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Assessment of dizzinessOverview
Summary
Aetiology
Emergencies
Urgent considerations
DiagnosisStep-by-step
Differential diagnosis
Guidelines
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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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