Review Article

Vertigo and Dizziness — A Clinical Approach

A Mukherjee*, SK Chatterjee**, A Chakravarty***

Abstract
Dizziness is a term which is used to describe a variety of sensations. It is possible to group these
complaints into four types : a rotational sensation (Type I dizziness), impending faint (Type II dizziness),
dysequilibrium (Type III dizziness) and vague lightheadness (Type IV dizziness). Type I dizziness or
vertigo is due to disease of the vestibular system - peripheral or central, and is characterized by a feeling
of movement relative to one’s surrounding. The majority of dizzy patients, however, belong to Types II,
III and IV, collectively called the non-vestibular system disorders. The distinction is usually possible by
a detailed history and clinical examination, but some special bedside tests - the dizziness simulation
battery - are often required for properly distinguishing the various types of dizziness. Important causes
of vertigo and the non-vestibular system disorders have been discussed with focus on benign positional
vertigo, acute peripheral vestibulopathy, Menieres’ disease, toxic damage to labyrinths, perilymph fistula,
cerebrovascular disease, multiple sclerosis, cerebellopontine angle tumors, basilar migraine, vestibular
epilepsy, cervical vertigo and phobic postural vertigo.

INTRODUCTION is spinning. Vertigo is often accompanied by nausea, vomiting,

and a straggering gait. Oscillopsia, a visual hallucination of
T he perception of our head and body positions and
motions in space depend on fundamental types of
information provided by five sensory modalities : vision,
rotational movements of the environment, may occur. The
onset of vertigo is often instantaneous, and patients
sometimes describe a sensation of being hurled to the ground.
vestibular sensation, joint position sense, touch-pressure Whenever the patient’s dizziness is exclusively rotational, it
sensation, and hearing. These inputs are integrated in the is due to a disorder of the vestibular system : either the
central nervous system. Disturbances of any of these peripheral labyrinth or its central connections. Because of
information or of the integration there of result in a number of this close relationship, it is important to separate definite
uncommon sensations that are not part of daily experience. rotational vertigo accurately from other types of dizziness. It
Patients affected with such problems frequently complain of is extremely important to elicit this ‘dynamic’ component in
“dizziness”. Although they may suffer from a variety of the patient’s symptomatology.
symptoms, it is the thread of unfamiliar spatial disorientation
that binds these complaints together. Patients can use a Type II dizziness is a sensation of impending faint or loss
number of words to convey this sense : giddy, fainting, or consciousness. Pallor, dimness of vision, roaring in the
vertiginous, floating, light-headed, unsteady, clumsy, off- ears, and diaphoresis, with recovery upon assuming the
balance, swaying, spinning are few of the commoner ones. recumbent position, are common, Type II dizziness of
However, it is possible to group these complaints into four cardiovascular origin is of abrupt onset and short duration.
types; a rotational sensation, impending faint, dysequilibrium, When faintness is gradual in onset or persists despite lying
and vague lightheadedness. down, hypoglycemia or other disorders of cerebral metabolism
should be sought.
TYPES OF DIZZINESS The complaint of impending faint usually implies an
Type I dizziness is a definite rotational sensation (vertigo) inadequate supply of blood or nutrients to the entire brain,
in which the patient feels that either he/she or the environment such as occurs in postural hypotension. It is not a feature of
focal cerebral ischaemia.
Sudden alteration in the state of consciousness (“dreamy
*Reader; ***Professor and Head, Department of Neurology,
states”) may be due to temporal lobe seizures, occurring in
Vivekananda Institute of Medical Science, Kolkata. **Associate the absence of other, more obvious seizure phenomena.
Professor, Department of Medicine, BS Medical College, Bankura, Type III dizziness or dysequilibrium is loss of balance
West Bengal.
Received : 19.10.2002; Revised : 23.8.2003; Accepted : 12.9.2003
without an abnormal sensation in the head. This experience

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occurs only when the patient is walking and disappears upon or distractions, it is likely to be of psychological origin.
sitting down. It is due to a disorder of motor system control. Associated alterations in consciousness clearly implies a
Type IV dizziness is vague lightheadedness other than syncopal element and excludes an organic VSD. Although
vertigo, faintness or dysequilibrium. This designation pure hypoperfusion of the brain-stem due to any cause
includes dizziness that cannot be identified with certainty as secondary to hypotension can cause true vertigo, this is
any of the other types. When patients complain of usually associated with altered levels of consciousness and
lightheadedness, fractional or poorly described symptoms therefore fall under the category of NVDs. Relation of the
of vertigo, faitness or dysequilibrium must first be looked for, giddiness to meals may reveal hypoglycaemia or the early
e.g., a rocking sensation instead of spinning. This is often postprandial dumping syndrome.
aided by testing with the dizziness simulation battery The general physical examination is often not helpful but
described later. Evidence of hyperventilation symptoms BP measurement for asymmetry, orthostatic change, cardiac
should next be sought, as well as symptoms pointing to a irregularity and neck bruits are often detectable. A ‘sharpened
psychiatric disorder, particularly depression, anxiety, panic Romberg’ test is often very useful to exclude organic neural
states or agoraphobia. Finally, the evidence for multiple disease.1 This test comprises of standing tandem with eyes
sensory impairment should be examined, especially peripheral closed on either leg with arms folded across the chest for 30
neuropathy, cervical spondylosis, or visual impairment in an seconds. If an individual can perform this test it almost
elderly or diabetic patient. excludes organic neurologic disease.
The term vertigo seems to be much more specific to a A proper psychiatric and cognitive function test is
disorder of the vestibular balance system comprising of the essential in such dizzy patients although panic and anxiety
inner ear, vestibular nerve, brain stem, cerebellum and often often accompanies the organic vestibular disorders as well.
including the eyes and the neck proprioceptors. The most A new term ‘perceptual dizziness’ is much talked about these
important character is its ‘movement’ or its dynamic aspect. days.2 It encompasses the idea that the cortex plays a primary
So the most important task a neurologist has is to question role in integrating all sensory inputs and preparing and
the dizzy patient to bring out the sole fact of whether his response to it. In this task it frequently has to suppress some
problem has a component of movement in it or not. This information or increase the gain of another system. Any
alone distinguishes between two major groups of disorders - disorder in the ability of this function of the cortex to select
the vestibular system disorders-VSDs and the non-vestibular appropriate or reject inappropriate balance information may
system disorders - NVDs. result in the feeling of dizziness where no physical finding is
Once this distinction is achieved the task is much easy seen and neuro-otologic tests are normal. This form of
thereafter. The NVDs have large number of disorders in the dizziness probably occurs in the vast majority of patients
causative list but most of the patients have no detectable who complain of feeling dizzy following minor head trauma.
pathology and comprises almost 70-80% of dizzy patients This is certainly not true vertigo. Two other forms of NVDs
coming to a doctor. In this brief review we would like to deal seem worth mentioning in this context. The first is ‘cervical
a little about these NVDs and non-vertigo patients, before vertigo’ associated with neck (not body) movements. It is
embarking upon the true vertigo patients with some disorder too commonly seen in clinical practice to ascribe any form of
in their balance apparatus. loss of balance to cervical spondylosis specially in older
patients on the belief that vertebro-basilar insufficiency occurs
THE NON-VERTIGO DIZZY PATIENTS - THE in these individuals due to compression of vertebral arteries
NVD S in the neck. The literature had never been very clear about
this concept and the authors feel that cervical spondylosis is
The majority of dizzy patients presenting to a doctor falls too often made a ‘scapegoat’. Vertebrobasilar insufficiency
in this category. They describe their symptoms in various should better not be diagnosed unless the vertigo-dizziness
words but usually lack the rotatory component of movement is accompanied by other brainstem signs/symptoms.
either of self or of surroundings and do not have associated Dizziness (true vertigo unlikely) in such individuals mostly
features of nausea, vomiting etc. Giddiness is a favourite result from abnormal proprioceptive stimuli from diseased
term used by these patients, who on enquiry may be found to neck joints resulting in a mismatch at the final integrative
have antecedent history of other medical diseases, head or level. Such a situation also arises following neck injuries
neck injury, significant life stress or medications. specially of the whiplash variety.
Hypertension, diabetes, heart and lung diseases, Brandt and Dieterich3 described a syndrome of phobic-
endocrine disturbances and full check list of drugs used are postural vertigo which is distinguishable from agoraphobia
most important things to ask about. The behavior of the (fear of open space) and acrophobia (fear of heights). It is
symptoms with either exercise or valsalva maneuver often characterized by the combination of initial vertigo with
can give a clue to the diagnosis. Intracranial SOL, heart disease subjective postural and gait instability and the fear of
and hypotension are likely to worsen with valsalva, while impending death. Patients complain of vertigo rather than
cardiopulmonary disorders will result in exacerbation of the anxiety and feel physically ill. The illusory perception (vertigo)
symptoms with exercise. If symptom decreases with exercise can be explained by the hypothesis that an impairment of the

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 Table 1 : Non-Vertigo Dizziness - Causes EVALUATING THE DIZZY PATIENT
Cardiac / Vascular Non-Cardiac The history should explore four major questions that
Valvular heart disease Anaemia
distinguish the disorders producing dizziness :
Tachy Hyperviscosity
Arrhythmias 1. The type of dizziness (I to IV)
Brady
2. The abruptness of attacks or continuity of symptoms.
Heart failure Hypo- and hyperglycaemia
Carotid sinus hypersensitivity Hyperventilation 3. The relation or independence of dizziness to position or
Hypotension from any cause Medications and toxins motion (standing/sitting/lying; sudden change in
Miscellaneous position; walking)
Anxiety, phobias, depression
Perceptual or cortical disorders 4. The age of the patient.
e.g. post-head injury A good neurological examination is the cornerstone for
establishment of the site of lesion and guides our
space-constancy mechanism in these patients leads to partial investigations appropriately. The VSDs in contrast to the
uncoupling of the efferent copy for active head movements. NVDs at least provide one physical sign to identify itself
A short list of NVDs causing dizziness is given in Table 1, during physical examination - Nystagmus. In some patients
but the list is far from exhaustive. secondary to compensation, this sign may be masked. There
the use of ‘Frenzal glasses’ which impair the patients ability
THE PATIENT WITH VERTIGO - THE VSDS to fixate, (but still allows the examiner to observe the patient’s
eye motion), brings out the nystagmus. Another crude but
True vertigo has been variously described but the essence
very useful method of activating nystagmus is by vigorous
of all description is its dynamic nature - an illusion of
head-shaking. This often increases or results in emergence
movement with respect to one’s surrounding space. In most
of nystagmus in patients with VSDs whose signs are well
cases it has a rotatory component. A patient with vertigo
compensated. This is mostly true of central VSDs. Nystagmus
usually has the perception of movement with respect to a
is so vital in VSDs that if it is absent (while patient complaining
stationary state, i.e. either the person is moving with the
of vertigo) when observed with Frenzel’s glasses, the patient
surrounding static, a condition called subjective vertigo, or
with vertigo can safely be stated to have a psychogenic origin
vice-versa when it is called objective vertigo. However these
for the symptom.
distinctions are of no localizing value.4 Another clinically
distinguishing feature is its incapacitating effect on the A neurological examination usually allows the distinction
patient, who is almost bed-bound at least in the beginning between central and peripheral causes of dizziness, and may
and is accompanied by anxiety, nausea and vomiting. The reveal certain pattern of involment that point to the diagnosis;
patients with NVDs who continue complaining of dizziness e.g. brainstem syndrome, cerebellopontine angle syndrome,
however may be seen to carry out normal life activities despite multiple sensory impairment. A neuro-otologic evaluation
having their problem. should include tests of hearing and of vestibular function.
A brief history on confronting a patient with vertigo is Electronystagmography (ENG) may help to identity and
helpful in a big way in directing our search for the cause. distinguish disorders of the peripheral (labyrinth, eighth
Sudden onset of symptoms, episodic nature, and relatively nerve) and central vestibular systems. Recording of the
short duration of symptoms, localizes the lesion to the inner amplitude, speed, and duration of ocular movements is first
ear, particularly if there are associated features of tinnitus, made during a series of eye and head position maneuvers. In
hearing loss and violent nausea and vomiting. In general, the caloric test the patient is positioned so that the horizontal
continuous symptoms implies a CNS origin. Increase in semicircular canals are exactly vertical, and each ear is irrigated
vertigo with change of position or with eye closing is with cool and warm water (or air) to produce a convection
characteristic of all VSDs and is of no localizing value, however flow of endolymph, which mimics rotational stimulation of
if symptoms occur only in certain positions of head, it each canal. Observations on the speed, duration, and
suggests otolith dysfunction. Vertigo exacerbated by loud morphology of the nystagmus generated by this test provide
noise and valsalva maneuver denotes a peripheral inner ear information on the function of the vestibular apparatus and
disorder with a perilymphatic fistula (the Otolith - Tullio its central connections.
phenomenon).5,6 Audiometric studies are used to evaluate lesions of the
A history of unaccustomed activity like mountain climbing, middle ear, labyrinth, and cochlear nerve, particularly in
scuba diving or even holiday in a beach resort with sea- Meniere’s disorder and cerebellopontine angle tumours.
bathing, is often found in some patients with persistent Routine pure tone audiometry indicates the presence or
vertigo for a few days. It results from barotrauma. absence of a hearing loss and may also distinguish banal
causes (acoustic trauma, aging, otosclerosis) from specific
Other symptoms relating to the CNS, like visual disturbance
cochlear and nerve disorders. More elaborate “site of lesion”
(specially diplopia), motor or sensory problems, headache
studies, such as the speech discrimination, alternate binaural
etc. are often ‘fellow travellers’, suggestive of extra-vestibular
loudness balance (ABLB), and acoustic reflex tests, improve
brain stem problem.

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the accuracy of diagnosis; brainstem auditory evoked Table 2 : Positional vertigo and nystagmus
response (BAER) testing is useful in distinguishing between Peripheral or Central or
brainstem and peripheral disorders. benign malignant
Dizziness Simulation Battery 1. Latency Usual Unusual - vertigo and
This is a series of eight bedside maneuvers that have nystagmus starts
immediately.
proven valuable in distinguishing the various types of
2. Appearance Torsional, upbeat Pure vertical, usually
dizziness. Some produce dizziness in all patients, whereas or horizontal downbeat
others induce it only in patients with underlying disorders. geotropic
After each maneuver the patient is questioned as to the 3. Fatigue Usual Unusual
similarity of test-evoked sensation to his own dizziness. 4. Vertigo and Severe Mild
systemic
Identification of a provoked sensation as identical to the
symptoms
patients dizziness is often more reliable than a verbal 5. Localization Posterior or Brainstem or
description, particularly if a single maneuver exclusively horizontal cerebellum
reproduced the symptoms. semicircular canal
1. Orthostatic hypotension : Blood pressure is measured
supine, immediately on standing, and after three minutes. (BPPV) is probably the most frequent cause of vertigo,
2. Potentiated Valsalva maneuver : The patient squats for accounting for about 25 per cent of patients with this
30 seconds, then stands and strains against a closed complaint. The patient experiences a sensation of spinning
glottis, or blows into a mercury sphygmomanometer, when rolling over in bed or making other sudden head
raising the column to 40 mmHg for 15 seconds. movements. Symptoms are often greatest when the patient
lies on the side with the affected ear underneath. The vertigo,
3. Carotid sinus stimulation : The carotid sinus is
sometimes accompanied by nausea and vomiting, lasts for
unilaterally massaged for 15 seconds without continuous
less than five minutes, and between episodes the patient is
compression of the artery.
free of symptoms. This condition, brought about only on
4. Neck twist : The patient rotates the head in each direction change of position, differs from other vestibular disorders in
for 15 seconds. Dizziness may result from vestibular which vertigo is increased by head motion but is present at
disorder or cervicogenic dizziness. other times as well. Benign positional vertigo occurs at any
5. Walking and turning : The patient walks in one direction time during adult years; the cause is usually obscure, although
and then quickly turns, reversing direction. This test it occasionally follows head trauma. The diagnosis is based
reproduces dizziness occurring with multisensory deficits, on the typical history and on finding the “benign” type of
gait apraxia, and disorders of balance. vertigo and nystagmus on performing the Nylen-Barany
6. Hyperventilation : The patient breathes deeply for three maneuver (Table 2). This condition must be distinguished
minutes. from so-called “central” or “malignant” positional vertigo
and nystagmus (Table 2), which may occur with lesions
7. Nylen-Barany maneuver : The examiner carries the
(tumours, infarcts) involving posterior fossa structures;
patients head backward from a seated position, so that it
benign positional vertigo may be uncommonly associated
is hanging 45 degrees below the horizontal and turned
with such conditions.
45 degrees to one side. Vertigo accompanied by
nystagmus indicates positional vertigo. The Typical posterior canal BPPV is caused by canalolithiasis,
characteristics distinguishing a “benign” from a a free floating clot within the endolymph on the posterior
“malignant” form of this condition are listed in Table 2. semicircular canal. Some workers have hypothesized that
immune complexes in the inner ear have an influence on the
8. Barany rotation : The patient is seated in a rotating
macular organ and cause the otoconia to dislodge more
chair, head tilted 30 degrees forwards from the vertical.
easily.7
The examiner spins the patient in one direction ten times
within 20 seconds, then abruptly stop this rotation. Acute Peripheral Vestibulopathy ( Acute Labyrinthitis ;
Vestibular Neuronitis ) : This condition is defined as a single
A flow chart showing major pathways of approaching a
bout of spontaneous vertigo, lasting for hours or days.
dizzy patient is provided in Table 3.
Attacks occasionally follow a trivial respiratory or other
A brief resume of important conditions producing true infection, but the relation is not clear. Symptoms of vertigo,
vestibular vertigo follows. It is most important to distinguish nausea, and vomiting usually improve within 48 hours, but
between periperal (labynthine) abnormalities and those may persist for seven to fourteen days. On examination the
involving central vestibular connection. The key to this patient appears acutely ill, often pale and diaphoretic,
distinction is the neurologic evidence for or against resisting motion of the head. Nystagmus invariably
involvement of neighbouring brainstem structures. accompanies the vertigo. As recovery takes place the patient
may feel “off balance” for weeks or months owing to unilateral
PERIPHERAL CAUSES OF VERTIGO impairment of vestibular function, present in about 50 per
Benign Positional Vertigo : Benign positional vertigo cent of patients. Hearing is not impaired in this condition.

1098 JAPI • VOL. 51 • NOVEMBER 2003

 Several lines of evidence favour a viral hypothesis e.g. impairment of vestibular function, resulting in the syndrome
temporal bone pathology in patients with vestibular of vestibular imbalance. In many patients the recurrent
neuronitis or the wide spread detection of herpes simplex episodes of vertigo may “burn out” over the years.
virus type 1 DNA in human vestibular ganglia and nuclei.8 Diagnosis depends on the characteristic history and the
Some cases of acute rotational vertigo without hearing audiometric findings (low frequency pure tone impairment,
impairment are caused by unilateral central vestibular lesions poor speech discrimination comparable to the pure tone
in the pontomedullary brainstem.9 hearing loss, and recruitment). Caloric testing demonstrates
Acute and Recurrent Peripheral Vestibulopathy : Acute abnormal vestibular function in 80 percent of patients.
and recurrent peripheral vestibulopathy is clinically similar Pathologic studies have identified distention of the
to the entity described above, but consists of repeated bouts membranous labyrinth with endolymph as the immediate cause
of vertigo occurring over a period of months or years. This of this condition, but the explanation for the excess of
condition occurs in an older age group than acute peripheral endolymph remains obscure.
vestibulopathy, and is associated with less severe vestibular
In recent years, numerous papers have discussed the
impairment on caloric testing. Approximately half the patients
possibility of an immunological, infectious, vascular or genetic
presenting with a single attack of peripheral vestibulopathy
pathogenesis.
experience a recurrence linking this with the previous
condition. The absence of auditory impairment distinguishes Toxic Damage to the Labyrinths : Drugs of the
this condition from Meniere’s disorder. aminoglycoside group (e.g., streptomycin, gentamicin,
amikacin) may produce toxic damage to the peripheral
Meniere’s Disorder : Meniere’s disorder is widely
vestibular apparatus. Although toxicity is generally dose-
considered to be one of the most frequent causes of dizziness,
related, some patients develop labyrinthine damage after brief
but actually accounts for only about 5 percent of all dizziness
treatment with ordinary doses of these drugs, particularly if
and 10 to 15 per cent of vertigo. It usually occurs in adults
renal function is impaired. Tinnitus, hearing loss, or vertigo
and consists of recurring bouts of vertigo associated with
may be the presenting symptom, along with severe impairment
hearing loss and tinnitus which may precede or follow the
of balance, nausea, and vomiting. Vertigo continues for days
first bout of vertigo. Patients often complain of “fullness” in
or weeks. If the ototoxic drug is immediately discontinued,
the ears, and are sometimes aware of recruitment as a
damage to the labyrinth is usually arrested. A characteristic
sensation of auditory discomfort produced by loud noises.
loss of balance follows the acute stage of vertigo and may
Bouts of vertigo last from hours to days, recurring as often
include blurring of vision on motion owing to loss of the
as every week or as infrequently as every ten years. Hearing
vestibulo-ocular reflexes. With the loss of vestibular
loss is unilateral in 80 to 90 percent of patients, with a severe
sensation, these patients are dependent on visual cues to
deficit in half the patients. Most patients develop chronic

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maintain balance, and are unable to walk in the dark. After rarely does acute spontaneous vertigo occur. Hearing loss,
several months, adaptation to the loss of vestibular sensation tinnitus, facial numbness or weakness and cerebellar ataxia
develops, and many can lead fairly normal lives. complete the picture. Unilateral or bilateral acoustic neuromas
Perilymph Fistula (PF) and Superior Canal Dehiscence are especially common in von Recklinghausen’s disease
Syndrome : PF may lead to episodic vertigo and sensorineural (neurofibromatosis).
hearing loss as a result of pathological elasticity of the otic Basilar Migraine : In vertiginous migraine,vertigo may
capsule or leakage of the perilymph, usually at the oval or occur preceding the headache, during the headache phase,
round window. The fistula and the partial collapse of the or as a “migraine equivalent” in place of the headache. Since
membranous labyrinth permit the abnormal transfer of ambient both migraine and vertigo are common conditions, the
pressure changes to the maculae or capolae receptors. PF occurrence of vertigo without a constant time relation to
may be caused by barotraumas or e.g. cholesteotoma, in headache may represent only a coincidence in some
which case the horizontal canal is most often involved. The unfortunate patients. The diagnosis should be considered
clue to diagnosis is precipatation of vertigo by acts of straining only when vertigo is accompanied by other brainstem signs/
and can be simulated by asking the patient to perform the symptoms (e.g. diplopia) and associated with headache.
valsalva maneuver. Vestibular Epilepsy : It is a rare cortical vertigo syndrome
A new type of PF is the superior canal dehiscence secondary to focal epileptic discharges in either the temporal
syndrome caused by dehiscence of bone overlying the lobes or the parietal association cortex. Scanty information
superior (anterior) canal.10 As a result on this dehiscence a is available on this condition in recent literature and great
third mobile window is formed and changes in pressure are care need be taken to diagnose this condition. A new clinical
pathologically transduced to the anterior canal. The condition sign of vestibular epilepsy is skew deviation of eyes with
is diagnosed by high resolution temporal bone computed nystagmus during attacks.11
tomography which demonstrates the defect of the bone
overlying the superior semicircular canal. TREATMENT OF VERTIGO
Treatment of vertigo consists of symptomatic relief and
CENTRAL CAUSES OF VERTIGO treatment of the underlying disease. Central causes of vertigo
Cerebrovascular Disease : Cerebrovascular disease like cerebrovascular disease, multiple sclerosis or cerebello-
produces vertigo when basilar-vertebral artery ischemia pontine angle tumours require urgent institution of specific
damages the vestibular nuclei or their connections. In treatment. In vertigo due to peripheral causes, symptomatic
virtually all cases injury to adjacent brainstem structures treatment tends to get more importance. This is usually done
occurs, and vertigo is unlikely to be due to a stroke when only with drugs and less attention is given to other treatment
other neurologic symptoms or signs are absent. modalities. In a patient with acute or recurrent vertigo due to
Transient ischemic attacks producing vertigo may be peripheral cause it is important to see that appropriate
particularly difficult to diagnose, because at the time of symptomatic treatment is advised and potentially treatable
examination the patient may have recovered completely. They causes are not missed.
rely on a history of neighborhood brainstem symptoms, such Any patient with vertigo should be advised to take bed
as diplopia, dysarthria, weakness or clumsiness of the limbs. rest and avoid sudden head movement in the initial stage.
Multiple Sclerosis : Multiple sclerosis may produce Vestibular suppressant medicines including antiemetics,
vertigo in young patients, although this condition accounts antihistamines and other drugs are given. They should
for no more than 5 percent of acute vertigo in those below however be prescribed over a limited period of time following
age 40. an acute vestibular lesion. Chronic use is not advocated as it
probably retards the process of central vestibular
Further, although multiple sclerosis may begin with vertigo,
compensation.
this is far less common than onset with optic neuritis or
paresthesias. A process of rehabilitation should be started after the
acute phase and this includes vestibular rehabilitative
Vertigo associated with ocular motor disorders that cannot
exercise. Vestibular suppressants and other central
be caused by purely peripheral vestibular disease (e.g.
depressant medicine should be discontinued as both can
persistent diplopia, median longitudinal fasciculus syndrome,
interfere with the adaptive plasticity considered the basis for
ophthalmoplegia) is strongly suggestive of this condition.
successful rehabilitation. Patients must be motivated to
Cerebellopontine Angle Tumors : Cerebellopontine angle experience discomfort during the early stage of rehabilitation,
tumors are a rare cause of vertigo, but must not be overlooked with the expectation that they will benefit from markedly
early in their growth when they are readily removable. The reduced (or absent) symptoms later. The very movements
large majority are benign acoustic neuromas arising in the that precipitate dizziness should be encouraged, rather than
internal auditory meatus. These tumors develop in middle- avoided.
aged patients who experience vague unsteadiness that
Benign paroxysmal pontronal vertigo should be treated
progresses over a period of years. Vertigo when present may
with canalith repositioning procedure (Epley maneuwer). A
be of the “malignant” positional type (Table 1), and only
properly performed maneuver cures the disorder in 50%-80%
1100 JAPI • VOL. 51 • NOVEMBER 2003
cases of posterior canal BPPV. Schwinkscheoindel. Munchener Medizinische Woehenschift
1986;128:247-50.
Conservative medical management for Meniere’s disease
consists of low salt diet and treatment with a diuretic. 4. Smith D. Dizziness - A clinical perspective. Neurol Clin
1990;8:199-208.
For refractory cases in which the offending ear has been
5. Dieterich M, Brandt T, Fries S. Otolith function in man -
unequivocally determined, ablative therapy can be
Results from a case of Otolith-Tulio Phenomenon. Brain
considered. Destruction of the inner ear via a labyrinthectary 1989;112:1377-92.
result in hearing loss. Selective sectioning of the vestibular
6. Brandt T. Vertigo - a systematic approach. In Recent Advances
portion of the VIII th nerve ( vestibular neurectomy ) usually in Clinical Neurology g. Ed. Kennard C. 1990;69-84.
spares hearing. Chemical labyrinthotomy in which gentamicin
7. Modugno GC, Pirodda a, Ferri GG, et al. A relationship
injections are made into the middle ear, has recently been
between autoimmune thyroiditis and benign paroxysmal
shown to be effective, with hearing preserved in most cases. positional vertigo ? Med Hypotheses 2000;54:614-15.
Rare, but surgically treatable causes of peripheral vertigo 8. Abrusow V, Schulz P, Strupp M. Distribution of herpes simplex
like perilymphatic fistula and newly recognized superior virus type 1 in human geniculate and vestibular ganglia :
semicircular canal dehiscence syndrome, should be kept in implications for vestibular neuritis. Ann Neurol 1999;46:416-
mind and looked for by appropriate tests. 19.
9. Sdtrupp M, Brandt T. Vestibular neuritis. Adv Otorhinolaryngol
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Announcement
4th Congress of the Asian Pacific Society of Atherosclerosis and Vascular Disease, Bali,
Indonesia, to be held from May 6-9, 2004.
For details contact : Dr Slamet Suyono, MD, Pacto Convex Ltd., Lagoon Tower Level B-1, Jagarta Hils
International, Jl Gatot Subroto, Jakarta 10270, Indonesia.
Fax : 62-21 5705798; E-mail : pactoltd@idola.net.id

Sd/-
RB Singh

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