How is BPPV different from vertigo caused by something serious?

BPPV causes brief episodes of spinning — seconds to a minute — that are reliably triggered by specific head movements: rolling over in bed, lying down, sitting up, looking up at a high shelf. Between episodes, there is no vertigo. A stroke or cerebellar lesion typically causes constant, persistent vertigo that is present regardless of head position, often with other neurological signs — limb weakness, difficulty walking, double vision, swallowing problems, or severe headache. If vertigo is constant and severe, came on suddenly without obvious positional trigger, and is accompanied by any neurological symptom, this needs emergency assessment rather than waiting.

What happens during the Epley manoeuvre and is it safe at home?

The Epley canalith repositioning manoeuvre involves a sequence of four head and body positions held for about 30 seconds each. The positions guide the dislodged calcium crystals from the posterior semicircular canal into the utricle, where they no longer cause vertigo. It is effective in about 80% of cases in a single session when performed correctly. Your GP or vestibular physiotherapist can perform it in the clinic. Home versions are available and reasonable for confirmed BPPV, but should only be tried once the diagnosis has been confirmed by Dix-Hallpike — performing it without a diagnosis risks missing a stroke or other serious cause.

What is vestibular neuritis and how is it treated?

Vestibular neuritis is inflammation of the vestibular nerve, often following a viral respiratory illness by 1–2 weeks. It causes severe constant spinning vertigo, nausea, vomiting, and unsteadiness lasting days, with gradual improvement over 1–6 weeks. It is not BPPV — the vertigo is constant rather than triggered by head position, and the Epley manoeuvre does not help. Short-term medication (prochlorperazine or ondansetron) manages the acute nausea and vomiting for up to 72 hours. After that, vestibular rehabilitation — exercises to retrain the brain's balance processing — is the most important treatment for full recovery.

What is vestibular rehabilitation and who needs it?

Vestibular rehabilitation is a physiotherapist-led programme of exercises that promote central compensation — the brain learning to use alternative sensory inputs (vision, proprioception) to replace the lost vestibular signal from the damaged side. It typically involves gaze stabilisation exercises, balance exercises progressing from firm to unstable surfaces, and habituation exercises that deliberately provoke mild dizziness to promote adaptation. It is the standard of care for vestibular neuritis, and also useful for refractory or recurrent BPPV, persistent dizziness after any vestibular insult, and persistent postural perceptual dizziness. The earlier it starts, the faster the recovery.

Can I drive with BPPV or vestibular neuritis?

During an acute episode of BPPV or vestibular neuritis, driving is not safe — the unpredictability of a vertigo attack while at the wheel creates a serious road safety risk. Austroads guidelines for fitness to drive require a period of symptom stability before returning to driving. For BPPV, most people can return to driving once the Epley manoeuvre has been successful and they have been free of positional vertigo attacks for a few days. For vestibular neuritis, driving should be deferred until acute vertigo has settled substantially. Discuss timing with your GP and inform your insurer if appropriate.

Benign paroxysmal positional vertigo and vestibular neuritis

Vertigo: BPPV, vestibular neuritis, and when vertigo means stroke

By Dr HB Lo, FACRRM Reviewed 10 June 2026 11 min read

Vertigo needs systematic differentiation between benign peripheral causes (BPPV, vestibular neuritis) and dangerous central ones (posterior circulation stroke). BPPV is the most common cause — brief, position-triggered, diagnosed by Dix-Hallpike, and managed with the Epley manoeuvre, which resolves it in ~80% of cases in one session.

Vestibular neuritis causes days of constant severe vertigo after a viral illness; early vestibular rehabilitation promotes recovery.

The HiNTS examination (head impulse, nystagmus, test of skew) separates peripheral from central causes in acute vestibular syndrome, with sensitivity exceeding early MRI in trained hands.

What vertigo actually is — and the central versus peripheral distinction

“Dizziness” is a non-specific symptom encompassing several distinct experiences that require different assessments. Vertigo is the false sense that either the patient or the environment is spinning or moving. Presyncope is a light-headed, near-fainting sensation from cardiovascular causes. Disequilibrium is unsteadiness or imbalance without true spinning, common in older adults from multiple contributing factors. Persistent postural perceptual dizziness (PPPD) is a functional dizziness with anxiety overlay. Accurate characterisation of the symptom shapes the entire workup.

Within vertigo, the critical first step is distinguishing peripheral causes (inner ear or vestibular nerve pathology — BPPV, vestibular neuritis, labyrinthitis, Meniere’s disease) from central causes (brainstem, cerebellum, or cortical pathology — posterior circulation stroke or TIA, cerebellar mass, multiple sclerosis). Central vertigo can present with relatively mild dizziness and minimal objective signs — it should never be assumed benign based on symptom severity alone.

The eTG and RACGP guidelines on vertigo in general practice identify three steps: characterise the type of dizziness; screen for central (dangerous) features; then diagnose the specific peripheral cause.

Benign paroxysmal positional vertigo (BPPV) is the most common single cause of vertigo overall, accounting for 20–30% of all vertigo presentations in general practice. Vestibular neuritis is the most common cause of prolonged acute vertigo.

A. Core clinical — the AU general-practice framework

Red flags for central (dangerous) vertigo

Before assessing BPPV or vestibular neuritis, exclude dangerous central causes. Red flags requiring immediate emergency assessment:

Constant, persistent vertigo that does not abate with rest (versus BPPV, which is episodic and brief)
Sudden severe headache accompanying vertigo (posterior fossa haemorrhage, vertebral artery dissection)
Focal neurological signs: limb weakness, facial asymmetry, dysarthria, dysphagia, diplopia, cerebellar signs (dysmetria, ataxia, past-pointing), hemiparesis
Severe imbalance unable to stand — disproportionate to the vertigo (peripheral vertigo usually allows walking with caution; central cerebellar lesions often cause gait ataxia out of proportion to the vertigo)
Direction-changing nystagmus or pure vertical/torsional nystagmus
Skew deviation (vertical misalignment of the eyes on alternate cover testing)
Cardiovascular risk factors with new-onset vertigo — posterior circulation stroke is more common in older adults with hypertension, diabetes, dyslipidaemia, atrial fibrillation, or known vascular disease

If any red flag is present, call 000 or arrange immediate ED transfer. ASOHNS and RACGP both emphasise that posterior circulation stroke is under-diagnosed when presenting with isolated vertigo.

HiNTS examination in acute vestibular syndrome

For the patient with acute vestibular syndrome — sudden-onset constant vertigo that is not triggered by position changes, with nausea, vomiting, and gait deviation — the AAO-HNS BPPV guideline and Bárány Society criteria recommend the HiNTS exam (Head Impulse, Nystagmus, Test of Skew). Performed by a trained clinician, HiNTS has sensitivity exceeding early MRI for distinguishing peripheral vestibular neuritis from posterior circulation stroke:

H — Head Impulse Test: an abnormal corrective saccade (the eye overshoots and corrects) after a rapid small head movement towards the affected side = peripheral (the vestibulo-ocular reflex is impaired). A normal head impulse = central (the brainstem-mediated VOR is intact — this is the dangerous finding in the context of acute vestibular syndrome).

N — Nystagmus type: unidirectional horizontal nystagmus (same direction regardless of gaze) = peripheral. Direction-changing nystagmus (reverses direction with gaze change) or pure vertical or torsional nystagmus = central.

T — Test of Skew: vertical eye misalignment on alternate cover (skew deviation) = central. No skew = peripheral.

Peripheral pattern: abnormal HI + unidirectional nystagmus + no skew. Central pattern (posterior circulation stroke): normal HI + direction-changing or vertical nystagmus + skew present — “INFARCT” mnemonic.

Dix-Hallpike manoeuvre for BPPV

The Dix-Hallpike test is the gold-standard diagnostic manoeuvre for posterior canal BPPV — the most common type, accounting for approximately 85% of BPPV cases. It can be performed in the general practice consulting room with a standard examination couch.

Technique: Patient seated on the examination couch. Turn the patient’s head 45° to the side being tested. Rapidly lower the patient to the supine position with the head hanging 20–30° below the couch level. Observe both eyes for nystagmus and ask about vertigo. Hold for 30–60 seconds.

Positive result (posterior canal BPPV): after a 1–5 second latency, rotatory (torsional) upbeating nystagmus appears towards the lower (dependent) ear, lasts 20–60 seconds, and fatigues on repetition. The patient experiences vertigo that mirrors the nystagmus onset.

Repeat the test with the head turned to the other side to confirm laterality and check both sides.

If the Dix-Hallpike is negative but horizontal nystagmus is elicited in a different head position, consider horizontal canal BPPV (less common; managed with the Lempert barbecue roll manoeuvre).

B. Evidence for the Epley manoeuvre and BPPV management

Epley canalith repositioning manoeuvre

The AAO-HNS Clinical Practice Guideline Update 2017 and multiple Cochrane reviews establish the Epley manoeuvre as the definitive first-line treatment for posterior canal BPPV. Approximately 80% of patients are symptom-free after a single correctly performed Epley session, with success rates exceeding 95% by the third session.

Mechanism: the Epley guides the dislodged otoconia (calcium carbonate crystals) from the posterior semicircular canal back into the utricle through a sequence of four head and body positions, each held for 20–30 seconds while the crystals settle. Once in the utricle, the crystals no longer stimulate the cupula with positional movement.

Technique overview: starting from the positive Dix-Hallpike position (head 45° rotated to the affected side, hanging), rotate the head 90° to the opposite side, then rotate the body 90° further (patient now facing downward), then bring the patient to sitting with the head slightly chin-tucked. Specific step-by-step guides are available from AAO-HNS and ASOHNS.

For horizontal canal BPPV: the Lempert (barbecue) roll manoeuvre addresses canalithiasis type (geotropic nystagmus); the Gufoni manoeuvre addresses cupulolithiasis type (apogeotropic nystagmus). Refer to vestibular physiotherapy if uncomfortable performing these variants.

Brandt-Daroff exercises

Brandt-Daroff exercises are a home-based alternative for patients in whom in-office Epley is not possible, or as an adjunct for refractory BPPV. They are less effective than a single Epley session but provide independent patient control. The AAO-HNS guideline rates the Epley as superior and recommends Brandt-Daroff as an adjunct or when the clinical manoeuvre cannot be performed.

Antiemetics and vestibular suppressants — use and limits

For acute severe nausea and vomiting from BPPV or vestibular neuritis: short-term antiemetics (prochlorperazine, ondansetron) are appropriate for the first 24–72 hours. Per eTG, these are symptomatic tools, not disease-modifying agents.

Prolonged use is actively harmful: vestibular suppressants (prochlorperazine, diazepam) delay central compensation — the brain’s process of adapting to a unilateral vestibular deficit — when used beyond 72 hours. Encourage stopping vestibular suppressants as early as tolerable and beginning vestibular rehabilitation exercises.

C. Vestibular neuritis — management and rehabilitation

Acute management

Vestibular neuritis presents as sudden onset of severe constant rotatory vertigo lasting 24 hours to several days, with nausea, vomiting, and a tendency to fall or lean towards the affected (hypofunctional) side. Horizontal nystagmus is directed away from the affected side (fast phase away, slow phase toward the damaged side). Hearing is preserved (distinguishes vestibular neuritis from labyrinthitis, where hearing loss also occurs).

The HiNTS exam shows an abnormal head impulse toward the affected side (corrective saccade), unidirectional horizontal nystagmus, and no skew deviation — peripheral pattern. This is reassuring and appropriate for conservative management.

Per eTG:

Prochlorperazine 5–10 mg orally three times daily (or 12.5 mg intramuscularly for severe vomiting) for a maximum of 72 hours
Ondansetron 4–8 mg as an alternative antiemetic, particularly for patients who cannot tolerate prochlorperazine
Diazepam 5–10 mg short-term if distress is severe — limit to 3 days maximum

Corticosteroids in vestibular neuritis

The Strupp et al. NEJM 2004 trial found a modest improvement in canal function at 12 months with methylprednisolone, but no sustained benefit at 3 years. The Cochrane review concluded evidence for corticosteroids in vestibular neuritis remains inconclusive. Oral prednisolone (50 mg daily for 1 week, tapering over 3 weeks) may be considered in severe or persistent cases — discuss with ENT or neurology specialist.

Antivirals have no demonstrated benefit in vestibular neuritis and are not recommended.

Vestibular rehabilitation — the cornerstone of recovery

Early vestibular rehabilitation, starting within the first week of illness, promotes central compensation — the cerebellum and brainstem adapt to the asymmetric input from the damaged side by recalibrating balance processing. The AAO-HNS guideline and ASOHNS both designate vestibular rehabilitation as standard of care.

Components: gaze stabilisation exercises (focusing on a stationary target while moving the head); habituation exercises (repeated movement sequences that provoke mild dizziness, promoting adaptation); balance exercises progressing from firm to foam and unstable surfaces; and walking and dynamic activities as tolerated.

Accessible through physiotherapists with vestibular rehabilitation training, and via GP Chronic Condition Management Plan funding.

D. Australian operations

MBS funding and referral structure

Standard GP consultation items (23, 36, 44) cover vertigo assessment and Epley manoeuvre performance. The Epley is a GP-deliverable in-office procedure requiring no special equipment beyond the examination couch. Training resources from AAO-HNS and vestibular physiotherapy educators are freely available.

The GP Chronic Condition Management Plan (items 965 and 967) funds vestibular physiotherapy for chronic vertigo, persistent vestibular dysfunction, and BPPV with recurrence. Physiotherapy sessions (5 sessions per year, 10 for Aboriginal and Torres Strait Islander patients) can be directed to vestibular rehabilitation specialists through a management plan.

Diagnostic audiology: following the MBS restructure effective 1 March 2023, items 82300–82332 cover pure-tone audiometry, speech audiometry, tympanometry, and impedance audiometry by an eligible audiologist on any medical practitioner referral (no specialist prerequisite). Refer for any suspicion of hearing loss (Meniere’s, acoustic neuroma, labyrinthitis).

MRI internal acoustic meatus and posterior fossa (item numbers via specialist referral): for unilateral or asymmetric sensorineural hearing loss; persistent vertigo not resolving as expected; atypical features; or recurrent unexplained vertigo.

PBS medications

Per eTG and the Australian Medicines Handbook:

Prochlorperazine 5 mg tablets / 12.5 mg injection — PBS general benefit
Ondansetron 4–8 mg wafer or oral — PBS general benefit
Diazepam 5 mg tablets — PBS general benefit (short course only)
Betahistine 16 mg three times daily — PBS general benefit for Meniere’s disease (uncertain efficacy; see below)
Hydrochlorothiazide / amiloride combination — PBS general benefit; used in Meniere’s for endolymphatic pressure reduction (modest evidence)
Prednisolone — PBS general benefit; selective use in vestibular neuritis per above

Meniere’s disease — the broader vertigo differential

Meniere’s disease should be distinguished from BPPV and vestibular neuritis: it produces episodic attacks of vertigo lasting 20 minutes to 12 hours (not seconds as in BPPV, not days as in vestibular neuritis), combined with fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness. Diagnosis follows the Bárány Society consensus criteria. Management includes dietary sodium restriction (<1500 mg/day), betahistine trial, diuretic (limited evidence), and ENT referral for intratympanic steroid or gentamicin in refractory cases. Note: the large BEMED 2016 RCT found betahistine no better than placebo for Meniere’s — PBS listing remains despite uncertain efficacy.

Driving assessment

Per the Austroads Assessing Fitness to Drive 2022 guideline, patients with recurrent unprovoked vertigo (including recurrent BPPV, Meniere’s disease, and any uncontrolled vestibular disorder) should be advised against driving during symptomatic periods. Discuss the requirement to notify VicRoads / transport authorities in the relevant state or territory for conditions that affect driving safety. Document this discussion in the medical record.

E. Special populations

Older adults: BPPV is substantially more common in older adults due to age-related otoconial degeneration. Presentation may be atypical — patients may describe diffuse “dizziness” or unsteadiness rather than clear spinning. Falls risk is significant: vertigo contributes to a substantial proportion of falls in older adults (see the falls-in-older-adults page). Vestibular suppressants carry greater risk in older adults — prolonged use causes sedation, falls, and cognitive impairment. Vestibular rehabilitation is particularly important. Recurrent BPPV in older adults is associated with vitamin D deficiency; a small RCT (Jeong SH et al. Neurology 2020) showed vitamin D supplementation in deficient patients reduced recurrence. Check vitamin D level in recurrent BPPV.

Women around perimenopause: vestibular migraine is the most common cause of recurrent episodic vertigo with normal examination between attacks, and is increasingly recognised in women aged 35–55 years. It overlaps clinically with Meniere’s and BPPV. Diagnosis follows Bárány Society criteria (vestibular symptoms of moderate-severe intensity for 5 minutes to 72 hours, in the context of a current or past migraine history). Management follows migraine prophylaxis principles — beta-blockers (propranolol), amitriptyline, topiramate, candesartan — with ENT or neurology input.

Patients with diabetes: peripheral neuropathy can reduce the proprioceptive component of balance, making vestibular compensation harder. Vestibular rehabilitation should incorporate proprioception exercises explicitly. Hypoglycaemia can cause dizziness and must be excluded as a contributing factor.

Post-viral and long COVID: vestibular dysfunction is recognised as a component of post-COVID syndrome, with persistent dizziness and imbalance occurring in a subset. Management follows vestibular rehabilitation principles. The condition may include elements of PPPD (persistent postural perceptual dizziness) with anxiety overlay — a combined vestibular rehabilitation and psychological support approach is most effective.

When to escalate

Immediate ED transfer (call 000): constant acute vertigo with HiNTS findings suggesting central pattern (normal head impulse test, direction-changing nystagmus, skew deviation); any focal neurological sign (limb weakness, facial asymmetry, cerebellar signs, diplopia, dysarthria); severe headache with vertigo; inability to stand; high-risk cardiovascular profile with new vertigo.

Same-day ENT referral: sudden sensorineural hearing loss accompanying vertigo — this is a medical emergency requiring same-day steroid initiation (best response within 14 days); suspected Ramsay Hunt syndrome (herpes zoster — ear vesicles).

Urgent neurology or ENT referral (within days): atypical BPPV not responding after three Epley manoeuvres; progressive or persistent vertigo beyond 2 weeks not improving; bilateral hearing loss with vestibular symptoms; suspected acoustic neuroma (progressive unilateral hearing loss, tinnitus, balance symptoms — MRI internal auditory meatus).

Routine outpatient referral: recurrent BPPV (more than 3 episodes per year); suspected Meniere’s disease; vestibular migraine; persistent PPPD not responding to vestibular rehabilitation; audiometry requested.

What this article is and is not

This is general health information drawn from current Australian guidelines — eTG, RACGP, ASOHNS, AAO-HNS 2017, Bárány Society — and major trials including Strupp 2004 and the Jeong 2020 vitamin D RCT. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about manoeuvre selection, specialist referral, and medication are made with your own GP and treating clinicians.

For patient-facing information: HealthDirect — Vertigo, Better Health Channel — Vertigo.

For acute emergency: sudden severe vertigo with neurological symptoms — call 000.

Sources cited

Frequently asked questions

How is BPPV different from vertigo caused by something serious?

BPPV causes brief episodes of spinning — seconds to a minute — that are reliably triggered by specific head movements: rolling over in bed, lying down, sitting up, looking up at a high shelf. Between episodes, there is no vertigo. A stroke or cerebellar lesion typically causes constant, persistent vertigo that is present regardless of head position, often with other neurological signs — limb weakness, difficulty walking, double vision, swallowing problems, or severe headache. If vertigo is constant and severe, came on suddenly without obvious positional trigger, and is accompanied by any neurological symptom, this needs emergency assessment rather than waiting.
What happens during the Epley manoeuvre and is it safe at home?

The Epley canalith repositioning manoeuvre involves a sequence of four head and body positions held for about 30 seconds each. The positions guide the dislodged calcium crystals from the posterior semicircular canal into the utricle, where they no longer cause vertigo. It is effective in about 80% of cases in a single session when performed correctly. Your GP or vestibular physiotherapist can perform it in the clinic. Home versions are available and reasonable for confirmed BPPV, but should only be tried once the diagnosis has been confirmed by Dix-Hallpike — performing it without a diagnosis risks missing a stroke or other serious cause.
What is vestibular neuritis and how is it treated?

Vestibular neuritis is inflammation of the vestibular nerve, often following a viral respiratory illness by 1–2 weeks. It causes severe constant spinning vertigo, nausea, vomiting, and unsteadiness lasting days, with gradual improvement over 1–6 weeks. It is not BPPV — the vertigo is constant rather than triggered by head position, and the Epley manoeuvre does not help. Short-term medication (prochlorperazine or ondansetron) manages the acute nausea and vomiting for up to 72 hours. After that, vestibular rehabilitation — exercises to retrain the brain's balance processing — is the most important treatment for full recovery.
What is vestibular rehabilitation and who needs it?

Vestibular rehabilitation is a physiotherapist-led programme of exercises that promote central compensation — the brain learning to use alternative sensory inputs (vision, proprioception) to replace the lost vestibular signal from the damaged side. It typically involves gaze stabilisation exercises, balance exercises progressing from firm to unstable surfaces, and habituation exercises that deliberately provoke mild dizziness to promote adaptation. It is the standard of care for vestibular neuritis, and also useful for refractory or recurrent BPPV, persistent dizziness after any vestibular insult, and persistent postural perceptual dizziness. The earlier it starts, the faster the recovery.
Can I drive with BPPV or vestibular neuritis?

During an acute episode of BPPV or vestibular neuritis, driving is not safe — the unpredictability of a vertigo attack while at the wheel creates a serious road safety risk. Austroads guidelines for fitness to drive require a period of symptom stability before returning to driving. For BPPV, most people can return to driving once the Epley manoeuvre has been successful and they have been free of positional vertigo attacks for a few days. For vestibular neuritis, driving should be deferred until acute vertigo has settled substantially. Discuss timing with your GP and inform your insurer if appropriate.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.

T1 AU primary 7 sources
T2 International primary 3 sources
T3 Named-author reconstruction 2 sources
- Strupp M et al. — Methylprednisolone for vestibular neuritis (NEJM 2004)
- Jeong SH et al. — Vitamin D and recurrent BPPV (Neurology 2020)