Glossary

Acute-onset, sustained vertigo with nystagmus, nausea, head-motion intolerance and gait unsteadiness lasting hours to days. Differential is dominated by vestibular neuritis versus posterior-circulation stroke.

Infarct in the anterior inferior cerebellar artery territory — vertigo + ipsilateral hearing loss + facial paresis. Common stroke that masquerades as labyrinthitis.

Peripheral vestibular nystagmus increases when the patient gazes in the direction of the fast phase. Central nystagmus typically does not obey this rule.

Ondansetron (preferred in the ED) or prochlorperazine for symptomatic relief of vomiting. Watch for QT prolongation in elderly and frail.

Methylprednisolone taper for vestibular neuritis hastens caloric recovery but has modest effect on patient-reported outcome. Cochrane evidence remains contested.

Imaging of the cervical and intracranial arteries, helpful for vertebrobasilar stenosis, dissection or occlusion when MRI is contraindicated or delayed.

MRI sequence that detects acute infarction in minutes. False-negative rate for small posterior-fossa strokes is 12–20% in the first 24–48 hours.

Admit when: any central HINTS feature, suspicion of stroke or TIA, posterior-fossa imaging changes, refractory vomiting, persistent gait instability, Wernicke concern, isolated SSNHL with vertigo.

Safe-to-discharge: clear peripheral diagnosis, hydrated and able to mobilise, accompanied home, written warning signs, follow-up booked.

Diagnostic head-hanging position with the head turned 45°; provokes torsional-upbeat nystagmus in PC-BPPV after a latency of seconds.

Sequential head positions that walk otoconia out of the posterior canal back into the utricle. First-attempt resolution in ~80% of PC-BPPV.

Alternative treatment for HC-BPPV, with separate variants for canalithiasis (geotropic) and cupulolithiasis (apogeotropic).

Rapid passive head thrust ~15° to one side while the patient fixates a target. Normal: eyes counter-rotate so gaze stays locked. Abnormal: catch-up saccade indicates ipsilateral peripheral hypofunction.

Three-step bedside battery for AVS — Head Impulse, Nystagmus pattern, Test of Skew. A central pattern (normal HIT, direction-changing nystagmus, or vertical skew) is more sensitive than early DWI-MRI for posterior-circulation stroke.

Otoconia in the horizontal canal cause horizontal nystagmus on supine roll. Geotropic = canalithiasis (stronger side affected); apogeotropic = cupulolithiasis (weaker side affected).

Acute peripheral vestibulopathy with sensorineural hearing loss, often post-viral or following otitis media. Watch for intracranial complications.

Treatment for HC-BPPV canalithiasis: sequential 90° head rolls toward the unaffected ear.

Spontaneous episode of vertigo 20 min to 12 h with low-frequency fluctuating SNHL, tinnitus and aural fullness. Bárány criteria define definite vs probable.

First-line imaging in suspected stroke to exclude haemorrhage before thrombolysis. Poor for posterior-fossa infarction; cannot exclude ischaemic stroke.

Infarct in the posterior inferior cerebellar artery territory — lateral medullary syndrome with vertigo, dysphagia, Horner, ipsilateral facial/contralateral body sensory loss.

Brief, position-triggered vertigo from otoconia in the posterior semicircular canal. Diagnosed by Dix-Hallpike with torsional-upbeat nystagmus; treated by the Epley manoeuvre.

Ischaemia in the territory of the vertebrobasilar arteries — PICA, AICA, SCA — producing acute vertigo plus brainstem or cerebellar signs. Can mimic vestibular neuritis exactly in the first hour.

Recurrent episodes of vertigo that occur without an obvious trigger. Dominated by vestibular migraine and Ménière's disease, with vertebrobasilar TIA the can't-miss central cause.

Nystagmus present in primary gaze in the absence of provocation. Direction (horizontal, vertical, torsional), fixation suppression and whether it obeys Alexander's law all carry localising value.

≥30 dB SNHL across three contiguous frequencies developing in ≤72 h. When paired with acute vertigo, an AICA-stroke red flag — but high-dose steroid within 14 days improves outcome.

Alternate-cover test for vertical refixation. A vertical skew in the AVS patient indicates brainstem disease until proven otherwise.

Time-critical intervention for ischaemic stroke (≤4.5 h from onset). Posterior-circulation strokes presenting with vertigo are commonly missed; HINTS is the triage gate.

Structured triage approach for the dizzy patient organising the assessment around Timing, Triggers and Targeted Examination. Yields three syndromes — triggered EVS, spontaneous EVS, and AVS — each with a different work-up.

Brief episodes of vertigo provoked by a specific manoeuvre — most often head position or sit-to-stand. Dominated by BPPV and orthostatic causes.

Transient ischaemia in the vertebrobasilar territory — recurrent brief vertigo with associated brainstem symptoms (diplopia, dysarthria, weakness). High-risk for completed stroke.

Episodic vestibular syndrome attributable to migraine, by Bárány/IHS criteria — the commonest cause of recurrent episodic vertigo in under-50s.

Acute, isolated unilateral peripheral vestibulopathy presenting as AVS without hearing loss. Self-limiting; early vestibular rehabilitation hastens functional recovery.

Exercise-based therapy combining gaze stabilisation, habituation and balance retraining. Highest-evidence long-term intervention for peripheral vestibular hypofunction.

Antihistamines (meclizine, dimenhydrinate), benzodiazepines and anticholinergics that reduce vertigo intensity short-term but delay central adaptation. Use for ≤48 h only.

Goggle-mounted video version of the bedside HIT. Quantifies VOR gain for each semicircular canal and detects covert saccades the unaided eye misses.

Thiamine-deficiency triad of confusion, ataxia and ocular signs in at-risk patients. Empirical IV thiamine before glucose; do not wait for confirmation.