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Assessment of dizzinessOverview

Summary

Aetiology

Emergencies

Urgent considerations

DiagnosisStep-by-step

Differential diagnosis

Guidelines

Resources

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SummaryDizziness is a non-specific term and may be used by patients to indicate true vertigo, lightheadedness,

imbalance, or a form of syncope. The prevalence of dizziness in the general population ranges from 20% to

30%.[1] True vertigo is described as a rotary sensation of the patient or surroundings, and is often of vestibular

origin.

AetiologyThe aetiology varies from vestibular to neurological to cardiovascular pathology. The most common causes of

vertigo are migraine-related vertigo, benign positional paroxysmal vertigo (BPPV), and Meniere's disease.

Cerebellar infarct or vestibular schwannoma (acoustic neuroma) may also cause dizziness.

History and clinical findings

It is important to take a detailed history of the patient's symptoms. True vertigo often indicates vestibular

pathology (e.g., BPPV, labyrinthitis, or Meniere's disease). Central pathology, such as a cerebellar ischaemic

stroke, needs to be ruled out. A description of the typical attacks, including their nature, duration, and associated

auditory symptoms (e.g., hearing loss, tinnitus, and aural pressure), should be determined. Physical examination

includes an ear and neurological examination plus an examination of the vestibular system. Neurological

examination is important to rule out central pathology. The Dix-Hallpike test should be carried out if BPPV is

suspected.

Investigations

The diagnosis of dizziness is usually made on the basis of the history and examination only. Investigations may

not be necessary. Magnetic resonance imaging (MRI) of the brain and internal auditory meatus should be carried
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out if there is concern that there may be central pathology. Vestibular function tests are indicated in some cases.

Tests of cardiovascular function may be necessary if a cardiovascular cause is suspected.

AetiologyDizziness has a variety of aetiologies. True vertigo (spinning sensation)indicates a problem with the vestibular system (peripheral or central).Dizziness or lightheadedness may be cardiovascular in origin or associatedwith infectious, metabolic, or autoimmune disease or with medications.

Vestibular Benign positional paroxysmal vertigo: the most common cause of vertigo, affecting 107 cases per

100,000 per year.[2] The lifetime prevalence is 2.4%.[3] It is caused by loose otoconia particles in the semi-

circular canals, usually the posterior canal but sometimes the lateral canal. It is diagnosed by the Dix-Hallpike

test for posterior canal BPPV. If the Dix-Hallpike test is negative in a patient with a compatible history, a supineroll test should be done to assess the patient for horizontal canal BPPV.[4] [3]

Meniere's disease: occurs in 1% of the population and affects all ages.[5] It is idiopathic but is

associated with endolymphatic hydrops. Meniere's disease is characterised by episodic vertigo, fluctuating

hearing loss, tinnitus, and aural pressure or fullness.[5]

Other specific disorders affecting the inner ear and associated with hydrops are temporal bone fracture,

syphilis, hypothyroidism, Cogan's syndrome, and Mondini's dysplasia.

Labyrinthitis: an acute infection of the vestibular organs, most commonly bacterial or viral. The patient

often presents after an upper respiratory or ear infection.[6]

Vestibular neuritis (neuronitis): an acute peripheral vestibulopathy due to reactivation of a viral infection,

most commonly herpes simplex virus, which affects the vestibular ganglion, vestibular nerve, labyrinth, or a

combination of these sites.

Superior semi-circular canal dehiscence: characterised by episodes of vertigo associated with loud

sound and/or altered middle-ear pressure. Auditory complaints include hyperacusis to bone-conducted sounds, a

conductive hearing loss, and normal acoustic reflexes. Many patients with superior semi-circular canal

dehiscence present after head trauma, and their dizziness may initially be thought to be post-traumatic vertigo,

labyrinthine concussion, or perilymphatic fistula. The diagnosis is supported by evidence of bony dehiscence of

the superior semi-circular canal on high-resolution computed tomography scan of the petrous temporal bones. In

addition, the vestibular-evoked myogenic potential may be abnormal.[7]

Perilymphatic fistula: occurs either in the round or oval window. It may occur after stapes surgery or

head trauma or in divers. It is characterised by paroxysmal vertigo, imbalance, and a sensorineural hearing loss

with or without tinnitus.[8] The diagnosis is made at surgery (exploratory tympanotomy).
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Middle-ear disease: acute bacterial otitis media and labyrinthitis may present with dizziness.[6] Other

middle-ear disease, such as cholesteatoma, may be associated with vertigo. Patients who have had previous

mastoid surgery with a mastoid cavity are prone to dizziness with an ear infection.

Neurological Migraine-related vestibulopathy: often occurs in patients with a personal or family history of migraine. It

is one of the most common causes of vertigo and dizziness. There are different theories for the pathophysiology

of migraine-associated vestibulopathy. These include a spreading, global central nervous system (CNS)

depression to account for central findings, and vasospasm of the internal auditory artery to account for peripheral

cochleovestibular symptoms. Others attribute the central and peripheral symptoms to deficits in the release of

neuropeptides during an attack.[9]

Posterior fossa tumours: include vestibular schwannomas (acoustic neuroma), meningiomas, cerebellar

or brainstem tumours, and epidermoid cysts.

Multiple sclerosis: vertigo is an initial symptom in 5% of patients and occurs at some point during the

disease in 50% of patients. Prolonged spontaneous attacks of vertigo occur if a demyelinating plaque occurs at

the root entry zone of the vestibular nerve or nucleus, and this presents as an acute peripheral vestibular

disorder, such as vestibular neuritis.[1]

Cerebellar stroke: may be due to infarction or haemorrhage. It may present in a similar fashion to

vestibular neuritis. Magnetic resonance imaging (MRI) demonstrates the infarction or haemorrhage. It is

important that MRI be done early, as one third of people with cerebellar infarction will develop acute, potentially

lethal posterior fossa oedema requiring emergency neurosurgical decompression.[10]

Vertebrobasilar ischaemia (usually affecting the anterior inferior cerebellar artery): these patients present

with episodic vertigo lasting 1 to 15 minutes, with diplopia, dysarthria, ataxia, drop attack, and clumsiness of the

extremities.

Wallenberg's syndrome: lateral medullary infarction, caused by occlusion of the ipsilateral vertebral

artery that supplies the posterior inferior cerebellar artery and thereby causes prolonged vertigo lasting several

days.

Hereditary ataxias: a heterogeneous group of inherited genetic disorders. The most common autosomal

recessive ataxia is Friedreich's ataxia, usually presenting with symptoms before 20 years of age.[1] The familial

episodic ataxias are rare.

Benign intracranial hypertension (pseudotumor cerebri): characterised by raised intracranial pressure

that is not caused by a mass lesion (e.g., a tumour); associated with headache and transient poor vision. These

patients are often obese and complain of clumsiness, imbalance, and dizziness rather than true vertigo. Some

patients present with bilateral 6th nerve palsy or tinnitus. This may be associated with hypervitaminosis A.[11]

Normal pressure hydrocephalus: associated with normal intracranial pressure and enlarged ventricles

(hydrocephalus). Patients present with ataxia, urinary incontinence, and cognitive dysfunction. The diagnosis

may be difficult to establish.[11]
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Mal de debarquement syndrome: thought to be due to a conflict between the sensory inputs from the

visual, vestibular, and somatosensory systems and the central vestibular nuclei, cerebellum, and parietal cortex.

It refers to the complaints of swinging, swaying, unsteadiness, and disequilibrium after exposure to motion.

There may be a history of a long voyage, air travel, or space flight.

Paraneoplastic cerebellar degeneration: a rare complication of cancer of the ovary, breast, or lung, or of

Hodgkin's lymphoma. Autoantibodies are thought to be directed against Purkinje cells. The anti-Yo antibody can

present years before tumour detection. Anti-Tr antibody is associated with Hodgkin's lymphoma.

Cardiovascular Syncope: defined as a sudden transient loss of consciousness with simultaneous diminution of postural

tone, followed by spontaneous recovery.[12] The differential diagnosis includes vasovagal attacks, orthostatic

hypotension, and medication-related and neurological causes, such as transient ischaemic attacks,

cardiopulmonary disease, and arrhythmias.

Presyncope: refers to lightheadedness without an illusion of movement and occurs prior to fainting or

losing consciousness. It is a more common occurrence than syncope and is a prodromal symptom of fainting or

near-fainting. Patients present with generalised weakness, giddiness, headache, blurred vision, and diaphoresis.

There may also be paraesthesia, nausea, and vomiting prior to losing consciousness. The mechanism is almost

always a reduction in blood supply to the brain. The symptoms may be spontaneous, positional, or associated

with various triggers, depending on the cause.[1] [13]

Orthostatic (or postural) hypotension: one of the most common causes of syncope and can be attributed

to impaired peripheral vasoconstriction or a reduction in intravascular volume. It is defined by the American

Autonomic Society as a decrease in systolic blood pressure (BP) of at least 20 mmHg or a decrease in diastolic

BP of at least 10 mmHg within 3 minutes of standing.[14] This may occur in hypotensive patients or those onantihypertensive medication. Patients complain of dizziness on standing.[12]

Autonomic dysregulation: patients present with exertional dizziness. Provocative activities include

standing upright for prolonged periods, swimming, or running. Patients complain of feeling "spacey" or "foggy"

during exertion without vertigo. Tilt-table testing may provoke symptoms.[15] [16]

Psychological Psychophysiological dizziness (mixed physiological and psychogenic aetiology): may occur

spontaneously or after a labyrinthine disorder. Patients complain of a variety of symptoms, such as rocking,

floating, or swimming sensations. The symptoms may worsen with stress or fatigue.[1]

Psychogenic dizziness: panic disorder with agoraphobia, personality disorders, or generalised anxiety is

often present in patients complaining of dizziness. If the dizziness is psychogenic, patients may demonstrate

inappropriate or excessive anxiety or fear. Phobic postural vertigo is characterised by dizziness in standing and

walking despite normal clinical balance tests. Patients may demonstrate anxiety reactions and avoidance

behaviour to specific stimuli.[17]
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Metabolic Diabetes mellitus: dizziness may be associated with episodes of hypoglycaemia. Also, diabetic patients

with peripheral neuropathy may have more difficulty in recovering from a peripheral vestibular disorder.[18]

Hypothyroidism: the prevalence of hypothyroidism has been found to be higher in patients diagnosed

with Meniere's disease compared with a control group.[19]

Autoimmune Systemic lupus erythematosus: patients may complain of vertigo or hearing loss and may have

abnormal nystagmography.[20]

Rheumatoid arthritis: patients are more likely to perceive themselves as having hearing loss, even with

normal audiometry.[C Evidence]

Cogan's syndrome: an inflammatory disorder resulting in interstitial keratitis and audiovestibular

dysfunction. The pathology involves plasma cell and lymphocyte infiltration of the spiral ligament, endolymphatic

hydrops, and degenerative disease of the organ of Corti. There is also demyelination of the 8th cranial nerve andinner ear osteogenesis.[21]

Wegener's granulomatosis (granulomatosis with polyangitis): characterised by granulomatous lesions of

the upper respiratory tract, necrotising vasculitis, and glomerulonephritis.[22]

Behcet's disease: a generalised systemic relapsing vasculitis of the arteries and veins of unknown

aetiology.[23]

Medication- or drug-related Ototoxic drugs: aminoglycoside antibiotics such as gentamicin and neomycin are ototoxic.

[24] [25] Ototoxicity has been described for topical as well as parenteral use. These drugs are vestibulotoxic and

cochleotoxic. They may result in vertigo without causing hearing loss. Toxicity with parenteral use is related to

the total dose administered. The risk factors are age >60 years, high serum drug levels, previous sensorineural

hearing loss, concomitant renal impairment, attendant noise exposure, duration of therapy >10 days, and

simultaneous administration of other ototoxic agents, such as loop diuretics or aspirin. Some patients have a

genetic predisposition that makes them susceptible to ototoxicity secondary to aminoglycoside exposure. This is

due to a mutation of the mitochondrial DNA m.1555A>G. This mutation accounts for 33% to 59% of

aminoglycoside ototoxicity.[26]

Chemotherapeutic drugs such as cisplatin are also ototoxic.[27] Cisplatin is widely used in various soft-

tissue neoplasms. It causes sensorineural hearing loss and tinnitus. The severity of the sensorineural hearingloss is related to the magnitude of the cumulative dose.

Alcohol: ingestion may cause patients to report feeling "high", dizzy, and intoxicated.[28]

Other drugs: antihypertensive medication, anaesthetic medication, antiarrhythmic medication, drugs of

abuse and various other drugs may cause patients to feel dizzy. Antihypertensive drugs may be associated with

orthostatic hypotension.[12] Second-generation antiepileptic drugs such as oxcarbamazepine and topiramate at

standard doses increase the risk of imbalance. This effect is not found at standard doses with gabapentin or

levetiracetam.[29]
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Most vertigo causes are peripheral and non-life-threatening. However, those few vascular CNS causes are

emergencies that should not be overlooked. Cerebellar stroke (cerebellar infarction or haemorrhage) may

present in a similar fashion to vestibular neuritis, with sudden intense vertigo, nausea, and vomiting. Nystagmus

is present and may be bilateral or vertical (suggesting a central cause of the vertigo). The patient may have other

neurological signs, such as limb ataxia and impaired gait. Patients with cerebellar stroke usually cannot stand

without support, even with the eyes open, whereas a patient with acute vestibular neuritis or labyrinthitis is

usually able to do so.

The head-impulse test is negative (no saccadic adjustment of the eyes on sudden head twisting), ruling out

acute vestibular neuritis or labyrinthitis. Recent studies have suggested that this test should be combined with

other tests of oculomotor function, including an examination of nystagmus and test of skew.[35] [36] Nystagmus,

which changes direction on eccentric gaze, is a predictor of central pathology. Skew deviation is vertical ocular

misalignment resulting from a right-left imbalance of vestibular tone (neural firing), such as otolithic inputs to the

oculomotor system. This can be shown during an alternate cover test. Skew has been identified as a central sign

in patients with posterior fossa pathology. These 3 tests identify stoke with a high degree of sensitivity and

specificity in patients with acute vestibular symptoms, and they may rule out stroke more effectively than early

diffusion-weighted MRI.

MRI demonstrates the infarction or haemorrhage. It is important that an MRI is done early, as one third of these

patients will develop acute, potentially lethal posterior fossa oedema, requiring emergency neurosurgical

decompression.[10] Urgent MRI should be requested in all patients with acute vertigo who have significant risk

factors for a cerebellar stroke, such as hypertension, diabetes mellitus, smoking, and cardiovascular disease,

because it is possible that central signs on examination may not present.[37] Close neurological observation is

important, as neurosurgical intervention may be required.[38]

Cardiovascular diseaseDizziness with syncope and chest pain may be related to cardiopulmonary disease such as myocardial

ischaemia (spasm or infarction), obstructive (aortic or mitral stenosis) hypertrophic cardiomyopathy, pulmonary

embolism, or hypertension. It is important to consider a history of associated chest pain, exertional syncope, and

dyspnoea.[12] Urgent treatment may be required (e.g., aspirin, emergency revascularisation in some cases of

acute coronary syndrome, anticoagulation, thrombolysis, or surgery for pulmonary embolism).

Vestibular neuritis and labyrinthitis

It is important to consider the diagnosis of vestibular neuritis and labyrinthitis, not because these conditions are

life-threatening but because there may be long-term functional impairment if a correct early diagnosis is not

made. Early treatment with corticosteroids has been shown to accelerate recovery of vestibular function in

patients with vestibular neuritis.[37] Treatment may also be considered in people with labyrinthitis.

Corticosteroid therapy within 3 days of onset of symptoms in people with vestibular neuritis may shorten the

attack. Corticosteroids may or may not influence the long-term outcome.

More serious conditions may also be mistakenly diagnosed as viral neuritis or labyrinthitis due to similar

presenting symptoms. It is important to recognise that any patient presenting with unilateral or asymmetrical
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sensorineural hearing loss (as may occur with labyrinthitis) needs to be investigated with MRI of the brain and

internal auditory meatus to rule out a posterior fossa tumour (e.g., acoustic neuroma).[39]

Red flags

Meniere's disease

Vestibular neuritis

Syncope or presyncope

Labyrinthitis

Cholesteatoma

Posterior fossa tumour

Multiple sclerosis

Cerebellar stroke

Vertebrobasilar insufficiency

Wallenberg's syndrome

Paraneoplastic cerebellar degeneration

Lyme disease

Syphilis

HIV

Step-by-step diagnostic approachThe clinical history and examination are most important in arriving at adifferential diagnosis for each patient. The history should be detailed withregard to the patient's dizziness, and the examination should includeotoscopy, CNS examination, and specific tests depending on the patient'spresentation.[40]

History: characteristics of the current episodeThe most important features in the patient's history of current complaint areas follows.

Differentiating between dizziness and vertigo

Vertigo is a spinning or rotatory sensation of the patient or his or her surroundings, and is often in

keeping with a vestibular event.

Dizziness or unsteadiness is a more generalised term and may not indicate vestibular pathology.

Patients who feel faint (presyncope) or actually have had syncopal attacks are more likely to have a

cardiovascular problem such as orthostatic hypotension, cardiac ischaemia, or arrhythmia.[41] [12] However, a

systematic review has shown that 63% of patients with cardiovascular causes of dizziness also report vertigo
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and that, in 37%, vertigo is the only type of dizziness described.[42] Syncope is defined as a sudden transient

loss of consciousness with simultaneous diminution of postural tone, followed by spontaneous recovery.[12] It

has also been recently described as a transient loss of consciousness due to transient global cerebral

hypoperfusion characterised by rapid onset, short duration, and spontaneous complete recovery. [43] Patients

with presyncope may have generalised weakness, giddiness, headache, blurred vision, and diaphoresis. There

may also be paraesthesia, nausea, and vomiting prior to losing consciousness. The mechanism is almost always

a reduction in blood supply to the brain. The symptoms may be spontaneous, positional, or associated with

various triggers, depending on the cause.[1] [13]

Determining whether the vertigo is better with the eyes open or closed

Patients who describe horizontal or rotational vertigo that decreases with visual fixation are more likely

to have a vestibular complaint.

Vertigo that does not lessen with visual fixation is more likely to be central in origin.[41]

Determining the duration of the vertigo

Vertigo lasting seconds and induced by positional change such as rolling over in bed is likely to be due

to benign positional paroxysmal vertigo (BPPV). Vertigo lasting seconds and induced by loud sounds or

coughing may be due to semicircular canal dehiscence. Vertigo lasting seconds with a history of trauma may be

secondary to a perilymphatic fistula.[44]

Vertigo lasting minutes to hours is suggestive of migraine, Meniere's disease, or cardiovascular disease

such as a transient ischaemic attack.

Vertigo lasting hours-to-days is suggestive of labyrinthitis, vestibular neuritis, central pathology such as

multiple sclerosis or a stroke, or an anxiety disorder.[44]

Checking for positional triggers

Vertigo associated with BPPV occurs on head movement (e.g., rolling over in bed, bending down, or

looking up quickly) and lasts seconds. Uncompensated unilateral vestibular loss may cause unsteadiness on

head movement. Both are relieved by keeping the head still.

Dizziness on getting up quickly may be associated with orthostatic hypotension and

presyncope.[15] There may also be a history of antihypertensive medication use or a history of cardiac disease

such as cardiac arrhythmia or cardiac failure.[12] Mild attacks of vertebrobasilar insufficiency may be associated

with orthostatic hypotension. People with autonomic dysregulation present with dizziness (but not true vertigo)

on standing upright for prolonged periods, swimming, or running.

Asking about the presence of other otological symptoms, such as tinnitus orhearing loss

Meniere's disease is associated with low-frequency hearing loss and tinnitus, both of which may

fluctuate, as well as aural fullness.[45] The vertigo is frequently associated with nausea and vomiting. The
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American Academy of Otolaryngology-Head and Neck Surgery has produced diagnostic guidelines.[46]A

definite diagnosis is made on the basis of:[45]

o At least 2 attacks of spontaneous rotational vertigo, lasting at least 20 minutes

o Audiometric confirmation of sensorineural hearing loss, tinnitus, and/or a perception of aural

fullness.

Labyrinthitis results in sudden hearing loss and/or tinnitus with acute vertigo lasting hours, and nausea

and vomiting.[6] It is important to try to differentiate between labyrinthitis and vestibular neuritis. Vestibular

neuritis is more common than labyrinthitis and presents with recurrent attacks of disabling vertigo, with no

associated hearing loss or tinnitus.

Superior semi-circular canal dehiscence is characterised by episodes of vertigo associated with loud

sound and/or altered middle-ear pressure, hyperacusis to bone-conducted sounds, and a conductive hearing

loss.

The presentation of posterior fossa tumours is typically with unilateral hearing loss, and imbalance rather

than true vertigo.[39]

Acute onset of dizziness may be associated with a bacterial otitis media and labyrinthitis.[6]In this case

there may be fever, irritability, and otalgia. Patients who have had previous mastoid surgery with a mastoid

cavity are prone to dizziness with an ear infection. Other middle-ear diseases such as cholesteatoma may be

associated with vertigo. Typically, there is a malodorous ear discharge and hearing loss with or without tinnitus.

There may be an associated hearing loss in people with systemic lupus erythematosus or multiple

sclerosis.

People with rheumatoid arthritis are more likely to perceive themselves as having hearing loss, even

with normal audiometry.[C Evidence]

Otological manifestations of Wegener's granulomatosis (granulomatosis with polyangitis) include vertigo,

serous otitis media, chronic otitis media, sensorineural hearing loss, and facial nerve palsy.[47]

Hearing loss may also occur following syphilis infection, HSV-1 infection, and in-utero exposure to CMV

infection, as well as with perilymphatic fistula, Mondini's dysplasia, Cogan's syndrome, and exposure to ototoxic

drugs or medications.

Determining how the episodes began

Patients with a preceding upper respiratory infection may have viral neuritis or labyrinthitis.[41]

Patients with a history of sea, air, or train travel prior to the onset of symptoms and with symptoms

occurring on disembarking may have mal de debarquement (MDD) syndrome.[48] Patients with MDD complain

of swinging, swaying, unsteadiness, and disequilibrium after exposure to motion. The symptoms commonly last

for only a few hours, but some patients may continue to experience symptoms for months or even years. The

symptoms differ from motion sickness that occurs after disembarking and are not associated with nausea or

vomiting.[48]
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Patients with a history of trauma or barotraumas (e.g., scuba divers or pilots) may have a perilymphatic

fistula.[44]

Asking about other more general symptoms associated with the vertigo

It is important to consider a history of associated chest pain, exertional syncope, and dyspnoea that may

be related to a cardiovascular aetiology.[12] Vestibular migraine may be associated with aura, visual disturbance, photophobia, or phonophobia, with

or without headaches.[41] Patients have varied symptoms, including true episodic vertigo, movement-provoked

disequilibrium, lightheadedness, and symptoms similar to BPPV.[9] They may also present with symptoms

similar to Meniere's disease.

Nausea is often associated with peripheral vestibular disorders as a part of the autonomic response.

Neurological symptoms such as gait disturbance, limb weakness, or dysarthria may indicate neurological

pathology, such as cerebellar infarction[10] or cerebellar pathology.

Patients with vertebrobasilar insufficiency present with episodic vertigo lasting 1 to 15 minutes, with

diplopia, dysarthria, ataxia, drop attack, and clumsiness of the extremities.

Patients with normal pressure hydrocephalus present with ataxia, urinary incontinence, and cognitive

dysfunction. The diagnosis may be difficult to establish.[11]

Patients with benign intracranial hypertension are often obese and complain of clumsiness, imbalance,

and dizziness rather than true vertigo; benign intracranial hypertension is associated with headache and

transient poor vision. Some patients present with bilateral 6th nerve palsy or tinnitus.

Patients with Cogan's syndrome and associated audiovestibular dysfunction present with ocular and

audiovestibular symptoms including photophobia, ocular discomfort, ocular redness, fluctuating sensorineural

hearing loss, and imbalance or vertigo.[49]

Patients with Wegener's granulomatosis (granulomatosis with polyangitis) may present with limited

forms of the disease, usually with head and neck involvement. Otological manifestations include serous otitis

media, chronic otitis media, sensorineural hearing loss, and facial nerve palsy.[47]

Audiovestibular manifestations of Behcet's disease include hearing impairment, tinnitus, and dizziness,

but it is also characterised by recurrent genital and oral ulceration and uveitis.

Asking about psychiatric symptoms

Panic disorder with agoraphobia, personality disorders, or generalised anxiety is often present in

patients complaining of dizziness.

If the dizziness is psychogenic, patients may describe symptoms of excessive anxiety or fear. A hospital

and anxiety depression scale of >8 is diagnostic.[50]

Phobic postural vertigo is characterised by dizziness on standing and walking, despite normal clinical

balance tests.
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Patients may describe avoidance behaviour to specific stimuli.[17]

Patients with psychophysiological dizziness may describe an initial labyrinthine disorder with persisting

symptoms.

History: identification of causeHistory of trauma or surgery

Dizziness may be a complication of middle-ear surgery such as stapedectomy. Patients may complain of

vertigo, which occurs because of a stapedectomy prosthesis that is too long or because of a perilymphatic fistula

at the oval window.[31]

Vertigo and balance disturbance may also occur after cochlear implantation and may be an immediate

transient short-lived vertigo or episodic vertigo of delayed onset.[32]

A perilymphatic fistula may occur after stapes surgery or head trauma or in divers. It is characterised by

paroxysmal vertigo, imbalance, and a sensorineural hearing loss with or without tinnitus.[8]

Post-traumatic vertigo generally occurs as a result of blunt head trauma such as a fall, an assault, or a

motor vehicle accident. Presenting symptoms may be of a traumatic perilymphatic fistula or post-traumatic

Meniere's disease. Patients may complain of vertigo, disequilibrium, tinnitus, pressure, headache, and

diplopia.[30]

Many patients with superior semi-circular canal dehiscence present after head trauma, and their

dizziness may initially be thought to be post-traumatic vertigo, labyrinthine concussion, or perilymphatic fistula.

History of other medical illnesses

Diabetes mellitus may be associated with attacks of dizziness associated with hypoglycaemic

episodes.[18]

Hypothyroidism,[19] rheumatoid arthritis,[51] or systemic lupus erythematosus[20] may also be

associated with dizziness.

Dizziness occurs as an initial symptom in 5% of people with multiple sclerosis and occurs at some point

during the disease in 50% of patients. Patients may present with a variety of neurological findings, such as

nystagmus, ataxia, and cranial nerve palsies.[1]

Patients with a history of migraine are more likely to have migraine-associated vertigo. Migraine or

Meniere attacks may be clustered.

Family history of illness

There may be a family history of migraine.

There may be a family history of hereditary ataxias. Most commonly, Friedreich's ataxia presents with

symptoms of ataxia, vertigo, nausea and vomiting, dysarthria, and nystagmus before the age of 20 years.[1]

Known or contact with infectious disease
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A patient with dizziness associated with Lyme disease has a history of outdoor exposure in areas with

high tick populations. Symptoms include rash, headache, neck pain and stiffness, sore throat, dizziness, otalgia,

tinnitus, facial and motor dysfunction, hearing loss, and facial palsy.[52]

Congenital syphilis may result in deafness. Secondary syphilis may present with bilateral sensorineural

hearing loss or vertigo. Patients with otosyphilis often present with vertigo. Late neurosyphilis may present with

hearing loss, fluctuating hearing, or vestibular symptoms.[21] Exposure in utero to CMV for the first time during pregnancy is associated with profound hearing and

vestibular loss in the infant.[21]

Audiovestibular symptoms (including sensorineural hearing loss) may be caused by reactivation of latent

HSV-1 infection and may be preceded by herpetic skin lesions.[21]

People with HIV infection may also describe onset of dizziness and difficulty with balance.[21]

Medication and drug history

There may be a history of medication or drug use associated with ototoxicity. Examples include

aminoglycoside antibiotics such as gentamicin and neomycin (particularly if these have been administeredconcomitantly with loop diuretics or aspirin), chemotherapeutic agents (e.g., cisplatin), antihypertensives,

anaesthetics, or antiarrhythmics.

There may also be a history of associated acute intoxication with alcohol.

Risk factors for cardiovascular disease or stroke

Assessment of a patient with vertigo should include assessment for risk factors for stroke, such as

hypertension, hyperlipidaemia, diabetes mellitus, smoking, or heart disease.[1]

A cardiovascular cause, vertebrobasilar insufficiency, Wallenberg's syndrome, and cerebellar stroke are

all more likely if there are risk factors present.

Patients with cerebellar stroke may present in a similar fashion to vestibular neuritis, with sudden intense

vertigo, nausea, and vomiting. Urgent MRI should be considered in all patients with acute vertigo who have

significant risk factors for a cerebellar stroke such as hypertension, diabetes mellitus, smoking, and

cardiovascular disease, because it is possible that central signs on examination may not present.[37]

History of neoplastic disease

Paraneoplastic cerebellar degeneration is a rare complication of cancer of the ovary, breast, or lung, or

of Hodgkin's lymphoma.

Patients present with dizziness, nausea and vomiting, gait instability, diplopia, nystagmus, gait and

appendicular ataxia, dysarthria, and dysphagia.[1] [53]

Physical examination: earEar examination
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Acute onset of dizziness may be associated with a bacterial otitis media with labyrinthitis.[6]Acute otitis

media does not usually result in dizziness, but where there is complicating labyrinthitis it may occur. The

tympanic membrane in acute otitis media is erythematous, opaque, and bulging.View image

Other middle-ear diseases such as cholesteatoma may be associated with vertigo. Otoscopy reveals

crust or keratin in the attic (upper part of the middle ear), pars flaccida, or pars tensa (usually posterior superior

aspect), with or without perforation of the tympanic membrane. View image

Patients who have had previous mastoid surgery with a mastoid cavity are prone to dizziness with an

ear infection or when swimming in cold water.

There may be evidence of fluid or blood in the middle ear and/or cerebrospinal fluid (CSF) otorrhoea if

the dizziness is related to trauma.

People with Wegener's granulomatosis (granulomatosis with polyangitis) may have signs of serous otitis

media or chronic otitis media.

The fistula test

Performed by applying pressure on the tragus to occlude the ear or by pneumatic otoscopy (exerting

pressure on each ear canal with a rubber bulb attached to an auriscope), thereby putting pressure on the middle

ear.

A positive result of induced dizziness and nystagmus occurs with superior semi-circular canal

dehiscence, post-surgical dizziness, or perilymphatic fistula.

Fistula test may be positive in people with cholesteatoma.

A positive fistula test provides support for doing a temporal bone CT.

Physical examination: eyeObservation for nystagmus

The presence of nystagmus may indicate peripheral or central pathology.

A central vestibular lesion produces vertical, bidirectional, or pure rotatory nystagmus. Abnormal

saccades and smooth pursuit may also indicate central pathology.

Observation of the eyes may lead to suspicion for other ophthalmological conditions, such as interstitial

keratitis in Cogan's syndrome or uveitis in Behcet's disease.

Observation of eye movements
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Ophthalmoplegia with palsies of cranial nerves III, IV, or VI may occur with multiple sclerosis or with an

intracranial lesion.[1]

Neurological signs such as diplopia, disconjugate gaze, Horner's syndrome, and gait ataxia are in

keeping with a central lesion.

Examination of the eyes with Frenzel glasses

These glasses use +30 diopter lenses to blur the patient's vision, remove optical fixation, and uncover

vestibular nystagmus.[10] [54]

It may be possible to use an ophthalmoscope instead of the Frenzel glasses to blur vision.

Infrared video goggles may be used instead of Frenzel glasses.

Examination of dynamic visual acuity

This tests the vestibulo-ocular reflex by observing the effect of head rotation on visual acuity (e.g., byreading the letters on a Snellen chart).[41]

Abnormal results indicate a bilateral vestibular failure.

Physical exam: clinical balance testsThe head impulse test

Particularly useful to differentiate between acute vestibular neuritis and cerebellar stroke in patients with

acute vertigo.[10]

The examiner turns the patient's head as rapidly as possible 15 degrees to one side and observes the

patient's ability to keep fixating on a distant target. With a peripheral vestibular lesion, a saccade occurs as the

vestibulo-ocular reflex fails, the patient cannot keep focusing on the target, and a catch-up movement occurs.

After a cerebellar stroke, no catch-up saccade occurs. The head-impulse test is negative (no saccadic

adjustment of the eyes on sudden head twisting) in people with cerebellar stroke, ruling out acute vestibular

neuritis or labyrinthitis.

The Dix-Hallpike test

This is useful in patients with a history suggestive of BPPV.

The test is performed by sitting the patient upright on a bed; for the right side, the examiner stands on

the patients right side, rotates the patients head 45 to the right, and then moves the patient, whose eyes are

open, to the supine right-ear down position, and then extends the patients neck slightly so that the chin points

slightly upwards. Patient's symptoms are noted and any nystagmus is observed.[3] [54] This manoeuvre is

associated with strong subjective symptoms, and the patient may cry out.
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Classically, peripheral nystagmus and symptoms are delayed by about 15 seconds, peak in 20 to 30

seconds, and then decay with complete resolution of the episode of vertigo. The test is repeated on the left with

the examiner standing on the patients left side. The nystagmus fatigues on repeat testing.[55]

BPPV is typically due to posterior canal pathology. If the pathology affects the horizontal canal, the

nystagmus may be more persistent and less fatigable.

When symptoms are due to central pathology, the test causes nystagmus that is not fatigable, is down-

beating, and is associated with minimal vertigo.

The Dix-Hallpike test has been shown to have a positive predictive value of 83% and a negative

predictive value of 52% for the diagnosis of BPPV.[56]

Supine roll test

If the Dix-Hallpike test is negative in a patient who has a history suggestive of BPPV, a supine roll test

should be performed.[3] [4] This supine roll test is performed by positioning the patient supine with the head in

the neutral position, then quickly rotating the head 90 to one side while the clinician observes the patients eyes

for nystagmus. The head is returned to the face up position, allowing all dizziness and nystagmus to subside; the

head is then turned rapidly to the opposite side.[3] [57]

Physical examination: CNSExamination of the other cranial nerves

Other cranial nerve palsies such as facial weakness or numbness may occur with cerebellopontine

angle tumours.

Tongue weakness with limb weakness may be a feature of a cerebral stroke.

Facial nerve palsy may occur with Wegener's granulomatosis (granulomatosis with polyangitis).

Neurological examination

Examination of cerebellar function is usually tested with the finger-to-nose test and rapid alternating

hand movements.[54] This may be abnormal in cerebellar lesions.

Gait should be checked for any disturbance, along with examination for limb weakness or dysarthria.

These may indicate a neurological pathology such as cerebellar infarction or other cerebellar pathology.[10]

Wallenberg's syndrome (lateral medullary infarction caused by occlusion of the ipsilateral vertebral artery

that supplies the posterior inferior cerebellar artery) causes prolonged vertigo, abnormal eye movements,

ipsilateral Horner's syndrome, ipsilateral limb ataxia, and loss of pain and temperature sensation of the ipsilateral

face and contralateral trunk.[13]
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