Neurological differential diagnosis...Vertigo

1. DIFFERENTIAL DIAGNOSIS OF VERTIGO
Synonyms: dizziness, imbalance, disequilibrium
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INTRODUCTION
Background: Symptoms of vertigo are nonspecific. Vertigo occurs when there is an imbalance or disturbance
in vestibular function anywhere in the peripheral or central vestibular system (labyrinth, vestibular nerve,
brainstem, cerebellum, cortex). Etiology of vertigo includes familial, infectious, neoplastic, metabolic, toxic,
vascular, autoimmune, and traumatic causes. Distinguishing the site and cause of lesion resulting in vertigo is
important because some causes of central vertigo can be life threatening and require immediate attention.
Pathophysiology: Sensation of balance is the result of appropriate information from vestibular, ocular, and
proprioceptive sensory receptors that is properly integrated within the cerebellum and brainstem. Gait,
posture, and visual focus during head movement are all dependent on an intact sense of balance. Loss of
sensory information, central integration, or output control mechanisms all result in a sense of imbalance.
Central causes of vertigo result from a disruption of central integrators (brainstem, cerebellum) or a sensory
information mismatch (cortex). Lesions affecting the vestibular nerve or root entry zone (cerebello-pontine
angle lesions) result in imbalance by affecting primary vestibular sensory information.
Race: There is no racial predilection for CNS causes of vertigo.
Sex: Both men and women are equally affected.
Age: CNS causes of vertigo typically affect the older population groups because of the associated risk factors of
vascular causes of vertigo (hypertension, atherosclerosis, diabetes).
 Younger age group is more commonly affected by migraine and multiple sclerosis.
 Cerebellar tumors affect a bimodal population - children and adults.
 Cerebello-pontine angle tumors typically affect people in the fifth to the eighth decade.
CLINICAL
History:
 CNS causes of vertigo can present in a variety of ways. Vertigo can be sudden and severe in onset and
last for days or it may comprise recurrent attacks that last for minutes to hours. Less often central
vertigo presents as brief episodes of vertigo brought on by changes in head or body position.
 Patient may describe an intense sensation of movement or tilting, or a severe sensation of imbalance;
sensation is aggravated by movement and improved by remaining stationary. It is important to
discriminate between vertigo (the sensation of movement or spinning) and lightheadedness.
Lightheadedness is often a symptom of a metabolic or cardiovascular abnormality.
 Cause of vertigo often is revealed by history and physical examination.
 In migraine-associated vertigo the patient gives a history of acute-onset vertigo that lasts either
minutes to a few hours or many hours to even days. Vertigo may precede, follow, or simultaneously

2. present with the headache (migraine without aura). Vestibular symptoms range in severity from
mild to severe. Vertigo may occur with other symptoms of aura (visual and somatosensory
paresthesias) before a headache (migraine with aura). Less commonly vertigo is a symptom of
basilar migraine. Basilar migraine is suspected when the vertigo is accompanied by binocular
visual deficits, diplopia, dysarthria, hearing loss, ataxia, or decreased consciousness.
 Patients with presyncopal lightheadedness describe a sensation of wooziness, lightheadedness, or
unsteadiness. Sensations result from diffuse cerebral ischemia. Symptoms may occur
spontaneously if secondary to cardiac arrhythmia, or can be precipitated by activity (postural
hypotension, hyperventilation).
 Vertebrobasilar artery (VBA) insufficiency - Vertigo is sudden in onset, lasts only minutes, is
associated with nausea and vomiting, and is accompanied by a range of neurological deficits
(extremity weakness, numbness, incoordination, dysarthria; diplopia, field defects; tinnitus,
hearing loss; loss of consciousness, drop attacks). Few or no residual signs or symptoms remain
after the TIA has resolved.
 Symptoms and signs of posterior fossa cerebrovascular disease include vertigo, tinnitus, and ataxia.
Symptoms may be transient, permanent, recurrent, or isolated. Stroke syndromes involving the
posterior circulation are varied depending upon the involved territory. Wallenburg syndrome
(lateral medullary syndrome) presents with vertigo, nausea, vomiting, imbalance, ipsilateral facial
numbness and weakness, diplopia, dysphagia, and dysphonia. Infarction of the dorsolateral
pontomedullary region results in labyrinthine injury (severe vertigo, nausea, vomiting, hearing
loss) in addition to the signs and symptoms of Wallenburg syndrome. Cerebellar infarction also
presents with severe vertigo, nausea, vomiting, and ataxia. Basilar artery syndrome results from
infarction of the pons. Symptoms include vertigo, hearing loss, ataxia, ophthalmoplegia, blindness,
and regional sensory losses.
 Cerebellar tumors may present with positional vertigo, imbalance while walking and standing, and
headaches. Specific features are dependent on tumor location (lateral, medial, ventricular), tumor
size, and growth rate. Primary cerebellar tumors typically occur in children. In adults, cerebellar
tumor usually results from metastasis.
 Temporal lobe tumors may present as recurrent brief attacks of vertigo lasting minutes; it may be
followed by transient disorientation, amnesia, and dysphasia.
 Brainstem lesions (neoplastic, vascular, posttraumatic) can have vertigo as a presenting symptom.
It may be brief or prolonged, depending on the extent of damage to the brainstem structures.
 Cerebello-pontine angle (CPA) tumors typically result in disequilibrium or unsteadiness rather
than a sensation of vertigo. However, sudden change in tumor size with hemorrhage or disruption
of regional blood flow to the labyrinth may precipitate vertigo. Majority of tumors in the CPA are
vestibular schwannomas, followed by meningiomas, lipomas, cholesteatomas, and metastatic
tumors.
 Vertigo is the initial presenting symptom in 5% cases of multiple sclerosis. The vertigo may last
several days to weeks; it may be positional in nature and is often associated with facial numbness
and weakness, and diplopia.
 Posttraumatic vertigo may be peripheral in origin (benign paroxysmal positional vertigo,
perilymphatic fistula, labyrinthine concussion, labyrinthine fracture) or central (cerebral
concussion). Postconcussion syndrome usually follows a mild head injury. Symptoms are
characterized by vertigo, headaches, blurred vision, diplopia, fatigue, and personality changes.

3.  Familial periodic ataxia syndromes represent a rare form of chronic recurring bouts of episodic
vertigo. There is a family history of recurrent spells of vertigo. Patients present with recurrent
vertigo, prominent nausea and vomiting, diplopia and dysarthria with the spells, and a progressive
truncal ataxia. Spells are precipitated by physical exertion or emotional stress. Acetazolamide is
effective in controlling episodic vertigo.
 Rarely does central nervous system infection cause vertigo. Lyme neuroborreliosis can have vertigo
as a presenting feature of Lyme disease encephalopathy.
 Psychogenic vertigo is a manifestation of panic or anxiety disorder. Patients will describe a
sensation of unsteadiness, vertigo, lightheadedness, and less often nausea and vomiting with the
symptoms.
Physical:
 During asymptomatic periods, patients with migraine-associated vertigo have normal physical
examinations. During migraine, patients may exhibit motion-intolerance, diaphoresis, and vomiting.
Occasionally nystagmus is observed during an attack; rarely does the migraine include dysarthria,
aphasia, hemiparesis, or extremity ataxia.
 When symptomatic, a cardiac examination may reveal arrhythmia as the cause of symptoms. If
hyperventilation is suspected, having the patient hyperventilate may precipitate the symptoms.
Orthostatic changes in pulse and blood pressure should be documented if accompanied by symptoms of
lightheadedness.
 Direction changing, gaze-evoked nystagmus, and severe truncal ataxia with limb incoordination are
findings associated with cerebellar infarction. Lateral medullary infarction also will cause direction-
changing nystagmus, but there will be associated signs indicating brainstem damage such as decreased
gag reflex, facial numbness, Horner syndrome, and dysphonia. Saccadic eye movements are disrupted;
gait is ataxic. Lateral pontomedullary syndrome also presents with nystagmus, defective saccades, and
hearing loss.
 CPA tumors that cause vertigo will also cause unilateral hearing loss and may present with nystagmus.
Nystagmus may be evident only in the dark or with Frenzel glasses, which remove visual fixation. Head
thrust test may reveal unilateral vestibular weakness. Large tumors may cause subtle facial weakness,
decreased corneal reflex, and facial dysesthesia.
 Differentiation between central and peripheral causes of vertigo is facilitated by a precise oculomotor
examination. Spontaneous nystagmus that cannot be suppressed with visual fixation; nystagmus that
changes direction with gaze; purely vertical, horizontal, or torsional nystagmus; and saccade dysmetria
(overshoot and undershoot) are all signs of a potential central abnormality as the cause of vertigo.
 Paroxysmal positional nystagmus that is of central origin usually does not fatigue with repeated
positioning maneuvers, has no latency of onset, lasts longer than 60 seconds, is often vertical in direction,
and may change direction with different head positions.
 Vertigo of a panic attack can sometimes be elicited by having the patient hyperventilate. Most patients
with psychogenic vertigo do not have any pathological findings on otologic or neurologic examination.
Causes:
 Central vertigo syndromes resulting from acute vascular events most commonly result from a
combination of hypertension and regional atherosclerosis.

4.  Less commonly, arterial dissection secondary to neck extension, rotational injury, or osteoarthritic spurs
is the cause of disturbed posterior fossa blood flow.
 Migraine and presyncopal lightheadedness are two forms of regional and global ischemia that may
present with vertigo or imbalance as the primary symptom.
WORKUP
Lab Studies:
 Few laboratory studies facilitate the diagnosis of central causes of vertigo.
 If vertigo is accompanied by prolonged nausea and vomiting, monitoring and replacing fluids and
electrolytes in the elderly would be prudent.
 In the rare case of suspected neuroborreliosis, serology for Lyme disease with ELISA, Western blot, and
lymphocyte antigen stimulation assay would be indicated.
 Cerebrospinal fluid should be obtained for Lyme antibody and polymerase chain reaction analysis
for Borrelia burgdorferi DNA.
Imaging Studies:
 Imaging studies are indicated when there is a suspicion that the symptoms are the result of ischemia.
MRI and MR angiography are the most helpful studies in assessing posterior circulation disorders and
acute infarction.
Other Tests:
 Formal evaluation with vestibular testing is indicated if the diagnosis is not apparent after obtaining a
history and performing a physical examination.
 Caloric testing will reveal if there is a unilateral peripheral weakness.
 Oculomotor testing can detect saccade, pursuit, and optokinetic disturbances.
 Positional testing with infrared oculography can detect nystagmus and clearly define nystagmus
patterns.
 Complete cardiac and peripheral vascular examination (ECG, Holter, echocardiogram, carotid and
vertebral doppler) should be performed if symptoms suggest hypoperfusion, embolic events, or
arrhythmia as the cause.
TREATMENT
Medical Care:
 Medical treatment includes supportive care with fluid replacement and vestibular suppressants for
intractable vertigo with nausea and vomiting.
 Treatment of migraine-associated vertigo includes analgesics and vestibular suppressants. Drugs useful
in the treatment of migraine include sumatriptan, propranolol, imipramine, amitriptyline, and

5. nortriptyline and vestibular suppressants diazepam and alprazolam. For further information on the
diagnosis and treatment of migraine headache please refer to the chapter Migraine Headache.
 Control of hypertension, diabetes, and atherosclerosis is indicated for long-term prevention of further
complications. Cardiac arrhythmia should be controlled.
 Drugs useful in the treatment of vertebrobasilar insufficiency include aspirin, ticlopidine, pentoxifylline,
heparin, and warfarin.
 Acetazolamide is indicated for the treatment of familial ataxia syndrome.
Surgical Care:
 Surgical treatment of central vertigo is limited to urgent posterior fossa decompression of cerebellar and
brainstem edema complicating the infarction.
 Cerebello-pontine angle tumors are surgically removed on an elective basis. If there is a medical
contraindication, radiotherapy for tumor control is an option.
MEDICATION
The goal of pharmacotherapy is to reduce morbidity and prevent complications.
Drug Category: Antihistamines -- Prevent the histamine response in sensory nerve endings and blood
vessels. Are effective in treating vertigo.
Meclizine (Antivert, Antrizine, Meni-D) -- Decreases
excitability of middle ear labyrinth and blocks conduction in
Drug Name middle ear vestibular-cerebellar pathways. These effects are
associated with therapeutic effects in the relief of nausea
and vomiting.
Adult Dose 25 mg PO q4-6h
<12 years: Not established
Pediatric Dose
>12 years: Administer as in adults
Contraindications Documented hypersensitivity
May increase toxicity of CNS depressants, neuroleptics, and
Interactions
anticholinergics
Pregnancy B - Usually safe but benefits must outweigh the risks.
Caution in angle-closure glaucoma, prostatic hypertrophy,
Precautions pyloric or duodenal obstruction, and bladder neck
obstruction
Dimenhydrinate (Dimetabs, Dramamine) -- A 1:1 salt of 8
chlorotheophylline and diphenhydramine thought to be
useful in the treatment of vertigo.
Drug Name Diminishes vestibular stimulation and depresses
labyrinthine function through central anticholinergic effects.
However, prolonged treatment may decrease rate of
recovery of vestibular injuries.
Adult Dose 50 mg PO or IM q4-6h or 100 mg supp q8h

6. <2 years: Not established
2-5 years: Up to 12.5-25 mg PO q6-8h; not to exceed 75
mg/24h
6-12 years: 25-50 mg PO q6-8h; not to exceed 150 mg/24h
Pediatric Dose
>12 years: Administer as in adults
Alternatively, 1.25 mg/kg or 37.5 mg/m2 IM qid; not to
exceed 300 mg/d
Documented hypersensitivity; do not administer to
neonates; IV products may contain benzyl alcohol, which
Contraindications
has been associated with fatal quot;Gasping syndromequot; in
premature infants and low birth weight infants
Alcohol or other CNS depressants may have additive effect
Interactions on dimenhydrinate; may mask ototoxic symptoms, caused
by certain antibiotics and irreversible damage may result
Pregnancy B - Usually safe but benefits must outweigh the risks.
Do not treat severe emesis with antiemetic drugs alone; may
contain either sulfites or tartrazine, which may cause
allergic-type reactions in susceptible persons; may impede
Precautions
diagnosis of conditions, such as brain tumors, intestinal
obstruction and appendicitis; may obscure signs of toxicity
from overdosage of other drugs
Drug Category: Anticholinergics -- Work centrally by suppressing conduction in the vestibular cerebellar
pathways.
Scopolamine (Isopto) -- Blocks action of acetylcholine at
parasympathetic sites in smooth muscle, secretory glands
and the CNS. Antagonizes histamine and serotonin action.
Drug Name
Transdermal scopolamine may be the most effective agent
for motion sickness. Its use in vestibular neuronitis is
limited by its slow onset of action.
Adult Dose 0.6 mg PO q 4-6h or 0.5 mg transdermally q3d
6 mcg/kg/dose IM/SC/IV; not to exceed 0.3 mg/dose, or 0.2
Pediatric Dose
mg/m2 and repeat q6-8h
Documented hypersensitivity; primary glaucoma (including
initial stages), pyloric obstruction, toxic megacolon, hepatic
Contraindications
disease, paralytic ileus, severe ulcerative colitis, renal
disease, obstructive uropathy, and myasthenia gravis
Antipsychotic effectiveness of phenothiazines may be
decreased by coadministration with scopolamine;
anticholinergic side effects may be increased by concurrent
therapy and phenothiazine dosages should be adjusted as
Interactions necessary; coadministration with tricyclic antidepressants,
may increase anticholinergic side effects (eg, dry mouth,
constipation, urinary retention) due to additive effect
(tricyclic antidepressants with less anticholinergic activity
may be beneficial)
C - Safety for use during pregnancy has not been
Pregnancy
established.
Caution in the elderly because of increased incidence of

7. glaucoma; large doses may suppress intestinal motility and
precipitate or aggravate toxic megacolon; anticholinergics
may aggravate hiatal hernia associated with reflux
Precautions esophagitis; patients with prostatism can have dysuria and
may require catheterization; use cautiously in patients with
asthma or allergies; a reduction in bronchial secretions can
lead to inspissation and formation of bronchial plugs
Drug Category: Benzodiazepines -- By binding to specific receptor-sites these agents appear to potentiate
the effects of gamma-aminobutyrate (GABA) and facilitate inhibitory GABA neurotransmission and other
inhibitory transmitters. These effects may prevent vertigo and emesis.
Diazepam (Valium) -- Depresses all levels of CNS (eg,
limbic and reticular formation), possibly by increasing
Drug Name activity of GABA.
Individualize dosage and increase cautiously to avoid
adverse effects.
Adult Dose 5-10 mg PO/IV/IM q4-6h
<6 months: Not recommended
>6 months: 0.05-0.3 mg/kg/dose IM/IV over 2-3 min; repeat
Pediatric Dose in 2-4 h prn
Alternatively, 0.12-0.8 mg/kg/24h PO divided q6-8h; not to
exceed 10 mg/dose
Documented hypersensitivity; narrow-angle glaucoma;
Contraindications
children <3 mo
Increases toxicity of benzodiazepines in CNS with
Interactions coadministration of phenothiazines, barbiturates, alcohols,
and MAO inhibitors
Pregnancy D - Unsafe in pregnancy
Caution with other CNS depressants, low albumin levels, or
Precautions
hepatic disease (may increase toxicity)
Drug Category: Phenothiazines -- Effective in treating emesis possibly due to effects in dopaminergic
mesolimbic system.
Promethazine (Phenergan) -- For symptomatic treatment of
nausea in vestibular dysfunction.
Drug Name Antidopaminergic agent effective in treating emesis. Blocks
postsynaptic mesolimbic dopaminergic receptors in brain
and reduces stimuli to brainstem reticular system.
Adult Dose 25-50 mg PO/IM/PR q4-6h
<2 years: Not recommended
Pediatric Dose
>2 years: 0.25-1.0 mg/kg PO/IV/IM/PR 4-6 times/d prn
Contraindications Documented hypersensitivity
May have additive effects when used concurrently with
Interactions other CNS depressants or anticonvulsants; coadministration
with epinephrine, may cause hypotension
C - Safety for use during pregnancy has not been
Pregnancy
established.
Some of the adverse effects include CNS depression, dry
mouth, extrapyramidal symptoms, hypertension, and skin
rash Caution in cardiovascular or hepatic disease, seizures,

8. sleep apnea, and asthma; may enhance effects of other
Precautions medications that cause CNS depression including alcohol,
narcotics, sedatives, hypnotics, etc
Prochlorperazine (Compazine) -- May relieve nausea and
vomiting by blocking postsynaptic mesolimbic dopamine
Drug Name
receptors through anticholinergic effects and depressing
reticular activating system.
Adult Dose 5-10 mg PO/IM q6h 25 mg supp PR q12h
2.5 mg PO/PR q8h or 5 mg q12h, prn; not to exceed 15
mg/d
Pediatric Dose
0.1-0.15 mg/kg/dose IM; change to PO as soon as possible
IV dosing not recommended for children
Documented hypersensitivity; bone marrow suppression,
narrow angle glaucoma, severe liver or cardiac disease;
comatose patients or patients with large amounts of central
Contraindications
nervous system depressants in their system (eg, alcohol or
barbiturates); do not use in surgery in children <2 y or that
weigh <20 lb
Coadministration with other CNS depressants or
Interactions anticonvulsants may cause additive effects; with
epinephrine may cause hypotension
Pregnancy D - Unsafe in pregnancy
Side effects include CNS depression, blurred vision, and
hypotension; neuroleptic malignant syndrome and
extrapyramidal dystonic reactions may rarely occur
Drug-induced Parkinson’s syndrome or
Precautions
pseudoparkinsonism occurs quite frequently; akathisia is
most common extrapyramidal reaction in elderly; lowers
seizure threshold and should be used cautiously in patients
with a history of seizures
Drug Category: Monoaminergics -- May treat vertigo possibly through modulating the sympathetic
system.
Ephedrine (Pretz-D) -- Stimulates release of epinephrine
Drug Name
stores, producing alpha- and beta-adrenergic effects.
Adult Dose 25 mg PO q4-6h
< 2 years: Not recommended
Pediatric Dose 2-5 years: 3 mg q6-8h
>5 years: 6.25 mg PO/SC q6-8h
Documented hypersensitivity; angle-closure glaucoma, and
Contraindications
cardiac arrhythmias
Theophylline, atropine, or MAO inhibitors may increase
toxicity; alpha- and beta-blockers decrease vasopressor
Interactions
effects of ephedrine; cardiac glycosides and general
anesthetics increase cardiac stimulation of ephedrine
Pregnancy B - Usually safe but benefits must outweigh the risks.
Side effects include excitation, tremulousness, insomnia,
nervousness, palpitation, tachycardia, and symptoms
associated with sympathetic activation; bladder sphincter

9. spasm can occur and cause transient acute urinary retention;
caution in the elderly and patients with diabetes mellitus,
Precautions
hyperthyroidism, hypertension, cardiovascular disease,
prostatic hypertrophy, and cerebrovascular insufficiency
FOLLOW-UP
Further Outpatient Care:
 After the underlying cause of vertigo has been identified and treated, supportive care with vestibular
suppressants and antiemetics are indicated for relief of vertigo.
BIBLIOGRAPHY
 Asmundson GJ, Larsen DK, Stein MB: Panic disorder and vestibular disturbance: an overview of
empirical findings and clinical implications. J Psychosom Res 1998 Jan; 44(1): 107-20.
 Curless RG, Schatz NJ, Bowen BC, et al: Lyme neuroborreliosis masquerading as a brainstem tumor in
a 15-year- old. Pediatr Neurol 1996 Oct; 15(3): 258-60.
 Cutrer FM, Baloh RW: Migraine-associated dizziness. Headache 1992 Jun; 32(6): 300-4.
 Davies RA, Luxon LM: Dizziness following head injury: a neuro-otological study. J Neurol 1995 Mar;
242(4): 222-30.
 Stewart WF, Lipton RB, Celentano DD, Reed ML: Prevalence of migraine headache in the United States.
Relation to age, income, race, and other sociodemographic factors. JAMA 1992 Jan 1; 267(1): 64-9.
 Welsh LW, Welsh JJ, Jaffe SC, Healy MP: Syndromal vertigo identified by magnetic resonance imaging
and angiography. Laryngoscope 1996 Sep; 106(9 Pt 1): 1144-51.
THE AUTHOR
Professor Yasser Metwally
Professor of neurology, Ain Shams University, Cairo, Egypt
http://yassermetwally.com