Vertigo and dizziness

Vertigo and dizziness account for up to 5 per cent of emergency department attendances and are deceptively heterogeneous: at one end sits a self-limiting bppv that a single bedside manoeuvre cures, at the other a posterior-circulation stroke whose only feature is vertigo. The Fellowship task is not to classify every dizzy patient but to make one decision reliably — is this a central (potentially dangerous) or a peripheral (usually benign) vestibular problem? — because that decision determines whether the patient is discharged to vestibular rehabilitation or admitted to a stroke pathway. The single most reliable tool for that decision in the acute vestibular syndrome is the HINTS examination, which in the hands of a trained clinician is more sensitive for stroke than early MRI.[1][2]

Definition and classification

Dizziness is the patient's word and is deliberately broad; vertigo is the physician's term for the illusion of motion (spinning, swaying, tilting) of either the self or the surroundings. The standard teaching framework, the Drachman quartet, divides dizziness into vertigo (a vestibular problem), presyncope (cardiovascular, near-faint), disequilibrium (a gait/balance disorder, often neurological), and light-headedness (psychiatric, hyperventilation). The first job at the bedside is to decide which quartet the patient is in, because each has a different dangerous differential: presyncopal dizziness is worked up for a cardiac cause, while true vertigo is worked up for a central-versus-peripheral cause. [1]

Vertigo itself is classified by its temporal pattern into the acute vestibular syndrome (AVS) — continuous vertigo lasting days to weeks with nausea, vomiting and gait instability, typically vestibular neuritis, labyrinthitis or a posterior-circulation stroke — the triggered episodic pattern, where vertigo is provoked by a specific movement or position (BPPV, orthostatic hypotension) — and the spontaneous episodic pattern (Meniere disease, vestibular migraine, TIA). The pattern plus the HINTS examination localises the lesion: the AVS is the high-stakes presentation, because its differential includes stroke. [1]

Pathophysiology — the vestibular apparatus and the VOR

The inner ear houses the vestibular end organ — three semicircular canals (horizontal, anterior, posterior) sensing angular acceleration, and two otolith organs (utricle and saccule) sensing linear acceleration and gravity. Each canal drives the vestibulo-ocular reflex (VOR), the reflex that keeps the visual world stable during head movement: when the head turns, the canals signal the brainstem to drive the eyes equally and oppositely, holding gaze steady. The head impulse test is a direct bedside test of the horizontal canal's VOR: a rapid turn of the head to the side of a deafferented canal produces no opposing eye movement, so the eyes slip off target and a corrective catch-up saccade snaps them back — a positive (abnormal) test. A normal head impulse test (no catch-up saccade) in AVS therefore means the peripheral horizontal canal and its nerve are intact, which points the lesion centrally. [1]

The common peripheral mechanisms are: canalithiasis in BPPV — loose otoconia displaced from the utricle settle into a semicircular canal (the posterior in roughly 85 per cent) and, on head movement, drag the endolymph and produce a false signal of rotation; viral inflammation of the superior vestibular nerve in vestibular neuritis; endolymphatic hydrops — a distension of the endolymphatic space — in Meniere disease; and acute bacterial or viral labyrinthitis when both the vestibular and the auditory apparatus are inflamed together. Central lesions (AICA, PICA, or vertebral artery territory stroke, or a cerebellar/brainstem tumour) interrupt vestibular processing in the brainstem and cerebellum but spare the peripheral VOR — which is exactly why a normal head impulse test is a red flag. [1]

Clinical presentation — the four disorders an examiner rewards

BPPV presents with brief (under one minute) episodes of spinning vertigo provoked by a specific change in head position — rolling over in bed, looking up to a high shelf, bending forward — with no vertigo between attacks and no hearing loss. Vestibular neuritis presents with the acute vestibular syndrome: continuous severe vertigo, nausea and vomiting, gait unsteadiness and a strong preference to lie still, building over hours and peaking within a day, without hearing loss. Labyrinthitis is vestibular neuritis plus acute sensorineural hearing loss and tinnitus on the affected side. Meniere disease presents with the characteristic triad of episodic vertigo (each attack lasting 20 minutes to 12 hours), fluctuating low- to medium-frequency sensorineural hearing loss, and fluctuating aural symptoms (fullness, tinnitus, hearing) in the affected ear.[6] Atypical features that should always trigger a search for a central cause are: vertigo with new headache or neck pain (vertebral dissection), vertigo with diplopia, dysarthria, dysphagia or dysmetria (brainstem/cerebellar signs), vertigo in a patient with vascular risk factors, and any vertical or downbeat nystagmus.

The HINTS examination — the central-versus-peripheral discriminator

In the AVS the HINTS examination is the discriminator, and reproducing its three components and their interpretation is a Fellowship-examined core. The mnemonic is H-I-N-T-S, with any one of the three central findings being central.[1][2]

In Kattah's 101-patient AVS cohort, the HINTS examination was 100 per cent sensitive and 96 per cent specific for stroke — more sensitive than early MRI diffusion-weighted imaging, which returned a false negative in 12 per cent of strokes within the first 48 hours.[1] The 2011 systematic review and the 2023 meta-analysis confirmed that a central HINTS pattern is highly specific for stroke and that, unlike imaging, its accuracy holds at the bedside on day one.[2][3]

The ED approach to the dizzy patient

Differential diagnosis — distinguishing the dangerous from the benign

The differential of acute vertigo is the differential the examiner tests relentlessly, and the can't-miss member is the posterior-circulation stroke that mimics a peripheral vestibulopathy. The discriminating moves are the temporal pattern, the HINTS examination, the hearing, and the vascular risk profile. [1]

Two mimics are particularly dangerous because the history is misleading. Cardiac presyncope frequently presents as "dizziness" — the patient uses the word the ED also uses for vertigo, but the symptom is a near-faint with greying vision, not a spin. Failing to take the symptom apart converts a high-risk cardiac presentation into a benign vertigo discharge. Posterior-circulation TIA may produce brief vertigo that mimics BPPV in timing — the give-away is the absence of a positional trigger, the presence of any brainstem sign, and vascular risk factors. Vertebrobasilar TIA causing isolated vertigo is rarer than once thought and is a diagnosis of exclusion after a clean HINTS, but the threat it carries (impending basilar occlusion) means any patient with high vascular risk and recurrent brief vertigo is imaged. [1]

The central causes in depth — the dangerous differentials

The central causes of vertigo are best remembered by the three vascular territories of the posterior circulation plus the three structural mimics. The vascular strokes are PICA (lateral medullary / Wallenberg), AICA (lateral pontine), and the vertebral/basilar perforator and superior cerebellar artery territories; the structural mimics are multiple sclerosis, the cerebellopontine-angle tumour, and vestibular migraine. Each has a signature that the bedside examination can separate.[13]

Investigations — HINTS first, then MRI

The investigations run in parallel with the bedside examination. The finger-prick glucose excludes hypoglycaemia (a vertigo and ataxia mimic). The ECG is mandatory — atrial fibrillation drives a cardioembolic posterior-circulation stroke, and the patient who says "dizzy" may have a primary cardiac rhythm. Bloods include full blood count, electrolytes and a coagulation screen; these are baseline rather than diagnostic. [1]

The pivotal imaging question is central versus peripheral, and the answer rests on HINTS, not on CT. Non-contrast CT of the brain is insensitive for posterior-fossa stroke — the dense petrous temporal bones produce beam-hardening artefact that obscures the brainstem and cerebellum, and early ischaemia is missed. A normal CT in AVS therefore excludes neither stroke nor a cerebellar haemorrhage reliably. MRI with diffusion-weighted imaging is the gold standard, but even MRI DWI returns false-negative in roughly 12 to 20 per cent of posterior-circulation strokes within the first 48 hours, which is the entire rationale for trusting the HINTS examination over early imaging.[1] The practical rule: a patient with a central HINTS pattern is managed as a stroke regardless of a normal CT or an early normal MRI, and is admitted to the stroke pathway. Audiometry, when available, characterises the hearing loss in Meniere disease and labyrinthitis; caloric testing and formal vestibular function tests are outpatient evaluations, not ED tests.

Immediate management — symptomatic control and the disposition split

Resuscitation is rarely required for vertigo itself, but vomiting and dehydration often are: establish intravenous access, give fluids (for example 1 litre of normal saline over an hour with antiemetic cover), and treat the nausea. The antiemetic of choice in the acute phase is prochlorperazine 5 mg orally or buccally (repeat if needed), or 12.5 mg intramuscularly for a vomiting patient, or ondansetron 4 mg intravenously as an alternative. The critical principle is that vestibular suppressants are a short-course symptomatic tool — three days at most in vestibular neuritis — because prolonged use impairs central vestibular compensation and prolongs recovery. [1]

Definitive management — the four disorders

BPPV (posterior canal). The diagnosis is made at the bedside by the Dix–Hallpike manoeuvre — sitting the patient up, turning the head 45 degrees to one side, then rapidly lying them back with the head extended 20 degrees over the end of the bed; a positive test reproduces the vertigo after a brief latency (1 to 5 seconds) with a characteristic torsional upbeating nystagmus fatiguing within a minute.[7] Treatment is the Epley canalith repositioning manoeuvre, which rotates the head through a sequence of positions that walk the loose otoconia out of the posterior canal and back into the utricle. The Cochrane review confirms the Epley is significantly more effective than sham or no treatment for resolving symptoms and converting a positive Dix–Hallpike to negative.[4] Horizontal-canal BPPV (the second commonest) is diagnosed by the supine roll test and treated with the Barbecue (Lempert) or Gufoni manoeuvre.

Vestibular neuritis. Symptom control is with a short course of prochlorperazine or an alternative antiemetic (three days, then stop). A tapering course of oral corticosteroids — for example prednisolone 1 mg per kilogram (maximum 60 mg) daily for three to five days then taper over two to three weeks, started within 72 hours of onset — modestly improves long-term caloric recovery, although the modern meta-analyses show inconsistent benefit on symptomatic outcomes and the practice is guideline-variable.[5] Antivirals alone are not effective. Early vestibular rehabilitation (graded head-movement exercises) accelerates central compensation and is the most evidence-based long-term intervention.

Labyrinthitis. Managed as vestibular neuritis with attention to the hearing loss: urgent audiology, and consider corticosteroids (systemic, and in some pathways intratympanic) for the sudden sensorineural hearing loss, which has its own time window. [1]

Meniere disease. Acute attacks are managed with bed rest, antiemetics and a short vestibular suppressant. Maintenance therapy is betahistine (a histamine analogue that improves cochlear microcirculation), a low-salt diet, and a diuretic (for example hydrochlorothiazide 25 to 50 mg daily or acetazolamide 250 mg twice daily) to reduce endolymphatic hydrops. Refractory disease is treated with intratympanic corticosteroids or gentamicin, and surgery (endolymphatic sac decompression, vestibular nerve section) in the small minority with refractory disabling vertigo. [1]

The functional and chronic vestibular disorders

Not every dizzy patient has an acute peripheral or central lesion. Two chronic, episodic-then-persistent disorders are common, frequently mislabelled as "psychogenic", and missed in the ED: vestibular migraine (the commonest central cause of recurrent vertigo) and persistent postural-perceptual dizziness (PPPD), the new consensus term for the chronic functional dizziness formerly called chronic subjective dizziness or phobic postural vertigo. Both are diagnoses of inclusion (against defined Bárány criteria) made after the dangerous and acute peripheral causes are excluded, and both are managed primarily WITHOUT vestibular suppressants. [1]

Complications and pitfalls

The complications of mismanaged vertigo are, in order of danger, the missed posterior-circulation stroke (the leading cause of vertigo-related litigation and mortality), prolonged vestibular suppressant use impairing central compensation, recurrence of BPPV (which can be re-treated), and the progression of sudden hearing loss in labyrinthitis when corticosteroids are withheld. The classic pitfalls at the bedside are: trusting a normal non-contrast CT in a patient with central HINTS; failing to perform the head impulse test in any AVS patient (and therefore defaulting to a neuritis diagnosis); prescribing long-term prochlorperazine or diazepam for vestibular neuritis; treating recurrent brief vertigo in a vascular patient as BPPV without excluding vertebrobasilar TIA; and forgetting the ECG in the elderly dizzy patient. [1]

Prognosis and disposition

Peripheral vestibular disorders do well with the right intervention: BPPV resolves in the great majority after one or two Epley manoeuvres; vestibular neuritis improves over weeks with vestibular rehabilitation (residual symptoms reflect delayed compensation, often from prolonged vestibular suppressants). Central HINTS carries the prognosis of its underlying stroke and is admitted. The disposition rules are: any central HINTS, any brainstem sign, true gait ataxia, severe headache, or a first attack of Meniere with new hearing loss — admit for imaging and specialist review; a clear peripheral pattern with normal gait — discharge with vestibular rehabilitation, a short antiemetic/steroid course, and a written safety-net for new neurological symptoms. [1]

Special populations

The elderly dizzy patient has a broader and more dangerous differential — posterior-circulation stroke, orthostatic hypotension from polypharmacy, carotid sinus hypersensitivity, cardiac arrhythmia — and the threshold for imaging, ECG monitoring and admission is lower. Polypharmacy (antihypertensives, sedatives, anticonvulsants) is a leading cause of dizziness in this group and is reversible. The anticoagulated patient with vertigo carries a higher risk of posterior-fossa haemorrhage (cerebellar haematoma presenting with vertigo and ataxia) and of cardioembolic stroke, and warrants early imaging even with a clean HINTS. Pregnancy is usually managed without vestibular suppressants (prochlorperazine is generally avoided in the first trimester); positional manoeuvres for BPPV are safe. [1]

Evidence and regional guidelines

The diagnostic evidence base is dominated by the HINTS examination. Kattah and colleagues (2009) showed that the three-step bedside HINTS examination was 100 per cent sensitive and 96 per cent specific for stroke in AVS, and more sensitive than early MRI DWI within 48 hours.[1] Tarnutzer's 2011 systematic review confirmed the high specificity of central ocular motor findings at the bedside,[2] and the 2023 meta-analysis extended this to show that diagnostic accuracy depends on clinician training and stroke location, but remains high in expert hands.[3] The Cochrane review of the Epley manoeuvre (Hilton and Pinder, 2014) confirms its efficacy for posterior-canal BPPV.[4] Corticosteroid meta-analysis for vestibular neuritis (Bogdanova, 2022) shows modest and inconsistent benefit.[5] The Bárány Society International Classification of Vestibular Disorders provides the operational diagnostic criteria for both Meniere disease (Lopez-Escamez, 2015)[6] and BPPV (von Brevern, 2015).[7]

Exam pearls

• Central HINTS = NORMAL head impulse + direction-changing (or vertical/downbeat) nystagmus + skew deviation — ANY one central sign is central. The candidate who states this rule wins the vertigo SAQ.
• HINTS is more sensitive than early MRI within 48 hours of AVS onset — a normal head impulse test in a vertiginous patient is a red flag, not reassurance.
• BPPV = brief positional vertigo reproduced by Dix–Hallpike → Epley manoeuvre. The nystagmus is torsional and upbeating on the dependent side, with a brief latency and fatigability.
• Vestibular neuritis = continuous vertigo + PERIPHERAL HINTS (abnormal head impulse) + no hearing loss. Labyrinthitis = neuritis + sudden SNHL.
• Meniere triad = episodic vertigo 20 min–12 h + fluctuating low-frequency SNHL + aural fullness/tinnitus (Bárány 2015).
• Prochlorperazine and other vestibular suppressants are short-course (≤3 days) — prolonged use delays central compensation.
• Never trust a normal non-contrast CT in a suspected posterior-circulation stroke — CT is insensitive in the posterior fossa; pursue MRI or admit.
• Nystagmus reading — direction-fixed horizontal is peripheral; direction-changing (gaze-evoked) or vertical/downbeat is central. Read the eyes in primary gaze then ±30 degrees lateral; never interpret end-point nystagmus.
• A purely vertical or downbeat nystagmus is central — full stop. A downbeat nystagmus worsened by lateral gaze or convergence points to a craniocervical junction lesion (Arnold–Chiari, cerebellar degeneration).
• The AICA stroke produces vertigo + ipsilateral sudden SNHL (AICA supplies the labyrinth); PICA (Wallenberg) spares the hearing. A hearing loss with a normal HIT and direction-changing nystagmus is AICA stroke, not labyrinthitis.
• Horizontal-canal BPPV (10–15%) = horizontal nystagmus on the supine roll test → Barbecue (Lempert) or Gufoni manoeuvre — NOT the Epley. The Epley only treats the posterior canal.
• A positional vertigo that is NON-fatiguing, persistent, or has downbeat nystagmus is a central positional lesion, NOT BPPV — do not reposition, image.
• Vestibular migraine = ≥5 episodes of vertigo 5 min–72 h + migraine history + ≥1 migraine feature per attack (Bárány/IHS, Lempert 2012); headache is NOT required during every attack.
• PPPD = ≥3 months of non-rotational dizziness provoked by posture/motion/visual stimuli after an acute vestibular event; treat with SSRI/SNRI + vestibular rehab, NOT suppressants.
• The corneal reflex (CN V) is the forgotten bedside sign — an absent reflex with a progressive unilateral hearing loss and imbalance is a vestibular schwannoma until MRI proves otherwise.
• Methylprednisolone (Strupp 2004, NEJM) improves objective recovery in vestibular neuritis; valacyclovir does NOT — do not add antivirals.
• A sudden SNHL (≥30 dB over three frequencies in 72 h) gets high-dose oral prednisolone within 7–14 days — this is an ENT emergency, not an outpatient referral.
• The eye-movement examination in AVS is the "eye ECG" — a mandatory first-line test that, in trained hands, outperforms early MRI (Newman-Toker 2015).
• A bilateral abnormal head impulse test with oscillopsia (the world jumping when walking) is a bilateral vestibulopathy — think aminoglycoside vestibulotoxicity. [1]

Red flags