Plain-language definitions of every clinical and physiological term used in the atlas. Cross-referenced and chapter-tagged. Hover an underlined term anywhere in the atlas for a quick definition; click through to here for full context.
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Acute, persistent vertigo with nystagmus, lasting days, with nausea and gait unsteadiness. Differentiated into peripheral (vestibular neuritis, labyrinthitis) and central (posterior circulation stroke, MS). HINTS exam is the initial bedside discriminator.
The electrical discharge rate of a sensory neuron. Vestibular afferents have a tonic resting discharge (~90 spikes/sec) that is modulated up or down by head motion; the brain compares left vs right firing rates to derive head velocity.
Spontaneous peripheral nystagmus intensifies on gaze toward the fast phase, attenuates on gaze toward the slow phase. Classified in three degrees: 1° (only on gaze toward fast), 2° (also primary), 3° (even on gaze toward slow). Higher degree = stronger drive.
The bulbous expansion at one end of each semicircular canal. Houses the cupula and crista ampullaris (where hair cells reside).
Endolymph flow away from the ampulla. Inhibits horizontal canal hair cells (and excites anterior/posterior canal hair cells).
Endolymph flow toward the ampulla. Excites the horizontal canal hair cells (and inhibits anterior/posterior canal hair cells).
Beating away from the ground (away from the dependent ear in the supine roll test). In horizontal canal BPPV, apogeotropic = cupulolithiasis variant.
Caudal displacement of the cerebellar tonsils through the foramen magnum. Classic VNG findings: downbeat nystagmus, periodic alternating nystagmus. Surgical decompression can dramatically improve symptoms.
Reduced vestibular function on both sides. On caloric, the sum of all four responses is markedly reduced (often <12°/s total). Patients have oscillopsia with head movement and worse imbalance in the dark. Confirm with rotational chair and video HIT.
Benign paroxysmal positional vertigo. Brief (<60s) episodes of vertigo triggered by head position changes, caused by otoconia free-floating in (canalithiasis) or stuck to (cupulolithiasis) a semicircular canal. The most common cause of vertigo in adults.
A vestibular test in which warm and cool water (or air) is irrigated into the external ear canal, producing a thermal gradient across the horizontal canal. The resulting endolymph convection drives nystagmus. Used to assess each ear separately at very low frequency (~0.003 Hz).
BPPV variant in which dislodged otoconia free-float in the semicircular canal. Produces brief (<60s) nystagmus with latency, crescendo-decrescendo, and fatigue on repeated positioning. Treated with the Epley maneuver.
The "little brain" attached to the brainstem. Critical for oculomotor control: the floccus and paraflocculus tune VOR gain and pursuit; the nodulus and uvula process velocity-storage; the dorsal vermis controls saccade accuracy.
Onset before 6 months. Increasing-velocity (accelerating) slow phase — the pathognomonic feature. Brief foveation periods between beats explain the relatively preserved visual acuity. Often a null point with head turn.
Cold Opposite, Warm Same — the mnemonic for caloric nystagmus direction. Cold water → endolymph falls → ampullofugal flow → inhibition → fast phase OPPOSITE the irrigated ear. Warm water reverses everything → fast phase SAME side as irrigated ear.
A ridge of sensory epithelium inside the ampulla, containing the hair cells whose stereocilia project up into the cupula.
The gelatinous flap inside the ampulla of each semicircular canal. It deflects when endolymph flows past it, bending the hair cells embedded in it. Has the same density as endolymph, so gravity acts equally on both — making the cupula gravity-insensitive in normal anatomy.
BPPV variant in which otoconia adhere to the cupula itself. Nystagmus has no latency, is sustained as long as the position is held, and does not fatigue. Treated with the Semont liberatory maneuver.
A rise in the cell membrane voltage toward zero. In hair cells, depolarization releases neurotransmitter onto afferent terminals, increasing afferent firing.
A measure of the asymmetry between right-beating and left-beating responses on caloric. DP = |(RW + LC) − (RC + LW)| ÷ total × 100. Less specific than unilateral weakness; values <30% usually not clinically significant in isolation.
The provocative test for posterior canal BPPV. The patient is rapidly moved from sitting to head-hanging-right (or left), and the examiner observes for upbeating-torsional nystagmus with the upper poles beating toward the dependent ear.
Nystagmus with a downward fast phase, present in primary gaze. Localises to cervicomedullary junction or cerebellar floccus. Classic association: Arnold-Chiari I. Also drug-induced (lithium, anticonvulsants), Wernicke encephalopathy.
A normal physiologic nystagmus that appears at extreme lateral gaze (>30°), is low amplitude, and fatigues within 20-30 seconds. Should not be mistaken for pathologic gaze-evoked nystagmus.
The potassium-rich fluid filling the membranous labyrinth, including the semicircular canals and otolith organs. Its inertia is what allows it to flow past the cupula during head rotation, providing the mechanical signal for angular acceleration.
A sequence of head positions that uses gravity to roll free-floating otoconia out of the posterior canal and back to the utricle. First-line treatment for posterior canal canalithiasis; 80-90% effective in 1-2 cycles.
Three classical observations: (1) eye movements occur in the plane of the canal being stimulated; (2) ampullopetal endolymph flow is more effective in horizontal canals (excitation > inhibition for horizontal); (3) ampullofugal flow is more effective in vertical canals.
The brainstem-generated saccade that resets the eye after a slow phase. Its direction names the nystagmus by convention (right-beating = fast phase to the right) — but it is not the diagnostic signal.
The ratio of nystagmus SPV with visual fixation to SPV without (in goggles). <0.5 = good suppression (peripheral). ≥0.7 = poor suppression (central red flag).
The reduction of nystagmus when the patient fixates a visual target. Peripheral nystagmus typically suppresses by ≥50%; central nystagmus does not. The fixation index (SPV with fixation ÷ SPV without) <0.5 suggests peripheral, ≥0.7 suggests central.
A small lobe of the cerebellum critical for VOR adaptation, smooth pursuit, and gaze-holding. Lesions produce a host of oculomotor abnormalities including downbeat nystagmus and rebound nystagmus.
A brief flat segment in the congenital nystagmus waveform during which the eye is essentially still on the target. Allows surprisingly good visual acuity despite the constant ocular oscillation.
The ratio of eye velocity to head velocity during the VOR. Normal ≈ 1.0 (eyes move equal and opposite to head). Reduced in vestibular hypofunction; restored by adaptation, vestibular rehab, or substitution.
Nystagmus that appears when the eye is held in eccentric gaze, beating in the direction of gaze. Reflects neural integrator dysfunction. Common in cerebellar disease and many drugs (anticonvulsants, sedatives).
Beating toward the ground (toward the dependent ear in the supine roll test). In horizontal canal BPPV, geotropic = canalithiasis variant.
The mechanoreceptor of the vestibular and auditory systems. Has stereocilia and one kinocilium; deflection toward the kinocilium opens transduction channels and depolarizes the cell, increasing afferent firing.
A bedside test of high-frequency VOR. The examiner unpredictably thrusts the patient's head ~10° while the patient fixates on a target. A positive (abnormal) test shows a corrective saccade after the thrust, meaning the VOR could not keep the eyes on target.
A bedside exam (Head Impulse, Nystagmus pattern, Test of Skew) used to differentiate peripheral from central causes of acute vestibular syndrome. Central pattern (HINTS+): NORMAL head-impulse + DIRECTION-CHANGING nystagmus + SKEW present. More sensitive than early MRI for posterior circulation stroke.
The semicircular canal oriented in the horizontal plane (when the head is tilted 30° down, as in caloric testing). Detects rotation about the vertical axis (head turning side to side).
A brainstem syndrome from MLF lesion: the abducting eye shows dissociated jerk nystagmus, while the adducting eye is slowed or fails to fully adduct, with preserved convergence. Bilateral INO in a young adult is multiple sclerosis until proven otherwise; unilateral INO in older adults suggests brainstem stroke.
Nystagmus with an asymmetric beat — slow drift in one direction followed by a fast resetting saccade. Most peripheral and central vestibular nystagmus is jerk in form.
The standard formula for unilateral weakness (UW) on caloric: UW = |(RW + RC) − (LW + LC)| ÷ (RW + RC + LW + LC) × 100. Values use peak slow-phase velocity. UW ≥ 25% is the conventional threshold for clinically significant peripheral asymmetry.
The single tallest "hair" on a vestibular hair cell, located at one edge of the stereocilia bundle. Its position defines the polarity of the hair cell — deflection toward it excites, away inhibits.
Vestibular neuritis with associated hearing loss (because the labyrinth as a whole, including the cochlea, is involved). Otherwise clinically similar to vestibular neuritis.
The conversion of mechanical movement (here, stereocilia deflection) into electrical signals via ion channels. The fundamental physical event of vestibular and auditory sensation.
A white-matter tract connecting the abducens (CN VI) and oculomotor (CN III) nuclei in the brainstem. Carries the signal that yokes the two eyes during conjugate gaze. A lesion here produces internuclear ophthalmoplegia (INO).
Episodic vertigo (20 min – 24 h), fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness. Pathology: endolymphatic hydrops. First-line: low-sodium diet + diuretic; intratympanic dexamethasone or gentamicin if refractory.
Middle temporal area and medial superior temporal area. Cortical regions essential for motion perception and smooth pursuit. Lesions impair pursuit toward the side of the lesion.
The brainstem-cerebellar circuit (medial vestibular nucleus + nucleus prepositus hypoglossi + cerebellar floccus) that converts the saccadic 'pulse' into a sustained 'step', holding the eye in eccentric gaze. A leaky integrator causes the eye to drift back to primary, producing gaze-evoked nystagmus.
The gaze position at which nystagmus is least intense — usually with best visual acuity. Patients with congenital nystagmus often turn their head to use this position for visual tasks.
Rhythmic, involuntary oscillation of the eyes. Most often described as having a slow phase (the actual drive) and a fast phase (a corrective saccadic reset). Named by the direction of the fast phase by convention.
INO + ipsilateral horizontal gaze palsy. The patient can only abduct one eye (with nystagmus); the other eye is locked at midline. From a larger pontine lesion involving both the MLF and the abducens nucleus.
A reflex eye movement that stabilizes the retina during sustained motion of the visual world (e.g. looking out a moving train window). Produces alternating slow phases (in the direction of motion) and fast resetting saccades.
The illusion that the world is moving when it is not. Caused by VOR failure (e.g. bilateral vestibular hypofunction) or by acquired nystagmus. Patients with congenital nystagmus typically do NOT have oscillopsia — a useful distinguishing feature.
Microscopic calcium carbonate crystals (about 2-3× denser than endolymph) embedded in the gel layer above otolith hair cells. When dislodged from the utricle, they can drift into a semicircular canal and cause BPPV.
Either the utricle or saccule. Detects linear acceleration (including gravity-induced) using calcium carbonate crystals (otoconia) embedded in a gel layer above the hair cells. The mass of the otoconia produces shear during linear motion.
Sinusoidal nystagmus — both 'phases' have similar velocity profiles, no clear slow/fast distinction. Usually congenital; in adults, suggests acquired central pathology (MS, brainstem stroke, oculopalatal myoclonus).
The sodium-rich fluid surrounding the membranous labyrinth, between it and the bony labyrinth. Continuous with cerebrospinal fluid via the cochlear aqueduct.
Horizontal jerk nystagmus that periodically reverses direction every 90-120 seconds, with a brief null period between reversals. Localises to cerebellar nodulus and uvula. Often baclofen-responsive.
The most gravity-dependent canal when the head is upright — which is why ~85-90% of BPPV occurs here, otoconia preferentially settling into it.
Paramedian pontine reticular formation. The brainstem horizontal saccade generator. Lesions slow horizontal saccades but not vertical.
The two components of a saccadic motor command. The 'pulse' is a brief high-frequency burst that moves the eye fast; the 'step' is a sustained tonic signal that holds the eye in the new position. Failure of the step produces gaze-evoked nystagmus.
Gaze-evoked nystagmus that briefly reverses direction when the eyes return to primary. Highly specific for cerebellar dysfunction, particularly the floccus. Cogan's classic sign.
Rostral interstitial nucleus of the MLF. The midbrain vertical saccade generator. Lesions slow vertical saccades.
A test of vestibular function at mid-frequencies (0.01–0.64 Hz). The patient sits in a chair that rotates sinusoidally; the resulting eye movements are recorded. Useful when calorics are absent or to characterize bilateral vestibular hypofunction.
A rapid, ballistic eye movement (up to 600°/s) that jumps the eye between targets. Generated by burst neurons in the brainstem (PPRF for horizontal, riMLF for vertical).
The other otolith organ. Detects vertical linear acceleration. Its hair cells are oriented mostly vertically.
A pendular waveform in which one eye intorts and elevates while the other extorts and depresses, then alternates. Localises to chiasmal/parasellar region. Bitemporal hemianopsia is the companion sign.
One of three orthogonal canals (horizontal, anterior, posterior) in each inner ear. Each detects rotation in its own plane. The canals on the two sides work in pairs (e.g. right horizontal pairs with left horizontal) to encode rotation about every axis.
A rapid side-to-side maneuver intended to dislodge otoconia from the cupula. Used for cupulolithiasis variants of BPPV when Epley is ineffective.
Vertical misalignment of the eyes (one higher than the other) due to brainstem (utriculo-ocular pathway) injury. A central sign. Tested with alternate cover test in HINTS.
The portion of a nystagmus beat where the eye drifts under vestibular drive. Its shape (linear, decelerating, accelerating) localises the lesion and is the diagnostic signal of the waveform.
The slope of the slow phase, in degrees per second. The most important quantitative measurement in VNG. Used in the Jongkees formula and in defining clinical thresholds (e.g. spontaneous nystagmus <6°/s is normal).
The slow eye-movement system that keeps a moving target on the fovea. Velocity-matched to the target. Generated cortically (MT/MST → DLPN → cerebellum). Slowed by sedatives, age, and almost any diffuse CNS process — so symmetric pursuit problems are often nonspecific.
Small, involuntary saccades away from fixation followed by a corrective saccade back, ~200 ms later. A few per minute is normal; many per minute suggests cerebellar disease or progressive supranuclear palsy.
The shorter, graded "hairs" projecting from the apical surface of a hair cell. Connected by tip links — fine filaments that pull open ion channels when the bundle deflects toward the kinocilium.
The provocative test for horizontal canal BPPV. Patient supine, head rotated 90° to each side. Geotropic nystagmus (toward the ground) suggests canalithiasis; apogeotropic suggests cupulolithiasis.
A fine filament connecting the tip of one stereocilium to the side of its taller neighbor. When the bundle bends toward the kinocilium, the tip links stretch and pull open mechanotransduction channels, depolarizing the hair cell.
The continuous baseline firing of vestibular afferents at rest, even with no head motion. About 90 spikes per second in humans. This baseline is what allows hair cells to encode both excitation (firing increase) and inhibition (firing decrease) — without a baseline they could only signal in one direction.
A measure of side-to-side caloric asymmetry, computed by the Jongkees formula. Compares total right-ear response (warm + cold) vs total left-ear response. ≥25% is conventionally clinically significant.
Nystagmus with an upward fast phase, present in primary gaze. Localises to brainstem (pons, medulla) or anterior cerebellar vermis. Wernicke encephalopathy and brainstem stroke are common causes.
One of the two otolith organs (the other is the saccule). Detects horizontal linear acceleration and head tilt. Source of the otoconia that, when dislodged, cause BPPV.
Episodic vertigo (5 min - 72 h) with at least one migrainous feature (photophobia, phonophobia, aura, or headache) during episodes. Audiogram normal. Treated with migraine prophylaxis (propranolol, topiramate, etc.).
Acute peripheral vestibulopathy from inflammation of the vestibular nerve. Acute persistent vertigo for days, no hearing loss (distinguishing from labyrinthitis). HINTS-peripheral pattern, decreasing-velocity slow-phase nystagmus.
The fast eye-movement reflex that keeps the eyes pointed at a target while the head moves. The eyes counter-rotate at equal and opposite velocity to head rotation. Essential for clear vision during head movement; failure causes oscillopsia.
A rapid head-thrust test that measures VOR gain at high frequencies (~5 Hz). Detects covert and overt corrective saccades using video. Positive result (corrective saccade after thrust) indicates VOR loss in the canal of the head-thrust direction.