Module 7 · Disease pages

Vestibular neuritis

Acute superior and inferior vestibular nerve loss
Clinical vignette
A 42-year-old man wakes with severe spinning vertigo, nausea, and unsteadiness. Symptoms began over minutes and are continuous. There is no hearing loss and no headache. Examination shows left-beating horizontal-torsional spontaneous nystagmus that intensifies on left gaze (Alexander's law), an abnormal bedside head impulse to the right, and a negative test of skew. MRI brain is normal.
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What it is

Vestibular neuritis is the second most common cause of peripheral vertigo after BPPV. It is a sudden, prolonged unilateral loss of vestibular nerve function that produces severe vertigo, nausea, and gait unsteadiness lasting days. Hearing is preserved. The acute syndrome is now formally termed acute unilateral vestibulopathy (AUVP) by the Bárány Society[Strupp M 2022], with vestibular neuritis retained as a clinical synonym. Both names refer to the same clinical entity.

The pathology preferentially affects the superior vestibular nerve in approximately 90% of cases, sparing the inferior division. This anatomy explains the canonical vHIT signature: reduced gain in the lateral and anterior canals with a preserved posterior canal on the affected side. Inferior vestibular neuritis — affecting only the posterior canal and saccule — is a much rarer entity that is easily missed without vertical-canal testing[MacDougall HG 2013].

The vHIT signature

The signature pattern of superior vestibular neuritis is shown below. Reduced VOR gain in the ipsilateral lateral and anterior canals; large overt corrective saccades after the head returns to rest; the posterior canal (innervated by the inferior division) is preserved. Compare against the normal-side panel that follows.

Right superior vestibular neuritis — affected side
0100200R latg=0.320100200R antg=0.400100200R postg=0.85
Right lateral and right anterior canals: reduced gain with large overt saccades. Right posterior canal preserved. This is the superior nerve pattern.
Left (unaffected) side for comparison
0100200L latg=0.960100200L antg=0.890100200L postg=0.87
Contralateral side: all three canals show normal gain with no corrective saccades.

Audiogram companion

Hearing is preserved in vestibular neuritis. If sudden hearing loss accompanies the vertigo, the diagnosis is labyrinthitis (or, in older patients with vascular risk factors, AICA-territory stroke must be excluded). The audiogram below shows the expected normal hearing thresholds.

2505001k2k4k8k020406080100120Frequency (Hz)Hearing level (dB HL)○ right× left
Normal pure-tone audiogram in both ears, as expected in pure vestibular neuritis.

Saccade pattern over time

In the acute phase, overt saccades dominate the picture: large, late, and obvious at the bedside. With recovery and central compensation, the saccadic strategy shifts. Covert saccades (during head movement) increasingly substitute for overt ones, and the overall pattern looks "compensated" even when canal function has not fully recovered[Manzari L 2013]. The bedside head impulse test, which can only see overt saccades, may look reassuringly normal at three months even though the underlying canal deficit persists. This is the principal reason vHIT replaced bedside HIT as the standard of care.

Inferior vestibular neuritis

A rarer presentation: isolated posterior canal deficit, often with torsional/down-beat spontaneous nystagmus rather than horizontal-torsional. The pattern on vHIT is unilateral reduced posterior canal gain with preserved lateral and anterior canals on the same side. Before vertical-canal vHIT was validated, this entity was nearly invisible to clinical testing. Inferior vestibular neuritis affects the saccule (ocular VEMPs are usually abnormal) and spares the utricle (cervical VEMPs intact), the mirror image of the superior form[MacDougall HG 2013].

Key teaching points

  • Reduced gain in lateral + anterior canals with preserved posterior canal = superior vestibular neuritis (~90% of cases).
  • Isolated reduced posterior canal gain = inferior vestibular neuritis (rare; vertical-canal testing is essential to catch it).
  • Overt saccades dominate acutely; covert saccades emerge with central compensation over weeks to months.
  • Hearing is preserved — sudden hearing loss with vertigo is labyrinthitis or AICA stroke until proven otherwise.
  • HINTS-plus is the bedside test that differentiates neuritis from stroke; an abnormal HIT alone is not enough.

References

  1. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Archives of Neurology 1988;45:737–9. doi:10.1001/archneur.1988.00520310043015
  2. Strupp M, Bisdorff A, Furman J, Hornibrook J, Jahn K, Maire R, Newman-Toker D, Magnusson M. Acute unilateral vestibulopathy/vestibular neuritis: diagnostic criteria — consensus document of the Bárány Society. Journal of Vestibular Research 2022;32:389–406. doi:10.3233/VES-220201
  3. Manzari L, Burgess AM, MacDougall HG, Curthoys IS. Vestibular function after vestibular neuritis. International Journal of Audiology 2013;52:713–8. doi:10.3109/14992027.2013.809485
  4. Weber KP, Aw ST, Todd MJ, McGarvie LA, Curthoys IS, Halmagyi GM. Head impulse test in unilateral vestibular loss: vestibulo-ocular reflex and catch-up saccades. Neurology 2008;70:454–63. doi:10.1212/01.wnl.0000299117.48935.2e
  5. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke 2009;40:3504–10. doi:10.1161/STROKEAHA.109.551234
  6. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology 2008;70:2378–85. doi:10.1212/01.wnl.0000314685.01433.0d
  7. MacDougall HG, McGarvie LA, Halmagyi GM, Curthoys IS, Weber KP. The video head impulse test (vHIT) detects vertical semicircular canal dysfunction. PLoS One 2013;8:e61488. doi:10.1371/journal.pone.0061488
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