Benign paroxysmal positional vertigo
Brief positional vertigo provoked by head movement, lasting seconds. The most common cause of vertigo at any age. HINTS is the wrong tool — Dix-Hallpike is the right one.
Clinical picture
Patients describe brief attacks of spinning vertigo — seconds to under a minute — provoked by specific head movements: lying down, rolling over in bed, looking up, or bending forward. Between episodes, the patient is asymptomatic or has only mild residual disequilibrium. There is no hearing loss, no tinnitus, no continuous vertigo, and no central oculomotor abnormality between episodes13.
Posterior canal BPPV accounts for the great majority of cases. Horizontal canal BPPV is less common but well described; anterior canal BPPV is rare. The pathology is displaced otoconia from the utricular macula entering a semicircular canal — most commonly free-floating in the canal (canalolithiasis) and less commonly adherent to the cupula (cupulolithiasis).
Why HINTS is not the right tool
HINTS is validated for the continuous acute vestibular syndrome3. BPPV is the opposite clinical phenotype: episodic, positional, brief, with a well-patient between attacks. Applying HINTS to a BPPV patient yields a normal head impulse, absent spontaneous nystagmus, and absent skew — but this pattern is uninformative because BPPV is not in the differential of acute vestibular syndrome.
The right bedside test is the Dix-Hallpike manoeuvrefor posterior or anterior canal BPPV, and the supine roll test for horizontal canal BPPV. Both work by positioning the head so that gravity acts on the otoconia in the suspected canal — the resulting endolymph flow generates the brief, short-latency, fatigable positional nystagmus that is the diagnostic finding13.
The Dix-Hallpike manoeuvre
Seat the patient on the couch with the head turned 45° toward the tested ear. Quickly move them from sitting to supine with the head extended approximately 20° below the horizontal, maintaining the head turn. Watch the eyes for at least 30 seconds. A positive test shows a typical positional nystagmus after a short latency (~1–5 seconds) with a torsional component (upper poles of the eyes beating toward the dependent ear) and an upbeating vertical component, lasting under one minute and fatiguing on repeat positioning. The vertigo is reproduced. This is the canonical pattern of posterior canal canalolithiasis.
Bárány Society 2015 criteria
The Committee for Classification of Vestibular Disorders defines several BPPV syndromes13. The two you will see most are:
Posterior canal BPPV — canalolithiasis. Recurrent attacks of positional vertigo provoked by lying down or turning over in supine. Dix-Hallpike provokes upbeating torsional nystagmus toward the dependent ear with a short latency, duration under one minute, and fatigue on repetition. No better explanation by another disorder.
Horizontal canal BPPV — canalolithiasis (geotropic).Recurrent attacks of positional vertigo provoked by rolling supine in bed. The supine roll test provokes horizontal nystagmus beating toward the lower ear that reverses direction on rolling to the other side. The affected ear is the side with the more intense nystagmus.
Treatment — canalith repositioning
The Epley manoeuvre (for posterior canal) and theLempert / barbecue roll (for horizontal canal) use gravity to walk the otoconia out of the affected canal back into the utricle. Both are highly effective in a single treatment session; repeat treatment is reserved for incomplete response.
Atypical and emerging BPPV syndromes
The 2015 criteria recognise additional syndromes that the bedside clinician should be aware of13:
Horizontal canal BPPV — cupulolithiasis (apogeotropic).Persistent positional nystagmus beating toward the upper ear during the supine roll test, which does not fatigue. The affected ear is the side with the less intense apogeotropic response.
Anterior canal BPPV. Rare; Dix-Hallpike provokes downbeating nystagmus with a torsional component. Anterior canal findings warrant a low threshold for central pathology because downbeat nystagmus is a central red flag — imaging is reasonable before committing to a repositioning manoeuvre.
Probable BPPV — spontaneously resolved. History consistent with BPPV but no positional nystagmus on examination.
Possible BPPV. Atypical features that do not meet the strict criteria but cease after a therapeutic positioning manoeuvre.
Differentiating central positional nystagmus
Persistent positional nystagmus that does not fatigue, pure vertical (downbeat) nystagmus without a torsional component, nystagmus with direction-changing features that do not fit canal mechanics, and the presence of other central oculomotor signs (gaze-evoked nystagmus, abnormal smooth pursuit, INO) all raise the suspicion of central positional nystagmus — typically from a posterior fossa lesion. Imaging is indicated.
When BPPV and stroke coexist
Patients with vascular risk factors can develop BPPV at the same time as a posterior fossa event. A positional manoeuvre that fully resolves both vertigo and nystagmus is reassuring; persistent symptoms, atypical nystagmus, or any continuous component require further workup.