Glossary

The cranial nerve innervating the lateral rectus, which abducts the eye. Its nucleus in the pons also contains interneurons that drive the contralateral medial rectus via the MLF, making it the hub of horizontal conjugate gaze.

Sudden, continuous vertigo or dizziness lasting more than 24 hours, with nausea, nystagmus, and gait unsteadiness. About one in four cases are posterior-circulation strokes rather than vestibular neuritis.

Peripheral vestibular nystagmus increases in intensity when the patient gazes in the direction of the fast phase, and decreases on gaze the other way. Central nystagmus typically does not obey this rule.

Potassium-channel blockers that enhance cerebellar Purkinje-cell activity. 4-aminopyridine can reduce downbeat nystagmus and episodic ataxia type 2, improving gaze stability and oscillopsia.

A peripheral disorder of brief, position-triggered vertigo from displaced otoconia in a semicircular canal. Its positional nystagmus shows latency, a crescendo–decrescendo course, and fatigability — features absent in central positional nystagmus.

Loss of vestibular function in both labyrinths — from ototoxicity, autoimmune disease, or CANVAS — producing oscillopsia and imbalance that worsen in the dark and on uneven ground.

Cerebellar ataxia, neuropathy, and vestibular areflexia syndrome — a slowly progressive disorder combining bilateral vestibular failure with sensory neuropathy and cerebellar signs, a recognised cause of chronic oscillopsia.

Positional nystagmus of central origin: immediate onset with no latency, non-fatiguing, persistent, often direction-changing or purely vertical, and unresponsive to canalith repositioning — distinguishing it from BPPV.

Vertigo from pathology in the brainstem, cerebellum, thalamus, or cortex, often accompanied by neuro-ophthalmological signs (vertical/direction-changing nystagmus, skew, INO) and other neurological deficits.

A vestibulocerebellar region that calibrates VOR gain, enables fixation suppression and smooth pursuit, and holds eccentric gaze. Floccular dysfunction produces gaze-evoked and downbeat nystagmus and saccadic pursuit.

The hindbrain structure coordinating movement, gaze-holding, and vestibular-reflex modulation. The flocculus/paraflocculus and nodulus/uvula are central to pursuit, VOR calibration, and velocity storage; their lesions cause gaze-evoked and downbeat nystagmus.

Herniation of the cerebellar tonsils through the foramen magnum, crowding the cervicomedullary junction. A classic structural cause of downbeat nystagmus and central vertigo.

Perceived double image from misalignment of the visual axes. In vertigo it is usually binocular and central — from skew deviation, INO, ocular tilt reaction, or a cranial-nerve palsy.

Nystagmus whose fast-phase direction reverses with the direction of gaze (gaze-evoked) — a strong pointer to a central lesion, and more sensitive than early DWI-MRI for posterior-circulation stroke in acute vestibular syndrome.

Vertical nystagmus with slow upward drift and fast downward corrective phases. Highly suggestive of a cerebellar (flocculus/nodulus) or craniocervical-junction lesion such as Chiari malformation; may respond to aminopyridines.

Visual acuity measured during head movement. A drop of more than two Snellen lines compared with the static chart indicates an inadequate VOR — a bedside test for oscillopsia and bilateral vestibular loss.

Nystagmus appearing or worsening on eccentric gaze, from a failing neural integrator (nucleus prepositus hypoglossi, medial vestibular nucleus, flocculus). Non-fatiguing and without latency — a hallmark of central, usually cerebellar, dysfunction.

A rapid, small-amplitude passive head turn while the patient fixates a target. A corrective catch-up saccade signals a peripheral VOR deficit; a normal (negative) HIT in a patient with ongoing AVS paradoxically points to a central lesion.

A three-step bedside oculomotor battery — Head Impulse, Nystagmus, Test of Skew — for acute vestibular syndrome. A central pattern (normal HIT, direction-changing nystagmus, or skew) is more sensitive than early MRI for posterior-circulation stroke.

Impaired adduction of one eye with abducting nystagmus of the other on horizontal gaze, from a lesion of the MLF. Convergence is typically spared. Nearly pathognomonic for a central (brainstem) lesion — MS in the young, stroke in the old.

A midbrain integrator for vertical and torsional gaze and a relay in the graviceptive (otolith-ocular) pathway. Lesions contribute to the ocular tilt reaction, skew deviation, and vertical gaze defects.

A heavily myelinated brainstem tract linking the abducens nucleus to the contralateral oculomotor nucleus to yoke horizontal conjugate gaze, and carrying ascending vertical/torsional signals. Its lesion causes internuclear ophthalmoplegia.

A central demyelinating disease that frequently affects brainstem and cerebellar ocular-motor tracts, causing INO (often bilateral in the young), skew deviation, gaze palsy, and nystagmus — sometimes presenting as vertigo.

The brainstem–cerebellar circuit (nucleus prepositus hypoglossi, medial vestibular nucleus, flocculus) that converts eye-velocity commands into the tonic position signal needed to hold gaze. Its failure produces gaze-evoked nystagmus.

The interface of neurology and ophthalmology concerned with vision and eye movement controlled by the nervous system — here, the ocular-motor signs that localise vestibular lesions.

Midline vestibulocerebellar lobules governing velocity storage and the processing of gravity-dependent (otolithic) signals. Their dysfunction underlies central positional and periodic alternating nystagmus.

Involuntary rhythmic oscillation of the eyes, classically a slow drift away from target with a corrective fast phase (jerk nystagmus). Its plane, direction, and modulation by gaze and fixation localise the lesion.

A triad of head tilt, conjugate ocular torsion, and skew deviation, all toward the side of a graviceptive (otolith-ocular) pathway lesion. A strongly localising sign of brainstem, cerebellar, or thalamic disease.

Passive head rotation evoking compensatory eye movement via the VOR. In supranuclear gaze palsy these reflexive movements are preserved even though voluntary gaze is lost — confirming the lesion is above the ocular-motor nuclei.

A pontine lesion of the PPRF/abducens nucleus plus the adjacent MLF: an ipsilateral horizontal gaze palsy combined with an INO, leaving only contralateral abduction. Adding a facial palsy gives the 'eight-and-a-half' syndrome.

Chaotic, large-amplitude, multidirectional saccades without intersaccadic intervals, from failure of brainstem omnipause-neuron control. Associated with paraneoplastic and parainfectious encephalitis.

The illusion that the stationary visual world is moving or bouncing, typically during head movement. It reflects inadequate gaze stabilisation — from VOR failure (bilateral vestibulopathy) or pathological nystagmus.

The pontine generator of ipsilateral horizontal saccades, projecting to the adjacent abducens nucleus. Its lesion causes a horizontal gaze palsy; combined with an MLF lesion it produces the one-and-a-half syndrome.

Vertigo from the labyrinth or vestibular nerve. Its nystagmus is unidirectional and horizontal-torsional, obeys Alexander's law, is suppressed by fixation, and is accompanied by a positive head impulse test — without other neuro-ophthalmological signs.

Nystagmus provoked by a change in head or body position. Peripheral (BPPV) forms show latency, a crescendo course, and fatigue; central forms are immediate, persistent, and often direction-changing.

A tauopathy presenting with vertical supranuclear gaze palsy (early downgaze limitation), slowed saccades, postural instability with falls, and axial rigidity. Unsteadiness often predates the eye signs by months.

The midbrain burst-neuron generator for vertical and torsional saccades. Lesions impair vertical gaze and contribute to vertical supranuclear palsy, often alongside thalamic-mesencephalic infarcts.

Inappropriate involuntary saccades that interrupt steady fixation — square-wave jerks, macrosaccadic oscillations, and opsoclonus — reflecting impaired cerebellar and brainstem fixation control.

Vertical misalignment of the eyes from imbalance in central otolith-ocular (graviceptive) input, detected as a vertical corrective movement on alternate cover testing. The third limb of the HINTS exam and a pointer to brainstem/cerebellar disease.

The eyes' ability to track a slowly moving target smoothly, depending on cortical eye fields, the cerebellar flocculus/vermis, and brainstem nuclei. Cerebellar or brainstem disease replaces it with catch-up (saccadic) pursuit.

Nystagmus present at rest in primary gaze. Peripheral forms are unidirectional, horizontal-torsional, fixation-suppressed, and obey Alexander's law; central forms can be vertical, purely torsional, or direction-changing and resist fixation.

Small, paired horizontal saccades that take the eye off the target and back after a brief interval. Frequent or large ones suggest cerebellar disease, PSP, or other degenerations.

The patient's perceived orientation of 'upright'. A tilt of the SVV reflects an imbalance in otolith (graviceptive) input and accompanies the ocular tilt reaction and skew deviation.

Loss of voluntary gaze with preserved reflex (vestibulo-ocular, oculocephalic) eye movements, from lesions above the ocular-motor nuclei — cortical eye fields, riMLF, PPRF, or their pathways. Vertical forms typify PSP.

Alternate cover-uncover testing for vertical ocular misalignment. A vertical refixation movement confirms skew deviation and, in acute vestibular syndrome, supports a central cause.

Vertical nystagmus with fast phases beating upward, pointing to lesions of the pontomesencephalic junction, medulla, or anterior cerebellar vermis.

A brainstem–nodulus mechanism that prolongs and integrates rotational vestibular signals beyond the canal afferents' time constant. Its dysregulation contributes to central positional and periodic alternating nystagmus.

Episodic vertigo meeting Bárány/IHS criteria, often with migraine features. Attacks may show central oculomotor signs — spontaneous, positional, or gaze-evoked nystagmus — with normal imaging, distinguishing it from peripheral vestibulopathy.

The reflex that stabilises gaze during head movement by driving the eyes equal and opposite to the head. Its peripheral sensors, brainstem relays, and cerebellar calibration are the substrate of nearly every sign in this chapter.

A goggle-mounted, camera-based head impulse test that measures VOR gain for individual semicircular canals and captures covert and overt catch-up saccades, sharpening the central-versus-peripheral distinction.

Infrared-camera recording of eye movements, quantifying nystagmus, saccades, pursuit, and VOR gain. It documents subtle catch-up saccades and adduction lag missed at the bedside.

A thiamine-deficiency emergency presenting with the classic triad of ophthalmoplegia/nystagmus, ataxia, and confusion. Gaze palsy and gaze-evoked nystagmus reflect involvement of brainstem ocular-motor and vestibular structures; high-dose IV thiamine can reverse it.