Vestibular Neuritis and Labyrinthitis

Introduction

Vestibular neuritis and labyrinthitis are closely related causes of acute, severe, continuous vertigo, typically arising after a viral upper respiratory tract infection. Vestibular neuritis is inflammation confined to the vestibular portion of the eighth cranial nerve, sparing hearing. Labyrinthitis involves the whole labyrinth, including the cochlea, and so additionally causes hearing loss and/or tinnitus.¹

The most important clinical task is not simply naming the condition, but distinguishing it from a posterior circulation stroke, which can present in an almost identical way. A structured bedside examination - the HINTS exam - is central to making this distinction safely.

Aetiology and pathophysiology

Most cases are presumed viral, either from direct viral infection of the vestibular nerve or ganglion, or from a post-viral immune-mediated process; herpes simplex virus reactivation has been implicated by analogy with Bell's palsy, though a causative organism is rarely confirmed in practice.^1,2

Bacterial labyrinthitis is a distinct and more serious entity, arising from direct bacterial spread into the labyrinth from acute or chronic otitis media, cholesteatoma, or meningitis. It carries a much higher risk of permanent hearing loss and needs urgent treatment of the underlying infective source, unlike the self-limiting viral form.²

Risk factors

• Recent upper respiratory tract or other viral infection
• Age 30-60 years, though it can occur at any age
• Concurrent or recent acute otitis media or cholesteatoma (risk factor for bacterial labyrinthitis specifically)
• Immunocompromise

Clinical features

The onset is acute, with severe, continuous vertigo that is present even at rest and worsened by any head movement, in contrast to the purely positional trigger of BPPV. Symptoms typically peak within the first 24-48 hours and then gradually improve over 1-6 weeks as the brain compensates centrally for the loss of peripheral vestibular input.¹

Nausea, vomiting and marked gait unsteadiness are prominent, and patients often prefer to lie still. Labyrinthitis additionally causes hearing loss and/or tinnitus in the affected ear, which is the key clinical feature separating it from vestibular neuritis.

Examination: the HINTS exam

In a patient with acute, continuous vertigo ("acute vestibular syndrome"), the HINTS exam is a validated bedside tool that outperforms early MRI for distinguishing a peripheral cause from a posterior circulation stroke, and should be performed in anyone with vascular risk factors or where the diagnosis is not obviously benign.³

Counterintuitively, a normal head impulse test in a patient with severe ongoing vertigo is the concerning finding, because it suggests the vestibular pathway is intact and the problem lies centrally. Gait should also be assessed: a patient who is unable to walk at all, or walks with marked truncal ataxia out of proportion to the vertigo, raises concern for a cerebellar stroke.³

Differential diagnosis

• Posterior circulation stroke or TIA: particularly in patients with vascular risk factors - excluded using the HINTS exam and, if uncertain, MRI
• BPPV: brief, positional vertigo rather than continuous vertigo lasting days
• Meniere's disease: episodic (not continuous) vertigo with fluctuating hearing loss and aural fullness
• Vestibular migraine: associated headache, photophobia or personal/family history of migraine
• Bacterial labyrinthitis: distinguished by an identifiable source of infection (otitis media, cholesteatoma, meningitis) and a more unwell, septic patient

Investigations

Vestibular neuritis and viral labyrinthitis are clinical diagnoses. Audiometry confirms and quantifies any hearing loss, distinguishing labyrinthitis from neuritis. MRI brain is indicated if the HINTS exam suggests a central cause, if there is diagnostic uncertainty, or if vascular risk factors make stroke a significant concern.^1,3

If bacterial labyrinthitis is suspected, investigate as for the underlying source - otoscopy, inflammatory markers, blood cultures, and CT temporal bones or lumbar puncture as clinically indicated - and involve ENT urgently.

Management

Management of viral vestibular neuritis and labyrinthitis is supportive. Short courses (ideally no more than 3 days) of a vestibular sedative such as prochlorperazine or cyclizine control acute nausea and vertigo; treatment is deliberately kept brief because prolonged use can slow the central compensation process that ultimately resolves symptoms.¹

Corticosteroids are sometimes used for vestibular neuritis with the aim of speeding recovery of vestibular function, though evidence for a clear long-term benefit is mixed, and their use should be individualised. Admission is considered for patients unable to tolerate oral fluids because of vomiting, or where the diagnosis remains uncertain and observation or urgent imaging is needed.

Vestibular rehabilitation exercises, ideally started once the acute nausea has settled, actively promote central compensation and are particularly valuable for patients with persistent imbalance beyond the initial acute phase.

Complications

• Chronic unilateral vestibular hypofunction with persistent imbalance, particularly if central compensation is incomplete
• Secondary BPPV, which can develop following an episode of vestibular neuritis
• Permanent sensorineural hearing loss, particularly with bacterial labyrinthitis
• Anxiety related to the fear of further attacks
• Missed stroke if a central cause is not adequately excluded

Red flags

Prognosis

Most patients improve substantially within days and continue to recover over 1-6 weeks as central compensation occurs, even though the peripheral vestibular deficit itself may not fully resolve. A minority experience persistent imbalance, particularly with exertion or in visually complex environments, which usually responds well to vestibular rehabilitation.¹ Labyrinthitis carries an additional risk of permanent hearing loss in the affected ear, which should be monitored with follow-up audiometry.