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1 · Introduction
The rotational chair test measures the vestibulo-ocular reflex across a band of frequencies (0.01–0.64 Hz) that caloric and vHIT cannot reach. Its three classical roles — confirming bilateral loss, characterising the low-mid frequency band, and tracking central compensation — define its niche in modern vestibular practiceWang Y 2022.
2 · Anatomy & physiology
The lateral canal lies at ~30° above horizontal in upright posture; the head is therefore tilted 30° forward during testing to bring it into the rotation plane. The superior division of CN VIII supplies the lateral and anterior canals plus the utricle; the inferior supplies the posterior canal and saccule. Central velocity-storage neurons in the medial and superior vestibular nuclei prolong the cupula's 4–6 s decay to a measurable VOR Tc of 15–25 sRaphan T 2002.
3 · Recording technique
SHA delivers sinusoidal rotation at 0.01–0.64 Hz with peak velocity 50–60°/s. The step test holds the chair at a constant velocity and measures the exponential decay of slow-phase eye velocity. Vision is denied throughout; the patient is alerted continuously; spectral purity below 60 % requires a re-test of that frequencyInteracoustics A/S (technical reference). 2023.
4 · Normal waves
Gain rises with frequency from ~0.35 at 0.01 Hz to ~0.75 at 0.32 Hz. Phase lead decays from 20–65° at the lowest frequencies to near zero at 0.32 Hz. Symmetry remains within ±22 %. Step-test Tc is 12–25 sWang Y 2022.
5 · Disease patterns
Superior vestibular neuritis (uncompensated)
Tc: 8.0 s · Step gain: 0.45
Acute unilateral peripheral loss reduces gain, increases phase lead, produces directional preponderance and shortens Tc. RCT confirms whether the lesion is compensating.
Inferior vestibular neuritis
Tc: 16.0 s · Step gain: 0.75
Inferior nerve supplies posterior canal + saccule; horizontal RCT is typically normal. Suspect from cVEMP loss with intact horizontal vHIT and SHA.
Ménière's disease, early/interictal
Tc: 16.0 s · Step gain: 0.72
Between attacks SHA is often near-normal; mild asymmetry may emerge. Caloric paresis appears earlier than SHA changes.
Ménière's disease, advanced
Tc: 11.0 s · Step gain: 0.58
Cumulative endolymphatic damage produces a fixed unilateral pattern resembling slowly compensating neuritis.
Bilateral vestibulopathy
Tc: 4.0 s · Step gain: 0.18
Gold-standard finding for BVP: gain < 0.2 across frequencies with marked phase lead and Tc collapsing toward the cupula value (~5 s). Bárány criteria 2017.
Vestibular schwannoma
Tc: 12.0 s · Step gain: 0.60
Slow-growing CN VIII lesion. RCT typically shows unilateral pattern; gradual onset gives time for compensation, so phase/asymmetry recover earlier than gain.
Superior canal dehiscence
Tc: 18.0 s · Step gain: 0.82
Horizontal SHA is typically normal in isolated SCD. Diagnosis hinges on VEMP thresholds + CT; RCT helps exclude a co-existing horizontal canal lesion.
Vestibular migraine
Tc: 22.0 s · Step gain: 0.78
Inter-ictally RCT is usually normal; subtle finding is *reduced* phase lead at high frequencies, attributed to a hyperactive velocity-storage mechanism.
Central / cerebellar lesion
Tc: 32.0 s · Step gain: 0.95
Velocity-storage disinhibition → very long Tc; visual suppression of nystagmus fails. Gain may be normal or *increased*. A peripheral test that looks normal but with failed suppression is the giveaway.
Presbyvestibulopathy
Tc: 14.0 s · Step gain: 0.65
Age-related decline is greatest at the lowest frequencies (0.01–0.04 Hz). The post-rotational Tc is the first to drift downward (Wang 2022).
Post-labyrinthectomy, acute
Tc: 6.0 s · Step gain: 0.35
Surgical deafferentation produces the deepest acute deficit; RCT documents the baseline against which central compensation is tracked.
Post-labyrinthectomy, compensated
Tc: 14.0 s · Step gain: 0.62
Months after the insult, the SHA pattern *recovers toward normal* even though the labyrinth is gone — a unique advantage of RCT over caloric testing for monitoring.
6 · Clinical cases (vignettes only)
Two-year history of oscillopsia after gentamicin
A 58-year-old man treated with intravenous gentamicin for endocarditis 18 months ago reports difficulty reading street signs while walking and a sensation of the world bouncing. No vertigo, no hearing loss. Romberg is positive with eyes closed.
Sudden vertigo, three days ago
A 35-year-old woman presents 72 hours after sudden-onset spinning vertigo with vomiting. She has spontaneous left-beating horizontal-torsional nystagmus. Hearing is preserved. Right horizontal vHIT gain is 0.4 with overt catch-up saccades.
Episodic vertigo with fluctuating hearing loss
A 47-year-old woman has had 7 episodes over the past year of spinning vertigo lasting 30–90 minutes, with low-frequency fluctuating hearing loss and aural fullness on the right. Audiogram between attacks shows a 35 dB low-frequency loss on the right.
Asymmetric high-frequency hearing loss
A 52-year-old man with two years of progressive right-sided tinnitus and high-frequency hearing loss has an MRI showing a 12 mm intracanalicular vestibular schwannoma on the right. He denies vertigo.
Sound-induced dizziness and autophony
A 38-year-old singer reports dizziness with loud sounds and hearing her own footsteps and heartbeat in the right ear. Audiogram shows a low-frequency conductive loss on the right with intact stapedial reflexes. Right oVEMP amplitude is 28 µV; right cVEMP threshold is 65 dB nHL.
Persistent vertigo and double vision
A 64-year-old woman has 6 weeks of unsteadiness, episodic diplopia and downbeat nystagmus. MRI shows a small infarct in the cerebellar nodulus. RCT gain is normal but Tc is 34 s and she cannot suppress nystagmus when asked to fixate.
Translabyrinthine schwannoma resection nine months ago
A 60-year-old man who underwent a left translabyrinthine resection nine months ago reports near-normal function. SHA shows symmetric gain within the normal band and almost no phase lead. Caloric testing shows complete left areflexia.
Mild unsteadiness, age 72
A 72-year-old woman has mild unsteadiness without falls. She has no acute vertigo. SHA shows gain of 0.18 at 0.01 Hz (below the normal band of 0.25–0.55 at that frequency) but normal gain from 0.04–0.64 Hz, with normal Tc and symmetric responses.
7 · Glossary
Vestibulo-ocular reflex (VOR). 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.
VOR gain. 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.
Phase lead. 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.
Symmetry / directional preponderance. Computed as (peakR − peakL)/(peakR + peakL) × 100. Values within ±22 % are normal. Larger values usually indicate an uncompensated unilateral lesion or an irritative state.
Time constant (Tc). 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.
Velocity storage. 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).
Sinusoidal harmonic acceleration (SHA). 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.
Step velocity test. 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.
Visual suppression / fixation. A normal subject can suppress > 60 % of nystagmus by fixating during chair rotation. Cerebellar lesions characteristically impair this.
Slow-phase velocity (SPV). 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.
Central compensation. 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.
Spectral purity. 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.
Alerting task. 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.
Jongkees formula. Originally for caloric responses: UW = ((R-warm + R-cool) − (L-warm + L-cool)) / Σ × 100. The same arithmetic is used for symmetry in RCT.
Cupula. Hair-cell stereocilia project into the cupula. Cupular deflection in the direction of the kinocilium depolarises the horizontal canal hair cells.
Semicircular canals. 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.
Hair cell. 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.
Cerebellum (flocculus / nodulus). The flocculus calibrates VOR gain; the nodulus/uvula controls velocity storage and visual suppression. Lesions here lengthen Tc and impair fixation suppression.
Vision denied / darkness. 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.
8 · References
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- Strupp M, Kim JS, Murofushi T, et al. (2017). Bilateral vestibulopathy: Diagnostic criteria — Consensus document of the Classification Committee of the Bárány Society, Journal of Vestibular Research, 27 (4), 177–189.
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- Hain TC, Cherchi M, Yacovino DA. (2013). Bilateral vestibular loss, Seminars in Neurology, 33 (3), 195–203.
- Raphan T, Cohen B. (2002). The vestibulo-ocular reflex in three dimensions, Experimental Brain Research, 145 (1), 1–27.
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- Agrawal Y, Van de Berg R, Wuyts F, et al. (2019). Presbyvestibulopathy: Diagnostic criteria — Consensus document of the Classification Committee of the Bárány Society, Journal of Vestibular Research, 29 (4), 161–170.
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- BalanceMD Clinical Group. (2024). Acoustic neuroma — rotational chair patterns (clinical resource).
- Duke University Department of Head & Neck Surgery. (2024). Vestibular Disorders Clinic — clinical resource on rotational testing.
- ENT & Audiology News editorial. (2015). Rotational chair testing: 'to rotate, or not to rotate, that is the real question', ENT & Audiology News.
- Interacoustics A/S (technical reference). (2023). VisualEyes SHA and Velocity-Step Test — clinical guidance.
- Barin K. (2009). Background and technique of rotational testing.