What are the distinguishing clinical features of vestibular neuritis versus labyrinthitis and the recommended management for each?

Vestibular Neuritis vs Labyrinthitis: Clinical Differentiation and Management

The single most critical distinguishing feature between vestibular neuritis and labyrinthitis is the presence or absence of hearing loss: vestibular neuritis presents with acute, severe rotatory vertigo lasting days without any auditory symptoms, while labyrinthitis presents with identical vertigo plus profound sensorineural hearing loss. 1, 2

Key Clinical Differentiators

Vestibular Neuritis

• Presents with sudden severe rotatory vertigo lasting 12-36 hours with decreasing disequilibrium over 4-5 days, accompanied by severe nausea and vomiting. 1
• Completely absent auditory symptoms—no hearing loss, no tinnitus, no aural fullness. 1, 3
• Horizontal spontaneous nystagmus with rotational component beating toward the unaffected ear. 4
• Positive head-impulse test toward the affected ear. 4
• Postural imbalance with falls toward the affected ear. 4

Labyrinthitis

• Sudden severe vertigo with profound hearing loss and prolonged vertigo lasting more than 24 hours. 1
• Vertigo and nausea occur simultaneously with hearing loss. 1
• Not episodic, not fluctuating—symptoms are continuous and persistent. 1
• Sensorineural hearing loss documented on audiometry of the affected ear. 2

Critical Diagnostic Pitfall: Ruling Out Stroke

Approximately 25% of patients presenting with acute vestibular syndrome have cerebellar or brainstem stroke, not peripheral vestibular disease—this rises to 75% in high vascular risk populations. 2

Red Flags Requiring Immediate MRI

• Severe postural instability with actual falling during gait testing. 2
• Direction-changing nystagmus without head position changes. 5
• Purely vertical nystagmus without torsional component. 5, 2
• Any additional neurologic symptoms (dysarthria, dysphagia, diplopia, limb weakness). 5
• New-onset severe headache concurrent with vertigo. 5, 2
• Nystagmus not suppressed by visual fixation. 5

Do not assume peripheral vestibular disease in patients with significant vascular risk factors (hypertension, diabetes, smoking, atrial fibrillation) even if the presentation appears typical for vestibular neuritis. 3, 6

Diagnostic Workup

Essential Clinical Assessment

• Perform comprehensive audiologic examination to definitively distinguish between the two conditions—labyrinthitis will demonstrate sensorineural hearing loss on the affected side. 2
• Document nystagmus characteristics: peripheral causes produce horizontal-rotatory nystagmus that is unidirectional and suppressed by visual fixation. 5
• Perform head-impulse test: positive (corrective saccade) indicates peripheral vestibular loss. 4

When Imaging Is NOT Indicated

• No neuroimaging is required for typical vestibular neuritis or labyrinthitis if the neurologic exam is completely normal and no red flags are present. 2
• Diagnostic yield of CT in isolated dizziness is less than 1%. 5

When Imaging IS Mandatory

• Obtain urgent MRI brain with diffusion-weighted imaging if any red-flag features are present or if clinical differentiation between peripheral and central vertigo is uncertain. 5, 2

Management

Vestibular Neuritis Treatment

• Oral corticosteroids within 3 days of onset accelerate recovery of vestibular function: methylprednisolone 100mg daily for 3 days, then taper over 7-10 days. 2, 6
• Corticosteroids achieve 62% recovery rate of labyrinthine function within 12 months. 4
• Withhold steroids in patients at higher risk of complications (uncontrolled diabetes, immunosuppression, active infection). 6

Symptomatic Management (Both Conditions)

• Antiemetics and vestibular suppressants (meclizine, diazepam) should be used sparingly and discontinued after 3 days maximum—prolonged use impedes central vestibular compensation. 1, 2, 6
• Vestibular suppressants are useful only for acute severe nausea/vomiting, not as primary treatment. 1

Rehabilitation

• Early resumption of normal activity should be encouraged immediately to promote central compensation. 6
• Directed vestibular rehabilitation therapy accelerates recovery, particularly for persistent imbalance. 6, 7
• Recovery occurs through three mechanisms: incomplete peripheral restoration, somatosensory/visual substitution, and central compensation. 4

Prognosis

• Most patients recover well from vestibular neuritis even without treatment, though peripheral vestibular function may never fully return. 6, 7
• Static symptoms (vertigo, nausea, spontaneous nystagmus) invariably resolve, though often not completely. 7
• Dynamic symptoms (impaired vestibulo-ocular reflexes on head-impulse testing) improve only slightly if at all. 7
• Persistent imbalance after acute phase may be due to inadequate central compensation or incomplete peripheral recovery. 7

Common Clinical Pitfalls

• Do not rely on absence of focal neurologic deficits to exclude stroke—75-80% of posterior circulation strokes present without focal findings. 5
• Do not prescribe vestibular suppressants beyond the first few days—they prevent the central compensation necessary for recovery. 1, 2, 6
• Do not assume vestibular neuritis in elderly patients with vascular risk factors without considering stroke. 3, 6
• Recognize that 10% of cerebellar strokes present identically to peripheral vestibular disorders. 5