📋 Key Information Summary
- Dizziness is a common presenting complaint in Australian general practice and emergency departments, accounting for approximately 3–5% of ED presentations and 1–2% of GP consultations annually.
- Always distinguish true vertigo (illusion of movement) from presyncope, disequilibrium, and non-specific dizziness — each has a distinct differential diagnosis and management pathway.
- The HINTS exam (Head Impulse, Nystagmus, Test of Skew) is a bedside examination that can differentiate central from peripheral causes with high sensitivity and specificity when performed acutely by a trained clinician.
- Red flags for central pathology include new-onset severe headache, focal neurological deficits, dysarthria, diplopia, ataxia, crossed signs, cardiovascular risk factors, and anticoagulant use — these mandate urgent neuroimaging (CT/CTA ± MRI).
- Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo (20–30% of cases), diagnosed with the Dix–Hallpike test, and treated with the Epley maneuver — an effective, low-cost, office-based treatment.
- Posterior canal BPPV accounts for ~85% of cases and produces torsional-upbeating nystagmus on Dix–Hallpike; lateral canal BPPV produces direction-changing horizontal nystagmus and is managed with the barbecue roll or Lempert maneuver.
- Vestibular neuritis presents with acute-onset, prolonged (days to weeks) spontaneous vertigo, unilateral vestibular hypofunction, and a positive head-impulse test — there is no cochlear involvement.
- Labyrinthitis is vestibular neuritis with concurrent hearing loss or tinnitus, suggesting cochlear involvement; it may be viral or bacterial (the latter requires urgent ENT referral).
- Early corticosteroids (methylprednisolone 100 mg IV then oral taper, or prednisolone 1 mg/kg PO daily tapered over 3 weeks) may improve vestibular recovery in vestibular neuritis, though evidence is mixed.
- Vestibular rehabilitation therapy (VRT) accelerates central compensation and recovery and should be offered to all patients with vestibular neuritis and labyrinthitis.
- Meclizine and other vestibular suppressants provide symptomatic relief but should be used short-term only (48–72 hours) as they impair central compensation.
- Aboriginal and Torres Strait Islander peoples in remote communities may have limited access to specialist vestibular assessment and imaging; culturally safe education, community-based rehabilitation, and telehealth pathways are essential.
Initial Assessment — Timing, Triggers, HINTS Exam, and Red Flags
History: Characterising the Dizziness
A structured history is the single most important diagnostic step. Ask the patient to describe their symptoms in their own words and then clarify using the following framework.
| Dizziness Type | Description | Typical Causes |
|---|---|---|
| Vertigo | Illusion of rotational or linear movement of self or environment | BPPV, vestibular neuritis, labyrinthitis, Ménière disease, vestibular migraine, posterior fossa stroke |
| Presyncope | Feeling of impending faint or blackout | Orthostatic hypotension, cardiac arrhythmia, vasovagal syncope, PE |
| Disequilibrium | Unsteadiness or imbalance without true vertigo, worse with walking | Peripheral neuropathy, cerebellar disease, vestibulopathy, medication effects |
| Non-specific dizziness | Lightheadedness, floating, vague sense of disorientation | Anxiety, hyperventilation, medication side effects, metabolic causes |
Key History Features — Timing and Triggers
- Onset: Sudden (seconds — BPPV, TIA/stroke) vs acute (minutes to hours — Ménière, vestibular migraine) vs gradual/subacute over hours to days (vestibular neuritis, labyrinthitis).
- Duration of individual episodes: Seconds (BPPV), 20 min to 12 h (Ménière), hours to days (vestibular neuritis, stroke).
- Positional provocation: Turning in bed, looking up, bending forward → suggests BPPV or positional central vertigo.
- Associated symptoms: Hearing loss or tinnitus (labyrinthitis, Ménière, AICA stroke), nausea/vomiting (all vestibular causes), headache (vestibular migraine, SAH), diplopia or dysarthria (central pathology).
- Precipitants: Recent upper respiratory tract infection (vestibular neuritis), head trauma (BPPV, perilymph fistula), Valsalva (superior canal dehiscence).
- Cardiovascular risk factors: Hypertension, diabetes, atrial fibrillation, smoking, hyperlipidaemia — increases suspicion for vertebrobasilar ischaemia.
- Medications: Aminoglycosides, loop diuretics, anticonvulsants, antihypertensives, SSRIs — can cause vestibulotoxicity or orthostatic symptoms.
Red Flags Requiring Urgent Evaluation:
- New severe headache, particularly "thunderclap" onset → consider SAH
- Focal neurological deficit (hemiparesis, ataxia, dysarthria, dysphagia)
- Diplopia, bilateral visual changes, or loss of vision
- Crossed signs (ipsilateral facial and contralateral body symptoms)
- Hearing loss with acute vertigo in presence of cardiovascular risk factors (AICA territory infarct)
- HINTS exam with normal head-impulse test + direction-changing nystagmus or skew deviation → central until proven otherwise
- Anticoagulant or antiplatelet use with new vertigo and neurological signs
- Progressive unilateral hearing loss with vertigo → acoustic neuroma exclusion
HINTS Examination — Head Impulse, Nystagmus, Test of Skew
The HINTS exam should be performed at the bedside in any patient presenting with acute continuous vertigo and nystagmus. It can be more accurate than early diffusion-weighted MRI (< 48 hours) for identifying posterior fossa stroke. It requires training and should be performed by experienced clinicians (emergency physicians, neurologists, or vestibular physiotherapists).
| Component | Technique | Peripheral Pattern | Central Pattern (Red Flag) |
|---|---|---|---|
| H — Head Impulse Test | Patient fixates on examiner's nose; examiner turns head 10–20° rapidly to one side; observe for corrective saccade | Positive — corrective saccade present (vestibular hypofunction) | Negative — no corrective saccade (normal or bilateral); a negative HIT in acute vertigo is concerning for stroke |
| I — Nystagmus Direction | Observe nystagmus in primary gaze, rightward gaze, and leftward gaze | Unidirectional, horizontal-torsional, beating away from lesion side, suppressed with fixation | Direction-changing (beats one way on right gaze, opposite on left gaze) or purely vertical/torsional nystagmus in primary gaze |
| N — Test of Skew | Cover–uncover test alternating eyes; look for vertical corrective refixation | No skew deviation | Skew deviation present — vertical misalignment of the visual axes, indicates brainstem/cerebellar pathology |
Interpretation warning: The HINTS exam has a sensitivity of ~97% and specificity of ~99% for stroke when performed by trained examiners. It should not be relied upon if the clinician is inexperienced with vestibular examination. Any uncertainty warrants neuroimaging (CT with CTA or MRI with DWI). The HINTS exam is only valid when there is spontaneous nystagmus present at the time of examination — it is not applicable to BPPV or asymptomatic patients.
Additional Bedside Tests
- Dix–Hallpike test: Provokes posterior canal BPPV — see BPPV section below.
- Romberg and tandem gait: Impaired tandem gait with eyes open may indicate central pathology; bilateral vestibular loss causes unsteadiness with eyes closed (positive Romberg).
- Fukuda stepping test: Patient marches on the spot with eyes closed; > 30° rotation suggests unilateral vestibular hypofunction.
- Auditory assessment: Whispered voice test or finger rub — hearing loss with vertigo suggests labyrinthitis, Ménière, or AICA stroke.
Benign Paroxysmal Positional Vertigo (BPPV)
BPPV is the most common vestibular disorder, accounting for 20–30% of all vertigo presentations in Australian emergency departments and general practice. It is caused by displaced otoconia (calcium carbonate crystals) from the utricle that migrate into the semicircular canals, most commonly the posterior canal (~85% of cases).
Aetiology and Risk Factors
- Most cases are idiopathic; age > 50 years is the strongest risk factor.
- Head trauma (even minor) — post-traumatic BPPV accounts for ~20% in younger populations.
- Associated with vestibular neuritis, Ménière disease, prolonged bed rest, and inner ear surgery.
- Vitamin D deficiency is emerging as a risk factor; studies show lower serum 25-OH vitamin D in recurrent BPPV patients.
Dix–Hallpike Test — Diagnostic Technique
The Dix–Hallpike test is the gold standard for diagnosing posterior canal BPPV. It should be performed in all patients with positional vertigo.
1
Position the patient
Patient sits upright on the examination couch with legs extended. Turn the head 45° toward the side being tested.
2
Lie the patient back rapidly
With head maintained at 45° rotation, guide the patient backwards so that the head hangs ~20° below horizontal over the end of the couch.
3
Observe for nystagmus and symptoms
Watch for latency of 1–5 seconds, then torsional-upbeating nystagmus lasting < 60 seconds, with reproduction of vertigo. The fast phase beats toward the undermost ear.
4
Return to upright and observe reversal
Sit the patient up and observe for reverse nystagmus. Repeat for the other side.
Posterior vs Lateral Canal BPPV: Posterior canal BPPV produces torsional-upbeating nystagmus with the Dix–Hallpike test. Lateral (horizontal) canal BPPV produces direction-changing horizontal nystagmus on the supine head-turn test (roll test) and is often more intense but less position-specific. Lateral canal BPPV accounts for ~10–15% of cases and is managed with the barbecue roll or Lempert (Gufoni) maneuver.
Epley Maneuver — Canalith Repositioning
The Epley maneuver is the first-line treatment for posterior canal BPPV. It has a single-treatment success rate of approximately 80% and a cumulative success rate of ~92% after three treatments. It can be performed in general practice, emergency departments, or by vestibular physiotherapists.
1
Dix–Hallpike position (affected side down)
Begin from the positive Dix–Hallpike position. Head turned 45° to the affected side, reclined with head hanging. Hold for 30–60 seconds after nystagmus resolves.
2
Rotate head 90° to opposite side
Without raising the head, rotate it 90° so it faces the opposite (unaffected) side. Hold for 30–60 seconds.
3
Roll onto the side
Roll the patient onto their side, keeping the head rotated, so they face the floor. The head should be at 135° from the original supine position. Hold 30–60 seconds.
4
Sit upright
Return to sitting. May briefly provoke vertigo — reassure the patient. Avoid lying flat for 48 hours afterward; sleep elevated on 2–3 pillows.
Pharmacotherapy — Symptomatic Relief
Meclizine (Meclozine)
Sea-Legs® · Postafen® · H₁ antihistamine / vestibular suppressant
Adult dose
25–50 mg PO TDS PRN (max 150 mg/day)
Paediatric dose
≥ 6 years: 12.5–25 mg PO TDS PRN
Duration
Short-term only (48–72 hours) — impairs central vestibular compensation
Renal adjustment
No specific adjustment; use with caution in severe renal impairment
PBS status
✔ PBS General Benefit
Prochlorperazine
Stemetil® · Dopamine antagonist / antiemetic
Adult dose
5–10 mg PO/IM/IV TDS; buccal Stemetil® 3 mg TDS
Paediatric dose
≥ 10 kg: 0.1–0.15 mg/kg/dose PO TDS (max 10 mg TDS)
Duration
48–72 hours maximum; risk of extrapyramidal side effects with prolonged use
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Avoid prolonged vestibular suppressants in BPPV. Meclizine and prochlorperazine suppress central vestibular compensation and may delay recovery. They are for short-term symptomatic relief only while the canalith repositioning maneuver is being performed or repeated. The definitive treatment is the Epley maneuver — not medication.
Patient Education — Self-Treatment and Recurrence
- Teach patients the home Epley maneuver for self-treatment of recurrences. The Brandt–Daroff exercises can also be prescribed as an alternative home exercise program.
- Recurrence rates are approximately 30–50% within 5 years — counsel patients that recurrence is common and manageable.
- Avoid head-hanging positions for 48 hours after treatment (e.g., hairdresser basins, gardening, bending).
- Sleep with 2–3 pillows for 48 hours post-maneuver; avoid sleeping on the affected side for one week.
- Consider checking serum vitamin D levels and supplementing if deficient (especially in recurrent cases).
- Referral to a vestibular physiotherapist is recommended if two or more Epley treatments are unsuccessful, if the canal involved is lateral (requires different maneuver), or if the patient cannot tolerate the procedure.
When to refer: Refer to an ENT specialist or neuro-otologist if BPPV recurs frequently (> 4 episodes/year), symptoms persist beyond 4 maneuvers, or if the Dix–Hallpike test is negative despite a convincing history. Also refer if there are concurrent audiovestibular symptoms (hearing loss, tinnitus, aural fullness) that may suggest an alternative diagnosis.
Vestibular Neuritis & Labyrinthitis
Definitions and Pathophysiology
Vestibular Neuritis
Inflammation of the vestibular nerve (superior branch most commonly affected), likely viral in aetiology (HSV-1 reactivation from the vestibular ganglion is the leading hypothesis). Presents with acute vertigo, nausea/vomiting, and unilateral vestibular hypofunction. No hearing loss.
Labyrinthitis
Inflammation involving both the vestibular nerve and cochlea (labyrinth). Viral labyrinthitis is the most common form. Concurrent sensorineural hearing loss or tinnitus differentiates it from vestibular neuritis. Bacterial labyrinthitis (secondary to otitis media or meningitis) is a medical emergency requiring urgent antibiotics.
Clinical Presentation
- Onset: Acute, often upon waking, or developing over hours. Severe rotational vertigo with nausea and vomiting.
- Duration: Spontaneous vertigo lasts days to 2 weeks, gradually improving. Residual imbalance may persist for weeks to months.
- Examination findings:
- Spontaneous horizontal-torsional nystagmus beating away from the affected side (unidirectional).
- Positive head-impulse test toward the affected side (corrective saccade).
- No skew deviation; unidirectional nystagmus → peripheral pattern on HINTS.
- Falls toward the affected side on Romberg and tandem gait.
- Labyrinthitis additionally: Ipsilateral sensorineural hearing loss and/or tinnitus. If hearing loss is profound and sudden → consider bacterial labyrinthitis or inner ear ischaemia (AICA territory stroke).
Exclusion of Stroke
Stroke mimicking vestibular neuritis: Approximately 10–25% of patients presenting with isolated acute vertigo to Australian EDs have a posterior fossa stroke. Posterior fossa strokes (particularly PICA territory cerebellar infarcts and lateral medullary infarction) can present with isolated vertigo and nausea — clinically indistinguishable from vestibular neuritis in the early phase. The HINTS exam is the most sensitive bedside tool, but:
- If any red flags are present → proceed to urgent CT with CTA (or MRI with DWI if available and not delayed).
- If HINTS exam shows central pattern (normal HIT, direction-changing nystagmus, or skew deviation) → urgent neuroimaging and neurology/stroke unit referral.
- If HINTS cannot be performed (clinician inexperience, patient unable to cooperate) → neuroimaging.
- If stroke is confirmed → manage per Australian Clinical Guidelines for Stroke Management (Stroke Foundation, 2023).
Investigations
Essential
Bedside examination (HINTS, Dix–Hallpike, hearing assessment)
Primary diagnostic tool; distinguishes peripheral from central and BPPV from neuritis.
Available
CT Brain (non-contrast)
MBS Item 56000 · Sensitivity for acute posterior fossa stroke is low (16–42%) in first 24 hours. CT with CTA is preferred if posterior fossa stroke is suspected. Available in most Australian EDs.
Available
CT Angiography (CTA) — Head and Neck
MBS Item 56100 · Identifies vertebrobasilar occlusion/dissection. Available at metropolitan and many regional hospitals.
Referral
MRI Brain with DWI
Gold standard for posterior fossa stroke detection (sensitivity > 95% even in first 24 hours). May require transfer to metropolitan centre. Refer if HINTS is central pattern or red flags present.
Specialist
Video Head Impulse Test (vHIT) / Electronystagmography (ENG)
Quantifies vestibular function. Available at tertiary vestibular centres (Royal Victorian Eye and Ear Hospital, RPAH, Princess Alexandra Hospital, etc.). Not routinely required for diagnosis of vestibular neuritis.
Available
Pure Tone Audiometry
MBS Item 82200 · Essential if labyrinthitis suspected (sensorineural hearing loss). Can be arranged through GP referral to audiologist or ENT.
Available
FBC, ESR/CRP, glucose, BSL, electrolytes
Rule out metabolic and infectious causes. Available in all settings.
Pharmacological Management
Symptomatic Treatment (Vestibular Suppression — Short-Term)
Ondansetron
Zofran® · 5-HT₃ antagonist / antiemetic
Adult dose
4–8 mg PO/IV/ODT every 8 hours PRN (max 24 mg/day)
Paediatric dose
≥ 4 weeks: 0.1–0.15 mg/kg/dose IV or PO every 8 hours (max 4 mg/dose in children < 12 years)
Duration
48–72 hours; does not impair vestibular compensation
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Promethazine
Phenergan® · H₁ antihistamine / vestibular sedative
Adult dose
12.5–25 mg PO/IM every 6–8 hours PRN (max 50 mg/day)
Paediatric dose
≥ 2 years: 0.1 mg/kg/dose PO TDS (max 12.5 mg/dose); generally avoid < 2 years
Duration
48–72 hours only; sedation impairs compensation
Renal adjustment
Use with caution in severe renal impairment
PBS status
✔ PBS General Benefit
Prochlorperazine
Stemetil® · Dopamine antagonist
Adult dose
5–10 mg PO/IM TDS; buccal 3 mg TDS; 12.5 mg IM for acute severe vomiting
Paediatric dose
≥ 10 kg: 0.1–0.15 mg/kg/dose PO TDS (max 10 mg TDS)
Duration
48–72 hours; risk of extrapyramidal symptoms and tardive dyskinesia
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Corticosteroid Therapy — Vestibular Recovery
Evidence from randomised controlled trials (Strupp et al., 2004; Fishman et al., 2011) suggests that early corticosteroid administration may improve vestibular recovery in vestibular neuritis, although the evidence is not definitive and practice varies. Current recommendations from international vestibular guidelines are to consider corticosteroids within the first 72 hours of symptom onset.
Prednisolone
Solone® · Redsolone® · Oral corticosteroid
Adult dose
1 mg/kg PO daily (max 60 mg) for 5 days, then taper over 2–3 weeks
Paediatric dose
1–2 mg/kg PO daily (max 60 mg); specialist guidance recommended
Duration
5 days at full dose then taper over 2–3 weeks; must be initiated within 72 hours of onset
Renal adjustment
No dose adjustment; monitor for fluid retention
Hepatic adjustment
No specific adjustment; prednisolone is the preferred form in hepatic impairment (vs prednisone which requires hepatic conversion)
PBS status
✔ PBS General Benefit
Methylprednisolone
Depo-Medrol® · Solu-Medrol® · IV corticosteroid
Adult dose
100 mg IV daily for 3 days, then switch to oral prednisolone taper
Indication
Severe presentation with intractable vomiting preventing oral intake; typically administered in ED
PBS status
✔ PBS General Benefit (IV form authority required for some indications)
Evidence summary for corticosteroids: Strupp et al. (2004) demonstrated improvement in vestibular function at 12 months with methylprednisolone vs placebo. However, Fishman et al. (2011) did not find significant benefit. A 2019 Cochrane review concluded there is low-to-moderate evidence that corticosteroids may improve vestibular recovery. Current consensus in Australian practice favours offering a short course of prednisolone to patients presenting within 72 hours, particularly with severe or complete vestibular loss on examination.
Vestibular Rehabilitation Therapy (VRT)
Vestibular rehabilitation therapy is an evidence-based exercise program designed to promote central vestibular compensation. It should be offered to all patients with vestibular neuritis and labyrinthitis, ideally starting within the first 1–2 weeks once nausea is controlled.
- Components of VRT:
- Gaze stabilisation exercises: VOR x1 (fixate on target while moving head) and VOR x2 (moving target and head simultaneously).
- Habituation exercises: Repeated exposure to provocative movements to reduce motion sensitivity.
- Balance and gait training: Static and dynamic balance tasks with progressively reduced base of support and visual input.
- Access in Australia: Vestibular physiotherapists are available in most metropolitan areas and some regional centres. Referral can be made directly from GP. The Australian Physiotherapy Association maintains a directory of vestibular-trained physiotherapists.
- MBS Items for physiotherapy: Medicare-subsidised physiotherapy may be available through a GP Management Plan (GPMP) and Team Care Arrangement (TCA) — MBS Item 10960 (up to 5 allied health sessions per calendar year). Enhanced Primary Care (EPC) referrals are commonly used.
- Duration: Typically 6–12 weeks of supervised sessions with a home exercise program. Most patients with vestibular neuritis recover substantially within 3–6 months, though residual dizziness may persist.
Monitoring and Follow-Up
- Review at 1–2 weeks to assess symptom trajectory, check for BPPV development (secondary BPPV occurs in ~15% of vestibular neuritis cases), and reinforce vestibular rehabilitation exercises.
- Audiometry at 2–4 weeks if labyrinthitis (to document hearing recovery or identify permanent sensorineural loss).
- If symptoms are not improving by 4–6 weeks → consider MRI brain, specialist referral, or re-evaluation of diagnosis.
- Driving safety: Advise patients not to drive until vertigo has resolved and they can perform a rapid head turn without triggering symptoms. Austroads guidelines for medical fitness to drive should be followed.
Bacterial Labyrinthitis — An Urgent Distinction
Bacterial labyrinthitis is a surgical and medical emergency. It occurs secondary to acute otitis media, cholesteatoma, or meningitis. Features include profound hearing loss, severe vertigo, high fever, and possible mastoid tenderness. Management: Urgent ENT referral, IV antibiotics per eTG (e.g., IV ceftriaxone 2 g daily + metronidazole 500 mg TDS if otogenic), and CT temporal bones. Do not delay treatment for imaging.
Ceftriaxone (empirical for bacterial labyrinthitis)
Rocephin® · Third-generation cephalosporin
Adult dose
2 g IV once daily
Paediatric dose
50–100 mg/kg IV daily (max 2 g)
Duration
10–14 days (initially IV, switch to oral when clinically stable per ENT guidance)
Renal adjustment
No adjustment required (biliary excretion predominant)
PBS status
✔ PBS General Benefit (inpatient IV use)
Special Populations
Paediatrics
BPPV is rare in children; consider vestibular migraine, benign paroxysmal vertigo of childhood, or central pathology as the leading differential.
Vestibular neuritis occurs in children but is under-recognised. Presentation is often with nausea, vomiting, and refusal to walk rather than a clear vertigo complaint.
The Dix–Hallpike test can be adapted for children; use distraction and allow extra time for the procedure.
Corticosteroids: Use specialist guidance; prednisolone 1–2 mg/kg/day is generally safe but vestibular neuritis in children should prompt specialist referral.
Meclizine: Use with caution in children < 6 years; not recommended under 2 years due to potential CNS depression.
Pregnancy
BPPV is the most common vestibular cause of vertigo in pregnancy and is safe to treat with the Epley maneuver at any gestation.
Distinguish from pre-eclampsia-associated symptoms (headache, visual disturbance, hypertension) and hyperemesis gravidarum.
Meclizine/Prochlorperazine: Category A (TGA) — considered safe in pregnancy. However, minimise use and prefer non-pharmacological measures first.
Corticosteroids: Prednisolone is Category A (TGA) — can be used when clinically indicated. First-trimester use should be discussed with the patient due to small risk of cleft palate (controversial data).
Ondansetron: Category B1 (TGA) — use only if other antiemetics are inadequate.
MRI (without gadolinium) is the preferred neuroimaging modality if central pathology is suspected.
Elderly
Vertigo in the elderly is associated with increased fall risk — falls are the leading cause of injury-related hospitalisation in Australians aged ≥ 65 years.
BPPV is very common but often misattributed to "old age," medications, or cervical spondylosis. Always perform Dix–Hallpike.
Multifactorial dizziness is common — polypharmacy, orthostatic hypotension, peripheral neuropathy, and vestibular dysfunction often coexist.
Prochlorperazine: Use with extreme caution — high risk of extrapyramidal side effects and falls. Avoid if possible.
Meclizine: Increased sedation and anticholinergic effects in the elderly. Use lowest effective dose, short duration only.
Corticosteroids: Monitor blood glucose (risk of steroid-induced hyperglycaemia), consider bone health with prolonged use.
Consider home-based vestibular rehabilitation if mobility is limited.
Renal Impairment
Most vestibular drugs (meclizine, prochlorperazine, ondansetron) require no significant renal dose adjustment.
Aminoglycoside vestibulotoxicity risk is elevated in renal impairment — if concurrent aminoglycoside use is necessary, monitor vestibular function and drug levels.
Corticosteroids: No dose adjustment, but monitor for fluid retention and hypertension.
Hepatic Impairment
Prochlorperazine is hepatically metabolised — use with caution in significant hepatic impairment; risk of accumulation.
Meclizine: Use with caution.
Corticosteroids: Prefer prednisolone (active form) over prednisone (requires hepatic conversion). Consider dose reduction in severe hepatic impairment.
Immunocompromised
Consider a broader infectious differential: CMV, VZV (Ramsay Hunt syndrome), syphilitic labyrinthitis, cryptococcal meningitis, and opportunistic infections.
HIV-positive patients with vertigo should be assessed for CNS toxoplasmosis, primary CNS lymphoma, and cryptococcal meningitis.
Herpes zoster oticus (Ramsay Hunt syndrome) presents with vertigo, hearing loss, and vesicular eruption in the ear canal — treat with oral aciclovir 800 mg 5 times daily for 7–10 days + prednisolone. PBS: Aciclovir is Authority Required for zoster.
Organ transplant recipients: consider opportunistic causes and drug-related vestibulotoxicity (calcineurin inhibitors may cause vestibular side effects).
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health — Vestibular and Balance Disorders
Aboriginal and Torres Strait Islander peoples experience a disproportionate burden of ear disease and its complications, which directly impacts vestibular health. Otitis media with effusion (OME) and chronic suppurative otitis media (CSOM) are highly prevalent in remote Aboriginal and Torres Strait Islander communities, particularly in children, and can lead to conductive hearing loss, labyrinthine complications, and vestibular dysfunction. These conditions are driven by socioeconomic disadvantage, overcrowded housing, limited access to primary healthcare, and environmental factors.
Key awareness: Otitis media affects up to 90% of Aboriginal and Torres Strait Islander children in some remote communities by age 2 years, compared to ~25% of non-Indigenous children. CSOM prevalence in remote communities is 10–20 times higher than the national average. Labyrinthitis secondary to CSOM may present more frequently in this population, and the diagnosis may be delayed due to healthcare access barriers.
Barriers to Care and Considerations
Quick Reference — Vestibular Syndrome to Treatment
BPPV (posterior canal)
Epley maneuver (first-line); meclizine 25 mg PO TDS PRN × 48 h
Single session; repeat if needed
Dix–Hallpike confirms; teach home Epley for recurrence
Vestibular neuritis
Prednisolone 1 mg/kg/day PO (max 60 mg) × 5 days + taper; ondansetron 4 mg PO TDS PRN × 48 h
Steroids within 72 h; VRT 6–12 weeks
HINTS exam peripheral pattern; exclude stroke; start VRT early
Viral labyrinthitis
Prednisolone 1 mg/kg/day PO × 5 days + taper; ondansetron/prochlorperazine PRN
Steroids within 72 h; audiometry at 2–4 weeks
Document hearing; refer if hearing loss persists > 2 weeks
Bacterial labyrinthitis
IV ceftriaxone 2 g daily ± metronidazole 500 mg TDS; urgent ENT referral
10–14 days IV then oral
Medical/surgical emergency; secondary to CSOM or meningitis
Central vertigo (stroke)
Acute stroke pathway (thrombolysis if within window); secondary prevention per Stroke Foundation guidelines
Time-critical; Code Stroke activation
HINTS central pattern; urgent CT/CTA → MRI DWI; admit to stroke unit
📚 References
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