Vestibulum — Vertigo Teaching Atlas

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.

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

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

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

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 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)

Right Warm (RW)Right Cool (RC)Left Warm (LW)Left Cool (LC)

Butterfly plot

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].

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

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

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].