
zz Are there any cardiac signs?

—— Yes.
—— Like dysrhythmia, murmurs, cardiac failure, abnormal ECG.
—— Refer to cardiologist for treatment.
zz Are there features suggestive of epilepsy?

—— Yes.
—— Symptoms may reflect: Aura or fits especially temporal lobe
epilepsy, anticonvulsant toxicity.

—— EEG may be required and neurology consultation.
zz Is there evidence of anemia or polycythemia?

—— Yes.
—— Check full blood count, blood film.
—— Investigate further as appropriate.
zz Do symptoms suggest hypoglycemia?

—— Yes.
—— Is patient taking insulin or sulfonylureas?
Yes.
—— Is patient: Taking the correct dose? Receiving insufficient
food? Taking inappropriate exercise? Is control too tight?

—— Modify treatment and improve patient education.
zz Symptoms of hypoglycemia:
—— Patient is not taking insulin/sulfonylureas.
—— Consider: Reactive hypoglycemia, e.g. postgastrectomy,
Addisson’s disease, hypopituitarism, insulinoma.

—— Investigate and treat as appropriate.
zz Are symptoms related to neck movements?

—— Yes.
—— This may reflect cervical spondylosis, carotid sinus
hypersensitivity (rare).
—— If association is definite, collar may help.
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zz Are there features of psychiatric disturbance?

—— Yes.
—— Anxiety disorders or panic attack with hyperventilation are
most common.
—— Are symptoms reproduced by voluntary overbreathing?
No.
—— Consider: Depression, psychosis, hypochondriasis.
—— Consult psychiatrist.
zz If above symptoms are reproduced by voluntary overbreathing?

—— Hyperventilation confirmed.
—— Treatment: Controlled breathing training.
GUIDING FOR EVALUATION OF DIZZY PATIENTS

(FLOW CHART 10.1)
History
zz Description:
—— Vertigo: Sensation of motion or spinning.
—— Presyncope: Blacking out or loss of consciousness.
—— Disequilibrium: Loss of balance or woobly.
—— Lightheadedness.
zz Duration:
—— Seconds-minutes.
—— Hours.
—— Days.
zz Onset:
—— Sudden.
—— Chronic.
zz Frequency:
—— Acute.
—— Episodic.
—— Persistent.
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Flow chart 10.1 Guide for vertigo practice by general practitioner
zz Aggravating factors:
—— Position.
—— Coughing.
—— Loud sounds.
—— Stress, fatigue, hunger, emotional upset and menses.
zz Associated symptoms:
—— Otologic symptoms: Hearing loss, tinnitus, ear fullness or
pain or ear discharge.

—— Neurological symptoms: Headache, aura, visual disturbance,
numbness, weakness, speech and swallowing difficulties.

zz Past medical history:
—— Cardiovascular disease.
—— Endocrine and metabolic disease.
—— Migraine.
—— Psychiatric illness.
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zz Drug history:
—— Ototoxic drugs: Antimlarial, antituberculous, topical
antibiotic eardrops, aminoglycosides and chemo

therapeutic drugs.
—— Antihypertensives.
—— Antiepileptics.
—— Sedatives and drugs acting on the central nervous system.
Examinations
General Examination
zz Pallor.
zz Blood pressure.
zz Pulse.
zz Temperature.
zz Postural hypotension.
ENT Examination
zz Otoscopy.
zz Rinne’e and Weber’s test.
Neurologic Examination
zz Cranial nerve examinations: Normal/abnormal.
zz Upper and lower limb examination: Tone, power, sensation,
reflexes.
Neurotologic Examination
zz Spontaneous and gaze-evoked nystagmus.
zz Oculomotor tests: Fixation, smooth pursuit, saccades,
convergence—positive in central lesions.
zz Special vestibular tests (VOR): Head shake test, Halmagyl, VOR
suppression, oscillopsia.
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zz Tests for vestibulospinal tract: Gait, Romberg’s test.

zz Cerebellar test: Past pointing/Dysdiadochokinesia.
zz Tests for mechanical disorders of the semicircular canals: Dix-
Hallpike test, fistula test, Valsalva. These are positive in
peripheral lesions.
zz Tests for utricular dysfunction (otolith-ocular reflexes): Skew
deviation, Ocular tilt reaction, subjective visual vertical. These
are seen in both peripheral and central lesions.
Investigations
zz Audiological test:
—— Pure tone audiometry.
zz Hematolgical tests:
—— Full blood count.
—— Fasting blood sugar.
—— Thyroid function test.
—— Venereal disease research laboratory (VDRL).
—— Cardiac enzymes.
—— Blood urea and serum electrolytes.
—— Autoimmune screening.
zz Cardiological test:
—— Electrocardiogram (ECG).
zz Radiological tests:
—— CT scan.
—— MRI.
zz Special vestibular tests:

—— ENG/VNG.
—— Video head impulse test.
—— Vestibular evoked myogenic potentials (VEMP).
—— Caloric tests.
—— Electrocochleography.
—— Dynamic posturography.
—— Rotatory chair.
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CHAPTER 11
Interesting Case Series
CASE 1: VESTIBULAR NEURONITIS

Case Presentation
A 60-year-old housewife presented with complaints of severe
rotator, spinning sensation since one week. She had nausea and
vomiting during the episodes. She had also instability on walking
since one week. After taking by a general practitioner, she had an
improvement in her symptoms. However, instability while walking
persisted. She had no hearing loss or tinnitus.
Past History
zz She is not diabetic and hypertensive.
zz She was not taking any ototoxic medication before attack.
zz She gave history of viral rhinitis about 15 days prior to
presentation.
Clinical Examination
zz Both tympanic membranes are normal.
zz Tuning fork tests are normal.
zz All cranial nerves, motor, sensory systems and reflexes are
found to be normal.
zz No cerebellar signs seen.
zz Horizontal nystagmus of first degree beating to the left.
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zz Unterberger’s stepping test: Abnormal deviation and rotation

to the left.
zz Gaze test, positional test and Dix-Hallpike test are normal.
Investigations
zz Pure tone audiometry is within normal limit.
zz Electronystagmography (ENG) done at the time of presentation
showed spontaneous nystagmus to the left. Caloric test
showed right-sided hypoactive responses to warm and cold
water irrigation.
Diagnosis and Discussion

This is a typical case of vestibular neuronitis. Patient presents with
severe rotator vertigo along with nausea and vomiting lasting for a
week. There are no ear symptoms such as deafness, tinnitus, aural
fullness, headache, diplopia or any sensory-motor loss. Classically,
it is preceded by an attack of upper respiratory tract infection,
yet in most cases (70%), this history may not be present. So, the
absence of history of upper respiratory tract infection does not
rule out vestibular neuritis.
Treatment
zz The drug therapy for vestibular neuritis comprises of vestibular
sedatives and antiemetics, primarily to provide symptomatic
relief. The patient may be started with antivertigo drugs.
zz The mainstay of therapy for long-term relief is early mobi
lization and vestibular rehabilitation exercises.
CASE 2: MÉNIÈRE’S DISEASE

Case Presentation
A 35-year-old man presented with recurrent attacks of giddiness
for last 5 years. The attacks were infrequent initially, but over the
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Interesting Case Series 121
last 1 year, the attacks have occurred at gradually shorter intervals.

The attacks were accompanied by severe nausea, occasionally
with vomiting, tinnitus and heaviness of the right ear. Each of the
attacks lasted for 1 to 6 hours, but the patient’s uneasiness and
sense of instability persisted for about a day. In between two
consecutive attacks, the patient was normal, but for last 6 months
he experienced persistent heaviness in the right ear.
General ENT Examination

zz General condition of patient is normal.
zz Clinically ENT examination did not reveal any remarkable
abnormality.
zz No facial weakness was noted.
zz Corneal reflex was normally bilateral.
Clinical Neurotological Examination

zz Standing test and stepping test are normal.
zz Positional test normal.
zz No nystagmus obtained in headshaking test.
Investigations
zz Pure tone audiometry test showed a mild-to-moderate degree
of sensorineural deafness slightly more marked in the lower
frequencies on the right side with normal hearing level on the
left.
zz Tone decay test was negative bilaterally.
zz ABLB test showed complete recruitment.
zz Glycerol test was positive.
zz Electronystagmography (ENG) showed a hypoactive caloric
response in right side with normal response on the left side.
Diagnosis
This typical case of Ménière’s disease of the right side.
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CASE 3: BENIGN PAROXYSMAL

POSITIONAL VERTIGO (BPPV)
Case Presentation
A 50-year-old male presented with repeated attacks of occasional
rotator vertigo with severe nausea but no vomiting. Each attack
lasting for about 1 minute for 2 weeks. Symptoms induced on
turning usually in bed but sometimes even while sitting. Several
times, the symptoms were elicited when the patients tried to
get up from bed. He has no deafness, tinnitus, aural fullness and
muscular weakness.
Examinations
zz Otoscopic examination—normal.
zz Tuning fork test—normal.
zz No cranial nerve palsy.
zz No motor/sensory deficit.
zz Plantar flexor and deep tendon reflex normal.
zz No spontaneous nystagmus.
zz Dix-Hallpike test showed definite rotatory left beating
nystagmus (anticlockwise direction) in left lateral position
of head. Nystagmus started after about 10 seconds and
accompanied by severe vertigo and mild nausea. The
nystagmus and vertigo subsided after about 30–40 seconds.
Repeating the position reduced the vertigo significantly.
zz Unterburger’s stepping test, standing test and cerebellar tests
were all normal.
Investigations
Pure tone audiometry—normal.
Diagnosis
This is classical case of left side BPPV.
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CASE 4: MÉNIÈRE’S DISEASE

A 45-year-old man working as a clerk in a office presented with
frequent attacks of severe giddiness with nausea and vomiting,
each attack persisting for about 2 to 5 hours and on occasion, it
continues for nearly day. The patient has been experiencing these
attacks of giddiness for about 3 to 4 years. Initially, these attacks
used to occur once every 2 to 3 months, but lately the frequency
has been increased and now these attacks of giddiness occur
3 to 4 times a month. Now, he finds difficult to attend office, feels
incapacitated, has become extremely depressed and frustrated,
stays at home more than 10 days a month. Additionally, the
patient has deafness and tinnitus in right ear, which has been
there for the last 3 years so, but during the attacks of giddiness, the
tinnitus increases, and there is also a definite sense of fullness and
blockage of the right ear just prior to and during attack. Very often,
he can predict an impending attack as the sense of blockage of the
right ear and the increase of tinnitus usually starts as few hours
before the onset of giddiness.
Clinical Diagnosis: Ménière’s Disease

Explanations
The typical triad of vertigo-deafness-tinnitus accompanied by
a sense of aural fullness and the episodic nature of the attack is
by itself very typical of Ménière’s disease. The patient is perfectly
normal in between two successive attacks (except for deafness
and mild tinnitus) proves the episodic nature of the disease, which
is the very characteristic of Ménière’s disease.
CASE-5: MIGRAINE-RELATED VERTIGO

A 40-year-old male executive reported with recurrent attacks
of vertigo each attack persisting for 2 to 4 hours with no
accompanying symptoms. There were no precipitating factors that
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the patient could recall on asking leading questions about any ear
symptoms such as tinnitus, deafness or aural fullness, the patient
categorically denied any related ear symptoms. The vertiginous
attacks had been occurring once every 2–3 months for the last
2 years but for the last 3 months, it is much more frequent occurring
once or twice every week.
Important History Noted

zz Recurrent attacks of vertigo with no accompanying symptoms.
zz No ear symptoms noted.
zz Duration of each symptom is 2–4 hours.
zz Patient state in between two attacks—Nothing specified.
Past History
zz Patient had undergone angioplasty 5 years back for cardiac
problems.
zz He has a mild persistent pain in shoulder 2 years back
diagnosed cervical spondylosis for which he is using cervical
collar.
zz History of motion sickness in childhood.
zz Family history of migraine.
zz No other relevant past family history.
On Examination
zz Bilateral normal intact tympanic membrane.
zz Rinne’s test positive in both sides.
zz Weber central.
zz ABC normal.
CNS Examination
zz No motor/sensory loss.
zz No cranial nerve palsies.
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zz No abnormal cerebellar signs.

zz Plantar flexor, knee jerk normal.
zz Corneal reflex—normal in both sides.
Balance System
zz Stepping test—slight rotation and deviated to right side more
or less within normal limits.
zz Gait—normal.
zz Romberg’s test—normal.
zz Head shaking test—normal.
zz No spontaneous, gaze and positional nystagmus.
Investigations
zz Cardiac examinations—normal.
zz Routine blood test—normal.
zz Pure tone audiometry—within normal limit.
zz ENG, ECG, VEMP—normal.
zz MRI brain—normal.
Diagnosis
Migraine-related vertigo (MRV) as there is family history of
migraine and a past history of motion sickness. Both these
factors and the episodic vertigo with no aural symptoms suggest
possibility of MRV.
Treatment
Since there is no definite clinical test to confirm it, a therapeutic
trial with prophylactic antimigraine drugs such as flunarizine,
amitryptyline and propranolol was instituted.
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CASE 6: PERILYMPH FISTULA

A 45-year-old male patient met with a road traffic accident where
he injured his head. CT head was normal. There was a transient loss
of consciousness. There was no history of any ear bleeding. The
patient was kept for observation overnight. He was discharged
on the next day. He felt a little unstable but could walk. After
2 days, he started feeling unsteady while walking. There was mild
rotator vertigo with no nausea or vomiting. The ear examination
was essentially normal. Fistula sign was negative. Valsalva
response was not recorded. He had tinnitus on the left side and
high frequency sensorineural hearing loss (SNHL). Tympanogram
showed a shallow A-type curve. High resolution computed
tomography (HRCT) was repeated which showed no fracture
lines or any damage to the otic capsule. He was initially treated
on symptomatic treatment hoping that he will recover of his
vestibular symptoms. However, his symptoms persisted. During
this period, he had to travel by air. Though it was a short flight,
his symptoms worsened and he had strong vertigo. He sought
medical help and had to return by road. The sudden aggravation
of symptoms raised suspicion of perilymph fistula. He was taken
up for left exploratory tympanotomy. There was thin-fluid noted
in the middle ear. It was sucked clear but re-accumulated within
few minutes. On close observation, it was detected to be coming
through fracture at the foot plate of stapes. The ossicles otherwise
were intact. The fracture was not very obvious because of mucosal
folds which were hiding the crack and the leak. The mucosa was
swollen. It was divided and raised to either side. A small piece of
tragal perichondrium was placed and mucosa replaced. It was not
perfect cover by mucosa but enough to hold the graft position.
A piece of gel foam under the crura through obturator foramen
provided additional support to keep the tissues pressed against
the foot plate at least for a few days. He was kept on bed rest with
head elevated by 30° for 5 days. He was a Muslim by religion but
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was asked to avoid bending down during his prayers for a period of
3 weeks. His vestibular symptoms started improving the next day
and became almost vertigo free in 2 weeks. He was not allowed
to fly for 1 month. His hearing showed no improvement for the
following 3 months. His tinnitus slowly reduced but did not go
completely.
Point to learn in this case
zz Post-head injury instability/vertigo can have varied
presentations and causes including postconcussion syndrome.

Some of them have confusion symptomatology. Often the
investigations may not clinch the diagnosis.
zz The aggravation of symptoms subsequent to sustained
pressure variations are strong suggestion towards the

diagnosis of perilymph fistula. Probably while testing fistula
sign the pressure variations are not sustained long enough.
zz Proactive approach towards exploratory tympanotomy should
be the right way to manage these patients. Endomeatal

tympanotomy is such a safe procedure that one can afford to
have some negative explorations which should be acceptable.
zz Hearing improvement and response to tinnitus may be poor.
However, some patients do improve significantly, if intervened

early.
CASE 7
A 42-year-old patient came to ENT-OPD with history of recurrent
bouts of decreased hearing, tinnitus and vertigo. From history, it
came to know that he has been suffering from recurrent bouts
of vertigo for over 3 years and during this time, had consulted
a number of general physicians, neurologists and general
practitioners. He was told that there was an ear problem, but he
was never referred to any ENT specialist. It was only now when his
tinnitus became complicated did he come for an ENT check-up. On
enquiry, he confessed to a feeling of aural fullness.
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He had undergone different investigations and the only

significant finding was a mild SNHL on audiometry.
He was advised a glycerol dehydration test and it came positive,
confirming the diagnosis of Ménière’s disease. He was advised
proper medication like beta-histine/cinnarizine/prochlorperazine,
mild diuretics and physiotherapy.
Comments
This patient was under treatment for long period, where every bout
of vertigo of him was treated symptomatically with cinnarizine,
beta-histine or prochlorperazine; however a diagnosis was never
reached or attempted by the treating physicians. A simple test
like audiometry was overlooked whereas MRI was done. This is a
common scenario where the physicians fails to follow a protocol
as far as both diagnosis and treatment are concerned.
CASE 8
A 55-year-old patient attended ENT-OPD with severe vertigo
and hearing loss for only 1 day. Symptomatic treatment with
intravenous prochlorperazine was given and an audiological
evaluation was ordered. Pure tone audiometry revealed unilateral
profound hearing loss. The treating doctor labeled it as Ménière’s
disease and put him on beta-histine and prochlorperazine.
Eventually even when the vertigo subsided, the patient’s hearing
loss did not improve.
Comments
This is a patient of sudden sensorineural hearing loss who presented
with acute vestibulocochlear pathology. The differentiating point
here from Ménière’s disease is the immediate development of
profound hearing loss. Hearing could have possibly salvaged, if
the patient was put on high dosage of steroid or intratympanic
steroid.
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CASE 9
A 50-year-old male executive reports with 3 episodes of sudden
severe vertiginous sensations over a period of about a year, one
of which lead to a fall. In that episode, the patient had fallen in the
toilet and had sustained minor head injury for which he had to
be hospitalized. Detailed history taking revealed that though he
complained of vertigo, he did not actually have a typical rotating/
spinning sensation. In the episode when he had fallen in the toilet,
he had gone to the toilet at night, but after voiding, he suddenly
fell down and all he could remember was that, he was lying flat
on the floor of the toilet. Different clinical tests and investigations
including MRI of the brain, MR angiography of the brain, ENG, CCG,
carotid Doppler studies and EEG revealed nothing significant. On
the two other occasions, he had a feeling of blankness in the head,
profuse sweating, a sensation of nausea with spinning sensation
in the head, a blurring of vision which gradually increased over
a period of 1–2 minutes and finally a complete blackout. He did
not have a fall but had lied down on the floor and after about
3–4 minutes, the symptoms subsided. All the attacks were
aggravated while the person was standing. One of these episodes
had taken place in his office while he was delivering a lecture. His
friend reported to his wife that while lecturing he had suddenly
complained that he was not feeling well and asked for a chair, but
even before the chair could be brought, he lay down on the floor. He
had become very pale in the face, with cold sweat in the forehead
and his radial pulse had become very feeble and slow and later
on was not palpable. After 15 minutes, when examined, nothing
was abnormal except low blood pressure of 96/64 mm Hg. The
patient complained of generalized weakness but no drowsiness at
the time of examination.
General examination: It did not show any abnormality. Clinical
neurotological tests were normal. Test for orthostatic hypotension,
hyperventilation test and other dizziness revealed no abnormality.
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Comments: This appears to be a case of syncope and not true

balance disorder.
CASE 10
A 45-year-old male businessman, complained of instability,
headache and vomiting for the last 3 months. He had an ataxic
gait, ataxia in the left upper limb and papilledema.
Findings
zz Caloric test findings showed a butterfly pattern of 1221.
zz There is a left beating spontaneous nystagmus and gaze
nystagmus to the left.
zz The pendular eye tracking was grossly disorganized.
zz The optokinetic nystagmus to the left was fairly normal while
that to the right was grossly affected.
Comments
zz Both the left beating caloric responses, e.g. L 440C and R
300C are hyperactive (directional preponderance to the left),
while both the right beating caloric responses, e.g. R 440C and
L 300C are hypoactive (inhibitory preponderance to the right).
zz The directional preponderance suggests a disinhibitory lesion
involving the temporal lobe of fibers projecting from it onto
the left nystagmus generator in the brainstem.
zz The suppression of the right beating caloric responses
indicates a lesion in the brainstem involving the nystagmus
generator on the right side responsible for producing right
beating nystagmus.
zz The patient was subsequently found to have a large brainstem
tumor.
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CHAPTER 12
Vertigo Clinic
Evaluation Format
HISTORY
zz Patient details
—— Name
—— Age
—— Sex
—— Address.
zz Presenting complaint
—— Vertigo (surrounding/head-rotating),
—— Light headedness
—— Imbalance
—— Others.
zz Duration of vertigo
—— Seconds
—— Hours
—— Days
—— Months
—— Years.
zz Mode of onset
—— Sudden
—— Gradual.
zz Associated symptoms
—— Nausea
—— Vomiting
—— Tinnitus
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—— Hearing loss
—— Fullness in ear
—— Blurring of vision
—— Slurring of speech
—— Headache
—— Photophobia
—— Others.
zz Description of first attack.

zz Frequency of each attack.
zz Periods in between attacks.
—— Free of symptoms
—— Not free of symptoms.
zz Warning signs before attack

—— Nil
—— Fullness in ear
—— Aura
—— Others.
zz Aggravating factors
—— Nil
—— Coughing
—— Sneezing
—— Loud sounds
—— Specified food
—— Specific head position
—— Standing from sitting position
—— Turning in bed
—— Raising hands
—— Menstruation
—— Others.
zz Relieving factors
—— Nil
—— Yes.
zz Any URI/Fever before attack.
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Vertigo Clinic Evaluation Format 133
zz Headache
—— Yes
—— No.
zz Cervical pain
—— Yes
—— No.
zz Head injury/any trauma

—— Yes
—— No.
zz Difficulty walking in the dark/streets/open spaces.

zz Cardiovascular disorders
—— Yes (Hypertension/past history of MI/Palpitations/Chest
pain/leg pain on walking or at rest/others)

—— No.
zz Medical problems
—— No
—— Yes (Thyroid/diabetes mellitus/anemia/polycythemia/auto-
immune/tuberculosis/smoking/alcohol/loss of weight/
appetite/blood in stools/diarrhea/food intolerance/
indigestion/bleeding disorders/microglobulinemia/
others).
zz Eye problems
—— No
—— Yes (Loss of vision/pain/discharge or tearing/glaucoma/
diplopia/refractory errors/new glasses/others).

zz Tullio phenomenon
—— Present
—— Absent.
zz Ototoxic drugs/other medications

—— No
—— Yes.
zz Acoustic trauma
—— No
—— Yes.
12.indd 133 9/7/2015 3:52:55 PM

zz Motion sickness
—— No
—— Yes.
zz Psychiatric history
—— No
—— Yes (Insomnia/depression/conversion reaction/agora-
phobia/others).
zz Family history of giddiness/psych disease
—— No
—— Yes.
zz History of unconsciousness
—— Yes
—— No.
If Patient Presents Like Near Faint

Sensation of impending faint (light headedness).
Mechanism: Diffuse cerebral ischemia (tunneling/dimming of
vision, shortness of breath, air hunger, perioral numbness).
zz History of orthostatic hypotension: Reduced blood volume,
hypotensive drugs, autonomic dysfunction.

zz History of vasovagal attack: Prolonged standing in hot sun, fear,
severe pain, acute vertigo.

zz History of hyperventilation: No/Yes (Anxiety, stress, panic
attacks/associated symptoms-frequent sighing, air hunger/

tightness in chest/perioral numbness/paresthesia of
extremities).
zz History of reduced cardiac output: No/Yes (Arrhythmia/valvular
disease/heart failure).
Examinations
Systemic
zz Pallor: Yes/No.
12.indd 134 9/7/2015 3:52:55 PM

Vertigo Clinic Evaluation Format 135
zz Blood pressure: Lying/standing.

zz Bruits carotids: No/Yes and Right/Left.
Ears
zz Tympanic membrane: Right/Left.
zz Tuning fork test: Right/Left, Webers-Right/Left, ABC-Right/Left.
zz Cranial nerves:
—— Corneal reflex—right/left.
—— Eye movements—normal/abnormal.
—— Ptosis—no/Yes.
—— 7th, 9th, 10th, 11th, 12th cranial nerve examinations.
zz Neurological examination:
—— Deep tendon reflexes—normal/abnormal.
—— Babinsky—normal/abnormal.
—— Muscle strength—normal/abnormal.
—— Sensation on face—normal/abnormal.
—— Sensation on limbs—normal/abnormal.
—— Cerebellar functions—finger to nose (with eyes open/eyes
closed).
zz Examination of vestibulospinal system:
—— Romberg’s test (eye closed/eyes open).
—— Tandem standing test (eyes open/eyes closed).
—— Walking-tandem (eyes open/eyes closed).
—— Examination of gait.
zz Examination of vestibulo-ocular system:

—— Opsoclonus—yes/no.
—— Ocular bobbing—yes/no.
—— Ocular flutter—yes/no.
—— Ocular myoclonus—yes/no.
—— Inspection of spontaneous nystagmus—no/yes

(Horizontal—right/left, rotatory—clockwise/anticlockwise,
vertical—up/down)—it is done with/without Frenzel lens
and with/without optic fixation.
12.indd 135 9/7/2015 3:52:55 PM

—— Saccades—no/yes.
—— Smooth pursuit—normal/abnormal.
—— Headshaking nystagmus—no/yes.
—— Positional testing—Dix-Hallpike maneuver.
—— Valsalva-induced nystagmus—no/yes.
—— Hyperventilation—dizziness (no/yes), nystagmus (no/yes).
—— Tullio phenomenon—no/yes.
—— Fistula test—no/yes.
Provisional diagnosis: We will get after history and examination.
INVESTIGATIONS
zz Pure tone audiometry.
zz Speech audiometry.
zz Impedence audiometry.
zz Acoustic reflex test.
zz ENG.
zz Blood tests—DC, TLC, Hb%, TSH, FBS, lipid profile, VDRL.
zz Imaging—MRI/CT.
zz Glycerol test (Right/Left).
Final diagnosis: We will get after all above steps.
MANAGEMENT
zz Medications.
zz Vestibular exercises.
zz Surgery.
12.indd 136 9/7/2015 3:52:55 PM

Points to Remember
PEARLS IN VERTIGO
zz Vertigo is a symptom and not a disease, and it accounts for
about 5% of all consultations with a general practitioner and
10–15% with an otorhinolaryngologist.
zz Vertigo may be defined basically as a data mismatch in the
sensory mechanism of the balance system consisting of
visual, vestibular, acoustic, proprioceptive, CNS and peripheral
nervous system.
zz Dizziness is a nonspecific term which includes sense
of imbalance (disequilibrium), blackout (presyncope),
lightheadedness, floating sensation or vertigo.
zz Balance is a complex interaction between the vestibular, ocular,
proprioceptive and central nervous systems (CNS) to maintain
head and body position in relation to the environment.
zz Peripheral vestibular system is the vestibular apparatus which
consists of the semicircular canals, utricle, saccule and the
vestibular nerve.
zz Central vestibular system includes vestibular nuclei and its
central connections in the brainstem and cerebellum.
zz Benign paroxysmal positional vertigo (BPPV) is the most
frequent vestibular end organ disorder accounting for 20% of
all dizziness cases.
zz Dix-Hallpike test is the diagnostic test for BPPV.
zz Medicines do not cure benign paroxysmal positional vertigo
(BPPV) but are useful in controlling severe symptoms.
zz Benign paroxysmal positional vertigo (BPPV) is often described
self-limiting, because the symptoms subside or disappear
even without treatment but, the recurrence rates are high.
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zz Epley maneuver is very beneficial in the management of BPPV.

zz Tullio’s phenomenon means feeling of vertigo on exposure
to loud sounds. It may be seen Ménière’s disease, perilymph
fistula, fenestration and vestibulofibrosis.
zz Oscillopsia is blurring of vision with head movement. It occurs
with bilateral vestibular loss.
zz Nystagmus is an involuntary movement of the eyes due to
a disturbance vestibulo-ocular reflex (VOR). It can be due to
either a peripheral or central vestibular disorder.
zz Jerk nystagmus is the eye movement consists of a quick
movement followed by a slow phase. The direction of
nystagmus corresponds to the fast phase. Usually seen in
peripheral vestibular disorders.
zz Pendular nystagmus is the involuntary eye movement which
has equal velocity in either direction. A sign of a central
vestibular or congenital disorder.
zz Ménière’s disease is due raised endolymphatic pressure and
clinically presents with episodic vertigo, low-pitched roaring
tinnitus, fluctuating sensorineural hearing loss and sense of
aural fullness.
zz In early cases of Ménière’s disease low frequencies sounds
are affected more and the audiogram shows a rising curve. In
long-standing cases, low and high frequencies are affected,
audiogram becomes flat and then falling type.
zz BPPV presents mostly in the fifth decade. It can follow an
attack of vestibular neuronitis or head trauma or ear surgery.
This is no gender bias.
zz Acoustic neuroma is a slow growing tumor. There is
concomitant vestibular adaptation and therefore severe
vertigo does not occur.
zz Vascular occlusion of labyrinthine artery is seen in the elderly
with arteriosclerosis and those with hypercoagulation disease
and cause irreversible hearing loss and episodic vertigo.
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zz Otolithic crisis of Tumarkin or drop attacks are seen in early or

late Ménière’s disease. Patient feels as if pushed to the ground
without any vertigo or loss of consciousness. It is presumed
they are due to distortion of otolithic membrane of utricle or
saccule when endolymphatic pressure rises.
zz Positional nystagmus of peripheral origin occurs in a fixed
direction, i.e. towards the undermost ear. Nystagmus of
peripheral origin lasts only for a few seconds and is always less
than one minute.
zz On Dix-Hallpike testing, nystagmus of central origin appears
immediately as soon as head is in critical position without a
latent period.
zz Cold water irrigation of ear canal causes nystagmus to opposite
side and warm water to the same side (COWS).
zz Ménière’s disease is usually unilateral but other ear may
be affected after a few years. Males are affected more than
females.
zz In Ménière’s disease, during the initial vestibular excitation
phase, the nystagmus will be ipsilateral but the vestibular
depression phase, the nystagmus would beat towards the
opposite side.
zz Typically, a patient suffering from Ménière’s disease would
have a severe form of rotatory vertigo lasting a few hours with
associated nausea and vomiting. Most of the time, there would
not have been any precipitating factors. The attacks could
occur anywhere and at any time of the day or night. Some
patients might have a preceding sensation of fullness in the
ear.
zz In Ménière’s disease, in between attacks the patient may not
have any findings other than signs of sensorineural hearing
loss (which again would be difficult to confirm clinically in the
early stage of the disease).
13_PTR.indd 139 9/7/2015 3:52:46 PM

zz In vertigo patients, FTA-ABS should be done to rule out

syphilitic cause.
zz A vertical spontaneous nystagmus is always pathognomonic
of a central vestibular lesion.
zz Vestibular system generates the slow phase of nystagmus
which is directed to the opposite side. The fast phase of the
nystagmus is generated by the central nervous system.
zz ENG does not measure or record torsional eye movements,
which is characteristic of BPPV.
zz The basis of the ENG testing is the corneo-retinal dipole, the
cornea is the positive pole and the retina is the negative pole.
ENG is not recommended for patients with less corneo-retinal
potential difference (degenerative, diabetic or hypertensive
retinopathies and retinitis pigmentosa) as the eye movement
in these cases would be difficult to track by electrodes.
zz A broad and wide-based gait with a tendency to fall, suggests
the possibility of a cerebellar pathology.
zz The most important point in the diagnosis of vertigo is an
unhurried and detailed history (Professor Alan G Kerr).
zz Hyperactive caloric response is seen in early Ménière’s disease,
central vestibular dysfunction. Decrease caloric response on
the affected side is seen in unilateral vestibular dysfunction.
zz The finger nose test and heel-knee test are tests to detect
abnormalities of cerebellar function.
zz During walking test, falling or deviating repeatedly in the
same direction suggests an unilateral vestibular lesion on the
side of fall.
zz In Unterburger’s test, the blind-folded patient is asked to extend
his arms and step on the same spot alternately with each foot
for 90 times in 1 minute. In peripheral vestibular lesions, the
patient rotates/deviates to the side of the lesion; in central
vestibular lesions, the sway is abnormally high.
13_PTR.indd 140 9/7/2015 3:52:46 PM

zz The vestibular rehabilitation exercises (also called Cawthrone-

Cooksy exercises) are a must in the management of all patients
of vestibular neuritis.
zz Cinnarizine has a strong labyrinthine sedative effect and anti-
vasoconstrictive effect. It reduces sludging phenomenon of
blood in the narrow blood vessels and thereby reduces plasma
viscosity which enhances microcirculation in the inner ear and
in the brain.
zz Beta-histine is the only non-sedating anti-vertigo drug
available. It is used with caution in peptic ulcer and bronchial
asthma patients.
zz Use of cinnarizine in not contraindicated in peptic ulcer and
bronchial asthma like beta-histine. Cinnarizine is very safe
drug in geriatric patients.
zz The slow phase of nystagmus is generated by the vestibular
labyrinth (peripheral nervous system) and the fast phase of
the nystagmus is generated by the central nervous system. The
direction of the nystagmus is the direction of fast phase.
zz Videonystagmography (VNG) can record rotator eye movement
that is not possible by electronystagmography (ENG).
zz The utricle is sensitive to horizontal displacement and the
saccule is sensitive to vertical displacement.
zz Falling or deviating repeatedly in the same direction suggests
an unilateral vestibular lesion on the side of fall.
zz The accuracy of timing, preciseness and perfect coordination
of the muscular contraction of the extraocular and skeletal
muscles is maintained by the cerebellum.
zz Diuretics and low salt diet help in reducing the tension of
endolymph in Ménière’s disease.
zz Equilibrium is maintained primarily by the vestibular part of
labyrinth and is aided by visual and proprioceptive senses
distributed all over the body. Final control of equilibrium is
done by the cerebellum and cerebrum.
13_PTR.indd 141 9/7/2015 3:52:46 PM

zz Vertigo can occur from disorders of any of the three systems,

vestibular, visual or somatosensory. Normally, the impulses
reaching the brain from the three systems are equal and
opposite. If any component on one side is inhibited or
stimulated, the information reaching the higher center is
mismatched leading to vertigo.
zz Lermoyez syndrome has sensorineural hearing loss first
followed by attacks of vertigo.
zz Vestibular neuronitis is not accompanied by deafness but has
severe vertigo of sudden onset.
zz In acoustic neuroma, vertigo is not usually present or mild due
to central adaptation.
zz Any young adult presenting with unilateral sensorineural
hearing loss and or tinnitus must be investigated with MRI/CT
to rule out acoustic neuroma.
zz Key points of vestibular neuronitis:
—— Vestibular neuronitis has sudden onset.
—— Only vestibular system is affected.
—— There is severe rotatory vertigo at onset.
—— There is gradual recovery with time.
zz Key points of benign paroxysmal positional vertigo:

—— It is the most common vestibular disorder.
—— Rotatory vertigo is of short duration.
—— It is normally easy to provoke.
—— It is usually self-limiting.
—— It may be treated with rotator maneuver.
zz History taking remains the main weapon for diagnosis of a

patient with balance disorder.
zz Cardiovascular causes of dizziness are vasovagal syncope,
orthostatic hypotension, embolic disease and cardiac
dysrhythmias.
zz Endocrine causes of dizziness are hypoglycemia, adrenal
failure and pheochromocytoma.
13_PTR.indd 142 9/7/2015 3:52:46 PM

zz Presbystasis is the progressive loss of balance function

accompanies the normal aging process.
zz Hennebert’s sign: Nystagmus induced by pressure insufflations
against an intact tympanic membrane. It is a false positive
fistula sign. First described in patient with congenital syphilis
due to a hypermobile stapes foot plate. Also noted in Ménière’s
disease, where it causes stapes footplate movement, the
undersurface of which is adhered to the distended saccule.
zz Vestibular neuritis or neuronitis is a viral infection of the
vestibular nerve or vestibular (Scarpa’s) ganglion. It is most
commonly thought to be due to Herpes simplex type I viral
infection.
zz Electronystagmography (ENG) is not recommended for
patients with less corneo-retinal potential difference
(degenerative, diabetic or hypertensive retinopathies and
retinitis pigmentosa) as the eye movements in these cases
would be difficult to track by electrodes. ENG does not measure
or record torsional eye movements, which is characteristic of
benign paroxysmal positional vertigo.
zz Treatment of acute attack of Ménière’s disease is primarily
aimed at control of vertigo and vomiting. Prochlorperazine
and ondansetron are commonly preferred medications
for control of vomiting. Vertigo control requires the use of
vestibular suppressants like connarizine or prochlorperazine
for 3–5 days.
zz Prolonged use of vestibular suppressants is not advisable as
this may hamper vestibular compensation and thus delay
recovery.
zz People with Ménière’s disease are advised to avoid high salt
containing food like papad, pickles, etc. Consumption of
alcohol and chocolates, and nicotine use is discouraged.
zz In Ménière’s disease, diuretic whenever prescribed should
preferably be the potassium sparing variety triamterene.
13_PTR.indd 143 9/7/2015 3:52:46 PM

Loop diuretics are unsafe in our country for risk of hyponatremia

and hypokalemia. Many prefer to use acetazolamide for short
periods of time.
zz At least 2 definitive episodes of vertigo of at least 20 minutes
duration must have occurred to make the diagnosis of
Ménière’s disease. Duration is usually several hours long.
zz In Ménière’s disease, pure tone audiometry shows a low
frequency or mixed low and high frequency loss may develop.
Typically, lower frequencies are affected more often than
higher frequencies because of preferential sensitivity of the
apex to hydrops.
zz Dysdiadochokinesia is the inability to perform rapidly
alternating motor movements, a sign of cerebellar disease.
zz The characteristic of the nystagmus that is diagnostic of BPPV
is that it is latent (starts after 10–15 seconds), short lasting (lasts
for about 15–20 seconds), rotatory (is mixed vertical-torsional),
geotropic (the direction of rotation of eyeballs is towards the
floor with the affected ear down), fatigable (tends to fade away
on repeating the test multiple times) and reversible (upon
rapidly bringing the patient to sitting position, many times a
milder rotator nystagmus is elicited opposite to that in supine
head-hanging position).
zz Before doing Dix-Hallpike test, it is important to rule out, if the
patient is having any significant complaint of cervical spine or
any history of coronary artery disease, in which cases the test
is modified.
zz Wallenberg’s syndrome (Lateral medullary syndrome or PICA
syndrome; most common brainstem stroke): The patient
presents with vertigo, ataxia, dysarthria and unilateral Horner’s
syndrome (ptosis, meiosis and anhidrosis). Anterior cerebellar
artery (AICA) strokes: The patient presents with vertigo and
unilateral deafness. Isolated pontine infarcts may present with
vertigo alone and may mimic vestibular neuritis.
13_PTR.indd 144 9/7/2015 3:52:46 PM

zz In Ménière’s disease, medical therapy has been the mainstay

of treatment and surgical option is reserved for the cases that
did not improve with conservative therapy. Medical therapy
includes low-salt diet and diuretics.
zz In Ménière’s disease, smoking and excessive stress are
discouraged as these are precipitating factors. The patient is
also instructed to avoid canned foods, cheese and pickles.
zz In Ménière’s disease, surgery is considered in cases with
rapid progression of the disease and in those who did not
respond to conservative therapy. Surgical options include
hearing preservation surgeries such as endolymphatic sac
decompression and retrolabyrinthine or middle fossa selective
vestibular nerve section. Hearing destructive surgeries can be
performed in patients with severe to profound hearing loss
and include labyrinthecomy and translabyrinthine VIII nerve
section.
zz Endolymphatic sac surgery is widely used as the primary
surgical procedure at various centers around the world and
success for the surgery has been reported to be between 60%
and 80% by various authors.
zz Migraine is the most common cause of headache in the world.
Prevalence studies have shown that 14–22% of women and
5–8% of men suffer from migraine.
zz Blood tests can be advised when the clinical diagnosis is
Ménière’s disease to distinguish between syphilis—a condition
in which ear symptoms resemble Ménière’s. However, this does
not mean that every Ménière’s patient should be suspected for
syphilis.
zz A unilateral or asymmetrical sensorineural hearing loss is an
indication for imaging to exclude a tumor of the VII cranial
nerve. Gadolinium MRI is the imaging of choice.
zz The vestibular apparatus consists of the semicircular canals,
utricle, saccule and the vestibular nerve. The otolithic organs
13_PTR.indd 145 9/7/2015 3:52:46 PM

consist of the utricle, which is adjacent to the semicircular

canals and the saccule which is close to the cochlea.
zz The sensory neuroepithelium is called the crista in the
semicircular canals and the macula in the otolithic organs.
zz The crista within the ampula consists of hair cells embedded
in a gelatinous substance called the cupula. The semicircular
canals determine rotational velocity in three dimensions.
zz The macula within the utricle and saccule contain hair cells
coupled to calcium carbonate crystals called otoconia or
otoliths. They sense gravity and linear accelerations.
zz A defect in the vestibule-ocular reflex results in nystagmus.
Nystagmus consists of involuntary eye movements with a fast
and a slow component. The direction of the nystagmus follows
the direction of the fast phase.
zz Pendular nystagmus: Beats of similar velocity each direction
(central cause). Jerk nystagmus: Quick and slow phase
(Peripheral vestibular or central cause).
zz In a peripheral vestibular lesion, where there is hyperactivity
on the side of the lesion the nystagmus beats towards the side
of the lesion (the stronger ear).
zz In Ménière’s disease, there is an initial irritative phase where
the nystagmus beats towards the side of the lesion. The
direction of the nystagmus changes to beat away from the side
of the affected ear later in the paretic phase, where there is
hypoactivity of the affected side.
zz Horizontal nystagmus of peripheral origin (Labyrinth or VIII
nerve) obeys Alexander’s law which states the nystagmus: It
always in one direction, irrespective of the direction of gaze
and Intensity of the nystagmus is greatest when looking in the
direction of the fast phase.
zz Prochlorperazine is the most effective drug for controlling
acute vertigo. This drug is best used for a very short course to
relieve acute symptoms, but should preferably be discontinued
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as soon as the acute symptoms subside such that the vestibular

compensation is not inhibited.
zz Beta-histine is used with caution in peptic ulcer and bronchial
asthma patients.
zz A nystagmus generated by a central vestibular pathology
often (but not always) increases in intensity when the eyes
are open (i.e. optic fixation) and decreases when the eyes are
closed. If intensity of nystagmus decreases on optic fixation, it
is usually a peripheral vestibular lesion but a central lesion is
also possible.
zz A broad and wide-based gait with a tendency to fall, suggests
the possibility of a cerebellar pathology. Falling or deviating
repeatedly in the same direction suggests an unilateral
vestibular lesion on the side of fall.
zz Onset of vertigo is sudden in peripheral vestibular lesion
whereas gradual onset in central pathology.
zz If the positional nystagmus does not have a latent period, then
its direction changing, not accompanied by an appreciable
sensation of vertigo and is not fatiguable, then this is expected
to be of central origin.
13_PTR.indd 147 9/7/2015 3:52:46 PM

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Index
Page numbers followed by f refer to figure and t refer to table
A Brainstem
concussion 27
ABC test 40
hemorrhage 12
Agoraphobia 4, 12
infarct 33
Alexander’s law 41
ischemia 106
American Institute of Health
Statistics 4 tumors of 13, 19
Aminoglycosides 30 Brandt-Daroff exercise 78, 78f
Amitriptyline 73
Ampullary nerve section 83 C
Anemia 21 Calcium channel blocker 72-75
Anxiety neurosis 4 Caloric test 21, 59, 60f, 118
Arrhythmias 12 Cardiovascular disease 116
Arthritis 30 Cardiovascular system 10
Asthma, bronchial 74 Cawthrone-Cooksey exercises 79,
Ataxia 10 86, 141
cerebellar 31 Central nervous system 2, 10, 21,
Atrophy, cerebellar 33 137
Audio-evoked response 60 Cerebellar artery syndrome,
Audiological test 55 posterior-inferior 13, 18
Autophony 102 Cerebellar function tests 40, 135
Cerebellar test 53, 118
B Cerebrovascular disease 22
Babinski’s test 40 Cervical pain 133
Barbiturates 30 Chiari malformations 44
Bechterew’s nucleus 7 Claussen butterfly chart 58f
Blood pressure 30, 37, 117, 135 Cogan’s syndrome 104
Blood sugar, fasting 55, 118 Corneal reflex 43, 135
Blood urea 55, 118 Cranial nerve 117, 135
Brain tumor 30 Craniocorpography 57, 58
15_Index.indd 151 9/7/2015 3:52:24 PM

D convergence 86, 88f

eye 86
Diabetes mellitus 12
head and neck 88
Diplopia 12, 32, 33
vestibular 136
Dix-Hallpike test 47, 49f, 118, 120,
137 Eye cover test 53
steps of 48f
F
Dizziness 23, 25, 113
common causes of 12 Fistula
episodic 110 labyrinthine 66
Drop attacks 32 perilymph 11, 12, 15, 26, 27, 36,
Dysarthria 32, 33 65, 100, 126
Dysdiadochokinesia 53, 118 sign
Dysesthesia 32 false negative 44
Dysmetria 32 false positive 44
Dysphagia 32, 33 test 43, 102, 118, 136
Flunarizine 73
E Fluorescent treponemal antibody
55, 68
Electrocardiogram 118
Fluoxetine 73
Electrocochleography 60, 118
Frenzel’s glass 41, 41f
Electronystagmography 57, 120,
Friedreich’s ataxia 12
141, 143
Endolymphatic sac surgery 82 G
Enzymes 55, 118
Epilepsy 13 Gait 118
temporal lobe 20 ataxia 31
Epley maneuver 66, 76, 138 examination of 135
steps in 77f Gaze test 120
Epstein-Barr virus 12 Glycerol test 56, 121, 136
Erythrocyte sedimentation rate
55, 104
H
Eustachian tube 102 Halmagyi test 51
Exercises Head impulse 51
adaptation 86 Head injury 15, 30, 133
compensation 86 Head movements 81
15_Index.indd 152 9/7/2015 3:52:24 PM

Index 153
Head shake test 46, 47f, 117 unilateral incomplete

Headache 132, 133 depression of 17
Heart disease 30 Labyrinthectomy 82
Hemorrhage 105 Labyrinthine artery, vascular
cerebellar 33 occlusion of 138
Hennebert’s sign 101, 102, 143 Labyrinthitis 11-13, 15, 26, 30, 33,
36, 102
Horner’s syndrome 105
autoimmune 104
Human immune deficiency virus
12 infective 71
Hydrochlorothiazide 73 syphilitic 12, 68
Hypertension 30 Lermoyez syndrome 142
Hyperventilation 31, 134, 136
M
syndrome 12
Ménière’s disease 11-13, 16, 17, 26,
Hypoglycemia 21, 30, 114
29, 33, 34, 36, 56, 63, 65, 67, 68,
Hypotension 12
70, 73, 82, 83, 96, 97, 111, 112,
orthostatic 21, 50, 134 120, 123, 138, 139, 140, 141, 143
postural 31, 37, 117 Ménière’s triad 96t
Metabolic disease 116
I
Metoclopramide 73
Infarction, cerebellar 22, 105 Metronidazole 15
Inflammatory diseases 64 Migraine 12, 30, 33, 34, 116
Inner ear disease, autoimmune 33 basilar artery 19
Ischemia Motion sickness 22, 36, 107, 134
cerebral 107 Muscle strength 135
labyrinthine 33 Multiple sclerosis 12, 13, 19, 26, 33,
vertebrobasilar 33 71, 106
Myoclonus, ocular 42, 135
L
Labyrinth N
bilateral complete depression Nalidixic acid 15
of 18 Nausea 10
intermittent failure of 65 Neuritis, vestibular 12, 33, 70, 73,
irritation of 65 143
unilateral complete depression Neuroma, acoustic 11, 13, 16, 36,
of 17 102, 103f, 138
15_Index.indd 153 9/7/2015 3:52:24 PM

Neuronitis, vestibular 11, 13, 14, 17, Polyarteritis nodosa 104

26, 30, 36, 99, 119, 142, 143 Positron emission tomography 55
Nystagmus 10, 138 Postconcussion syndrome 27
central and peripheral 41, 42, Prednisolone 73
42t Presbystasis 143
gaze-evoked 117 Presyncope 12
head shaking 136 Promethazine 73
jerk 138, 146 Psychiatric disorders 12
pendular 138, 146 Ptosis 135
peripheral 42 Pure tone audiometry 55, 118, 136
pure vertical 40
spontaneous 40, 42f, 117 R
Valsalva induced 136
Red blood cells 74
Rehabilitation exercises, vestibular
O
85
Ocular dysfunction, vestibular 12 Rehabilitation therapy, vestibular
Oculomotor tests 52, 117 79
Opsoclonus 42, 135 Rinne’s test 39, 117
Optokinetic test 59 Romberg test 45, 118, 135
Oscillopsia test 50 Rotation test 46
Otolith-ocular reflexes 118 Rotation, sensation of 3
Otorrhea 30
Otoscopy 117 S
Ototoxicity 23, 36 Saccades 52, 136
Scarpa’s ganglion 7
P Schwalbe’s nucleus 7
Pallor 37, 117 Selective serotonin reuptake
Panic disorders 12 inhibitor 73
Peptic ulcer 74 Semont maneuver 79
Pheochromocytoma 74 Sensorineural hearing loss 126
Photophobia 132 Single photon emission
Pinna and external auditory canal, computerized tomography 55
examination of 38 Speech audiometry 136
Plantar flexor 122 Spinal nucleus 7
15_Index.indd 154 9/7/2015 3:52:24 PM

Index 155
Spondylosis, cervical 30 Unterburger’s test 45, 46f, 120, 140

Spondylotic myelopathy, cervical Utricular dysfunction 118
31
Steroids, intratympanic 82 V
Stimulation
Valsalva maneuver 44
caloric 17
Vascular diseases 64
labyrinthine 16
Vascular insufficiency 107
Stroke
Vasovagal attack 31, 134
cerebellar 26
Venereal disease research
inferior cerebellar 12 laboratory 55, 118
Suppurative otitis media, chronic Vertebrobasilar insufficiency 13,
65 18, 66, 67, 71, 106
Syphilis 11, 16 Vertebrobasilar transient ischemic
Systemic lupus erythematosus 104 attack 34
Vertigo 3, 10, 35, 37, 55, 62, 74, 109,
T 111
Tandem standing test 135 alternobaric 12, 66, 67
Tendon reflexes, deep 40, 122, 135 benign paroxysmal 11-14, 17,
Thyroid dysfunction 12 36, 63, 99, 122, 137, 142
Thyroid function test 55, 118 benign positional 11-14, 17, 26,
Transient Ischemic attack 12, 106 36, 63, 66, 99, 122, 137, 142
Trauma 64 causes of 11, 20
acoustic 133 central causes of 32, 33, 104
labyrinthine 13, 36 cervical 12, 13, 20
Traumatic head injury 12 clinic evaluation format 131
Tricyclic antidepressants 73, 75 diagnosis 35
Trifluopromazine 73 epileptic 71
Tullio’s phenomenon 100-102, 133, labyrinthine 16
136, 138 migrainous 26, 105
Tumor, cerebellar 33 non-recurrent 30
Tuning fork test 39, 122, 135 ocular 20
onset of 29
U otologic 111
Unconsciousness 134 ototoxic 13
Unsteadiness, sensation of 3 peripheral 21, 34t
15_Index.indd 155 9/7/2015 3:52:24 PM

physiological 5, 22 Vestibulo-ocular reflex 9, 10, 51,

post-traumatic 25 138
psychogenic 20 assessment of 57
rotatory 66 Vestibulo-ocular system,
treatment of 62 examination of 135
true 112 Vestibulopathy, bilateral 12, 103
with deafness 13, 36 Vestibulospinal tract 10, 118
without deafness 13, 36 Vestibulotoxic drugs 11, 15
Vestibular disorders Video head impulse test 118
central 18 Videonystagmography 57, 141
peripheral 12, 13 Vision, blurring of 132
Vestibular evoked myogenic Vomiting 10
potentials 59, 118
Vestibular origin, peripheral 11
W
Vestibular system, disorders of 11
Vestibule-spinal reflex, assessment Walking test 45
of 57 Wallenberg’s syndrome 18, 105,
Vestibule-spinal system, 144
examination of 135 Weber’s test 39, 117
Vestibulocerebellar tracts 10 Whiplash injury 27
15_Index.indd 156 9/7/2015 3:52:24 PM

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MANAGEMENT OF VERTIGO

Prelims.indd 1 9/7/2015 3:24:45 PM

Santosh Kumar Swain

The Health Sciences Publisher

Prelims.indd 3 9/7/2015 3:24:45 PM

Inquiries for bulk sales may be solicited at: [email protected]

Management of Vertigo Made Easy ®

Prelims.indd 4 9/7/2015 3:24:45 PM

Prelims.indd 5 9/7/2015 3:24:45 PM

For the most medical practitioners, a heart-sinking moment is

Santosh Kumar Swain

Prelims.indd 7 9/7/2015 3:24:45 PM

I am deeply indebted to my teacher and mentor Professors

Prelims.indd 9 9/7/2015 3:24:45 PM

Prelims.indd 11 9/7/2015 3:24:45 PM

4. Diagnosis of Vertigo from History 28

5. Clinical Tests for Vertigo 37

6. Investigations for Vertigo 55

Prelims.indd 12 9/7/2015 3:24:45 PM

8. Vestibular Rehabilitation Exercises 85

9. Important Clinical Conditions of Vertigo 96

10. Approach to Vertigo by General Practitioner 110

Prelims.indd 13 9/7/2015 3:24:45 PM

Simplified Approach to Get a Diagnosis 111

11. Interesting Case Series 119

12. Vertigo Clinic Evaluation Format 131

Points to Remember 137

Prelims.indd 14 9/7/2015 3:24:45 PM

Vertigo and dizziness are extremely common problem, but are

zz If so, whether it is a central or peripheral disorder?

zz What is the probable etiology?

zz What is the best possible treatment?

1.indd 1 9/7/2015 3:55:23 PM

(subjective), or of the environment (objective), or sense of

is the patients feel that they or their environments are moving.

patient with respect to his environment. The patient feels that

an individual to feel unsteady when standing or walking and

1.indd 2 9/7/2015 3:55:23 PM

less or significantly longer. And of course the prolonged can last

—— Prolonged—weeks to months or forever.

The sensation of rotation most commonly arises from a problem

Remember during Managing the Vertigo Patients

1.indd 3 9/7/2015 3:55:23 PM

zz Judicious use of newer technology: Videonystagmography

Prevalence of Vertigo in Community

QUALITY OF LIFE IN VERTIGO PATIENT

zz Drug side effects.

zz 3Fs syndrome (Fear of frequent falling).

There is always a need to develop a systematic, efficient and

1.indd 4 9/7/2015 3:55:23 PM

The ability to maintain balance is essential to nearly all activities

2.indd 5 9/7/2015 3:55:10 PM

Figs 2.1A and B Inner ear and its parts

2.indd 6 9/7/2015 3:55:10 PM

Fig. 2.2 Vestibular nuclei and their connections (Vestibular pathway)

moves sideways. The utricle and saccule sense gravitational

2.indd 7 9/7/2015 3:55:11 PM

(nucleus of Deiters). Superior nucleus is situated at pons. Inferior

BASIC PHYSIOLOGY OF BALANCE DISORDER