Glossary

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. Central nystagmus typically does not obey this rule.

Rare variant of BPPV (~3% of cases) from otoconia in the anterior semicircular canal, provoked by head extension; characteristically produces transient downbeating-torsional nystagmus on the Straight Head Hanging Test.

A peripheral disorder of brief, position-triggered vertigo from displaced otoconia in a semicircular canal. Subtypes by canal: posterior (most common, ~85%), horizontal/lateral (~15%), anterior (rare). Diagnosed at the bedside; treated with canalith-repositioning manoeuvres.

Loss of vestibular function in both labyrinths — from ototoxicity, autoimmune disease, or CANVAS. At the bedside: bilaterally positive HIT, dramatically positive Romberg, oscillopsia, and gait worsened in the dark.

Seated manoeuvre that aids lateralisation in horizontal-canal BPPV. Bowing forward and leaning back change the orientation of the canal and the direction of the elicited horizontal nystagmus identifies the affected side.

Rotational vertebrobasilar insufficiency from mechanical compression of one vertebral artery on cervical rotation, usually at the C1–C2 articulation. Provocation produces vertigo, nystagmus, diplopia, or drop attacks; confirmed by dynamic vertebral-artery imaging.

Positional nystagmus of central origin: no latency, non-fatiguing, persistent, often direction-changing or pure vertical, and unresponsive to canalith-repositioning manoeuvres. Distinguishes from BPPV at the bedside.

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.

Dizziness or imbalance arising from disordered proprioceptive input from the upper cervical spine, often after whiplash or in cervical spondylosis. Diagnosis is clinical, supported by neck-restricted range of motion and reproduction with cervical positioning.

A destructive keratinising squamous epithelial growth in the middle ear, capable of eroding bone and producing a labyrinthine fistula. Vertigo with pressure-induced provocation in chronic otitis media should raise this suspicion.

Standardised six-condition test (firm/foam × eyes open/closed/visual conflict) that probes the relative reliance on visual, proprioceptive, and vestibular inputs to balance.

Structured psychological therapy effective for PPPD, anxiety, and panic-related dizziness. Combined with vestibular rehabilitation, it reduces visual dependence and motion provocation.

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

The gold-standard positional test for posterior-canal BPPV. Seated patient with head turned 45° toward the tested side is laid back quickly with the head extended ~20° below horizontal; provokes torsional-upbeat nystagmus toward the dependent ear.

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.

Sequence of head positions that relocates otoconia from the posterior semicircular canal back to the utricle, treating PC-BPPV. Diagnostic via Dix-Hallpike, therapeutic with Epley.

Patient marches in place 50–100 steps with eyes closed and arms outstretched. Rotational drift > 30° toward the hypofunctioning side suggests unilateral vestibular loss. Sensitive but non-specific.

Nystagmus appearing or worsening on eccentric gaze, from a failing neural integrator (cerebellar flocculus, medial vestibular nucleus, nucleus prepositus hypoglossi). Non-fatiguing — 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 HIT in a patient with ongoing AVS paradoxically points to a central lesion.

Vertigo and / or nystagmus provoked by pressure change in the external auditory canal (pneumatic otoscope, tragal compression). Signals an abnormal third window — superior canal dehiscence, perilymph fistula, large vestibular aqueduct.

Vertigo and nystagmus provoked by pressure changes in the external auditory canal (e.g., pneumatic otoscopy). Classically seen with perilymph fistula, superior canal dehiscence, or labyrinthine fistula in chronic otitis media.

Three-step bedside 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.

About 15–20% of BPPV. Diagnosed by the Supine Roll (Pagnini-McClure) test; geotropic nystagmus = canalithiasis (stronger side affected), apogeotropic = cupulolithiasis (weaker side affected). Treated with Lempert (barbecue roll) or Gufoni manoeuvres.

Inflammation of the membranous labyrinth, usually viral or bacterial; presents with continuous vertigo, spontaneous nystagmus AND sensorineural hearing loss. Vestibular neuritis spares hearing.

Three-word recall plus clock-drawing screen (0–5 total) for cognitive impairment. ≤ 2 flags a positive screen; in dizzy elderly, the result frequently reshapes the work-up around geriatric assessment rather than vestibular testing.

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.

Fall of ≥20 mmHg systolic or ≥10 mmHg diastolic blood pressure within three minutes of standing. A common, often missed mimic of vestibular vertigo, especially in older adults and patients on antihypertensives.

Coordination drift test: with eyes closed, the patient raises an arm overhead and lowers it to touch the examiner's finger. Consistent drift toward one side suggests ipsilateral peripheral vestibular hypofunction; asymmetric overshoot suggests cerebellar dysmetria.

Abnormal communication between the inner-ear perilymph and middle ear, typically at the oval or round window. Provoked by barotrauma, head trauma, or stapes surgery. Hennebert and Tullio may be positive; nystagmus tends to be more horizontal than in SSCD.

Vertigo from the labyrinth or vestibular nerve. Nystagmus is unidirectional, horizontal-torsional, fixation-suppressed, obeys Alexander's law; HIT is abnormal toward the affected side; no other neuro-ophthalmological signs.

A chronic functional vestibular disorder defined by Bárány Society criteria: persistent non-spinning dizziness ≥ 3 months, worsened by upright posture, motion, or complex visual stimuli, often arising after an acute vestibular insult.

Most common BPPV variant (~85%), from otoconia in the posterior semicircular canal. Diagnosed by Dix-Hallpike, treated with the Epley.

Sustained heart-rate rise of ≥30 bpm (≥40 bpm in adolescents) on standing without orthostatic hypotension. Presents as chronic light-headedness and exercise intolerance.

Bedside sign of upper motor neuron weakness: with arms outstretched, palms up, and eyes closed, the affected arm drifts downward and pronates. A red flag for central pathology in the dizzy patient.

Postural-stability test. Patient stands with feet together, eyes open then closed. A positive sign — instability emerging only with eyes closed — indicates sensory ataxia from vestibular or dorsal-column dysfunction.

Romberg performed in tandem (heel-to-toe) stance. Narrowing the base of support increases sensitivity to subtle balance deficits and unmasks compensated unilateral vestibular loss.

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 HINTS and a pointer to brainstem/cerebellar disease.

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.

Positional test for anterior-canal BPPV. Supine, the head is extended 30–45° below the horizontal in the midline; provokes transient downbeating-torsional nystagmus when AC-BPPV is present.

Absence of the bony roof over the superior semicircular canal, creating a third window into the membranous labyrinth. Presents with sound- or pressure-induced vertigo (Tullio, Hennebert), autophony, pulsatile tinnitus, and characteristically low VEMP thresholds.

Test for horizontal-canal BPPV. Supine with head flexed 30°, rotate the head 90° each way; the direction of horizontal nystagmus (geotropic vs apogeotropic) and the side of greater intensity localise the lesion.

Patient walks heel-to-toe along a straight line. Inability or instability suggests cerebellar disease, vestibular hypofunction, or functional gait disorder; the pattern (wide-based, cautious, or freezing) refines the differential.

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

A third opening into the membranous labyrinth (in addition to the oval and round windows), which transmits pressure and sound to the cochlea or vestibular end-organs abnormally. Underlies SSCD, perilymph fistula, and large vestibular aqueduct.

Functional balance test. Patient rises from a chair, walks 3 m, turns, walks back and sits. >12 s predicts increased fall risk in older adults.

Vertigo and/or nystagmus induced by loud sound; a hallmark of third-window lesions, most often superior semicircular canal dehiscence.

Sound-induced vertigo and / or nystagmus, classically vertical-torsional in superior canal dehiscence. Threshold low (often ≤ 80 dB) in SSCD; matched VEMP thresholds < 75 dB nHL are corroborative.

A variant of the Fukuda stepping test; some sources use the names interchangeably. Tests vestibulospinal tone asymmetry by stepping in place with eyes closed.

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

Transient ischaemia in the posterior circulation supplying the brainstem and cerebellum. Can cause positional vertigo (rotational head movements), drop attacks, dysarthria, diplopia, or ataxia. Imaging confirms.

Inflammatory disorder of the vestibular nerve (usually superior division) producing sudden continuous vertigo, unidirectional spontaneous nystagmus, positive HIT toward the affected ear, and intact hearing. Differentiated from labyrinthitis by hearing preservation.

Exercise-based therapy that drives central compensation for vestibular loss through adaptation, substitution, and habituation. First-line treatment for bilateral vestibulopathy, vestibular neuritis recovery, and PPPD.

Reflex that stabilises gaze during head movement by driving the eyes equal and opposite to the head. Tested at the bedside by the head impulse test.

A goggle-mounted, camera-based head impulse test that quantifies VOR gain for each semicircular canal and detects covert and overt catch-up saccades missed at the bedside.

Thiamine-deficiency emergency presenting with the classic triad of ophthalmoplegia/nystagmus, ataxia, and confusion. Treat empirically with IV thiamine BEFORE glucose — delay risks permanent Korsakoff syndrome.

Therapeutic counterpart to the SHHT: a four-position sequence (sit → supine head-hanging → chin-to-chest → return to sitting), each held ~30 s, that repositions otoconia from the anterior canal back to the utricle.