vestibular neuritis

**Definition:** Acute unilateral peripheral vestibulopathy due to inflammation of the vestibular nerve (superior division most commonly affected). When the labyrinth is also involved with hearing loss/tinnitus, it is termed labyrinthitis (vestibular neuritis = vestibular only; labyrinthitis = vestibular + cochlear).

**Pathophysiology:** Presumed viral etiology, most often reactivation of latent HSV-1 in the vestibular ganglion (Scarpa's ganglion); often follows a viral URI. Loss of unilateral tonic vestibular input causes a tone imbalance: the intact side dominates, driving the eyes slowly toward the lesion with corrective fast saccades away from the lesion.

**Clinical presentation:** - Abrupt-onset, severe, continuous vertigo (days; peaks in first 24 h, improves over days to weeks) - Nausea, vomiting, oscillopsia, postural imbalance (falls/veering toward the affected side) - NO hearing loss, tinnitus, or aural fullness - NO brainstem/cerebellar signs (diplopia, dysarthria, dysphagia, limb ataxia, facial numbness/weakness)

**Exam findings (HINTS exam – "INFARCT" = central):** - Head Impulse test: ABNORMAL (corrective saccade when head turned toward the affected side) – peripheral - Nystagmus: unidirectional, horizontal ± torsional, fast phase away from the lesion; suppressed by visual fixation, follows Alexander's law (intensifies when looking in direction of fast phase); never changes direction with gaze - Test of Skew: NORMAL (no vertical skew deviation) - Central pattern (concerning for posterior circulation stroke): normal head impulse, direction-changing nystagmus, or skew deviation. Remember: HINTS is only for patients with continuous vertigo + spontaneous nystagmus (acute vestibular syndrome). - Romberg/gait: falls toward the affected side but can usually walk (vs. central: unable to walk unaided).

**Diagnosis:** Clinical. Imaging (MRI brain) if any central features, vascular risk factors, or abnormal HINTS. Audiometry normal. Caloric testing shows reduced response on the affected side (canal paresis).

**Differential:** - Labyrinthitis (hearing loss) - Posterior circulation stroke/cerebellar infarct (AICA stroke causes vertigo + hearing loss + facial palsy) - BPPV: brief (<1 min) positional episodes, Dix-Hallpike positive, no hearing loss - Meniere disease: episodic vertigo (20 min–hours), fluctuating low-frequency sensorineural hearing loss, tinnitus, aural fullness; endolymphatic hydrops - Vestibular migraine - Acoustic neuroma (vestibular schwannoma): gradual unilateral hearing loss/tinnitus, NF2 association - Ramsay Hunt syndrome (VZV): vertigo + hearing loss + facial palsy + ear vesicles

**Management:** - Acute (first 1–3 days): vestibular suppressants (meclizine, dimenhydrinate, benzodiazepines) and antiemetics (ondansetron, promethazine) – short course only, because prolonged use impairs central compensation - Corticosteroids (e.g., prednisone taper) started early may improve recovery of peripheral vestibular function; antivirals are not helpful - Early vestibular rehabilitation therapy/ambulation to promote central compensation (key long-term intervention) - Prognosis: generally good, most recover; some have residual dizziness. Recurrence is uncommon (recurrent episodes should prompt reconsideration, e.g., Meniere or vestibular migraine).

**High-yield pearls:** - Acute vertigo + hearing loss = labyrinthitis (or AICA stroke, so look for other deficits) - Acute vertigo, no hearing loss, + normal head impulse = think central cause (stroke) - Nystagmus is named by its fast phase, which is directed away from the lesion in peripheral vestibular loss - Peripheral vertigo: horizontal/torsional, suppressed by fixation; central vertigo: vertical, pure torsional, or direction-changing, not suppressed by fixation