Posterior Circulation Stroke

The brainstem and the back of the brain — the cerebellum — receive their blood supply from two arteries that run up the back of the neck and join into a single artery called the basilar. A stroke in this circulation produces vertigo, imbalance, slurred speech, double vision, or weakness on one side of the face or body. Sometimes only vertigo, making it easy to mistake for an inner-ear problem.

This is the diagnosis behind every dizzy patient's emergency presentation. Most are not strokes. But missing a stroke is the worst possible outcome — both for the patient (because secondary prevention prevents a much bigger second stroke) and because some posterior strokes, particularly basilar artery occlusion, need urgent thrombolysis or clot retrieval that has a narrow time window.

The bedside examination — the HINTS test, plus a careful check of gait, hearing, and the rest of the neurology — done by a trained clinician within 24 hours of symptom onset, is the most reliable way to separate the inner-ear from the brainstem cause. An MRI in the first 24–48 hours misses up to 1 in 8 small posterior strokes; the bedside examination misses far fewer.

Posterior circulation strokes — affecting the brainstem, cerebellum, and posterior thalamus — account for approximately 20% of all ischaemic strokes, and are misdiagnosed at twice the rate of anterior circulation events.1 The Tarnutzer 2017 meta-analysis found that roughly 9% of cerebrovascular events are missed at the initial ED visit, with the misdiagnosis rate rising to 35% when the presenting complaint is dizziness or vertigo.2

The clinical challenge has three roots. First, the presentation overlaps with common benign vestibular disorders: vestibular neuritis, vestibular migraine, BPPV. Many posterior strokes — particularly small PICA-territory cerebellar infarcts — present with isolated vertigo indistinguishable from peripheral vestibulopathy on the vertigo axis alone.4 Second, the standard neurological screen is often unrevealing — there is no facial droop, no hemiparesis, no aphasia in many posterior strokes, and the NIH Stroke Scale (designed for cortical strokes) scores them as low. Third, diffusion-weighted MRI, the standard stroke imaging modality, has a false-negative rate of 12–20% in posterior strokes within the first 48 hours of onset, falling to nearly zero by day 7.

The combined effect is that frontline assessment requires a different toolset for the dizzy patient than for the hemiparetic patient. The HINTS examination, gait assessment, bedside hearing, and a structured central nystagmus look — all woven into a single 5-minute examination — outperforms early MRI for ruling stroke in or out at the bedside.

The diagnostic framework that has emerged from twenty years of vestibular medicine research (Newman-Toker, Edlow, Kerber, Tarnutzer) reframes acute dizziness around the timing and triggers of symptoms rather than the patient's description of the dizziness itself. Three clinical syndromes are differentiated: acute vestibular syndrome (AVS) — continuous vertigo lasting hours to days, in which the differential is neuritis vs. central infarction; episodic vestibular syndrome triggered (s-EVS) — short positional or exertional episodes, where the differential is BPPV vs. central positional vertigo or third-window pathology; andspontaneous episodic vestibular syndrome (s-EVS)— recurrent attacks without a clear trigger, where the differential includes vestibular migraine, Ménière's, posterior-circulation TIA, and panic disorder. Each syndrome calls for a different examination strategy.9

The GRACE-3 emergency department guideline, published in 2023, is the current authoritative document for the workup of acute dizziness in the ED. Its central recommendations: characterise the timing pattern first; use HINTS for the AVS group; do not over-rely on CT or early MRI for ruling out posterior stroke; and arrange expedited outpatient assessment with vascular imaging (CTA or MRA) for patients with suspected TIA.9

The vascular substrate matters. Vertebral artery dissection is the leading cause of posterior stroke in patients under 50, often following neck trauma (chiropractic manipulation, head turning, sports). Atherothrombosis is the leading cause in older patients with vascular risk factors. Top-of-basilar syndrome from cardioembolism is the emergency that justifies aggressive imaging and thrombectomy referral.5,10

The five territories above are the "named places" of posterior circulation stroke. Each one produces a slightly different mix of vertigo, balance, and other neurological signs. The two most important to know are PICA (the most common cerebellar stroke that can present with isolated vertigo) and AICA (the great mimic of vestibular neuritis because it also affects the inner ear).

Three points worth committing to memory. PICA infarction is the most common cerebellar stroke; Lee 2006 showed that 11% of cerebellar infarcts present with isolated vertigo, mostly from medial-PICA territory.4These are the patients most easily mistaken for vestibular neuritis — and the patients in whom HINTS pays its biggest dividend.

AICA infarction involves the labyrinth because the labyrinthine arteryis a terminal branch of AICA. The result is a stroke that can present like neuritis on every component of HINTS except the hearing — hence the "HINTS-Plus" modification that adds a bedside hearing check.8

Lateral medullary (Wallenberg) syndrome — usually from PICA or vertebral artery occlusion — is the named brainstem syndrome of vestibular medicine. Its clinical fingerprint (ipsilateral Horner, ipsilateral facial sensory loss, contralateral body sensory loss, dysphagia, hoarseness, ataxia) is so distinctive that HINTS becomes irrelevant — a Wallenberg patient is diagnosable on standard neurological examination alone.

The two cerebellar territories that warrant specific operational concern beyond diagnosis: large SCA infarction carries the highest risk of cerebellar oedema and brainstem compression within 24–72 hours, and may need decompressive suboccipital craniectomy.11Top-of-basilar embolic syndrome from cardioembolism (often atrial fibrillation, often poorly anticoagulated) presents with bilateral oculomotor and visual deficits, altered consciousness, and prominent vertigo — the window for endovascular thrombectomy is 4.5–24 hours depending on imaging selection. Any acute vertigo presentation with bilateral signs, oculomotor abnormalities, or altered consciousness should bypass standard HINTS and trigger immediate vascular imaging.10

The card above is a quick reference to the most common abnormal eye-movement patterns that indicate a brain (rather than inner-ear) cause. The most important takeaway: any purely vertical nystagmus (downbeat or upbeat) or any purely torsional nystagmus is a central sign that warrants urgent imaging.

Three nystagmus patterns deserve specific attention in the acute setting. Downbeat nystagmus localises to the cervicomedullary junction or vestibulocerebellum — the differential includes Chiari I malformation (often missed in young patients), cerebellar degeneration, posterior fossa stroke, and toxin exposure (lithium, anticonvulsants). It is worsened by downgaze and often increased by lying supine.

Periodic alternating nystagmus (PAN) — horizontal jerk nystagmus that reverses direction every 60–90 seconds — is highly specific for nodulus-uvula lesions or cervicomedullary pathology. It is easily missed if the examiner does not watch for several minutes. PAN is one of the few nystagmus patterns with a specific treatment: baclofen.

Pure torsional nystagmus (no horizontal or vertical component) is always central, almost always midbrain or medullary, and warrants urgent imaging regardless of the rest of the examination.

Two practical observations on bedside nystagmus discrimination. First, the corollary of "central nystagmus rules in central" is not "peripheral-looking nystagmus rules out central". A unidirectional horizontal-torsional nystagmus that obeys Alexander's law can still be cerebellar — the cerebellum can mimic peripheral patterns convincingly. Use the broader examination (gait, head impulse, hearing) to disambiguate. Second, the suppression-by-fixation test — using Frenzel goggles or a covered eye to remove visual fixation — separates peripheral nystagmus (suppressed by fixation) from central nystagmus (not suppressed). It's a five-second additional test that adds substantial discriminative power.12

Doctors examining a dizzy patient look for several specific things to decide whether the cause is the inner ear (most common) or the brain (much rarer but much more serious). The most important: can the patient walk or stand unsupported? Inner-ear vertigo patients are usually able to, even if they look unsteady. Patients with a cerebellar stroke often cannot stand at all without falling.

Other things to check: the HINTS examination (described in the Vestibular Neuritis module), hearing on each side, whether the patient's face moves normally, and whether there is any difference in feeling between the two sides of the body.

A structured 5-minute bedside examination for the dizzy patient covers the following. History: onset (sudden vs. gradual), duration (seconds vs. hours vs. days), triggers (positional, exertional, spontaneous), and associated symptoms (hearing, speech, swallowing, vision, weakness). The triggered/spontaneous distinction determines which examination sub-protocol applies.9

HINTS for the AVS patient — see the Vestibular Neuritis module for the full technique. Three steps; any one central finding makes the pattern central.6

Gait: the most useful single bedside discriminator after HINTS. A patient who cannot stand unsupported with eyes open is not a vestibular neuritis patient — that is a cerebellar truncal ataxia until proven otherwise. Romberg testing distinguishes proprioceptive ataxia (eyes-closed worse) from cerebellar ataxia (worse in both).

Bedside hearing: rub fingers near each ear and ask the patient to say which side they hear it better. Acute asymmetric hearing in an AVS patient is a red flag for AICA infarction.7,8

Cranial nerves and limbs: a screening examination — facial movement and sensation, palate elevation, tongue protrusion, limb power, sensation, and coordination (finger-to-nose, heel-to-shin). Any focal abnormality redirects the patient to a stroke pathway regardless of HINTS.

Three nuances of bedside discrimination at the clinician level. First, the head impulse test should be performed with the patient's head pre-positioned 30° forward of neutral (to align the lateral semicircular canals with the horizontal plane) and the patient instructed to fixate on the examiner's nose with eyes locked. A high-velocity, low-amplitude rotation (10–20° at >1000°/s) is required — a slow rotation produces false negatives. Covert saccades (compensatory saccades that occur during the head movement itself, invisible to the naked eye) require vHIT to detect; their presence is a peripheral finding, their absence in the right context is reassuring.

Second, the bedside head-shaking test (vigorous head-shaking 20 times then observation for nystagmus) adds supplementary information: a perverted (cross-coupled) vertical or torsional response after horizontal shaking is a central sign. Third, the test of skew should be done with alternate cover testing, watching for vertical refixation as fixation is transferred from one eye to the other — easily missed if the patient is looking down or if cover times are too short.

A patient who cannot sit unsupported but has otherwise preserved limb coordination, sensation, and strength is exhibiting truncal ataxia — a cerebellar-vermis or paravermal finding that points directly to PICA territory infarction. This sign is more useful than any single HINTS component and is missed if the patient is examined only in the recumbent position. Always test sitting balance with arms folded across the chest.

Early CT scans of the head are good at finding bleeds but miss almost all acute ischaemic strokes in the posterior circulation. Early MRI is better but still misses about 1 in 8. This is why the bedside examination is so important: a normal early scan does not rule out a posterior stroke. Patients with persistent symptoms or red flags often need repeat imaging at 48–72 hours.

The imaging hierarchy in suspected posterior circulation stroke:

• Non-contrast CT head — first-line in any acute stroke presentation. Sensitivity for acute ischaemic stroke is poor in the first 24 hours; sensitivity for posterior fossa lesions is even worse because of beam hardening artefact from the petrous bones. CT primarily excludes haemorrhage.
• CT angiography (CTA) — head and neck — evaluates the vertebral and basilar arteries for stenosis, dissection, or occlusion. Should be performed in any patient with red flags or any concern for vascular cause, irrespective of CT head findings.
• MRI with diffusion-weighted imaging (DWI) — the imaging modality with the highest sensitivity for acute ischaemic stroke. False-negative rate 12–20% in posterior strokes within 48 hours. Repeat at 5–7 days if clinical suspicion remains and initial DWI is negative.2
• MR angiography (MRA) — used as the vascular component when MRI is the chosen modality.

The 2019 AHA/ASA stroke management guideline calls for vascular imaging in any patient with suspected posterior-circulation TIA — particularly because vertebral artery dissection requires anticoagulation rather than antiplatelet therapy.10

The clinician's most important imaging decision is not what to order but what to do with a normal scan. A patient with persistent AVS, a central-looking HINTS, and a negative initial MRI should be admitted for monitoring and repeat imaging at 48–72 hours; the false-negative rate falls dramatically by day 7. Discharge with outpatient follow-up is appropriate only when the clinical examination is reassuring, HINTS is peripheral, gait is preserved, and there are no red flags. The cost of an unnecessary admission is far lower than the cost of a missed posterior stroke that returns with completed cerebellar infarction or basilar occlusion.1

One specific scenario deserves separate attention. A young patient (under 50) with acute vertigo and neck pain — even without a clear traumatic precipitant — should have CTA or MRA of the vertebral arteries to exclude dissection. Vertebral dissection accounts for up to 25% of strokes in young adults; the typical clinical picture is occipital or posterior neck pain preceding vertigo by hours to days, often after minor trauma or even routine activities like hairdressing or chiropractic manipulation.5