Vestibular Neuritis

1. 0:00Vestibular neuritis is the unilateral counterpart to bilateral vestibulopathy. In bilateral disease the DVA pattern is symmetric loss with no directional asymmetry. In neuritis the pattern inverts — directional asymmetry is the diagnostic clue, and the absolute loss may be modest once central compensation kicks in.
2. 0:25The Bárány Society in 2022 renamed the condition acute unilateral vestibulopathy — AUVP — keeping vestibular neuritis as an acceptable synonym. The new criteria require an acute or subacute spinning or non-spinning vertigo of moderate or severe intensity lasting at least 24 hours, spontaneous peripheral nystagmus appropriate to the canal afferents involved, unambiguous evidence of reduced VOR function on the side opposite the fast phase, and the absence of acute central or acute audiological symptoms.
3. 1:00Anatomy matters here in a way it doesn't for bilateral disease. The vestibular nerve has two divisions. The superior division carries the horizontal and anterior canals, plus the utricle. The inferior division carries the posterior canal and the saccule. Neuritis can be selective.
4. 1:25Superior division neuritis — the most common pattern — produces abnormal horizontal vHIT, abnormal caloric on the affected side, abnormal oVEMP, and preserved cVEMP. DVA shows asymmetric loss greater on head turns toward the lesioned side.
5. 1:55Inferior division neuritis is rare but instructive. Calorics and horizontal vHIT are normal — these test only the superior nerve. The posterior canal vHIT shows impulse deficit. The cVEMP, which depends on the inferior nerve, is absent. Patients can be told they have no vestibular lesion when in fact they do. Canal-specific head-thrust DVA is what catches it.
6. 2:30Recovery follows a predictable course. The acute symptoms — the spinning vertigo and the spontaneous nystagmus — subside over days to weeks as static compensation occurs in the vestibular nuclei. DVA recovers more slowly and incompletely. The Herdman 2003 trial showed that DVA improves with structured gaze-stabilisation exercise mainly through covert catch-up saccades, not through recovery of VOR gain.
7. 3:00Two practical points. First, an asymmetric DVA finding without documented unilateral VOR loss is not yet vestibular neuritis. Document the loss with caloric, vHIT, or both. Second, a normal-caloric patient with asymmetric DVA, ipsilateral hearing-spared vertigo, and absent cVEMP is inferior division neuritis. Look for it specifically.

What is vestibular neuritis?

Vestibular neuritis — also known as acute unilateral vestibulopathy (AUVP) — is an acute peripheral vestibular syndrome caused by sudden loss of vestibular function on one side, without hearing change. The patient presents with severe, sustained vertigo and unsteadiness, typically lasting days to a couple of weeks. The leading hypothesis is reactivation of latent herpes simplex virus type 1 in the vestibular ganglion, though several other mechanisms are recognised.²⁸

On examination there is a spontaneous peripheral vestibular nystagmus beating away from the affected side, made more obvious by removing visual fixation (Frenzel glasses, or M-shaped finger occlusion). Bedside head-impulse testing shows catch-up saccades when the head is thrust toward the affected ear. Hearing is preserved — this is the key distinction from labyrinthitis.²⁸

How common is it?

Vestibular neuritis is the second most common peripheral cause of acute prolonged vertigo after BPPV. The annual incidence is approximately 3.5 per 100,000 persons; the condition accounts for roughly 7% of patients presenting to vertigo clinics.²⁸

Bárány Society 2022 diagnostic criteria

The 2022 Bárány consensus introduced four diagnostic categories. The principal one is Acute Unilateral Vestibulopathy (AUVP), requiring all six criteria below.²⁸

1. Acute or subacute onset of sustained spinning or non-spinning vertigo of moderate or severe intensity, lasting at least 24 hours.
2. Spontaneous peripheral vestibular nystagmus appropriate to the canal afferents involved — generally horizontal-torsional, direction-fixed, enhanced by removal of visual fixation.
3. Unambiguous evidence of reduced VOR function on the side opposite the direction of the fast phase of the spontaneous nystagmus.
4. No evidence for acute central neurological, otological, or audiological symptoms (no hearing loss, no tinnitus, no otalgia).
5. No acute central neurological signs — no skew deviation, no gaze-evoked nystagmus, no audiological signs.
6. Not better accounted for by another disease or disorder.

The other three categories are AUVP in evolution (symptoms ≥3 hours but not yet 24 hours; used to enable specific treatment and central-stroke exclusion in the very acute window), probable AUVP (criteria met except the unilateral VOR deficit is not clearly documented), and history of AUVP (for patients seen long after the acute phase with documented unilateral VOR deficit).²⁸

Why one division gets hit more often

The vestibular nerve splits into a superior and an inferior division inside the internal auditory canal. The superior division carries afferents from the horizontal canal, the anterior canal, and the utricle; the inferior carries afferents from the posterior canal and the saccule. The two divisions take different paths through bony channels of slightly different size — the superior travels through a narrower, longer canal, which is the leading anatomical explanation for why neuritis preferentially affects the superior division.^29,31

Aw and colleagues studied 33 patients with acute unilateral peripheral vestibulopathy and found that most had abnormal lateral and anterior canal function — consistent with selective superior division involvement — while a small minority had all three canals affected, suggesting involvement of both divisions. Isolated inferior division involvement (normal calorics, abnormal posterior canal vHIT, absent cVEMP) is rare but recognised.^29,30

The DVA pattern in detail

In acute unilateral vestibulopathy, DVA is asymmetric: the loss is greater on head turns toward the affected ear than away from it. The rule comes from the canal-to-muscle wiring covered in the Anatomy module — a head turn to the right depends on the right horizontal canal driving the contralateral abducens. If the right canal is knocked out by neuritis, rightward head motion has nothing to drive the leftward eye rotation, the eyes lag, and the optotype blurs. Leftward head motion is largely intact, because it depends on the unaffected left horizontal canal.¹⁴

The clinical implications:

• Asymmetry ≥0.1 logMAR between directions is the most useful screening criterion in this population. It is robust to age, to floor effects in static acuity, and to bilateral symmetric noise. A patient with a unilateral lesion will fail this asymmetry test even when the absolute loss looks modest.^1,21
• Absolute loss on the affected side typically falls in the 0.2–0.5 logMAR range in the acute phase. Central compensation reduces the absolute loss over weeks; the asymmetry tends to persist longer than the absolute deficit and is therefore the more durable laboratory clue in the chronic phase.^3,5
• The unaffected side is rarely entirely normal in the acute phase. Patients may be too dizzy or nauseated to perform the test reliably; the bedside oscillation also affects neck and visual systems that themselves are stressed. Repeat the test once the patient can tolerate it.

Compensation and recovery

The acute symptoms — the spinning vertigo and spontaneous nystagmus — subside over days to weeks as static compensation occurs in the vestibular nuclei. The brain re-equalises the tonic firing rate between the two vestibular nuclei despite the persisting peripheral asymmetry. By two to three weeks, the spontaneous nystagmus is usually absent on direct gaze.²⁸

DVA recovers more slowly and incompletely. The Herdman 2003 trial randomised 21 patients with unilateral vestibular hypofunction to structured vestibular exercises versus placebo; the exercise group showed significant DVA improvement on the unpredictable head-motion paradigm.³ The Schubert 2008 mechanistic follow-up attributed improvement chiefly to covert catch-up saccades— well-timed, sub-200 ms saccades during the head motion — and only partly to a small rise in active VOR gain.⁵

Differential diagnosis

The most important miss is a posterior-circulation stroke presenting as an acute vestibular syndrome. The HINTS exam (Head-Impulse, Nystagmus, Test of Skew) is the bedside discriminator: peripheral patterns require a positive HIT, unidirectional nystagmus, and no skew. Any deviation from that pattern warrants imaging. Other differential considerations:

• Labyrinthitis — same picture plus hearing loss and/or tinnitus on the affected side. Outside the AUVP criteria.²⁸
• Ménière's disease (first attack) — fluctuating unilateral hearing loss is the discriminator. AUVP has stable, preserved hearing.
• Vestibular migraine — episodes usually shorter, with prior migraine history, headache features, and triggers. Spontaneous nystagmus is uncommon between attacks.
• Anterior vestibular artery infarct — produces an identical clinical picture but with central origin. Anterior vestibular artery distribution overlaps the superior division territory; ipsilateral hearing loss and additional central signs argue against AUVP.²⁸
• Selective inferior division neuritis — acute vertigo with normal calorics. Easy to miss if the test battery does not include cVEMP and posterior canal vHIT.^30,31

Reading the report

An asymmetric DVA loss greater on head motion toward the affected ear, combined with documented unilateral VOR loss on horizontal vHIT or caloric, in a patient with a self-limited acute vertigo episode lasting ≥24 hours and no hearing change, is sufficient for the diagnosis under the Bárány 2022 criteria.²⁸

When the asymmetric DVA is the only abnormal vestibular finding — calorics normal, horizontal vHIT normal — pursue the inferior division pattern explicitly: cVEMP, posterior canal vHIT, and saccule-specific symptoms. Failure to do so under-diagnoses up to several percent of neuritis cases that the routine battery would otherwise miss.^30,31