Central and cerebellar lesions
The chair test inverts everything you expect from peripheral disease. Gain is preserved, time constants lengthen, and the patient cannot stop the nystagmus by looking at a light.
Clinical picture
Patients present with persistent disequilibrium, ataxia, sometimes diplopia and downbeat nystagmus, and a clinical examination that shows central oculomotor signs — saccadic pursuit, square-wave jerks, gaze-evoked nystagmus, or impaired suppression on the head-impulse test. Multiple sclerosis, posterior circulation stroke, cerebellar atrophies and tumours of the cerebellopontine angle can all produce this pattern.
Pathophysiology
The cerebellar nodulus and uvula tonically inhibit the brainstem velocity-storage integrator and provide the substrate for visual fixation suppression Raphan T 2002. Lesions here release velocity storage from inhibition (very long Tc) and remove the brake on the VOR during fixation. Flocculus lesions calibrate VOR gain — chronically they can produce VOR gain that is either reduced or paradoxically increased.
RCT pattern
| Step Tc | 32.0 s |
|---|---|
| Step gain | 0.95 |
SHA gain is normal or slightly increased; phase lead can be reduced. The hallmarks are on the step test and the visual-suppression trial:
- Step-test Tc > 30 s (often well above).
- Fixation index near 1 — the patient cannot suppress nystagmus.
- Optokinetic-after-nystagmus prolonged.
Diagnosis & differential
- MRI of the brain with attention to the posterior fossa and brainstem.
- Look for accompanying oculomotor signs at the bedside.
- Beware vestibular migraine, which can mimic these findings between attacks.