Vertigo and facial nerve palsy

Definition / Overview

Vertigo is the illusion of rotational movement of the patient or their environment, arising from asymmetric signalling within the peripheral or central vestibular system. It is distinct from pre-syncope (reduced cerebral perfusion) and non-specific disequilibrium (multifactorial, often non-vestibular).

The three conditions covered here account for the majority of peripheral vestibular disorders encountered in otolaryngology practice:

• Benign paroxysmal positional vertigo (BPPV): the most common cause of vertigo at any age; otolith dysfunction causing brief, position-triggered episodes
• Menière's disease: endolymphatic hydrops producing episodic vertigo with low-frequency sensorineural hearing loss (SNHL), aural fullness and tinnitus
• Vestibular neuronitis (VN): acute unilateral vestibular deafferentation, typically viral or post-viral, producing a single prolonged episode of vertigo without hearing loss

Clinical Assessment of Vertigo

History Framework

The history alone discriminates peripheral from central causes in most cases. Key domains:

• Character: true rotational vertigo vs. light-headedness vs. oscillopsia
• Duration of each episode: seconds (BPPV), minutes-to-hours (Menière's), days (VN/labyrinthitis)
• Triggers: head position change (BPPV), stress/salt load (Menière's), spontaneous onset after viral illness (VN)
• Associated symptoms: hearing loss, tinnitus, aural fullness (cochlear = Menière's/labyrinthitis); headache, diplopia, dysphagia, dysarthria, limb ataxia (central)
• Recurrence pattern: single prolonged episode vs. episodic vs. chronic continuous

Encourage patients to describe the sensation without using the word "dizzy" to maximise diagnostic precision.

Examination

Central vs. Peripheral Differentiation

Must-not-miss: posterior fossa stroke mimicking acute peripheral vertigo. The HINTS battery has higher sensitivity for posterior circulation stroke than early MRI diffusion imaging within the first 24 hours. Any normal HIT, direction-changing nystagmus, or vertical skew mandates urgent neuroimaging.

Benign Paroxysmal Positional Vertigo

Pathophysiology

Free-floating calcium carbonate crystals (otoconia) detach from the utricular macula and migrate into a semicircular canal. The posterior canal is affected in ~85-90% of cases; horizontal canal in ~10%; anterior canal rarely. Two mechanisms:

• Canalolithiasis: free debris floating in the canal endolymph, causing cupular deflection with head movement; nystagmus has a latency and fatigues
• Cupulolithiasis: debris adherent to the cupula, causing continuous cupular deflection in provocative positions; nystagmus is immediate and non-fatiguing

Risk factors include head trauma, prolonged bed rest, Menière's disease, vestibular neuronitis, osteoporosis (particularly in older women), and vitamin D deficiency.

Clinical Features

• Episodes last $< 60$ seconds (typically $< 30$ s for posterior canal BPPV)
• Triggered by head position changes: lying down, rolling over, looking up, bending forward
• Rotational vertigo with associated nausea; no hearing loss or tinnitus
• Positive Dix-Hallpike: upbeat-torsional nystagmus, latency, and fatiguability are the diagnostic triad for posterior canal BPPV

Management of BPPV

Posterior Canal BPPV: Epley Canalith Repositioning Manoeuvre

The Epley manoeuvre is first-line treatment; reported resolution rates $> 80\%$ after one session.

1. Start in Dix-Hallpike position to the affected side (down ear)
2. Rotate head 90° toward the unaffected ear
3. Roll body with head to the lateral decubitus position (face-down 45°)
4. Return to seated upright, chin slightly tucked

Post-procedure activity restrictions are not routinely required. Repeat the manoeuvre if symptoms persist; $> 90\%$ of patients achieve resolution within one to three treatments.

Horizontal Canal BPPV

• Geotropic (canalolithiasis): Barbecue roll (360° rotation toward the unaffected ear) or Gufoni manoeuvre
• Apogeotropic (cupulolithiasis): Gufoni manoeuvre or forced prolonged positioning toward the unaffected ear

Adjuncts

• Vestibular rehabilitation (Brandt-Daroff exercises) as second-line or for refractory cases
• Vestibular sedatives (prochlorperazine, betahistine) are not effective for BPPV; avoid as they suppress central compensation
• Surgical: posterior semicircular canal occlusion or singular neurectomy reserved for intractable cases unresponsive to repeated repositioning; very rarely required

Recurrence

Recurrence rate is approximately 15-30% per year. Screen for osteoporosis and vitamin D deficiency in recurrent cases, particularly in older women. Treat underlying Menière's disease if coexistent.

Menière's Disease

Pathophysiology

Menière's disease results from endolymphatic hydrops: abnormal distension of the endolymphatic compartment of the membranous labyrinth. The mechanism is debated but likely involves impaired endolymph resorption by the endolymphatic sac, producing elevated endolymphatic pressure. Rupture of the Reissner's membrane mixes potassium-rich endolymph with perilymph, transiently depolarising hair cells and producing the acute attack.

Histopathological findings include ballooning of the scala media, displacement of Reissner's membrane, and eventual degeneration of cochlear hair cells with long-standing disease.

Diagnostic Criteria (AAO-HNS / Barany Society)

Definite Menière's disease:

• Two or more spontaneous episodes of rotational vertigo, each lasting 20 minutes to 12 hours
• Audiometrically documented low-to-medium frequency SNHL in the affected ear on at least one occasion before, during, or after a vertigo episode
• Fluctuating aural symptoms (hearing loss, tinnitus, or fullness) in the affected ear
• Symptoms not better explained by another diagnosis

Probable Menière's disease: meets criteria except audiometric documentation.

The tetrad of symptoms: episodic rotational vertigo + fluctuating low-frequency SNHL + tinnitus + aural fullness.

Clinical Features

• Episodes last 20 minutes to several hours (typically 2-4 hours)
• Hearing loss characteristically fluctuates early in the disease, recovers between attacks, then progressively worsens
• Low-frequency SNHL is the audiometric signature early; a "flat" or "ski-slope" pattern emerges later
• Unilateral in ~80-85% of cases; bilateral in 15-20% (consider autoimmune aetiology)
• Lermoyez variant: hearing improves at the onset of the vertiginous episode
• Drop attacks (Tumarkin otolithic crises): sudden falls without loss of consciousness, from sudden utricular dysfunction; occur in later disease

Investigations

Gadolinium-enhanced T1-weighted MRI (preferably at 3T, with delayed imaging at 4 hours after IV gadolinium or 24 hours after intratympanic gadolinium) demonstrates endolymphatic hydrops as expansion of the scala media.

Management of Menière's Disease

Lifestyle and Dietary Modification (First Line)

• Low-sodium diet ($< 1500\,\text{mg/day}$) with consistent fluid intake
• Avoidance of caffeine, alcohol, nicotine
• Stress reduction; sleep hygiene
• Explain the episodic natural history and counselling regarding driving during active disease

Medical Management

Intratympanic Therapy

• Intratympanic dexamethasone: preserves hearing; reduces vertigo frequency; repeatable; preferred when hearing preservation is the priority. Delivered 4 mg/mL via myringotomy or sustained-release device.
• Intratympanic gentamicin: chemical ablation of vestibular hair cells (partial or complete labyrinthectomy). Highly effective for vertigo control (~80-90%). Risk of additional SNHL (~20-30%). Reserved for patients with disabling vertigo and poor/non-serviceable hearing in the affected ear, or when dexamethasone fails. Low-dose titration protocol preferred to minimise SNHL.

Surgical Options (Refractory Disease)

Endolymphatic sac surgery is the least destructive operation but has the lowest vertigo control rate. Vestibular neurectomy offers high vestibular control while preserving cochlear function, at the cost of a posterior fossa approach and its associated risks.

Bilateral Menière's Disease

Requires particular caution with destructive procedures. Bilateral ablation risks bilateral vestibular failure, producing chronic oscillopsia and profound disequilibrium. Intratympanic dexamethasone and dietary/medical management preferred.

Vestibular Neuronitis

Pathophysiology

Vestibular neuronitis (VN) is acute unilateral peripheral vestibular failure, most commonly attributed to reactivation of herpes simplex virus type 1 (HSV-1) within the vestibular ganglion (Scarpa's ganglion), by analogy with HSV pathophysiology in Bell's palsy. The superior vestibular nerve is more frequently involved than the inferior, likely due to its longer bony canal with less room for ischaemic decompression.

The sudden loss of tonic vestibular afference from one labyrinth produces a dynamic asymmetry: the brainstem interprets the imbalance as rotational movement. Central compensation involving the cerebellum and brainstem occurs over days to weeks, restoring perceived balance even with persistent peripheral hypofunction.

Labyrinthitis is the closely related condition where inflammatory deafferentation also affects the cochlear division, producing associated hearing loss and/or tinnitus in addition to the vestibular syndrome.

Clinical Features

• Acute onset of severe, continuous rotational vertigo lasting days to weeks (typically 3-7 days severe phase)
• Spontaneous horizontal-torsional nystagmus beating toward the unaffected ear (fast phase away from the lesion)
• Nystagmus suppressed by fixation (peripheral pattern)
• Positive head impulse test toward the affected side
• Normal hearing (distinguishes VN from labyrinthitis)
• Absence of neurological signs
• Nausea and vomiting proportionate to the vertigo severity
• History of recent viral upper respiratory tract illness in up to 50%
• Recovery: acute vertigo resolves over days; subtle imbalance on dynamic tasks may persist for weeks to months; a minority develop chronic disequilibrium or secondary BPPV

Investigations

VN is a clinical diagnosis. Investigations are directed at excluding central pathology:

• HINTS battery: mandatory in any acute sustained vestibular syndrome. Normal HIT + direction-changing nystagmus + vertical skew = stroke until proven otherwise
• MRI with gadolinium: if HINTS suggests central cause, atypical features, vascular risk factors, or failure to improve within expected timeframe. Posterior circulation strokes can initially mimic VN; MRI may be false-negative in the first 24-48 hours (DWI limitations)
• Audiogram: to exclude cochlear involvement (labyrinthitis, Menière's)
• Caloric testing / vHIT: confirms unilateral canal paresis; low-frequency (caloric) deficit with preserved high-frequency (vHIT) response suggests partial lesion

Management

Acute Phase (Days 1-3)

1. Vestibular sedatives to control nausea and vertigo:
   • Prochlorperazine 12.5 mg IM or 10 mg oral TDS
   • Promethazine 25 mg IM/oral if prochlorperazine insufficient
   • Diazepam 5-10 mg oral/IV: for severe distress; short-term only
2. IV fluids if unable to tolerate oral intake
3. Reassurance regarding the benign, self-limiting nature
4. Limit vestibular sedative duration to 2-3 days maximum: prolonged use suppresses central compensation and prolongs recovery

Subacute Phase (Days 3 Onward)

• Vestibular rehabilitation: supervised exercises targeting gaze stabilisation, static and dynamic balance. Promotes central compensation. Evidence supports faster functional recovery compared to no rehabilitation.
• Cease all vestibular suppressants once acute nausea/vomiting resolves

Role of Corticosteroids and Antivirals

• Methylprednisolone: evidence from randomised trials supports improved recovery of peripheral vestibular function when commenced early (within 3 days). Recommended dose: 100 mg reducing over 3 weeks. Benefit on symptomatic recovery less clear but vestibular function recovery is supported.
• Aciclovir/valaciclovir: not demonstrated to improve outcomes in randomised trials; not routinely recommended in current evidence-based guidelines despite HSV aetiology hypothesis.

Prognosis

• Most patients achieve functional compensation within 6 weeks
• Recurrence of VN is uncommon (approximately 2-10%)
• Secondary BPPV develops in up to 10-15% of patients following VN; examine for this if symptoms recur or change character

Complications and Special Considerations

BPPV Complications

• Persistent BPPV despite multiple repositioning attempts: consider incorrect canal identification, cupulolithiasis variant, coexistent Menière's disease, or central mimicry
• Falls risk: counsel patients regarding driving and working at heights during active symptoms
• Anxiety and panic disorder are common comorbidities; address concurrent with vestibular rehabilitation

Menière's Disease Complications

• Progressive SNHL: the dominant long-term morbidity; hearing rehabilitation with hearing aids or, in advanced bilateral disease, cochlear implantation
• Bilateral involvement: worst prognostic outcome; monitor the contralateral ear with serial audiometry
• Gentamicin toxicity: bilateral ablation risk if disease becomes bilateral after unilateral IT gentamicin
• Surgical risks of vestibular neurectomy: sensorineural hearing loss (~5%), CSF leak, meningitis, facial nerve injury (rare but dependent on approach)

Vestibular Neuronitis Complications

• Failure to compensate: predisposed by anxiety, sedentary behaviour, older age, central nervous system disease; managed with structured rehabilitation
• Secondary BPPV: treat with repositioning manoeuvres
• Unrecognised posterior fossa stroke: the most critical complication of misdiagnosis; maintain a low threshold for neuroimaging in patients with vascular risk factors or atypical examination findings

Perioperative and Long-Term Management

Fitness to Drive

Patients with active disabling vertigo (BPPV, acute Menière's attack, acute VN) must not drive. AUSTROADS guidelines apply; patients should be counselled explicitly and documentation kept. Return to driving when episodes are controlled and the treating clinician is satisfied with symptom stability.

Occupational Considerations

Working at heights, operating heavy machinery, and aviation duties are contraindicated during active vestibular disease. Formal occupational health assessment may be required.

Hearing Rehabilitation in Menière's Disease

• Conventional hearing aids once the SNHL is stable
• Bone conduction devices if conductive component exists
• Cochlear implantation in patients with advanced bilateral SNHL; outcomes are comparable to other causes of SNHL and should be discussed early with the MDT

Audiological Monitoring

All three conditions require serial audiometry:

• BPPV: baseline only; no cochlear involvement expected
• Menière's disease: 6-monthly audiograms to monitor progression and guide management decisions
• VN / labyrinthitis: if hearing was affected at onset, monitor until stable

Patient Education and Self-Management

• Written information regarding trigger avoidance (Menière's), dietary modification, and rescue medication
• Explain the distinction between vestibular neuronitis and stroke clearly; provide documentation for emergency department presentations
• Menière's disease support groups and balance rehabilitation programmes are available through audiology and physiotherapy services in the Australian and New Zealand public hospital network