The conditions
Posterior-circulation stroke
Around one ischaemic stroke in five is in the posterior circulation — the territory that feeds the very structures that keep us balanced. Vertigo can be its only symptom, which is exactly what makes it dangerous.
Why it matters
A stroke happens when the blood supply to part of the brain is cut off. The posterior circulation supplies the back of the brain — the brainstem and cerebellum — which is where balance is controlled. A stroke here can make the room spin, sometimes with no other obvious sign at first.
The posterior circulation — the vertebral and basilar arteries and their branches — supplies the brainstem, cerebellum, thalamus and occipital lobes, and accounts for roughly 20% of ischaemic strokes.1,2 Of patients arriving at the emergency department with new vertigo, around 3–5% ultimately have vertebrobasilar ischaemia, so stroke must always be on the list for an acute presentation.
The crucial epidemiological fact is the miss rate. In one large series up to 35% of cerebellar infarcts were initially overlooked — most often relabelled as vestibular neuritis — and a substantial fraction of those patients later deteriorated.3,4 Isolated vertigo with no other deficit is a recognised stroke presentation, especially in the PICA and AICA territories.
Vascular territories and their syndromes
Three branches of the vertebrobasilar tree produce most vestibular strokes. Knowing which structures each one feeds lets you predict the accompanying signs — and explains why one of them (AICA) can masquerade as inner-ear disease.
Supplies: Dorsolateral medulla; inferior cerebellum (nodulus, uvula)
Syndrome: Lateral medullary (Wallenberg) syndrome; isolated cerebellar infarction
Vertigo + facial numbness, Horner's, dysphagia/dysarthria, limb ataxia, crossed sensory loss
Supplies: Lateral pons; flocculus; labyrinth & cochlea (internal auditory artery)
Syndrome: Lateral pontine syndrome; labyrinthine infarction
AVS that mimics neuritis but adds ipsilateral hearing loss, tinnitus and facial weakness
Supplies: Superior cerebellum (vermis); superior cerebellar peduncle
Syndrome: Superior cerebellar syndrome
Disequilibrium and gait ataxia, often with little or no nystagmus; dysmetria
The AICA is the great mimic: through the internal auditory artery it supplies the labyrinth and cochlea, so an AICA infarct can present as an acute vestibular syndrome with hearing loss — looking, at first, like labyrinthitis. PICA infarction gives the classic Wallenberg (lateral medullary) syndrome with hearing usually preserved, while superior cerebellar (SCA) lesions tend to cause disequilibrium and gait ataxia with little nystagmus.2
Pathophysiology
Vertigo follows ischaemia of the central vestibular apparatus: the vestibular nuclei of the dorsolateral medulla, the inferior and middle cerebellar peduncles, and the vestibulocerebellum (nodulus, uvula, flocculus). Damage here corrupts the integration of vestibular signals, so spatial orientation and gaze stabilisation fail — experienced as vertigo, imbalance and nystagmus. Unlike a peripheral lesion, the deficit is persistent and non-fatigable, and it usually comes with neighbouring brainstem or cerebellar signs that localise the lesion.2
Clinical features
Stroke vertigo characteristically begins suddenly, is maximal at onset, and comes with imbalance severe enough that the patient cannot stand or walk unaided — out of proportion to what a peripheral lesion would cause. Distinguishing features include:
- Nystagmus that is vertical (often downbeat), torsional, or direction-changing, and that is not suppressed by fixation — in contrast to the unidirectional, fixation-suppressed nystagmus of a peripheral lesion.
- Symptoms that worsen with eye closure and do not fatigue on repetition, because visual compensation has been removed.
- Preserved hearing in most brainstem infarcts — the important exception being AICA, where the labyrinth is also infarcted.
- Focal signs — diplopia, dysarthria, dysphagia, facial numbness, limb weakness, hemisensory loss or Horner’s — which are easy to overlook when vertigo dominates the picture.
Diagnosis
Diagnosis rests on disciplined bedside examination married to the right imaging — in that order.
Bedside: HINTS
In a patient with a genuine acute vestibular syndrome, the three-step HINTS battery — Head Impulse, Nystagmus direction, and Test of Skew — is more sensitive than early MRI for stroke.5,6 A central (dangerous) pattern is any of: a normal head impulse, direction-changing gaze-evoked nystagmus, or a skew deviation — captured by the mnemonic INFARCT (Impulse Normal, Fast-phase Alternating, Refixation on Cover Test). The interactive interpreter on the differential page works through every combination.
Caution: HINTS is valid only in continuous AVS with spontaneous nystagmus, and only in trained hands. It is not a test for episodic or positional vertigo, and a reassuring pattern never overrides other red flags.
Imaging
MRI with diffusion-weighted imaging is far superior to CT for posterior- fossa infarcts. But a normal early DWI does not exclude stroke — up to ~20% of small posterior-fossa infarcts are missed in the first 24–48 hours, so persistent or worsening symptoms justify repeat imaging.7 Vascular imaging — CTA or MRA — is essential to look for vertebral or basilar stenosis, occlusion or dissection, and to guide reperfusion decisions.
Red flags for a central cause
- Age > 50, or vascular risk factors (hypertension, diabetes, hyperlipidaemia, smoking).
- Vertigo persisting > 24 hours without settling, or sudden severe headache / neck pain.
- Any focal neurological sign, however subtle.
- Inability to sit or stand unaided — truncal ataxia out of proportion to vertigo.
- A normal head-impulse test in a patient with ongoing AVS.
Management
A posterior-circulation stroke is treated as an emergency, like any other stroke. The patient is admitted, scanned, and — if they arrive in time — may be given a clot- busting drug or have the clot removed. Afterwards, medicines to prevent another stroke and balance rehabilitation help recovery.
Management mirrors any acute ischaemic stroke, with added vigilance for posterior-fossa complications. Eligible patients within 4.5 hours receive intravenous thrombolysis with alteplase;8,9 selected large-vessel occlusions — particularly basilar occlusion — are candidates for mechanical thrombectomy.10 Outside the reperfusion window, antiplatelet therapy is the cornerstone: short-course dual antiplatelet therapy (aspirin + clopidogrel) reduces early recurrence after minor stroke or high-risk TIA.11,12
Secondary prevention adds a high-intensity statin and blood-pressure control once the patient is neurologically stable.13 Vestibular rehabilitation in the post-acute phase promotes central compensation and reduces falls.14
The point that distinguishes posterior-fossa stroke from anterior strokes is the threat of mass effect. A large cerebellar infarct can swell, compress the fourth ventricle and brainstem, and cause obstructive hydrocephalus within 2–4 days — so these patients need monitoring and a low threshold for neurosurgical referral (decompression or external ventricular drainage).4 Otherwise the algorithm follows standard practice: reperfusion when eligible,8 antithrombotic and risk-factor secondary prevention,11,13 and structured vestibular rehabilitation.14
Key points
- Posterior-circulation strokes are ~20% of ischaemic strokes and can present as isolated vertigo.
- PICA → Wallenberg / cerebellar infarct (hearing spared); AICA → AVS with hearing loss (mimics labyrinthitis); SCA → gait ataxia with little nystagmus.
- Central nystagmus (vertical/direction-changing, fixation-resistant), a normal head impulse, and gait failure are the warning signs.
- HINTS beats early MRI in AVS; a normal early DWI does not exclude posterior-fossa stroke.
- Treat as an emergency — reperfusion when eligible — and watch for cerebellar swelling and hydrocephalus.