Vestibular Neuritis and Labyrinthitis

Risk factors

• Preceding upper respiratory viral illness (1-2 weeks prior in many cases)
• Reactivation of latent HSV-1 within Scarpa's ganglion (leading hypothesis)
• Recent ear infection (bacterial labyrinthitis)
• Cholesteatoma or chronic otitis media (suppurative labyrinthitis)
• Autoimmune disorders
• Vascular risk factors (raise suspicion for stroke mimics)

Pathophysiology

Vestibular neuritis is most often attributed to viral (HSV-1) reactivation within the vestibular ganglion or post-infectious immune-mediated demyelination of the superior vestibular nerve (which supplies the horizontal and anterior semicircular canals and utricle). Labyrinthitis involves both vestibular and cochlear structures and may be viral (post-URI) or bacterial (from acute otitis media, meningitis, or cholesteatoma — a true emergency).

Clinical presentation

Differential diagnosis

• Posterior circulation stroke (especially PICA/AICA) — CRITICAL mimic — central HINTS pattern (normal head impulse, direction-changing nystagmus, skew deviation), other brainstem/cerebellar signs, vascular risk factors; MRI with DWI to exclude
• Ménière disease — Recurrent episodes 20 min-12 h with low-frequency hearing loss, tinnitus, aural fullness; not a single prolonged event
• BPPV — Brief (seconds) positional vertigo; Dix-Hallpike positive
• Vestibular migraine — Recurrent episodes with migraine features; vertigo duration variable
• Multiple sclerosis — Younger patients, recurrent or progressive course, other CNS findings, demyelinating MRI lesions
• Acoustic neuroma — Progressive unilateral SNHL, gradual imbalance, MRI confirms
• Ramsay Hunt syndrome (herpes zoster oticus) — Vertigo + hearing loss + ipsilateral facial palsy + vesicular ear-canal rash

Diagnostic workup

Treatment

Complications

• Persistent unilateral vestibular hypofunction with chronic imbalance
• Permanent hearing loss (labyrinthitis)
• Secondary BPPV (debris dislodged into posterior canal during acute event) — Dix-Hallpike at follow-up
• Persistent postural-perceptual dizziness (PPPD) — chronic functional dizziness after acute event
• Falls and injury
• Anxiety and avoidance behaviors
• Suppurative labyrinthitis: meningitis, intracranial extension

PANCE pearls

• The most important task in AVS is to distinguish vestibular neuritis from a posterior circulation stroke — use HINTS (head impulse, nystagmus direction, test of skew), not MRI alone (MRI DWI may be falsely negative in the first 24-48 h for posterior strokes).
• Peripheral pattern (consistent with neuritis): ABNORMAL head impulse (catch-up saccade toward affected side), UNIDIRECTIONAL nystagmus, NO skew deviation.
• Central pattern (consistent with stroke): normal head impulse, direction-CHANGING nystagmus, or skew deviation — refer urgently for stroke evaluation.
• Limit vestibular suppressants to ~3 days — chronic use impairs central compensation.
• Steroids accelerate recovery in vestibular neuritis (per Strupp NEJM 2004); antivirals do not.
• Pure hearing loss without vertigo is NOT labyrinthitis — consider sudden sensorineural hearing loss (SSNHL), an emergency requiring high-dose steroids.

References

• Bárány Society 2022 — Strupp M et al. Acute unilateral vestibulopathy/vestibular neuritis: Diagnostic criteria. J Vestib Res 2022;32:389-406.
• Strupp 2004 — Strupp M et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. NEJM 2004;351:354-361.
• HINTS — Kattah JC et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI DWI. Stroke 2009;40:3504-3510.