👁️ VOR & Vestibular Nystagmus — Interactive Teaching Tool

For therapist training · Press the buttons and watch the reflex happen

1 · The Vestibulo-Ocular Reflex (VOR)

Press the button: the head turns right → the endolymph lags behind (inertia) → the cupula in the ampulla bends → impulses travel to the vestibular nucleus → then to the eye-muscle nuclei (CN III / IV / VI) → the eyes move left, keeping the image stable on the retina.

Ready. Press the button to start the VOR sequence.

Top view of head & horizontal canals

NOSE (front of head)cupula in ampullaright horizontal canal + endolymph

Neural pathway & eye muscles

vestibular nervedirectindirectvia INT + contralateral MLFminor direct path (ATD)R horizontal canalampullacupula + cristaVestibular nucleus (R)L Abducens nucleus(CN VI)R Oculomotor nucleus(CN III · medial rectus)INTinternuclear neuronsClinically: MLF lesions cause internuclear ophthalmoplegia (INO) — impaired adduction with nystagmus of the abducting eye.R MLFiL Lateral RectusR Medial RectusSolid = direct projectionPurple = via MLF (indirect)Dashed = minor ATD pathEyes rotate LEFT → the image stays stable on the retina

2 · Testing — Vestibular: Nystagmus (V:N, EASI) / Post-Rotatory Nystagmus (PRN, SIPT)

Ayres protocol: rotate at 2 seconds per revolution, head tipped 30° down. Clockwise rotation excites the right horizontal canal → eyes drift left, then snap back. After ≈10 revolutions the endolymph has caught up and the reflex stops. Stop the chair and inertia keeps the fluid moving → reversed nystagmus = PRN. All stages below run from the same clock: physical input → central processing → observable eye response.

Scenario:
Normal fluid physics, vestibular-nucleus output and cortical inhibition.
Speed:2.00 s per revolution
Ready. At rest the endolymph, the canal wall and the cupula all sit still — no nystagmus.

1 · Physical input — same in every scenario

Revolutions: 0 / 10Ampulla + cupulaHorizontal canalblue = endolymph
Canal wall speed
Endolymph speed
Cupula: neutral
Revolutions: 0 / 10

2 · Central processing — scenario differs here

cupula inputVestibularnucleusVOR motor commandCorticalinhibition
Vestibular-nucleus output
The line marks the level the eyes need — below it there is no eye movement.
Cortical inhibition
Net eye-movement command
Vestibular nucleus: resting

3 · Observable response — what we time

Muscles: —
Nystagmus: absent

PRN timing follows the visible eye response. The fluid may continue settling after the eyes stop.

3 · Clinical Interpretation of PRN Duration

SHORT duration (< ~7 s)
The fluid stimulus may be physically normal, but the brief eye response points to a vestibular nucleus processing problem. Often co-occurs with eye-control, balance, postural-control and bilateral-coordination difficulties. If those signs are present AND duration is short → the vestibular system is one of the causes.
PROLONGED duration (≥ ~13 s)
The fluid stimulus may be physically normal. A prolonged eye response reflects delayed or weak cortical inhibition of the central reflex, not a vestibular-nucleus issue. Research found children with no other praxis problems but failing only praxis on verbal command (≤ −1 SD) plus prolonged PRN → Dyspraxia on Verbal Command, which is not sensory-integration based.
⚠ PRN duration times the eyes—not the fluid. Hyper/hypo-reactivity involves the reticular activating & limbic systems (awareness / over-response). Long PRN does not mean hyper-reactive; short or absent nystagmus does not mean hypo-reactive.

Norms: mean ≈ 10 s, SD ≈ 3 s (≈ 7–13 s normal). Note: standardized SCPNT/SIPT norms formally cover ages 4 years – 8 years 11 months; values outside that range are clinical extrapolations.