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Evaluation and management of the dizzy patient

Article  in  Journal of Neurology, Neurosurgery, and Psychiatry · January 2005

DOI: 10.1136/jnnp.2004.055285 · Source: PubMed

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 EVALUATION AND MANAGEMENT OF
THE DIZZY PATIENT
L M Luxon
iv45

J Neurol Neurosurg Psychiatry 2004; 75(Suppl IV):iv45–iv52. doi: 10.1136/jnnp.2004.055285

B
alance in man is a sophisticated and complex mechanism comprised of sensory inputs from
the vestibular apparatus, vision, and proprioception. These pass into the central nervous
system (CNS), are integrated and modulated by activity of the cerebellum, the
extrapyramidal system, the limbic system, and the cerebral cortex, and provide perception of
head and body position in space, eye movement control, and appropriate static and dynamic
postural function. Alterations in the sensory inputs, integrating mechanisms, or effector organs
can result in the perception of dizziness or vertigo, disordered eye movements and disequilibrium,
or instability. A wide variety of pathological processes may give rise to dizziness, such that
patients present to many different specialists, but most commonly to the ear, nose, and throat
(ENT) or neurology departments (table 1).
Dizziness is extremely common, both in primary care and at the tertiary level, and by the age of
60 years, one third of the population has suffered from a balance disorder. While in primary care
many cases of dizziness resolve spontaneously, in tertiary care dizziness is commonly associated
with significant morbidity and, in the older population, if compounded by falls, mortality. Thus, a
clear diagnostic strategy including a detailed neuro-otological examination, as outlined in the
previous article, is essential if an accurate diagnosis is to be made. Diagnosis is key to the
rehabilitation and management of the dizzy patient.
Three main groups of disorders giving rise to disequilibrium can be identified—general medical,
neurological, and otological—with a few other disorders such as visual vertigo, cervical vertigo,
and the multisensory dizziness syndrome in the elderly, falling outside this classification. A
detailed history and examination, as outlined in the preceding section, will usually point the
examiner in the correct direction for appropriate investigation. Inevitably there is some overlap
(fig 1), in as much as diffuse cerebrovascular disease may produce both neurological and neuro-
otological abnormalities, while general medical disorders, such as diabetes mellitus and
autoimmune syndromes, may give rise to both labyrinthine and/or central vestibular dysfunction.
Patients with persistent dizziness/vertigo/disequilibrium and evidence of vestibular dysfunction
on standard vestibular tests (see Davies, p iv32) fall into two main categories: those with specific
diagnoses (for example Menière’s disease and benign positional paroxysmal vertigo), for whom
there are standard established treatment regimens, and those with peripheral labyrinthine
pathology, in whom spontaneous adequate vestibular compensation does not take place, and
chronic vestibular symptoms become the overriding clinical presentation requiring management.
The scope of this article does not allow detailed consideration of visual, neurological or general
medical causes of dizziness, and will concentrate on the management of patients with peripheral
vestibular disorders and the general strategy for managing patients with neurological disorders
manifesting with vertigo.

c PERIPHERAL VESTIBULAR DISORDERS AND COMPENSATION

Epidemiological studies providing data on causation in ‘‘the dizzy patient’’ all highlight the
overriding importance of peripheral vestibular pathology, whether the patients present to an
otolaryngologist or a neurologist. The balance system in humans has a remarkable capacity to
adapt and to learn new behaviours, and this is characterised by the rapid symptomatic recovery
following peripheral vestibular pathology, referred to as ‘‘vestibular compensation’’. This is the
collective term given to a variety of processes including adaptation/habituation, leading to
recalibration of the gain of the vestibular reflexes and substitution of both sensory inputs and
_________________________
motor responses, together with alteration of strategies used for balance (fig 2). This process is
Correspondence to: independent of the causation of vestibular dysfunction, and the components of vestibular
Professor Linda M Luxon,
Academic Unit of Audiological compensation vary in their efficacy in facilitating symptomatic recovery of perception, oculomotor
Medicine, Institute of Child and postural stability from subject to subject. Thus, some patients recover stability with no head
Health, 30 Guildford Street, movement induced vertigo, but may suffer from pronounced visually induced dizziness, while
London WC1 1EH, UK;
l.luxon@ich.ucl.ac.uk others experience pronounced instability, but little disordered perception of imbalance (that is,
_________________________ dizziness).

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 NEUROLOGY IN PRACTICE

Table 1 Causes of dizziness spontaneous nystagmus with the fast phases directed away
from the affected ear, and postural instability (ataxia). These
General medical Otological
symptoms are related to the differences in the levels of tonic
c Haematological c Menière’s disease
Anaemia
activity in the central vestibular nuclei, resulting from the
c Post-traumatic syndrome
Hyperviscosity vestibular pathology. Static oculomotor recovery is a robust
c Positional nystagmus
Miscellaneous c Vestibular neuronitis
process that starts 3–4 hours after the onset of the lesion, and
iv46 c Cardiovascular c Infection is complete in a few days. It occurs in parallel with the
Postural hypotension c Otosclerosis and Paget’s disease reappearance of resting neural activity in the ipsilateral
Carotid sinus syndrome c Vascular accidents vestibular nuclei and ‘‘rebalancing’’ of the vestibular nuclei.
Dysrhythmia c Tumours Postural recovery, on the other hand, appears to rely more on
Mechanical dysfunction c Auto-immune disorders propriospinal mechanisms. Dynamic symptoms are conse-
c Metabolic c Drug intoxication
quent upon abnormalities of the gain, symmetry, and phase
Hypoglycaemia
Hyperventilation of the vestibular reflexes, and recovery continues over
Neurological Miscellaneous months or years, being faster for postural than for oculo-
c Supratentorial c Ocular motor symptoms.
Epilepsy c Cervical
Syncope c Multisensory dizziness syndrome FAILURE OF COMPENSATION AND
Psychogenic
DECOMPENSATION
c Infratentorial
Multiple sclerosis The majority of patients will ‘‘compensate’’ and function
Ischaemia virtually normally within six weeks to six months following a
Infective disorders peripheral vestibular disorder, although this symptomatic
Degenerative disorders
Tumours recovery does not parallel recovery of vestibular function.
Foramen magnum abnormalities Some patients demonstrate incomplete resolution of symp-
toms, with persistent failure of recovery from the initial
event, while other patients recovery normally, but then
demonstrate recurrent episodes of decompensation, with
Damage to the vestibular elements of the peripheral episodes of vertigo interspersed with periods during which
labyrinth results in a characteristic syndrome of acute vertigo, they are asymptomatic. The reasons for incomplete

Figure 1 Outline strategy for management of vertigo. Reproduced with permission from Luxon LM, Davies RA, eds. Handbook of vestibular
medicine. London: Whur Publishers, 1997.

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iv47

Figure 2 Diagram of the natural history of peripheral vestibular pathology. Reproduced with permission from Luxon LM, Davies RA, eds. Handbook
of vestibular medicine. London: Whur Publishers, 1997.

asymptomatic recovery may be single or multiple (fig 3), and TREATMENT OF THE VESTIBULAR PATIENT
evaluation of these factors is crucial in the management of a Successful management of the patient with dizziness
patient with a peripheral vestibular disorder (see Davies, depends upon accurate diagnosis, an understanding of
p iv32) and persistent chronic symptomatology. The most vestibular physiology, appropriate intervention strategies,
common causes of failure of compensation are psychological and the physician’s awareness of the overlap between
disorders, impairment of the other sensory inputs required vestibular, autonomic, and psychological aspects of vestibular
for balance (vision/proprioception), use of drugs with action pathology.
upon the central nervous system (importantly including Appropriate management for the dizzy patient of vestibular
vestibular suppressant drugs), and co-morbid systemic pathology results in the ability to control and coordinate eye,
disorders. head, and body movements in order to maintain gaze,

Figure 3 Factors affecting compensation. Reproduced with permission from Luxon LM, Davies RA, eds. Handbook of vestibular medicine. London:
Whur Publishers, 1997.

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 NEUROLOGY IN PRACTICE

stability, and posture. Management also aims to achieve dizziness, prevent vomiting, and promote vestibular compen-
appropriate vestibular perception without adverse symptoms, sation, but currently no such drug is available.
despite the persisting dynamic asymmetry in the gain of The drug treatment of a vestibular disorder is initiated for
vestibular reflexes. Evaluation and efficacy of intervention one of three main reasons:
are often difficult due to the dysynchrony between vestibular c treatment of the acute vestibular symptomatology

symptoms and signs and vestibular test results, and treat- c specific treatment of a condition that causes vestibular

iv48 ment should include validated psychological questionnaires symptoms—for example, Menière’s disease, migraine or
(in view of the high prevalence of psychological disorders in epilepsy
c non-specific but empirical treatment of a chronic vestib-
patients with chronic vestibular symptoms), together with
ular disorder—for example, central vestibular symptoma-
questionnaires evaluating vestibular symptomatology, dis-
tology.
ability, and handicap. Objectively, posturography results may
provide direction for intervention in terms of balancing
Symptomatic treatment of acute vestibular episode
strategies, and additionally provides objective quantification
Symptoms of vertigo, nausea, vomiting, sweating, pallor, and
of increasing stability.
diarrhoea are extremely alarming and debilitating to a
There are five main arms of management intervention:
patient, who commonly suspects that the symptoms are life
c general medical evaluation, with correction/amelioration
threatening. The initial step in the management of such a
of associated morbid conditions
patient must to be reassure and explain the nature of the
c pharmacological intervention
symptoms, together with providing hydration if necessary.
c vestibular rehabilitation with physiotherapy and specific
Antiemetics should be administered—for example, hyoscine,
physical manoeuvres for the management of benign
prochlorperazine, promethazine, cyclizine, dimenhydrinate,
positional paroxysmal vertigo
and metoclopromide—orally if feasible, intramuscularly, as a
c psychological intervention
c surgery.
suppository, or via the buccal membrane. Hyoscine adminis-
On the basis of the diagnosis, an appropriate rehabilitation tered transdermally and prochlorperazine administered via
the buccal membrane have been shown to be potent
plan should be constructed for each patient, and should be
antiemetics, with some evidence of efficacy in the suppres-
explained in detail to ensure understanding and active
sion of vertigo and/or dizziness.
compliance with the programme (table 2).
Calcium channel antagonists, cinnarizine and cyclizine,
have vestibulosuppressant effects, although cinnarizine is
General measures
less effective than hyoscine in controlling patients’ sickness.
In the dizzy patient, a general medical examination should
Both drugs may give extrapyramidal side effects, and should
identify co-morbid, systemic conditions such as hyperten- be used only briefly in older patients.
sion, vascular disease, diabetes, autoimmune disorders, and Diazepam has no specific action on the vestibular system,
psychological pathology, all of which may impact upon and acts by reducing neural activity and causing inhibition
vestibular compensation if appropriate treatment is not in throughout the CNS, including activity in the vestibular
hand. Specifically, ophthalmological and rheumatological/ nerve and vestibular nuclei. The role of this drug in the
orthopaedic problems should be addressed, to ensure optimal treatment of vestibular disorders is controversial, but it is
visual and proprioceptive input for vestibular rehabilitation. widely used for its anxiolytic activity in acute vestibular
crises.
Pharmacological treatment
Acute vestibular symptoms caused by either peripheral or Specific treatment of vestibular disorders
central vestibular disorders may be helped by use of anti- Migraine affects approximately a fifth of the population, is
emetic and vestibular suppressant drugs. Despite our current the most common cause of dizziness/vertigo in children, and
understanding of vestibular neurochemistry, treatment of is a common presentation both with headache and in the
vestibular disorders remains mostly empirical, often with headache-free periods in adults with migraine. Vestibular test
relatively poor understanding of the specific antivertiginous results are commonly normal, although approximately 20%
action of any particular drug, and a lack of appropriate of cases demonstrate a canal paresis on caloric testing.
clinical trials establishing efficacy, duration, and dosage of Diagnosis depends on the history based on the International
the drug. The ideal antivertiginous drug would suppress Headache Society criteria. The treatment of migraine asso-
ciated dizziness parallels the treatment of migrainous head-
Table 2 Rehabilitation programme ache. General measures include dietary restriction, lifestyle
adaptations, stress reduction techniques, and vestibular
1. Investigation and diagnosis rehabilitation in the presence of a fixed vestibular deficit.
2. Explanation
3. Rehabilitation plan The course of treatment includes simple over-the-counter
– correction of remediable problems analgesics, triptans, ergot derivatives, and acetozolamide.
– general fitness programme Prophylactic medication includes b blockers, calcium channel
– physical exercise regimens blockers, serotonin reuptake inhibitors, and amitriptyline.
– psychological assessment Episodic ataxia, while rare in comparison with migraine,
– medication may present with acute vertigo and ataxia, with or without
– realistic family/social/occupational goals interval symptoms, in both adults and children. Both
4. Monitoring/feedback/follow up
5. Discharge acetazolamide and 4-aminopyridine are effective in episodic
ataxia type II.
Reproduced with permission from Luxon LM, Davies RA, eds. Handbook Menière’s disease is perhaps the most commonly mis-
of vestibular medicine. London: Whurr Publishers, 1997.
diagnosed vestibular condition. Diagnosis should be based on

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NEUROLOGY IN PRACTICE

strict criteria as defined by the American Academy of Chronic vertigo

Ophthalmology and Otolaryngology (AAOO) committee on It cannot be overemphasised that chronic vertigo on the basis
hearing and equilibrium guidelines. The treatment of of a peripheral vestibular disorder should not be treated with
Menière’s disease remains controversial and empirical, not antiemetics and/or vestibular sedatives, as these drugs are
least because of the continuing quest to define the exact reported to impair vestibular compensation, and thus delay
underlying pathogenesis of this condition. There are few recovery. Regrettably, in practice these drugs are commonly
double blind randomised studies assessing treatment effi- prescribed for chronic vertigo both in primary and tertiary iv49
cacy, and it is important to recall an 80% placebo response in care.
this condition. Medical treatment aims to influence under- Central vestibular disorders occurring with demyelination,
lying pathology of endolymphatic hydrops or the postulated degeneration or vascular events are commonly associated
immunological pathogenesis of this disorder, while destruc- with persistent disequilibrium, nausea, and eye movement
tive surgery may either be medical (intratympanic injection disorders Such disorders are usually associated with un-
of aminoglycosides) or surgical (see below). pleasant perceptions of motion and vegetative symptoms
Clinical treatment normally includes institution of a low for which drug intervention (clonazepam, carbamazepine,
salt diet, although there are no double blind trials reporting flunarizine) may be helpful.
efficacy of this regimen. Notwithstanding this, the author’s
experience, like that of many other clinicians, is that strict VESTIBULAR REHABILITATION
The cornerstone of vestibular rehabilitation relies on the
adherence to a low salt diet, together with diuretics, is a
plasticity of the central nervous system, which enables
highly effective strategy in patients who can be persuaded to
reorganisation of the mechanisms subserving balance and
follow this regimen. Patient compliance depends upon
‘‘symptomatic vestibular compensation’’. When supervising
education about unexpected levels of salt in many foods
servicemen’s rehabilitation during the second world war, Sir
(for example, cornflakes, prepared foods, and tinned food).
Terence Cawthorne, an ENT surgeon, and Dr Harold Cooksey,
Diuretics have been reported in a small number of double
a rheumatologist, observed that soldiers with balance
blind trials to be effective in the long term control of vertigo,
disorders after head injury improved more rapidly if they
but not of auditory symptoms. The most common prescrip-
were active and mobile, than if they were inactive and
tion is for bendrofluazide 10 mg each day, together with
bedridden. They therefore empirically devised the vestibular
potassium supplements. Again, there are no data on the
exercise regimen known as the Cawthorne-Cooksey exer-
efficacy of this empirical treatment in Menière’s disease.
cises. These formed the basis of the multiplicity of phy-
More potent loop diuretics such as furosemide (frusemide)
siotherapy vestibular rehabilitation regimes currently
should be avoided because of potential ototoxicity.
available. In the 1970s and 1980s, scientists working on
Betahistine is a histamine analogue which is proposed to
animal models of vestibular compensation demonstrated that
have value in Menière’s disease, as a result of improving micro-
visual input and motor activity are indeed crucial for
vascular circulation in the stria vascularis of the cochlea,
symptomatic recovery from unilateral peripheral vestibular
thus reducing endolymphatic pressure. A number of trials of
disorders. There is now also some evidence that vestibular
this drug are reported, but none adhere to the AAOO criteria. exercises may be of value in more central lesions involving
Thus, there remains no definitive evidence for its use. the vestibular nuclei and cerebellum.
Steroid treatment has been proposed both systemically and As noted above, vestibular compensation relies on recali-
transtympanically in Menière’s disease, on the assumption of bration of the vestibular reflexes, and sensory and motor
an autoimmune pathogenesis. There are no double blind substitutions in terms of input and predictive activity. For
controlled studies demonstrating the clinical efficacy of this model to be effective, the vestibular disorder must be
steroids or other immunosuppressants, and their use remains stable. In relapsing conditions such as Menière’s disease,
open to question. where there is fluctuating vestibular function, rehabilitation
Management of Menière’s disease by destructive surgical physiotherapy is unhelpful until intervention or spontaneous
or medical treatments must be considered extremely carefully recovery brings about a stable vestibular situation. Thus, a
in view of the possibility of bilateral Menière’s disease, with correct diagnosis is essential to ensure appropriate treatment
subsequent bilateral loss of auditory and vestibular function. of conditions characterised by varying vestibular function—
Streptomycin and gentamicin have been used because of for example, migraine, benign positional vertigo of parox-
their selective vestibulotoxic effect, with gentamicin the drug ysmal type, vestibular Schwannoma, or vascular disease.
of choice. There is no consensus on optimal protocol, Moreover, as noted above, the sensory inputs required for
technique of administration, or end point of treatment. balance must be optimal, and thus if there are any remedial
Moreover, while this technique has been advocated in visual problems (for example, cataracts), or conditions which
patients with intractable vertigo unresponsive to medical may affect proprioception (for example, arthritis/autoim-
treatment with good auditory function, there are reports of mune disease), these must be optimally managed medically,
deafness developing in up to 30% of treated cases. in conjunction with vestibular rehabilitation programmes.
Surgical intervention includes the theoretical prophylactic Most importantly (see below), psychological factors play an
approach of endolymphatic sac decompression, but there is important part in the effectiveness of vestibular rehabilitation
no firm evidence on the efficacy of this intervention. therapies, and psychological disorders must thus be con-
Destructive procedures fall into two categories: those that sidered and treated where appropriate.
aim to preserve auditory function, such as vestibular In each individual patient, it is helpful to define the
neurectomy; and those in which the disease process has strategy used for balance (visual, vestibular, or proprioceptive
already caused profound hearing loss in addition to dominance) and the particular difficulties encountered by the
intractable vertigo. In the latter group, labyrinthectomy is individual. The rationale of the Cawthorne-Cooksey exercises
advocated, if medical treatment has failed. is to stimulate each of the sensory inputs in a progressively

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iv50

Figure 4 The Epley manoeuvre. Ant, anterior; Lat, lateral; Post, posterior. Reproduced with permission from Luxon LM, Davies RA, eds. Handbook of
vestibular medicine. London: Whur Publishers, 1997.

more difficult manner, to allow adaptation to occur. favour, as it explains more effectively the majority of the
However, some patients have very specific symptoms, which clinical features of BPPV.
are more amenable to ‘‘customised’’ exercises—that is, Most commonly (93%), this condition affects the posterior
programmes are specifically structured on an individual basis semicircular canal, but rarely (5%) the horizontal canal may
to address the specific limitations and symptoms experienced be involved, and extremely rarely (2%) the anterior canal. It
by that particular patient. As compliance and active is important that this condition is differentiated from central
collaboration with vestibular rehabilitation programmes are positional nystagmus (see Davies, p iv32), which is associated
required of the patient, such an individual approach may be with neurological pathology. The initial management of this
more effective than a generic regimen. A detailed explanation condition was habituation therapy with exercises, but in
of the mechanisms of balance and vestibular compensation 1980, Brandt and Daroff proposed specific repetitive posi-
is required for the patient to understand why physio- tional exercises based on the hypothesis of cupulolithiasis.
therapy should help them feel better from their dizziness/ Their initial report claimed a 98% success rate. However,
disorientation, rather than medication or an ear operation. more recently, specific repositioning manoeuvres (the Epley
There is some evidence in the literature that early interven- manoeuvre, the Semont manoeuvre) based on the hypothesis
tion following vestibular pathology is associated with a better of canalithiasis as the causation of BPPV have been intro-
outcome. More surprisingly, recent work has shown that duced. These repositioning manoeuvres involve a series of
older people may compensate as effectively as younger specific consecutive head movements, which allow the debris
people, and age per se is not a negative prognostic factor. in the canal being treated to gravitate out of the canal into
Importantly, a general exercise regimen relevant to the age the utricle, thus avoiding stimulation of the crista during
and ability of the patient should form part of the rehabilita- head movements (fig 4). Most reports cite success rates of
tion strategy. resolution of positional symptoms of between 80–95%
following the first manoeuvre, although patients may
PARTICLE REPOSITIONING PROCEDURES experience vague disorientation for 2–3 days after treatment.
In addition to systematic or customised exercise programmes Repeated manoeuvres, with mastoid vibration, may be
for a peripheral vestibular disorder, a number of specific necessary in a small percentage of patients, but currently
treatments aimed at treating benign positional vertigo of it appears that less than 5% of patients cannot be improved
paroxysmal type (BPPV) have been developed. This condition by one of these manoeuvres. Provided the diagnosis is
is characterised by acute vertiginous episodes that are certain, it may be appropriate to consider surgical interven-
triggered by changes in the position of the head relative to tions such as plugging the posterior canal to bring about
gravity. Until recently BPPV had been attributed to cupulo- resolution of the positional symptoms in the small percentage
lithiasis—that is, degenerative debris adhering to the cupula of patients in whom medical management fails.
of the posterior semicircular canal—making it gravity
sensitive. However more recently, the hypothesis of cana- PSYCHOLOGICAL TREATMENT
lithiasis—that is, degenerative debris floating freely in the The interaction of psychological factors in both the exacer-
endolymph of the posterior semicircular canal—has gained bation of symptoms of peripheral vestibular disorder and

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iv51

Figure 5 Diagram illustrating the interaction of autonomic, psychological, and vestibular symptoms.

failure of vestibular compensation cannot be overemphasised vertigo due to failure of compensation, there is no evidence to
(fig 5). Many studies have highlighted the association of suggest that labyrinthine destruction will result in improved
agrophobia, avoidance behaviour, anxiety states, panic compensation.
attacks, and depression with vestibular pathology. It is well ‘‘Failure’’ of medical management in Menière’s disease
recognised that in panic attacks autonomic symptoms and often reflects inadequate attempts at medical management,
dizziness are common, but equally in vestibular disorders, or failure of patient compliance. It must be remembered that
anxiety and autonomic symptoms are common. Thus there is between 10–50% of cases of Menière’s disease become
an intimate relation between these disorders and symptom bilateral, and, thus, labyrinthine destruction of one ear
complexes. should, if possible, be avoided. Both vestibular neurectomy
On initial assessment, it is helpful to consider psychological and transtympanic gentamicin—measures aimed at destroy-
factors and specifically to ask about anxiety, panic attacks, ing vestibular function in Menière’s disease, while preserving
and avoidance behaviour, together with mood change in a auditory function—may be effective, but both procedures
patient with dizziness. The presence of avoidance behaviour carry a small but significant risk of profound sensorineural
makes compliance with a vestibular physiotherapy rehabili- hearing loss. Surgical intervention may rarely be required for
tation programme unlikely and it is of value to address both intractable benign positional vertigo not amenable to particle
cognitive and physical symptoms in parallel. More severe repositioning procedures, but great care must be taken that
psychological disturbance should prompt immediate psychia- the diagnosis is absolutely accurate, and that an atypical form
tric referral, as vestibular recovery will not be possible until of central positional nystagmus does not explain the failure
the psychological factors have been appropriately managed. to respond to appropriate management.
In a young and otherwise healthy patient, who fails to Not infrequently, an appropriate understanding of vestib-
compensate from an apparently straightforward peripheral ular pathology, knowledge of the range of vestibular
vestibular disorder, the index of suspicion of an underlying disorders, and the rationale for management can lead to
psychological problem should be high. appropriate medical management of symptoms that have
initially appeared intractable.
SURGERY
It is now widely recognised that surgical intervention for
vertigo is extremely rarely required. Specific exceptions to OTHER FORMS OF CHRONIC VERTIGO
The management strategy set out above applies most
this rule include:
c life threatening complications of chronic middle ear
commonly to unilateral peripheral vestibular disorders of a
disease multiplicity of aetiologies: traumatic, infective, and vascular.
c neoplasia involving otological structures (for example, However it is equally applicable to bilateral vestibular failure
vestibular Schwannoma) of acquired type.
c trauma to the middle/inner ear (for example, a perilymph Children with congenital bilateral vestibular failure, caused
fistula). by either a genetic defect or anomalous inner ear develop-
In the past, therapeutic surgical intervention, particularly ment, compensate extremely well and can ski, swim, and
for Menière’s disease, has been advocated, but there is little skateboard, provided vestibular loss is an isolated abnorm-
evidence that any of these procedures are more effective than ality. If, however, there are other motor or cognitive defects
medical management. Destructive surgical procedures must or visual impairment, the effects of congenital bilateral
be undertaken with great care and very positive indications vestibular loss are profound.
as outlined above. In a patient with a clear cut peripheral Acquired bilateral vestibular failure is most commonly
vestibular disorder, who is continuing to experience disabling caused by gentamicin treatment, but also can be associated

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 NEUROLOGY IN PRACTICE

with trauma, bilateral Menière’s disease, or as an idiopathic, appropriate rehabilitation strategies which lead to sympto-
presumably late onset, genetic origin. This is extremely matic recovery and significant improvement in this large
disabling in the early stages with oscillopsia and gross ataxia, group of patients with low morbidity and few long term
though intensive vestibular rehabilitation can be highly sequelae. Perhaps most importantly, an understanding of
effective, and should be pursued aggressively. vestibular rehabilitation prevents patients from being
The most difficult form of chronic vertigo to treat is that referred from department to department in search of an
iv52 caused by central vestibular disorders, such as vascular explanation for their chronic symptoms.
events, multiple sclerosis, and spinocerebellar degenerations,
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of the pathophysiology of balance disorders and appro- c Excellent review of common presentation of vestibular symptoms and
priate management interventions is key to implementing migraine.

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