Key Facts

Vestibular neuritis (vestibular neuronitis) is an acute unilateral vestibular loss causing prolonged rotational vertigo. It is the most common cause of acute vestibular syndrome and must be differentiated from posterior circulation stroke.

Epidemiology

• Annual incidence: 3.5 per 100,000
• Peak age: 30-60 years
• No sex predominance
• Accounts for 5-10% of all vertigo presentations
• Often preceded by viral URTI (1-2 weeks before)

Aetiology

• Viral reactivation: HSV-1 reactivation in Scarpa's (vestibular) ganglion is the leading theory
• Post-infectious inflammation of the vestibular nerve
• Superior vestibular nerve affected more commonly than inferior division
• Vascular ischaemia of the vestibular nerve is an alternative hypothesis

Pathophysiology

• Unilateral vestibular nerve inflammation causes acute loss of vestibular input from one labyrinth
• Tonic vestibular imbalance: the intact contralateral vestibular system generates relative excitation
• This imbalance is perceived as rotation (vertigo) and drives spontaneous nystagmus towards the intact ear
• Central compensation begins within hours to days via cerebellar and brainstem adaptation
• Vestibular rehabilitation accelerates central compensation
• Incomplete compensation may result in chronic dizziness/imbalance

Typical Presentation

• Acute onset severe rotational vertigo (usually developing over hours)
• Duration: 24-72 hours of intense vertigo, then gradual improvement over 1-6 weeks
• Severe nausea and vomiting
• Postural instability: difficulty standing/walking, falling towards affected side
• May have preceding viral URTI symptoms
• No hearing loss, no tinnitus (if present, consider labyrinthitis or Ménière)

Examination Findings

• Spontaneous horizontal-torsional nystagmus: beating AWAY from the affected ear
  • Follows Alexander's law: increases when looking in direction of fast phase
  • Inhibited by visual fixation (use Frenzel glasses to unmask)
• Positive head impulse test (HIT): corrective saccade when head turned towards affected side
• Negative test of skew: no vertical misalignment (skew deviation suggests central cause)
• Romberg positive: falls towards affected side
• Gait deviation towards affected side

Red Flags (Suggesting Central Cause — Stroke)

• Negative head impulse test (normal) with acute vertigo — paradoxically suggests central lesion
• Direction-changing nystagmus (changes with gaze direction)
• Skew deviation (vertical misalignment on alternate cover test)
• Acute hearing loss with vertigo (consider AICA stroke)
• New headache, especially occipital
• Truncal ataxia unable to sit unsupported
• Other neurological signs (diplopia, dysarthria, dysphagia, limb ataxia)

Bedside

• HINTS exam (most important bedside assessment):
  • Head Impulse Test (HIT): positive (abnormal) = peripheral (reassuring)
  • Nystagmus: unidirectional, inhibited by fixation = peripheral
  • Test of Skew: negative = peripheral
  • HINTS positive for peripheral cause = safe to diagnose vestibular neuritis
  • HINTS suggesting central cause = urgent MRI/neurology
• Hearing assessment (whispered voice, tuning forks): should be normal
• Blood pressure, blood glucose
• Gait assessment

Bloods

• Not routinely required
• Consider glucose, lipids, coagulation if stroke risk factors

Imaging

• Not routinely required if HINTS confidently peripheral
• MRI brain (DWI): if any central features on HINTS exam, stroke risk factors, or diagnostic uncertainty
  • DWI-negative MRI within first 48 hours does NOT fully exclude posterior fossa stroke (sensitivity ~80% in first 24 hours)

Special Tests

• Caloric testing: absent or reduced vestibular response on affected side (canal paresis >25%)
• vHIT (video Head Impulse Test): quantitative assessment of VOR; reduced gain on affected side
• Pure tone audiometry: should be normal (if abnormal, diagnose labyrinthitis)
• Vestibular evoked myogenic potentials (VEMPs): assess inferior vestibular nerve function

Non-pharmacological

• Vestibular rehabilitation exercises: most important treatment; begin as soon as acute symptoms allow (usually 3-5 days)
  • Cawthorne-Cooksey exercises: head movements, balance exercises, gait training
  • Customised vestibular physiotherapy
  • Promote central compensation
• Early mobilisation (avoid prolonged bed rest)
• Adequate hydration (especially if vomiting)

Pharmacological

• Acute phase (first 3-5 days only):
  • Prochlorperazine 5-10mg TDS PO or buccal 3-6mg BD
  • Cyclizine 50mg TDS
  • Ondansetron 4-8mg for severe vomiting
  • STOP vestibular sedatives after 3-5 days — prolonged use delays vestibular compensation
• Corticosteroids: methylprednisolone starting at 100mg OD, tapered over 3 weeks (Strupp et al., NEJM 2004 — showed improved vestibular recovery)
  • Evidence is modest; not universally adopted
  • If used, start within 72 hours of symptom onset
• Antivirals (valaciclovir): no evidence of benefit; NOT recommended

Surgical

• Not applicable for vestibular neuritis

Referral Criteria

• Emergency assessment if central features on HINTS exam (stroke)
• ENT/audiovestibular referral if: not improving after 6 weeks, recurrent episodes, hearing loss develops
• Vestibular physiotherapy referral for rehabilitation
• Neurology referral if diagnostic uncertainty or atypical features

• Most patients recover well over 1-6 weeks with vestibular rehabilitation
• 50-70% achieve complete vestibular compensation within 3 months
• 30-50% have persistent mild imbalance or dizziness at 1 year
• Caloric testing: 50% show persistent canal paresis at 1 year (asymptomatic due to central compensation)
• 10-15% develop BPPV subsequently (otoconia displaced during acute illness)
• Recurrence of vestibular neuritis is rare (<2%)
• Incomplete compensation more likely in elderly patients and those with delayed mobilisation
• Prolonged use of vestibular sedatives significantly delays recovery

HINTS Exam Interpretation

Vestibular Neuritis vs Labyrinthitis

Strupp et al. (NEJM 2004) Key Findings