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Vestibulum
An atlas of eye movement & nystagmus
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01
Module

Neural Control of Eye Movement

From retina to extraocular muscle — the hierarchy that keeps the world stable on the fovea.

Contents
  1. 01The oculomotor systems
  2. 02Extraocular muscles
  3. 03Saccade system
  4. 04Pursuit system
  5. 05Gaze-holding (neural integrator)
  6. 06Optokinetic system
  7. 07Vestibulo-ocular reflex (VOR)
  8. 08Peripheral vestibular labyrinth
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Section 01

The four oculomotor systems

A single type of eye movement is inadequate to keep targets of interest on the foveae in all situations. The oculomotor system therefore consists of four functional classes, each with its own neural circuitry, that converge on a "final common pathway" — the cranial motor neurons of CN III, IV, and VI and the six extraocular muscles they innervate.

Cerebral cortex(FEF, PEF, MT/V5)Midbrain(Superior colliculus)Cerebellum(Flocculus, vermis)VestibularlabyrinthPremotor systems (brainstem tegmentum)PPRF · riMLF · NPH · MVN — burst/tonic neurons, neural integratorFinal common pathwayOculomotor neurons (CN III, IV, VI) · Extraocular muscles
The four primary control systems. Each detects a different aspect of visual/vestibular input and converges on the same brainstem motor neurons.
Saccade

Rapid (≤100 ms), ballistic eye movements that bring a peripheral target onto the fovea. Velocities up to 700°/s. The observer is briefly 'blind' during the saccade.

Smooth pursuit

Continuous, low-velocity tracking of a moving target. Generated by a feedback loop sampling target position/velocity. Saturates around 50°/s.

Gaze-holding

Maintenance of the eye at an eccentric position against the orbital elastic forces that would return it to primary gaze. Powered by the neural integrator.

Optokinetic & VOR

Stabilize the retinal image during head/world motion. OKN uses moving visual cues; VOR uses semicircular-canal signals about angular head velocity.

Section 02

The six extraocular muscles

Six striated muscles control each eye. They function as three agonist-antagonist pairs in three planes: horizontal (medial & lateral recti), vertical (superior & inferior recti), and torsional (superior & inferior obliques). To move the eye, an agonist contracts while its antagonist relaxes (Sherrington's law of reciprocal innervation).

MRLRSRIRSOIORIGHT EYE — view from front
MuscleCNPrimary action
Medial rectus
IIIAdduction (inward)
Lateral rectus
VIAbduction (outward)
Superior rectus
Intorsion + adduction
IIIElevation
Inferior rectus
Extorsion + adduction
IIIDepression
Superior oblique
Depression + abduction
IVIntorsion
Inferior oblique
Elevation + abduction
IIIExtorsion
Hover any row to highlight the muscle's primary direction of action. Note the rule: lateral rectus = VI, superior oblique = IV, all others = III.
Mnemonic
LR6 SO4 All3 — Lateral rectus = CN VI, Superior oblique = CN IV, All others = CN III.
Section 03

The saccade system

When a target is detected at the edge of vision, the saccade system makes a single rapid, ballistic eye movement to bring it onto the fovea. Most saccades last under 100 ms, reach peak velocities up to 700°/s, and are pre-programmed — once initiated, they cannot be corrected mid-flight.

Frontal eye field(contralateral saccade command)Superior colliculus(amplitude/direction)PPRF(horizontal burst)riMLF(vertical burst)Cerebellar vermis (calibration)Oculomotor neurons → EOMsBallistic saccade in <100 ms ↓
The saccade pathway from cortex (frontal eye field, FEF) through the superior colliculus to the brainstem burst generators (PPRF for horizontal saccades; riMLF for vertical/torsional).
Peak velocity
up to 700°/s
Duration
<100 ms
Latency
~200 ms
Horizontal generator
PPRF (pons)
Vertical generator
riMLF (midbrain)
Cortical drive
FEF, parietal eye field, SEF
Section 04

The smooth pursuit system

When a target moves smoothly, the pursuit system tracks it by continuously sampling retinal slip — the velocity difference between target and fovea — and feeding it back to drive a matching eye velocity. The system saturates around 50°/s; above that, the saccadic system takes over with catch-up saccades. Unlike saccades, smooth pursuit requires a visual stimulus.

Clinical signature
Saccadic ("cogwheel") pursuit is a classic sign of cerebellar disease or drug toxicity. It also occurs physiologically in the elderly, with sleep deprivation, with inattention, and as a normal pediatric variant.
Saturation velocity
~50°/s
Latency
~100 ms
Key structures
MT/V5, FEF, cerebellar flocculus, vestibular nuclei
Section 05

Gaze-holding: the neural integrator

After a saccade or pursuit movement places the eye eccentrically, a sustained tonic neural signal is required to hold it there against the spring-like elastic forces of the orbit. This signal is created by the neural integrator — velocity-coded input is mathematically integrated into a position signal. For horizontal gaze the integrator is the nucleus prepositus hypoglossi and the medial vestibular nucleus; for vertical gaze it is the interstitial nucleus of Cajal. The cerebellar flocculus tunes the gain.

Normal integrator

Eye holds steady at eccentric gaze.

Leaky integrator (gaze-evoked nystagmus)
Fast-phase: → right-beating horizontal · slow phase: decreasing-velocity

Decreasing-velocity slow phase + corrective saccade.

A 'leaky' integrator produces gaze-evoked nystagmus: the eye drifts back toward primary gaze along a decreasing-velocity exponential, with a corrective saccade restoring eccentric gaze.
Section 06

The optokinetic system

Optokinetic nystagmus (OKN) is a reflexive eye movement elicited by a moving full-field visual scene. The slow phase follows the scene; the fast phase resets the eye centrally. In humans, OKN works synergistically with the smooth-pursuit system for low-velocity stimuli and with the velocity-storage mechanism (a cerebellar gain control) for sustained stimulation.

Fast-phase: → right-beating horizontal
Optokinetic nystagmus: slow phase tracks the stimulus, fast phase resets.
Section 07

The vestibulo-ocular reflex (VOR)

The VOR is the fastest reflex in the body — latency ~7 ms. Angular head acceleration is transduced by the semicircular canals into firing-rate changes in the vestibular nerve, which drives a compensatory contraversive eye movement of equal velocity. The result: the image remains stable on the retina during head motion. Unlike pursuit and OKN, the VOR operates in the dark — it does not require vision.

Head, turning right →R horizontal canalR vestibular nucleus↑ firing rateL abducens nucleus→ L lateral rectusR oculomotor n.→ R medial rectusMLFL eyeR eyeConjugate eye movement ← left
The 3-neuron arc of the horizontal VOR. Rightward head rotation excites the right horizontal canal, drives the right vestibular nucleus, then excites the left abducens nucleus (left LR contraction) and right oculomotor nucleus via the MLF (right MR contraction) — a leftward conjugate eye movement.
T
The head impulse test
The clinical head impulse test directly probes the VOR. With the patient fixating, the examiner delivers a small, fast, unpredictable head turn. A normal VOR keeps the eyes locked on target; an impaired VOR produces a visible corrective saccade — the classical sign of peripheral vestibulopathy. The video head impulse test (vHIT) quantifies gain[19].
C

Frequency dependence of the VOR. The VOR is exquisitely tuned for the high-frequency, high-acceleration head movements of natural locomotion (1–10 Hz). vHIT probes ~3–5 Hz directly. The caloric test, by contrast, simulates ~0.003 Hz — a non-physiological low frequency. This frequency separation explains the increasingly recognized dissociation in early Ménière's disease: low-frequency caloric weakness can precede any measurable vHIT abnormality, because the hydropic compromise impairs low-frequency hair-cell signaling first[20]. The corollary is that a normal vHIT does not exclude vestibular hypofunction; the test you order has to match the question you are asking.

Section 08

The peripheral vestibular labyrinth

The peripheral vestibular apparatus comprises the three semicircular canals — horizontal (lateral), anterior (superior), and posterior — and the two otolith organs — utricle and saccule. The canals transduce angular acceleration via cupular deflection of stereociliated hair cells; the otoliths transduce linear acceleration (including gravity) via shear of an otoconia-laden gelatinous macula.

Horizontal (lateral) canalAnterior canalPosterior canalvestibulecochleautricle + saccule (otolith organs)Each canal has a swelling (ampulla) containing the crista ampullaris with hair cells and overlying cupula.
The membranous labyrinth: three roughly orthogonal canals and two otolith organs. Canals pair across the head: R lateral with L lateral; R anterior with L posterior (RALP); L anterior with R posterior (LARP).
Ewald's laws (paraphrased)
  1. Eye movement evoked by a canal occurs in the plane of that canal.
  2. In the horizontal canal, ampullopetal (toward the ampulla) endolymph flow is a more potent stimulus than ampullofugal flow.
  3. In the vertical canals, ampullofugal flow is the more potent stimulus.
Canal pairings
  • Horizontal pair: R lateral & L lateral (both in same yaw plane).
  • RALP plane: R Anterior & L Posterior — diagonal plane through the head.
  • LARP plane: L Anterior & R Posterior — the opposite diagonal.
These three plane-pairs allow vector decomposition of any angular head motion.
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Bedside Exam02
02
Module

The Bedside Examination

In skilled hands the eye exam outperforms early MRI for identifying posterior-circulation stroke. Here is how to do it.

Contents
  1. 01Approach to the dizzy patient
  2. 02Gross eye exam
  3. 03Head impulse test
  4. 04Examining for nystagmus
  5. 05Test of skew (cover test)
  6. 06Putting it together: HINTS+
  7. 07Dix-Hallpike maneuver
  8. 08Supine roll test
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Section 01

Approach to the dizzy patient

Dizziness accounts for ~3% of emergency-department visits. The most important branch-point is whether the presentation fits an acute vestibular syndrome (AVS) — rapid-onset vertigo lasting days, nausea/vomiting, gait unsteadiness, head-motion intolerance, spontaneous nystagmus. In AVS, the question becomes: is this peripheral (e.g., vestibular neuritis) or central (e.g., posterior fossa stroke)? The framework reframes the dizzy patient by Timing, Triggers and Targeted Exam — sorting presentations into four broad vestibular syndromes that drive very different workups.

Acute vestibular syndrome (AVS)
Duration: days–weeks
Trigger: spontaneous (continuous)
  • ·Vestibular neuritis
  • ·Labyrinthitis
  • ·Posterior fossa stroke
  • ·MS plaque
  • ·First migraine attack
Episodic vestibular syndrome — spontaneous
Duration: minutes–hours, recurrent
Trigger: no clear trigger
  • ·Vestibular migraine
  • ·Ménière's
  • ·TIA (vertebrobasilar)
  • ·Panic disorder
Episodic vestibular syndrome — triggered
Duration: seconds, with triggers
Trigger: head position changes
  • ·BPPV
  • ·Orthostatic hypotension
  • ·Central positional vertigo
  • ·SSCD (sound/pressure)
Chronic vestibular syndrome ()
Duration: weeks–months, persistent
Trigger: exacerbated by movement, upright posture, complex visual scenes
  • ·PPPD
  • ·Bilateral vestibulopathy
  • ·Cerebellar degeneration
  • ·Mal de débarquement syndrome
  • ·Post-concussive dizziness

is the bin most often missed in the emergency department because the patient is rarely in extremis: dizziness is constant but low-grade, and the bedside exam is often normal. These patients usually present to outpatient clinics, not the ED, and the diagnosis rests more on history pattern and vestibular function testing than on a single examination finding.

Section 02

Gross eye exam — what to look for first

  1. 1.
    Spontaneous nystagmus in primary gaze
    With fixation, then again after fixation is removed (Frenzel lenses, video-Frenzel, or look at the eyes with a +20 D lens / ophthalmoscope while the other eye fixates a target).
  2. 2.
    Range of EOM motion
    Test the 9 cardinal gaze positions. Look for an adduction deficit (INO), upgaze palsy (dorsal midbrain), or any restricted movement.
  3. 3.
    Ocular alignment
    Cover-uncover and alternate cover tests to detect tropias/phorias. Vertical misalignment (skew) is a central sign in AVS.
  4. 4.
    Pupils
    Anisocoria, light response, RAPD (Horner's accompanies Wallenberg lateral medullary syndrome).
  5. 5.
    Gaze-evoked nystagmus
    Hold gaze 15–20° eccentric for ≥10 seconds in 4 cardinal positions. A few unsustained beats at extremes = physiologic end-point; sustained = pathologic.
  6. 6.
    Saccades
    Quick gaze shifts between two targets. Look for slowing (INO, brainstem), inaccuracy (cerebellum: hypermetria), latency, or initiation difficulty.
  7. 7.
    Smooth pursuit
    Track a slowly moving finger. Saccadic ('cogwheel') pursuit = cerebellar/age/sedation.
Section 03

The head impulse test (Halmagyi-Curthoys)

With the patient fixating your nose, deliver a small (~15°), fast, and unpredictable head turn. Watch the eyes. A normal keeps the eyes locked on your nose (eyes counter-rotate equally to the head). An abnormal VOR produces a visible corrective ("catch-up") saccade back to the target after the head movement — the cardinal sign of peripheral vestibular hypofunction toward that side.

Examiner's nose (fixation target)
Phase: still · VOR gain: 1.00
Toggle sides to see the difference. The corrective saccade is the diagnostic finding — it tells you the VOR is impaired on the side the head was turned to.
What does it mean?
In a patient with acute vestibular syndrome, an abnormal head impulse test toward one side is REASSURING for peripheral disease (e.g., vestibular neuritis). A normal head impulse test in a patient with severe spontaneous vertigo and nystagmus is a DANGER sign — central causes (stroke) typically spare the VOR[1,2].
Section 04

Examining for nystagmus

To characterize nystagmus, observe in five conditions: primary gaze with fixation, primary gaze without fixation(Frenzel / video-Frenzel goggles), eccentric gaze in 4 directions, after head-shaking (15 cycles 2 Hz then watch), and in positions of provocation (Dix-Hallpike, roll test). Each tells you something different about where the lesion is.

Peripheral pattern
  • ·DIRECTION-FIXED (same fast-phase in all gaze)
  • ·Mixed horizontal-torsional
  • ·Suppressed by fixation
  • ·Intensity ↑ with gaze toward fast phase (Alexander)
  • ·Abnormal HIT on affected side
  • ·NO vertical or pure torsional nystagmus
Central pattern
  • ·DIRECTION-CHANGING (reverses with gaze)
  • ·Pure vertical or pure torsional
  • ·Not suppressed by fixation
  • ·Often accompanied by other signs (skew, dysmetria)
  • ·Normal HIT (usually)
  • ·Persistent positional without latency/fatigue
Congenital pattern
  • ·Lifelong history
  • ·Horizontal plane in ALL gaze (including vertical)
  • ·Increasing-velocity slow phase
  • ·Has a null zone (head turn adopted)
  • ·Dampens with convergence
Section 05

Test of skew — alternate cover test

Vertical ocular misalignment () is a hallmark of brainstem dysfunction, especially involving the otolith-ocular pathway from the utricle through the vestibular nuclei to the . Test by holding the patient's gaze on a target while alternately covering each eye every 1–2 seconds. A vertical refixation movement of the uncovered eye = skew.

TargetL eyeR eyeL eye covered → R eye visible refixates
In skew, when the cover moves from right to left eye, the previously covered eye refixates vertically. The pattern is conjugate (both eyes show similar offset) — distinct from a fourth-nerve palsy.
Skew vs CN IV palsy
Skew is comitant (similar magnitude in all positions) and lacks the torsional component and head tilt of fourth-nerve palsy. The hypertropic eye in skew often shows an excyclotorsion of the LOWER eye relative to the higher eye — opposite to trochlear palsy.
Section 06

Putting it together — HINTS+

= Head Impulse + Nystagmus + Test of Skew. In a patient with the, the combination distinguishes peripheral from central with sensitivity approaching 100% for stroke when performed by a trained clinician — exceeding early MRI-DWI[1]. "" adds a finger-rub hearing test (unilateral hearing loss in AVS suggests AICA stroke, since the cochlea is supplied by the internal auditory artery, a branch of AICA)[2,3].

TestPeripheral (benign)Central (dangerous)
Head Impulse TestABNORMAL — corrective saccade present (toward affected side)Normal — no corrective saccade
NystagmusDirection-fixed horizontal (with torsional component), suppressed by fixationDirection-changing, or pure vertical/torsional, not suppressed
Test of SkewAbsentPresent (vertical refixation on alternate cover test)
Hearing (the +)Symmetric (preserved)May have UNILATERAL hearing loss (AICA stroke)
A peripheral pattern requires ALL THREE to be benign. A central pattern is identified by ANY ONE dangerous feature.
Important caveats
  • HINTS is for AVS only — patients with acute, continuous vertigo + nystagmus + nausea. Do NOT use for episodic or triggered vertigo.
  • HINTS requires the examiner to be comfortable with all three components; sensitivity drops sharply in untrained hands.
  • An isolated cerebellar infarct without nystagmus or HIT abnormality may be missed — gait and truncal stability must also be tested[21,22].
  • HINTS does not replace neuroimaging when central signs are present.
Section 07

Dix-Hallpike maneuver

The diagnostic test for posterior (and anterior) canal BPPV. Move through the five steps; on the right is what you should see in the patient's eyes at each step.

head turned 45° to RIGHTPatient seated
Patient's eyes (close-up)

Patient seated. Patient sits with legs extended on table. Head turned 45° toward the side being tested (here: RIGHT).

Click the steps to walk through the maneuver and see what the eyes do.
Treatment: Epley maneuver
Once posterior canal BPPV is confirmed, Epley canalith repositioning is 80% effective on first attempt[4]. Sequence: Dix-Hallpike position (affected side) → rotate head 90° to opposite side (still supine) → roll body so head is face-down → sit up with head turned 45°. Hold each position 30–60 seconds[5].
Section 08

Supine roll test (Pagnini-McClure)

The horizontal canal is in the gravity plane when the patient is supine with head flexed ~30°. Rolling the head 90° to each side stimulates the affected horizontal canal. The nystagmus is purely horizontal[5,4].

Affected ear DOWN (geotropic)
Fast-phase: → right-beating horizontal · fatigable · latency 0.5s
Geotropic (canalithiasis): both directions provoke nystagmus beating toward the ground. The MORE intense side identifies the affected ear.
Affected ear DOWN (apogeotropic)
Fast-phase: ← left-beating horizontal · latency 0.5s
Apogeotropic (cupulolithiasis): both directions provoke nystagmus beating away from the ground. The LESS intense side identifies the affected ear.
Side identification
Geotropic: Affected side = side with STRONGER nystagmus on roll. Ewald's first law (ampullopetal flow excites the horizontal canal more strongly than ampullofugal).
Apogeotropic: Affected side = side with WEAKER nystagmus.
The "Bow & Lean" test (head pitched forward, then back, while seated) provides confirmatory lateralization in horizontal-canal BPPV.
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Atlas of Nystagmus03
05
Module

VNG / ENG Interpretation

Reading the tracings — saccade, pursuit, OKN, gaze, caloric, vHIT. The art of pattern recognition in vestibular laboratory studies.

Contents
  1. 01What is VNG/ENG?
  2. 02Saccade test
  3. 03Gaze test
  4. 04Smooth pursuit test
  5. 05Optokinetic test
  6. 06Caloric test
  7. 07vHIT (video head impulse)
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Section 01

What is VNG / ENG?

Electronystagmography (ENG) and videonystagmography (VNG) are laboratory techniques for recording eye movements. ENG uses the corneoretinal potential (the eye is an electrical dipole, positive at the cornea and negative at the retina); skin electrodes around the eyes detect changes as the eye rotates. VNG uses an infrared video camera mounted in goggles to track pupil position frame-by-frame and is now the standard.

VNG advantages

Detects torsional movements, records in complete darkness, no skin preparation, less artifact. Now the standard of care.

ENG advantages

Records with eyes closed (sleep studies, infants), no goggles needed, cheaper. Calibration depends on the corneoretinal potential — varies with light and time.

The standard VNG battery
Most labs run a standardized sequence: Oculomotor tests(saccade, gaze, pursuit, OKN) → Positional / positioning tests(Dix-Hallpike, roll, head-shake) → Caloric test (warm/cool irrigation of each ear). vHIT and VEMPs are usually separate.
Section 02

Saccade test — accuracy, velocity, latency

Patient fixates a target that jumps unpredictably between positions. The software measures three things for each saccade.

01
Accuracy

How close the eye lands to the target. Normal ≈ 90–110% of target amplitude.

When abnormal
  • ·Hypometria (consistent undershoot): basal-ganglia disease, fatigue, inattention
  • ·Hypermetria (overshoot): CEREBELLAR — dorsal vermis lesion, posterior fossa stroke
  • ·Asymmetric hypermetria → side of cerebellar lesion
02
Peak velocity

Should follow the 'main sequence' — larger saccades go faster. Normal 10° saccade ≈ 200–400°/s.

When abnormal
  • ·Slow saccades: INO (slow ADducting eye), PSP (slow vertical), spinocerebellar ataxia type 2, drug intoxication, myasthenia
03
Latency

Time from target jump to saccade onset. Normal 180–250 ms.

When abnormal
  • ·Prolonged: basal ganglia (Parkinson, Huntington), age, inattention
  • ·Reduced: 'express saccades' — frontal lobe disinhibition
— — target—— eyetime (s)
A normal random saccade paradigm. Each step in the target trace produces a near-vertical jump in the eye trace landing on target.
The signature of INO
On a saccade test, internuclear ophthalmoplegia produces a characteristic pattern: the ADducting eye is SLOW and undershoots on horizontal saccades, while the ABducting eye is normal velocity but may show dissociated nystagmus. Compare velocities side-by-side in monocular recording.
Section 03

Gaze test — looking for nystagmus at eccentric gaze

The patient holds gaze at ±20–30° horizontal, ±20° vertical, and primary gaze, each for ≥10 seconds. Look for nystagmus, and characterize the slow phase.

25° LEFT
Fast-phase: → right-beating horizontal
PRIMARY
Fast-phase: → right-beating horizontal
25° RIGHT
Fast-phase: → right-beating horizontal
Spontaneous (primary-gaze) peripheral right-beating nystagmus enhanced on rightward gaze (Alexander's law), suppressed on leftward gaze.
The 3 degrees of spontaneous nystagmus
1st degree: present only with gaze toward fast phase.
2nd degree: present in primary gaze and toward fast phase.
3rd degree: present in all gaze directions including AWAY from fast phase. Implies a larger imbalance.
Section 04

Smooth pursuit test

Patient tracks a target moving sinusoidally at 0.2–0.4 Hz (~20–40°/s peak velocity). The software computes pursuit gain(eye velocity ÷ target velocity). Normal > 0.8; reduced in cerebellar disease, brainstem lesions, drug toxicity, advanced age, and inattention.

NORMAL — smooth, gain ≈ 0.95SACCADIC — cerebellar / drug
Normal pursuit (top) follows the sinusoid smoothly. Saccadic ('cogwheel') pursuit (bottom) is interrupted by catch-up saccades.
Caveats
Saccadic pursuit is sensitive but non-specific. It is reduced in normal aging (age >60), with drowsiness, inattention, medications (benzodiazepines, anticonvulsants, alcohol). Interpret only with clinical context.
Section 05

Optokinetic (OKN) test

A moving striped or dot pattern (or a rotating drum) drives the eyes into reflexive nystagmus. The slow phase tracks the stimulus; the fast phase resets. OKN gain (slow-phase velocity ÷ stimulus velocity) is computed for both directions; asymmetry suggests deep parietal/occipital cortical disease.

Fast-phase: ← left-beating horizontal
Optokinetic nystagmus in response to a rightward-moving full-field stimulus.
Inverted OKN
Patients with congenital nystagmus paradoxically show OKN beating IN THE DIRECTION of stimulus motion (inverted), because their nystagmus 'locks on' to the stimulus and the entire pattern reverses. A pathognomonic finding.
Section 06

The caloric test

Each ear is irrigated with warm (44°C) and cool (30°C) water (or air). The temperature change creates a convection current in the horizontal canal endolymph, mimicking head rotation. Mnemonic: COWS — Cold, Opposite (fast phase away from irrigated ear); Warm, Same (fast phase toward irrigated ear). Slow-phase velocity is measured.

Slow-phase velocity (°/sec)
Butterfly plot
slow-phase velocity (°/s)LEFT EARRIGHT EARLW 10LC 8RW 22RC 20
UNILATERAL WEAKNESS
40.0%
→ LEFT peripheral hypofunction
DIRECTIONAL PREPONDERANCE
0.0%
Within normal limits
Total slow-phase: 60°/sec
The butterfly (Claussen) plot displays slow-phase velocity for each of the four irrigations. A unilateral weakness >25% is the threshold for clinically significant peripheral vestibular hypofunction.
Formulae

Unilateral weakness (UW) = |(RW + RC) − (LW + LC)| / (RW + RC + LW + LC) × 100%

Directional preponderance (DP) = |(RW + LC) − (LW + RC)| / (RW + RC + LW + LC) × 100%

RW = right warm slow-phase velocity; RC = right cool; LW = left warm; LC = left cool. UW >25% suggests peripheral hypofunction on the side with reduced response. DP >30% is non-localizing but suggests an asymmetry (peripheral or central).

Bilateral weakness
Total response (RW+RC+LW+LC) < 22°/s suggests bilateral vestibular hypofunction. Causes: ototoxicity (aminoglycosides), neurofibromatosis II (bilateral vestibular schwannomas), autoimmune inner ear disease, idiopathic. Rotational chair testing is needed for confirmation.
Section 07

Video head impulse test (vHIT)

vHIT extends the bedside head impulse test by recording head and eye velocity with high-speed video. It produces a numerical VOR gain(eye velocity ÷ head velocity) per canal and detects covert catch-up saccades not visible to the naked eye. All six semicircular canals can be tested[19].

01
Gain

Eye velocity ÷ head velocity. Normal ≥ 0.8 for lateral canals; ≥ 0.7 for vertical.

When abnormal
  • ·Reduced gain on the affected side in peripheral hypofunction
  • ·Bilateral reduction in BVH
02
Covert saccades

Catch-up saccades occurring DURING the head impulse — invisible at bedside but detected by vHIT.

When abnormal
  • ·Present in partial vestibular hypofunction; sensitivity higher than overt saccades alone
03
Overt saccades

Catch-up saccades AFTER the head impulse ends — what you see at bedside.

When abnormal
  • ·Hallmark of unilateral vestibulopathy
vHIT vs caloric
Both test the lateral canal, but at different frequencies. vHIT probes high-frequency (≈3–5 Hz) VOR; caloric simulates very low-frequency (~0.003 Hz). The two can dissociate: in early Ménière's, calorics may be abnormal while vHIT remains normal. Use both for a complete picture[20].
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Case Simulator06
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Module

References & Acknowledgements

Due credit to the primary sources from which Vestibulum's content was synthesized.

Primary textbook

McCaslin, D. L. (Ed.). Electronystagmography/Videonystagmography (ENG/VNG). Plural Publishing.

The primary source for the neuroanatomy, oculomotor systems, bedside examination, and VNG/ENG interpretation modules. Content has been synthesized and reorganized for interactive presentation; readers seeking depth, full waveform examples, and the technical underpinnings of recording montages should consult the original text.

Supporting peer-reviewed literature

For each topic, the most authoritative consensus criteria, clinical practice guidelines, and validation studies are listed. References use APA-style formatting; DOIs are provided where available and resolve to the canonical source.

HINTS / acute vestibular syndrome

  1. []Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y.-H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke, 40(11), 3504–3510. https://doi.org/10.1161/STROKEAHA.109.551234
  2. []Newman-Toker, D. E., Curthoys, I. S., & Halmagyi, G. M. (2015). Diagnosing stroke in acute vertigo: the HINTS family of eye movement tests and the future of the 'eye ECG.' Seminars in Neurology, 35(5), 506–521. https://doi.org/10.1055/s-0035-1564298
  3. []Edlow, J. A., Carpenter, C., Akhter, M., Khoujah, D., et al. (GRACE-3 / SAEM Guidelines committee) (2023). Guidelines for reasonable and appropriate care in the emergency department (GRACE-3): acute dizziness and vertigo. Academic Emergency Medicine, 30(5), 442–486. https://doi.org/10.1111/acem.14728

BPPV — diagnosis & management

  1. []Bhattacharyya, N., Gubbels, S. P., Schwartz, S. R., et al. (2017). Clinical practice guideline: benign paroxysmal positional vertigo (update). Otolaryngology–Head and Neck Surgery, 156(3 Suppl), S1–S47. https://doi.org/10.1177/0194599816689667
  2. []von Brevern, M., Bertholon, P., Brandt, T., et al. (2015). Benign paroxysmal positional vertigo: diagnostic criteria. Consensus document of the Committee for the Classification of Vestibular Disorders of the Bárány Society. Journal of Vestibular Research, 25(3–4), 105–117. https://doi.org/10.3233/VES-150553
  3. []Balatsouras, D. G., & Korres, S. G. (2011). Subjective benign paroxysmal positional vertigo. Otolaryngology–Head and Neck Surgery, 145(1), 98–103. https://doi.org/10.1177/0194599811402247
  4. []Anagnostou, E., Kouzi, I., & Spengos, K. (2015). Diagnosis and treatment of anterior-canal benign paroxysmal positional vertigo: a systematic review. Journal of Clinical Neurology, 11(3), 262–267. https://doi.org/10.3988/jcn.2015.11.3.262

Ménière's disease

  1. []Lopez-Escamez, J. A., Carey, J., Chung, W. H., et al. (AAO-HNS / Bárány Society / EAONO / JSER) (2015). Diagnostic criteria for Menière's disease. Journal of Vestibular Research, 25(1), 1–7. https://doi.org/10.3233/VES-150549
  2. []Basura, G. J., Adams, M. E., Monfared, A., et al. (2020). Clinical practice guideline: Ménière's disease. Otolaryngology–Head and Neck Surgery, 162(2 Suppl), S1–S55. https://doi.org/10.1177/0194599820909438

Vestibular migraine

  1. []Lempert, T., Olesen, J., Furman, J., et al. (Bárány Society & International Headache Society) (2012). Vestibular migraine: diagnostic criteria. Journal of Vestibular Research, 22(4), 167–172. https://doi.org/10.3233/VES-2012-0453
  2. []Lempert, T., Olesen, J., Furman, J., et al. (2022). Vestibular migraine: diagnostic criteria (update). Journal of Vestibular Research, 32(1), 1–6. https://doi.org/10.3233/VES-201644

Persistent postural-perceptual dizziness (PPPD)

  1. []Staab, J. P., Eckhardt-Henn, A., Horii, A., et al. (2017). Diagnostic criteria for persistent postural-perceptual dizziness (PPPD): consensus document of the Committee for the Classification of Vestibular Disorders of the Bárány Society. Journal of Vestibular Research, 27(4), 191–208. https://doi.org/10.3233/VES-170622

Vestibular neuritis & acute unilateral vestibulopathy

  1. []Strupp, M., Bisdorff, A., Furman, J., et al. (2022). Acute unilateral vestibulopathy/vestibular neuritis: diagnostic criteria. Journal of Vestibular Research, 32(5), 389–406. https://doi.org/10.3233/VES-220201

Superior semicircular canal dehiscence (SSCD)

  1. []Minor, L. B., Solomon, D., Zinreich, J. S., & Zee, D. S. (1998). Sound- and/or pressure-induced vertigo due to bone dehiscence of the superior semicircular canal. Archives of Otolaryngology–Head & Neck Surgery, 124(3), 249–258. https://doi.org/10.1001/archotol.124.3.249
  2. []Ward, B. K., van de Berg, R., van Rompaey, V., et al. (2021). Superior semicircular canal dehiscence syndrome: diagnostic criteria consensus document of the Committee for the Classification of Vestibular Disorders of the Bárány Society. Journal of Vestibular Research, 31(3), 131–141. https://doi.org/10.3233/VES-200004

Bilateral vestibulopathy

  1. []Strupp, M., Kim, J.-S., 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. https://doi.org/10.3233/VES-170619

Eye movement systems & neuroanatomy

  1. []Leigh, R. J., & Zee, D. S. (2015). The Neurology of Eye Movements (5th ed.). Oxford University Press.
    The definitive reference on oculomotor neuroanatomy and pathology. Used for cross-checks of saccade/pursuit/VOR/gaze-holding physiology.
  2. []Brandt, T., Dieterich, M., & Strupp, M. (2013). Vertigo and Dizziness: Common Complaints (2nd ed.). Springer.

Video head impulse test (vHIT) & high-frequency VOR

  1. []Halmagyi, G. M., Chen, L., MacDougall, H. G., Weber, K. P., McGarvie, L. A., & Curthoys, I. S. (2017). The video head impulse test. Frontiers in Neurology, 8, 258. https://doi.org/10.3389/fneur.2017.00258
  2. []McCaslin, D. L., Jacobson, G. P., Bennett, M. L., Gruenwald, J. M., & Green, A. P. (2014). Predictive properties of the video head impulse test: measures of caloric symmetry and self-report dizziness handicap. Ear and Hearing, 35(5), e185–e191. https://doi.org/10.1097/AUD.0000000000000047

Posterior circulation stroke

  1. []Tarnutzer, A. A., Berkowitz, A. L., Robinson, K. A., Hsieh, Y.-H., & Newman-Toker, D. E. (2011). Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ, 183(9), E571–E592. https://doi.org/10.1503/cmaj.100174
  2. []Saber Tehrani, A. S., Kattah, J. C., Mantokoudis, G., et al. (2014). Small strokes causing severe vertigo: frequency of false-negative MRIs and nonlacunar mechanisms. Neurology, 83(2), 169–173. https://doi.org/10.1212/WNL.0000000000000573

Multiple sclerosis — vestibular & oculomotor manifestations

  1. []Thompson, A. J., Banwell, B. L., Barkhof, F., et al. (2018). Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. The Lancet Neurology, 17(2), 162–173. https://doi.org/10.1016/S1474-4422(17)30470-2
  2. []Frohman, E. M., Frohman, T. C., Zee, D. S., McColl, R., & Galetta, S. (2005). The neuro-ophthalmology of multiple sclerosis. The Lancet Neurology, 4(2), 111–121. https://doi.org/10.1016/S1474-4422(05)00992-0
A note on the animations

The animated nystagmus patterns in Vestibulum are stylized representations generated parametrically from the kinematic features described in the source literature (fast/slow phase amplitudes, slow-phase shape, latency, fatigability, gaze modulation). They are not derived from patient recordings, and they intentionally exaggerate features for teaching clarity. For authentic recordings, readers should consult the McCaslin VNG textbook DVD and the published case libraries from the Bárány Society.

Acknowledgements

Vestibulum was conceived and designed by Dr. Prahlada N. B. for the educational use of medical students, ENT and neurology trainees, audiologists, and vestibular therapists.

Institutional support: Karnataka ENT Hospital and Research Center (R), Champions Educational and Medical Society (R), and Amogh Foundation.

Special thanks to the authors and editors of the source works cited above, whose careful clinical observation and rigorous criteria-building underpin every page of this atlas.

Educational use only

This material is for educational purposes only. Not for clinical use. Clinicians remain completely responsible for interpretation, formulation of differential diagnosis, and any clinical decision. Citations here support specific points in the atlas; they do not constitute clinical endorsement of any specific approach for any specific patient. Where guidelines and criteria have been updated since publication, the most recent version should be consulted.

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End of compiled atlas.

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Vestibulum

An interactive teaching atlas of eye movement examination and nystagmus in vertigo. Content synthesized from McCaslin's Electronystagmography/Videonystagmography, current Bárány Society criteria, and peer-reviewed sources.

→ Full references & acknowledgements
Built for

Medical students, ENT/Neurology/Audiology trainees, vestibular therapists, and clinicians who want to teach themselves the language of nystagmus.

GlossaryMy libraryCompareDDx toolFlashcardsReferencesMy progressPrint allBPPV maneuversPattern trainer
Concept & design

Dr Prahlada N.B

Karnataka ENT Hospital and Research Centre (R),
Champions Educational and Medical Society (R), and
Amogh Foundation, Chitradurga, Karnataka, India

Please share your valuable feedback to: prahladnb@kenthospitals.com

Disclaimer

For educational purposes only. Not for clinical use. Vestibulum is an instructional resource intended to support learning about eye movement examination and nystagmus. Clinicians remain completely responsible for the interpretation of findings, the formulation of a differential diagnosis, and any clinical decision. Nothing in this application replaces individualized assessment, hands-on training, expert consultation, or established practice guidelines.

© 2026 Dr Prahlada N.B · Karnataka ENT Hospital and Research Centre (R) · Champions Educational and Medical Society (R) · Amogh Foundation