Vertigo — Central and Peripheral

Vestibular System Anatomy and Function

• Peripheral vestibular dysfunction: Pathology of the labyrinth, vestibular nerve (CN VIII), or root entry zone results in asymmetric vestibular tone. The ipsilateral nucleus receives less inhibition, causing the eyes and posture to drift toward the lesion; central nervous system compensation generates slow-phase nystagmus away from the lesion (fast phase defines direction). Canal paresis produces vertigo proportional to the degree of asymmetry. Endolymphatic displacement (BPPV) mechanically stimulates cupulae, generating brief vertigo with characteristic latency and fatigability.

• Central vestibular dysfunction: Brainstem lesions (medial longitudinal fasciculus, vestibular nuclei, root entry zone of CN VIII) or cerebellar infarction/hemorrhage impair the VOR and gaze-holding mechanisms. Unlike peripheral causes, central lesions often produce direction-changing or purely vertical nystagmus, defective smooth pursuit, and additional neurologic deficits (cranial nerve palsies, motor/sensory findings). Cerebellar dysfunction specifically impairs temporal coordination of eye movements and produces dysmetria and dysdiadochokinesia.

• Adaptation and compensation: Central neural pathways (cerebellar flocculus, nodulus, uvula) dynamically recalibrate the VOR and substitute visual/proprioceptive cues after peripheral vestibular loss. This explains why peripheral vestibular symptoms improve over weeks to months despite permanent end-organ damage, whereas acute central lesions may produce persistent deficits.

PERIPHERAL CAUSES (80% of vertigo)

• Benign paroxysmal positional vertigo (BPPV): Calcium carbonate otoconia (otoliths) detach from the utricle and migrate into semicircular canals, most commonly the posterior canal (85–90% of cases). Predisposing factors include head trauma, prolonged immobility, osteoporosis, and aging. Idiopathic BPPV increases in prevalence after age 60.

• Vestibular neuritis (vestibular neuronitis): Presumed viral inflammation of the vestibular division of CN VIII, often preceded by upper respiratory infection. Sudden-onset severe vertigo persists 3–7 days with spontaneous nystagmus but no auditory symptoms (distinguishing from labyrinthitis).

• Labyrinthitis: Viral or bacterial inflammation of both vestibular and cochlear divisions; presents with concurrent vertigo and sensorineural hearing loss ± tinnitus. Bacterial labyrinthitis is a complication of meningitis or otitis media/mastoiditis.

• Ménière disease: Idiopathic endolymphatic hydrops causing episodic vertigo (minutes to hours), fluctuating sensorineural hearing loss, tinnitus, and aural fullness. Attacks increase with sodium intake and stress.

• Vestibular migraine: Vertigo lasting minutes to hours associated with migraine headaches; most common cause of recurrent vertigo in young patients.

• Ototoxicity: Aminoglycosides (especially gentamicin and tobramycin), vancomycin, loop diuretics (furosemide), and cisplatin damage vestibular hair cells; risk increases with renal impairment and concurrent nephrotoxins.

• Perilymphatic fistula: Abnormal communication between middle and inner ear perilymph following head trauma, barotrauma (diving), or chronic ear disease; causes positional vertigo and fluctuating hearing loss.

CENTRAL CAUSES (10–15% of vertigo)

• Brainstem infarction: Predominantly lateral medullary infarction (Wallenberg syndrome) affecting the nucleus tractus solitarius and inferior cerebellar peduncle; causes ipsilateral facial pain/thermoanesthesia, contralateral body pain/temperature loss, and vertigo with ipsilateral nystagmus. Basilar artery occlusion is life-threatening.

• Cerebellar stroke (infarction or hemorrhage): Acute cerebellar infarction (territory of PICA or AICA) or spontaneous cerebellar hemorrhage causes vertigo, ataxia, headache, and vomiting; risk of brainstem compression from edema requiring emergency decompression.

• Posterior fossa tumors: Vestibular schwannoma (acoustic neuroma), meningioma, medulloblastoma, or hemangioblastoma present with progressive vertigo, hearing loss, and ataxia.

• Multiple sclerosis: Demyelination of the medial longitudinal fasciculus (internuclear ophthalmoplegia) or brainstem nuclei; typically young patients with monocular vision loss, weakness, or prior neurologic events.

• Paroxysmal brainstem attacks: Vertebrobasilar insufficiency, Arnold-Chiari malformation, or syrinx produce episodic vertigo mimicking peripheral causes but with additional brainstem signs.

RISK FACTORS

• Peripheral: Age >60, female sex, head trauma, immobility, osteoporosis, viral illness, ototoxic medications, diving/pressure changes
• Central: Age >50, hypertension, diabetes, smoking, atrial fibrillation, prior stroke, MS, family history of migraine

PERIPHERAL VERTIGO

• Cardinal symptoms: Spinning sensation with rotatory illusion of environment; typically acute or subacute onset; severe and disabling; reproducible by positional changes (BPPV) or associated with specific triggers (migraine)

• Nystagmus characteristics: Unidirectional (beats in same direction regardless of gaze direction); rotatory or mixed component; no vertical component in pure peripheral disease; fatigues with repeated positional testing (nystagmus declines with each Dix-Hallpike); suppressed by visual fixation

• Associated symptoms:
• BPPV: Brief vertigo (seconds to 1 minute) triggered by position changes; latency of 5–20 seconds; fatigable nystagmus
• Vestibular neuritis: Sudden severe vertigo lasting days; unilateral hearing preserved; prominent horizontal-rotatory nystagmus; positive head impulse test
• Ménière disease: Episodic attacks (20 minutes to several hours); fluctuating low-frequency sensorineural hearing loss; tinnitus; aural fullness
• Vestibular migraine: Moderate vertigo; associated with migraine features; photophobia; phonophobia

• Physical exam findings:
• Positive Dix-Hallpike maneuver: Patient supine with head extended off table; if posterior canal BPPV, nystagmus develops with 5–20 second latency, beats toward affected ear
• Positive head impulse test (thrust test): Patient fixates on examiner's nose while head is rapidly moved; with peripheral vestibular loss, eyes lag behind head motion (corrective saccade required). Normal VOR prevents visual lag.
• Romberg test: May show increased body sway but patient typically maintains balance
• Fukuda stepping test: Deviation toward affected ear from baseline
• Gait: Wide-based, veering toward lesion; no true ataxia (coordinated limb movements preserved)

CENTRAL VERTIGO

• Cardinal symptoms: Spinning sensation typically less severe than peripheral; onset variable; often persistent rather than episodic; frequently accompanied by other neurologic deficits

• Nystagmus characteristics: Often direction-changing (e.g., rightward with rightward gaze, leftward with leftward gaze); may be purely vertical, upbeating, or downbeating; does not fatigue; not suppressed by fixation (present despite visual attention); may reflect underlying pathology (downbeating nystagmus = spinocerebellum pathology; upbeating = medial longitudinal fasciculus or rostral brainstem)

• Associated neurologic deficits (critical differentiator):
• Brainstem signs: Cranial nerve palsies (CN VII facial droop, CN XII tongue deviation, CN V trigeminal loss); contralateral motor/sensory loss; ataxia (limb coordination abnormality on finger-nose and heel-shin testing)
• Cerebellar signs: DANISH (Dysarthria, Ataxia, Nystagmus, Dysdiadochokinesia, headache, Intention tremor, Scan speech); no motor weakness but profound dysmetria; severe headache if hemorrhage; rapid neurologic deterioration if edema
• Posterior circulation: Headache; loss of consciousness; visual field defects; dysarthria

• Head impulse test: Normal or preserved in most central lesions (VOR intact via intact brainstem pathways), contrasting sharply with peripheral vestibular loss

• Smooth pursuit and saccades: Often abnormal with central lesions (pursuits irregular/fragmented; saccades dysmetric or slowed)

BEDSIDE EXAMINATION

• Dix-Hallpike maneuver: Most sensitive test for posterior canal BPPV (sensitivity 80%). Patient supine with head extended off edge; if positive, rotatory nystagmus toward affected ear with 5–20 second latency, duration <1 minute, fatigues with repeat testing. Repeat several times; fatigue is pathognomonic for BPPV and rare in other conditions.

• Head Impulse Test (vestibulo-ocular reflex test): Patient fixates on examiner's nose during rapid passive head rotations (~20° amplitude, 1–2 Hz). Positive test (corrective saccade) = impaired VOR, indicating peripheral vestibular loss. Negative test (smooth pursuit maintained) = preserved VOR, suggesting central pathology or intact peripheral system. Interpretation: absent saccade during head impulse = peripheral loss; catch-up saccade = peripheral loss; no saccade = normal VOR.

• Nystagmus characterization:
• Observe direction (rightward, leftward, vertical), velocity profile (exponential decay = peripheral; linear = central), fatigability (decreases with repetition = BPPV; persistent = central), fixation suppression (abolished by visual fixation = peripheral; persists = central)
• Vertical or direction-changing nystagmus is virtually always central and warrants urgent MRI

• Gaze-holding tests: Ask patient to sustain eccentric gaze. Gaze-evoked nystagmus (nystagmus develops during sustained off-center gaze) suggests cerebellar pathology or brainstem dysfunction.

• Smooth pursuit and saccadic testing: Fragmented or slowed pursuits or dysmetric saccades indicate central pathology

• Romberg test: Typically normal in peripheral vestibular disease (patient compensates); positive (cannot stand with feet together and eyes closed) suggests central pathology or severe proprioceptive loss

• Fukuda stepping test: Patient marches in place for 1 minute with eyes closed. Deviation >45° from baseline toward affected side suggests peripheral vestibular loss. Less sensitive than head impulse test.

DIAGNOSTIC CRITERIA & DECISION RULES

• ABCD² score (for posterior circulation stroke): Age ≥60 (1 point), blood pressure ≥140/90 (1 point), clinical features (unilateral weakness or speech disturbance = 2 points, other symptom = 1 point), duration ≥60 minutes (2 points), diabetes (1 point). Score ≥4 = ~10% 2-day stroke risk, requires urgent imaging.

• Vertigo Risk Stratification for Stroke (VARS): Focal neurologic deficits, history of stroke/TIA, age >60, and continuous vertigo (not episodic) identify patients at higher central stroke risk.

IMAGING & SPECIALIZED TESTING

• MRI brain with contrast (gold standard for central causes): Diffusion-weighted imaging (DWI) reveals acute brainstem or cerebellar infarction as hyperintense lesions within hours of symptom onset (more sensitive than conventional T2 for acute stroke). Fluid-attenuated inversion recovery (FLAIR) shows subacute/chronic changes. Gradient echo detects hemorrhage (hypointense). Contrast-enhanced T1 reveals mass lesions (schwannoma with characteristic "ice-cream cone" appearance), meningitis, or demyelination. Indicated in all suspected central causes and any atypical peripheral presentation.

• CT head (non-contrast): Less sensitive but excludes hemorrhage and acute large infarctions in stroke protocol settings. Useful when MRI contraindicated or unavailable.

• Audiometry: Sensorineural pattern (bone conduction better than air conduction at low frequencies = retrocochlear pathology) suggests vestibular schwannoma or labyrinthitis; flat low-frequency hearing loss typical of Ménière disease.

• Electonystagmography (ENG) and videonystagmography (VNG): Measure eye movements quantitatively; caloric testing (thermal stimulation of each ear with warm and cold water) assesses vestibular function bilaterally. Unilateral weakness (one side produces smaller nystagmus) indicates peripheral vestibular loss on that side. Less used acutely but helpful in chronic evaluation.

• Posturography (dynamic or static): Assesses balance and vestibular-proprioceptive integration; useful in vestibular rehabilitation assessment but not diagnostic acutely.

• Lumbar puncture (LP): Indicated when meningitis or leptomeningeal disease suspected (pleocytosis, elevated protein, low glucose); obtained before imaging if meningitis concern high.

LABORATORY TESTS

• CBC with differential: Elevated WBC suggests infection (labyrinthitis, meningitis)
• Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP): Elevated in infection or vasculitis
• Rapid plasma reagin (RPR)/VDRL: Syphilis can cause labyrinthitis
• Lyme serology (ELISA with Western blot confirmation): Lyme-related facial nerve palsy may accompany vertigo in endemic areas

DIAGNOSTIC APPROACH ALGORITHM

Acute vertigo with nystagmus

1. 1.Bedside exam (head impulse, Dix-Hallpike, nystagmus type, focal deficits)
2. 2.If normal head impulse + nystagmus = BPPV (posterior canal most common); positive Dix-Hallpike confirms
3. 3.If abnormal head impulse + horizontal nystagmus + no focal deficits = vestibular neuritis; supportive MRI shows normal brain
4. 4.If direction-changing or vertical nystagmus OR focal neurologic deficits = urgent MRI to exclude central cause
5. 5.**If imaging normal + episodic attacks

Immediate stabilisation (rule out the killer first)

• Acute vestibular syndrome with central features: treat as posterior circulation stroke. Per the AHA/ASA acute ischemic stroke guideline, obtain emergent imaging and give IV thrombolysis (tissue plasminogen activator, e.g., alteplase) if within the window and no contraindication; endovascular thrombectomy is indicated for basilar/vertebral large-vessel occlusion. Posterior-circulation deficits often score low on the NIHSS — do not let a low score exclude thrombolysis.
• Cerebellar infarct or hemorrhage with mass effect: neurosurgical emergency. AHA/ASA guidance supports suboccipital decompressive craniectomy ± external ventricular drain for brainstem compression or obstructive hydrocephalus; medical therapy alone is inadequate.

First-line therapy by peripheral etiology

• BPPV: canalith repositioning — the Epley maneuver for posterior canal, the Lempert/barbecue roll for horizontal canal. The AAO-HNS BPPV guideline (2017 update) recommends repositioning as initial treatment and recommends against routine vestibular suppressants and against routine imaging. Brandt-Daroff exercises are an adjunct for home use.
• Vestibular neuritis/labyrinthitis: brief symptomatic control with a vestibular suppressant — antihistamine (meclizine), benzodiazepine (diazepam), or antiemetic (ondansetron, promethazine) — limited to roughly the first 24–72 hours, plus fluids. Corticosteroids are sometimes used but the evidence is inconsistent. Vestibular rehabilitation is the definitive treatment because recovery depends on central compensation.
• Ménière disease: sodium restriction and a diuretic (thiazide or thiazide-like, e.g., hydrochlorothiazide-triamterene) per the AAO-HNS Ménière disease guideline; escalate to intratympanic corticosteroid, then ablative intratympanic gentamicin, endolymphatic sac surgery, labyrinthectomy, or vestibular nerve section for refractory disease.
• Vestibular migraine: trigger avoidance plus standard migraine prophylaxis (beta blocker propranolol, TCA amitriptyline, or topiramate).

Contraindicated / avoid

• Prolonged vestibular suppressants: blunt central adaptation and prolong disability; anticholinergic and sedative burden causes falls and delirium in older adults.
• Meclizine as a substitute for repositioning in BPPV — explicitly discouraged by AAO-HNS.
• Systemic aminoglycosides in a patient with vestibulotoxicity risk.

Emergencies

• Cerebellar edema with brainstem compression or obstructive hydrocephalus: peak swelling occurs a few days after a PICA/AICA infarct; signalled by declining consciousness, new gaze palsy, hypertension with bradycardia, or worsening headache/vomiting. Requires emergent decompression per AHA/ASA.
• Basilar artery occlusion: progressive thrombosis of the vertebrobasilar system; signalled by fluctuating vertigo with dysarthria, diplopia, quadriparesis, or depressed consciousness — the locked-in endpoint. Emergent CTA/MRA and thrombectomy.
• Bacterial labyrinthitis extending to meningitis: infection tracks through the cochlear aqueduct or internal auditory canal; signalled by fever, neck stiffness, and altered mental status in a patient with otitis media/mastoiditis. Emergent lumbar puncture and IDSA-guided antibiotics.
• Missed posterior-circulation stroke labelled "peripheral vertigo": the single most consequential complication of this presentation.

Disease-related

• Falls and fragility fracture: loss of vestibulospinal postural control, compounded by age and sedating drugs; signalled by recurrent unwitnessed falls.
• Permanent sensorineural hearing loss: progressive hair-cell and endolymphatic damage in Ménière disease and labyrinthitis; audiometry shows loss that no longer fluctuates.
• **Tumarkin otolithic crisis (drop attacks): sudden otolithic discharge in advanced Ménière disease causing abrupt collapse without** loss of consciousness — commonly mistaken for syncope or seizure.
• Persistent postural-perceptual dizziness (PPPD): failed central compensation with maladaptive visual dependence; nonvertiginous unsteadiness persisting months after a resolved acute event.
• Bilateral vestibulopathy: signalled by oscillopsia (bouncing vision when walking) and gait instability worse in the dark.

Treatment-related

• Canal conversion during repositioning: otoconia migrate from posterior to horizontal canal; signalled by new geotropic/apogeotropic horizontal nystagmus on supine roll test.
• Intratympanic gentamicin ablation: hair-cell death causing chronic imbalance, oscillopsia, and hearing loss.
• Vestibular suppressants: anticholinergic delirium, sedation, falls, and impaired central compensation prolonging symptoms.

• HINTS beats early MRI in acute vestibular syndrome: Head Impulse, Nystagmus, Test of Skew. A normal head impulse (no catch-up saccade), direction-changing nystagmus, or skew deviation on cover–uncover = central (INFARCT). Apply HINTS only to continuous vertigo with nystagmus, never to episodic positional vertigo. Diffusion-weighted MRI can be falsely negative in the first hours after a small brainstem/cerebellar infarct.
• Best next step in classic BPPV is the Epley maneuver, not a drug and not imaging — the AAO-HNS BPPV guideline recommends against routine vestibular suppressants and routine neuroimaging in unambiguous BPPV.
• The buzzword triad by duration: seconds with position change = BPPV; days, continuous, no hearing loss = vestibular neuritis; 20 minutes to hours with fluctuating low-frequency hearing loss, tinnitus, and aural fullness = Ménière disease.
• Hearing loss separates neuritis from labyrinthitis — and does not rule out stroke. An AICA infarct knocks out the labyrinthine artery, producing vertigo plus acute hearing loss, mimicking a peripheral lesion. This is the association examiners love.
• Vertical or purely downbeating nystagmus, or nystagmus not suppressed by fixation, is central until proven otherwise — think cerebellar/craniocervical junction pathology (Chiari malformation) and get MRI.
• Common distractor: non-contrast CT. CT is insensitive for posterior fossa ischemia; its only role is excluding hemorrhage. Ordering CT and calling it reassuring is the wrong answer.
• Truncal ataxia — inability to sit or walk unsupported — is central. Peripheral vertigo patients veer toward the lesion but can still ambulate.
• Progressive unilateral sensorineural hearing loss with poor speech discrimination and imbalance = vestibular schwannoma at the cerebellopontine angle; MRI with gadolinium; bilateral lesions mean NF2.
• Meclizine is a bridge, not a therapy — extended use delays central compensation and causes falls in the elderly.