Vestibular Neuritis: Diagnosis and Management
Definitive Diagnosis
Vestibular neuritis is diagnosed clinically in an adult presenting with acute, severe rotatory vertigo lasting 12–36 hours (with decreasing disequilibrium over 4–5 days), nausea, vomiting, and gait instability, in the complete absence of hearing loss, tinnitus, aural fullness, facial weakness, or focal neurological deficits. 1
The key discriminator is the absence of auditory symptoms—no hearing loss, no tinnitus, no ear fullness—which distinguishes vestibular neuritis from labyrinthitis (which presents with profound hearing loss) and Ménière's disease (which presents with fluctuating hearing loss and aural fullness). 1, 2
Clinical Presentation
- Severe rotational vertigo lasting 12–36 hours at peak intensity, followed by 4–5 days of gradually improving disequilibrium. 1
- Severe nausea and vomiting are typical. 1, 2
- Intolerance to head motion is prominent. 2
- Horizontal spontaneous nystagmus (with a rotational component) beating toward the unaffected ear. 3
- Postural imbalance with falls toward the affected ear. 3
- No auditory symptoms: no hearing loss, no tinnitus, no aural fullness. 1, 2
- No focal neurological deficits: no dysarthria, dysphagia, diplopia, limb weakness, or Horner's syndrome. 1, 2
Critical Differential: Ruling Out Stroke
Approximately 25% of patients with acute vestibular syndrome have cerebellar or brainstem stroke, not peripheral vestibular disease; this proportion rises to 75% in high-vascular-risk cohorts (age >50 years with hypertension, diabetes, atrial fibrillation, or prior stroke). 2, 4
Red Flags Requiring Urgent MRI Brain Without Contrast
- Age >50 years with any vascular risk factor (hypertension, diabetes, atrial fibrillation, prior stroke), even if neurologic exam is normal. 2, 5
- Severe postural instability with frequent falls. 2, 5
- New severe headache accompanying vertigo. 2, 5
- Any focal neurological symptoms: dysarthria, dysphagia, diplopia, limb weakness, sensory loss, Horner's syndrome. 2, 4
- Pure vertical nystagmus (up-beating or down-beating) without torsional component. 2, 4
- Direction-changing nystagmus without changes in head position. 2, 4
- Baseline nystagmus present without provocative maneuvers. 2, 4
- Normal head-impulse test (suggests central cause). 2, 4
- Skew deviation on alternate cover testing. 2, 4
If any red flag is present, obtain urgent MRI brain without contrast with diffusion-weighted imaging; CT head has <1% diagnostic yield for posterior-circulation stroke and should not be substituted for MRI. 2, 5
Diagnostic Testing
When Imaging Is NOT Indicated
No imaging is required for typical vestibular neuritis when the neurologic exam is normal, there are no red-flag features, and the clinical presentation is consistent with peripheral vestibular disease. 2, 5
Head-Impulse Test
- Pathologic head-impulse test toward the affected ear confirms ipsilateral vestibuloocular reflex deficit. 3, 6
Audiometry
- Comprehensive audiologic examination is mandatory to definitively exclude labyrinthitis; vestibular neuritis shows normal audiometry, whereas labyrinthitis demonstrates sensorineural hearing loss on the affected side. 2
First-Line Treatment
Corticosteroids (Within 3 Days of Onset)
Oral corticosteroids should be initiated within 3 days of symptom onset to accelerate recovery of vestibular function. 2, 7
- Recommended regimen: Methylprednisolone 100 mg daily for 3 days, then taper over 7–10 days. 2
- Evidence: Corticosteroids achieve a 62% recovery rate of labyrinthine function within 12 months, compared to incomplete recovery without treatment. 7, 3
- Withhold steroids in patients at higher risk of complications (e.g., uncontrolled diabetes, active infection, significant immunosuppression). 7
Symptomatic Management (Acute Phase Only)
Vestibular suppressants (e.g., meclizine, diazepam) and antiemetics should be used sparingly and discontinued after a maximum of 3 days; prolonged use impedes central vestibular compensation. 2, 8, 7
- Meclizine: 25–100 mg daily orally in divided doses for acute symptom relief only. 8
- Antiemetics (e.g., metoclopramide, prochlorperazine) for severe nausea/vomiting. 2
- Rationale for early discontinuation: Vestibular suppressants delay central compensation and prolong recovery. 2, 7
Vestibular Rehabilitation
Early resumption of normal activity should be encouraged to promote central vestibular compensation; directed vestibular rehabilitation therapy is indicated for persistent symptoms after the acute phase. 2, 7, 6
- Vestibular exercises (habituation, gaze stabilization, balance retraining) significantly improve gait stability and accelerate recovery. 2, 6
- Initiate rehabilitation as soon as acute nausea/vomiting resolves (typically after 3–5 days). 7, 6
Prognosis
- Most patients recover well, even without treatment, though recovery may be incomplete. 7, 3
- Peripheral restoration of labyrinthine function is usually incomplete but improved by early corticosteroid therapy. 3
- Central compensation (via somatosensory and visual substitution) is the primary mechanism of long-term recovery and is enhanced by vestibular rehabilitation. 3
Common Pitfalls
- Assuming absence of focal neurologic deficits excludes stroke: 75–80% of posterior-circulation strokes presenting with acute vestibular syndrome lack focal deficits. 2, 4
- Prolonged use of vestibular suppressants: Impedes central compensation and delays recovery; limit to 3 days maximum. 2, 7
- Failing to obtain audiometry: Hearing loss is the key discriminator between vestibular neuritis (no hearing loss) and labyrinthitis (profound hearing loss). 2
- Ordering imaging for typical vestibular neuritis without red flags: Diagnostic yield is <1%; imaging is unnecessary when clinical presentation is consistent with peripheral disease and neurologic exam is normal. 2, 5