Glossary

Reflex eye movement that stabilises vision during head rotation.

The angular VOR generates a compensatory eye movement equal in magnitude and opposite in direction to head rotation, with a latency of ~7–15 ms. It is driven by the semicircular canals and modulated centrally by velocity storage.

Ratio of peak slow-phase eye velocity to peak chair velocity.

Gain quantifies the magnitude of the VOR response. In healthy adults at 0.32 Hz it lies between ~0.55 and 0.95. Reduced gain across frequencies suggests bilateral peripheral loss; reduced gain on one side alone suggests unilateral loss not yet compensated.

Timing relationship between eye and head velocity.

Phase is positive (lead) when eye velocity peaks before chair velocity. In normals phase lead is large at low frequencies and approaches zero above 0.16 Hz. Elevated phase lead at all frequencies suggests peripheral hypofunction; reduced phase lead suggests over-active velocity storage.

Bias of nystagmus to one rotational direction.

Computed as (peakR − peakL)/(peakR + peakL) × 100. Values within ±22 % are normal. Larger values usually indicate an uncompensated unilateral lesion or an irritative state.

Decay time of nystagmus after a step in chair velocity.

After a velocity step the SPV decays exponentially. The cupula alone gives Tc ≈ 4–6 s; the central velocity-storage integrator prolongs this to 12–25 s in normals. Tc shortens with peripheral loss and lengthens with central disinhibition.

Brainstem integrator that prolongs the angular VOR response.

A central integrative network in the medial and superior vestibular nuclei that extends the cupular afferent time constant by combining canal, otolith and optokinetic inputs (Raphan & Cohen 2002).

Multi-frequency rotational VOR test (0.01–0.64 Hz).

The chair is oscillated sinusoidally across octave frequencies with vision denied. Gain, phase and symmetry are extracted at each frequency. SHA is the gold standard for bilateral vestibular loss.

Constant-velocity rotation used to measure VOR time constant.

After a rapid acceleration to constant velocity the SPV decays exponentially; the same occurs after deceleration to a stop. Per-rotational and post-rotational Tc are compared.

Cortical override of the VOR by an earth-fixed visual target.

A normal subject can suppress > 60 % of nystagmus by fixating during chair rotation. Cerebellar lesions characteristically impair this.

Velocity of the compensatory (slow) phase of nystagmus.

The slow phase reflects the VOR drive; the fast phase is a brainstem-generated re-fixation saccade. SPV — not nystagmus frequency — is the metric used by every RCT calculation.

Re-balancing of vestibular tonus after a unilateral peripheral loss.

Within weeks to months the brainstem and cerebellum restore resting tone and gain. Caloric asymmetry persists; SHA usually normalises — which is precisely why RCT is the test of choice for monitoring.

Goodness-of-fit of eye velocity to a sine wave.

Computed at each SHA frequency. A purity below ~60 % means the response is poorly described by a sinusoid (drowsiness, artefact, or sparse nystagmus) and the frequency should be re-tested.

Continuous cognitive task used to maintain VOR responsiveness.

Drowsiness collapses VOR gain. The tester engages the subject in arithmetic, naming, or country-listing to keep arousal up. Without alerting, gain may falsely appear reduced.

Asymmetry calculation borrowed from caloric testing.

Originally for caloric responses: UW = ((R-warm + R-cool) − (L-warm + L-cool)) / Σ × 100. The same arithmetic is used for symmetry in RCT.

Gelatinous mass in the ampulla that deflects with endolymph flow.

Hair-cell stereocilia project into the cupula. Cupular deflection in the direction of the kinocilium depolarises the horizontal canal hair cells.

Three orthogonal canals encoding angular acceleration.

Lateral (horizontal), anterior (superior) and posterior canals. The horizontal canal lies 30° above the earth-horizontal in upright posture, which is why the head is tilted 30° forward during RCT.

Mechanotransducer of the vestibular and auditory periphery.

Type I (flask-shaped, calyx ending) and Type II (cylindrical, bouton endings) hair cells convert stereociliary deflection into receptor potentials via mechanically gated potassium channels.

Modulates VOR gain and velocity storage.

The flocculus calibrates VOR gain; the nodulus/uvula controls velocity storage and visual suppression. Lesions here lengthen Tc and impair fixation suppression.

Light- and target-free recording condition.

Visual input both drives optokinetic responses and suppresses the VOR; recording in complete darkness isolates the pure vestibular contribution. Achieved with goggles covered or inside a light-tight booth.