Case report reveals post-stimulatory reversal afternystagmus in a patient with vestibular schwannoma, indicating coexisting peripheral and central vestibular dysfunction.
Skull vibration-induced nystagmus (SVIN) normally begins and ends abruptly, without post-stimulatory reversal, because the 100 Hz stimulus drives irregular afferents through the direct pathway and largely bypasses the velocity storage integrator. An 83-year-old woman with chronic gait instability, dizziness and no resting nystagmus underwent skull vibration-induced nystagmus testing, which produced high-intensity right-beating nystagmus (73°/s) that reversed to left-beating nystagmus (10°/s) for 6–8 s after stimulus cessation; the same pattern recurred at 3-month follow-up. Imaging showed a left vestibular schwannoma with floccular compression and diffuse parenchymal retraction, and temporal bone photon-counting-detector CT excluded semicircular canal dehiscence; testing indicated predominantly left hypofunction. We interpret the reversal, hypothetically, as a stimulus-facilitated, rebound-like central phenomenon—arising from the fixed left vestibular-tone asymmetry and the unusually intense vibratory drive on a permissive central substrate—and emphasize extending observation beyond the per-stimulatory period, where such post-stimulatory signs may reveal coexisting peripheral and central vestibular dysfunction.
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Palomino-Diaz et al. (2026) studied this question.
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