Vestibular neuritis
A unilateral, presumed-viral peripheral vestibular failure — the textbook acute peripheral pattern and the cleanest demonstration of how the chair tracks compensation.
Clinical picture
A previously well adult develops acute spontaneous spinning vertigo with vomiting and gait imbalance. Symptoms are present at rest and worsened by head movement. Hearing is preserved Le TN 2021. Spontaneous horizontal-torsional nystagmus beats away from the affected ear; head-impulse testing reveals a deficit in the ipsilateral lateral canal.
Pathophysiology
Most cases are presumed viral (HSV-1 reactivation in the vestibular ganglion is the leading hypothesis). The superior division of CN VIII is preferentially affected, sparing the posterior canal and saccule — hence the cVEMP is usually preserved. The acute asymmetric resting tonus drives both spontaneous nystagmus and the RCT pattern.
RCT pattern
| Step Tc | 8.0 s |
|---|---|
| Step gain | 0.45 |
Acute superior vestibular neuritis is the prototype of an uncompensated unilateral peripheral lesion: gain falls across all frequencies, phase lead climbs (most at the low frequencies), symmetry shifts toward the intact side, and the step-test Tc shortens toward the cupula value Le TN 2021.
Over the following weeks brainstem and cerebellar compensation re-balance resting tone. Phase and symmetry typically recover first; gain at the highest frequencies last. By six months SHA is often within normal limits, even though caloric paresis persists — the cardinal RCT lesson.
Diagnosis & differential
Inferior vestibular neuritis spares the lateral canal: horizontal SHA is normal, but cVEMP is absent and posterior canal vHIT is reduced. The chair report alone may look unremarkable — diagnosis is by combining tests.
- Stroke (PICA / AICA) — the HINTS triad and brainstem signs are essential to exclude; RCT cannot.
- Ménière's first attack — typically accompanied by hearing loss/fullness.
- Vestibular migraine — episodic, headache association, often normal interictal RCT.