Posterior circulation stroke

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The posterior circulation is supplied by the vertebral, basilar and posterior cerebral arteries. It serves the medulla, pons, midbrain, cerebellum, thalami and occipital and inferomedial temporal lobes. Because these structures contain compact cranial-nerve, long-tract, coordination, respiratory and consciousness pathways, a small lesion can produce a complex combination. Crossed findings—an ipsilateral cranial-nerve or facial deficit with contralateral limb sensory or motor deficit—strongly localise to the brainstem.

Recognition is difficult because vertigo, nausea, gait instability and headache overlap with benign vestibular disease and migraine. The clinician should define onset, continuity, triggers and ability to stand, then examine eye alignment and movements, nystagmus, speech, swallowing, face, limbs, sensation, coordination and gait when safe. A central syndrome is supported by direction-changing or vertical nystagmus, skew deviation, normal head impulse in the correct syndrome, severe truncal ataxia or any focal sign, but individual findings require expertise.

Imaging should answer both haemorrhage and occlusion. Non-contrast CT remains essential initially but has anatomical limitations in the posterior fossa. CTA should assess both vertebral arteries, basilar artery and posterior cerebral circulation, including dissection or stenosis. MRI is more sensitive for small infarcts but is not infallible in the first hours. Treatment follows reperfusion, stroke-unit and secondary-prevention principles, with additional attention to airway and swallowing, basilar deterioration and space-occupying cerebellar swelling.

Key points

Posterior circulation stroke can present with diplopia, dysarthria, dysphagia, vertigo, nystagmus, ataxia, visual field loss, crossed sensory findings or reduced consciousness and may be FAST-negative.
Basilar artery occlusion can fluctuate or progress to quadriparesis, coma or locked-in syndrome and requires immediate CTA and thrombectomy-centre discussion.
Isolated dizziness is usually not stroke, but an acute continuous vestibular syndrome with inability to stand, central eye signs, new headache or focal neurology demands urgent expert assessment.
HINTS is useful only in an appropriate continuous acute vestibular syndrome when performed and interpreted by a trained clinician; it is not a casual screening test for all dizziness.
Early non-contrast CT is insensitive to small posterior fossa infarction; add CTA for vertebrobasilar occlusion and obtain MRI with diffusion-weighted imaging when diagnostic uncertainty persists.
An early MRI can occasionally be diffusion-negative in a small brainstem infarct, so repeat imaging is appropriate when a persistent objective syndrome remains unexplained.
Apply the same urgent thrombolysis principles as other disabling ischaemic strokes, and consider mechanical thrombectomy for eligible vertebrobasilar occlusion according to the current specialist network protocol.
Cerebellar infarction can swell, compress the fourth ventricle and cause hydrocephalus or brainstem injury; worsening headache, vomiting or consciousness needs repeat imaging and early neurosurgical review.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Vertebrobasilar atherosclerosis

Atherosclerotic plaque can thrombose or embolise within vertebral, basilar or posterior cerebral arteries, causing brainstem, cerebellar or occipital infarction.

Cardioembolism

Atrial fibrillation, intracardiac thrombus and valve disease can send emboli into the posterior circulation, sometimes affecting several territories.

Small penetrating-artery disease

Hypertensive and metabolic arteriopathy can occlude perforators supplying the pons, thalamus and other compact deep structures.

Cervical artery dissection

Vertebral dissection is particularly relevant with new posterior neck or occipital pain, trauma or stroke in a younger person.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Arterial occlusion
Thrombus or embolus interrupts flow through vertebral, basilar, cerebellar or posterior cerebral arteries and downstream brain tissue.
2
Strategic network ischaemia
Energy failure affects densely packed cranial, long-tract, balance, visual and consciousness pathways, producing varied or crossed deficits.
3
Infarction and oedema
Persistent hypoperfusion causes neuronal death and swelling, with limited posterior-fossa space making cerebellar oedema especially dangerous.
4
Collateral-dependent evolution
Variable collateral supply permits fluctuating symptoms or delayed deterioration, particularly during progressive basilar occlusion over time.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Lateral medullary syndrome

Dysphagia, dysphonia, ipsilateral Horner syndrome, facial pain-temperature loss, limb ataxia and contralateral body pain-temperature loss suggests dorsolateral medullary ischaemia.

Lateral pontine syndrome

Facial weakness, vertigo, nystagmus, ipsilateral ataxia and possible hearing loss points towards an AICA or lateral pontine lesion.

Basilar occlusion

Fluctuating diplopia and dysarthria may progress to bilateral weakness, impaired consciousness, abnormal eye movements or locked-in syndrome with preserved vertical gaze.

Cerebellar infarction

Sudden vertigo, vomiting, severe gait or truncal ataxia, dysmetria and nystagmus may occur without limb weakness and can later deteriorate from swelling.

Posterior cerebral artery stroke

Contralateral homonymous hemianopia, visual agnosia, memory disturbance or thalamic sensory symptoms may be the only deficits and are easily missed by FAST.

Midbrain syndrome

An ipsilateral third-nerve palsy with contralateral weakness, tremor or ataxia localises to midbrain perforators and requires urgent vascular imaging.

Central vestibular pattern

Continuous vertigo with direction-changing nystagmus, skew, severe inability to sit or stand, new focal sign or high-risk headache is concerning for stroke.

Red flags requiring action

Reduced consciousness, bilateral weakness, new respiratory irregularity or rapidly evolving cranial-nerve signs suggests basilar occlusion or brainstem compression and needs immediate airway and thrombectomy-centre escalation.
Inability to sit or stand unsupported in an acute vestibular syndrome is a major central warning even when facial symmetry and arm strength are normal.
Progressive occipital headache, vomiting, drowsiness or sixth-nerve palsy after cerebellar infarction suggests swelling and obstructive hydrocephalus.
New dysphagia, wet voice, absent cough or pooling secretions creates aspiration and airway risk and requires nil-by-mouth care pending trained assessment.
Neck pain or occipital headache after trauma or manipulation with posterior symptoms suggests vertebral artery dissection and requires full head-and-neck angiography.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Non-contrast CT brainFirst step
Why
Exclude intracranial haemorrhage and detect a large established posterior infarct, hydrocephalus or another structural lesion.
Interpretation and limitations
Beam-hardening and early ischaemia reduce sensitivity in the posterior fossa; a normal CT cannot rule out brainstem or cerebellar stroke.
02
CT angiography of head and neck
Why
Detect vertebral or basilar occlusion, stenosis or dissection and identify a mechanical thrombectomy target.
Interpretation and limitations
Review the entire vertebrobasilar circulation and collateral anatomy; a basilar occlusion is time-critical even when symptoms have fluctuated.
03
MRI brain with diffusion-weighted imaging
Why
Identify small brainstem, cerebellar, thalamic or occipital infarcts and distinguish selected mimics.
Interpretation and limitations
Early posterior lesions can be diffusion-negative; persistent objective central signs may require repeat MRI or continued stroke management despite an initial negative scan.
04
Structured eye-movement and gait examination
Why
Differentiate central from peripheral acute vestibular syndromes and localise brainstem or cerebellar dysfunction.
Interpretation and limitations
HINTS applies only to continuous acute vestibular syndrome with spontaneous nystagmus and requires trained technique; do not use it for brief positional dizziness or inexpert reassurance.
05
NIH Stroke Scale plus posterior examination
Why
Quantify common stroke deficits while deliberately documenting cranial nerves, gait, truncal stability and swallowing.
Interpretation and limitations
A low NIHSS may coexist with disabling ataxia, diplopia, dysphagia or hemianopia and must not by itself exclude reperfusion assessment.
06
ECG and rhythm monitoring
Why
Detect atrial fibrillation or another cardiac mechanism after a posterior circulation infarct.
Interpretation and limitations
Paroxysmal AF may require longer monitoring; vertebral atherosclerosis and dissection remain alternative mechanisms requiring arterial review.
07
Repeat CT or MRI for deterioration
Why
Identify cerebellar swelling, hydrocephalus, haemorrhagic transformation, recurrent occlusion or infarct extension.
Interpretation and limitations
Do not wait for the scheduled follow-up scan when headache, vomiting, pupils or consciousness worsen.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Peripheral vestibular disorder

Unidirectional nystagmus, abnormal head impulse and preserved stance support peripheral disease; central eye signs or inability to stand favour stroke.

Vestibular migraine

Recurrent episodes with migraine features may mimic posterior ischaemia, but a first focal or persistent syndrome requires vascular assessment.

Brainstem demyelination

Symptoms developing over hours to days with characteristic inflammatory lesions and previous attacks support multiple sclerosis rather than maximal-at-onset stroke.

Toxic or metabolic ataxia

Sedative exposure, alcohol, hypoglycaemia and electrolyte disturbance can produce diffuse imbalance without a coherent vascular localisation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01VERTIGOAcute continuous vestibular syndromeFirst stepNew continuous vertigo, nausea, nystagmus and gait unsteadiness persist for hours rather than brief positional spells.

1Check glucose and observations and examine pupils, ocular alignment and movement, nystagmus, cranial nerves, speech, limbs, coordination and ability to sit or stand safely.
2Use HINTS only if trained and the patient meets its intended syndrome; any central sign or unresolved high-risk presentation needs urgent stroke assessment.
3Obtain brain and head-and-neck vascular imaging, recognising that early CT and occasionally early MRI may miss small posterior infarction.
4Admit or arrange specialist follow-up according to objective findings and diagnostic certainty, with explicit return advice if a peripheral diagnosis is made.

02BASILARSuspected basilar artery occlusionBilateral or fluctuating brainstem signs, reduced consciousness or quadriparesis suggests basilar thrombosis.

1Activate the hyperacute stroke and airway pathways, document last-known-well and premorbid function and obtain rapid focused neurological assessment.
2Perform non-contrast CT and immediate CTA, sending images and clinical details to the comprehensive stroke centre without transfer delay.
3Assess intravenous thrombolysis when eligible and mechanical thrombectomy using the current posterior circulation network criteria.
4Monitor breathing, consciousness, pressure and neurological change in a high-acuity environment before and after reperfusion.

03CEREBELLUMCerebellar infarct with swelling riskImaging shows a substantial cerebellar infarct or symptoms worsen over the following hours or days.

1Admit to a monitored specialist unit and track consciousness, pupils, headache, vomiting, eye movements and brainstem function frequently.
2Repeat CT urgently for deterioration and assess fourth-ventricular effacement, hydrocephalus and brainstem compression.
3Discuss early with neurosurgery because suboccipital decompression and/or ventricular drainage may be life-saving in selected patients.
4DefinitiveAvoid lumbar puncture and do not rely on temporary osmotic measures as a substitute for definitive surgical assessment.

04AFTERMechanism and recoveryThe posterior circulation infarct is stable after acute reperfusion and complication decisions.

1Review vertebral and basilar anatomy, dissection clues, cardiac rhythm and conventional vascular risk factors to define the most likely mechanism.
2Choose antiplatelet or anticoagulant secondary prevention according to that mechanism and begin high-intensity lipid and blood-pressure management.
3Assess swallowing, speech, vision, vestibular symptoms, gait and falls and provide targeted multidisciplinary rehabilitation.
4Address driving, work, recurrence symptoms and follow-up imaging or rhythm monitoring in a clear discharge plan.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces early recurrent thrombosis while the longer-term non-cardioembolic antiplatelet strategy is determined.

Aspirin

After haemorrhage has been excluded, give 300 mg once daily by a swallow-safe route for acute ischaemic stroke, delaying until 24-hour imaging after thrombolysis.

Do not give before haemorrhage exclusion or prematurely after thrombolysis; consider allergy, bleeding, planned anticoagulation and enteral access.

Provides time-dependent intravenous reperfusion when the specialist stroke team judges the posterior deficit disabling and treatment criteria are met.

Alteplase

For an eligible disabling posterior circulation ischaemic stroke, use 0.9 mg/kg intravenously to a maximum 90 mg, with 10% as a bolus and the remainder over 60 minutes.

Apply the complete thrombolysis protocol for imaging, pressure, anticoagulants, bleeding and follow-up; posterior location does not remove haemorrhage risk.

Controls severe nausea and vomiting accompanying acute cerebellar or vestibular stroke while diagnostic and reperfusion work proceeds.

Antiemetic therapy

Use an adult formulary dose by a safe route, selecting the agent around QT interval, extrapyramidal risk, sedation, swallowing and Parkinsonian features.

Do not allow symptom relief to postpone imaging, and reassess recurrent vomiting as a possible sign of swelling or raised intracranial pressure.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Basilar occlusion and locked-in syndrome

Progressive brainstem infarction can cause quadriplegia, anarthria, coma or death despite initially mild or fluctuating symptoms.

Cerebellar swelling and hydrocephalus

Posterior-fossa oedema can compress the fourth ventricle and brainstem, causing abrupt reduced consciousness and requiring neurosurgical review.

Dysphagia and aspiration

Bulbar pathway injury causes secretion, nutrition and airway problems with high pneumonia risk after brainstem infarction.

Visual, balance and cognitive disability

Occipital, thalamic and cerebellar injury can leave field loss, dizziness, ataxia, memory difficulty and loss of independence.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat consciousness, pupils, cranial nerves, limb signs, coordination and NIHSS while explicitly recording deficits not captured well by the scale.
Monitor respiratory pattern, oxygen saturation and secretion handling closely in bulbar or basilar disease and escalate airway risk early.
Perform a trained swallowing screen before oral food, drink or medicines and provide alternative hydration and treatment routes after failure.
Observe cerebellar infarcts for delayed headache, vomiting, sixth-nerve palsy or drowsiness and image immediately if these emerge.
Track cardiac rhythm, pressure, temperature and glucose and manage them according to the acute stroke and reperfusion plan.
During recovery, monitor gait, falls, visual field, diplopia, hearing, cognition and fatigue because apparently mild deficits can prevent safe independence.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

FAST has a blind spot

Eye movements, gait, coordination, swallowing and visual fields are essential additions when the vertebrobasilar circulation is clinically plausible.

Crossed signs localise

An ipsilateral cranial-nerve deficit with contralateral limb motor or sensory change points strongly towards a brainstem lesion.

HINTS needs the right patient

It was developed for continuous acute vestibular syndrome with spontaneous nystagmus, not for asymptomatic examination or brief positional vertigo.

MRI can be too early

Small medullary or pontine infarcts may remain diffusion-negative initially, so the examination should drive repeat imaging when signs persist.

Locked-in is conscious

A ventral pontine lesion may abolish speech and limb movement while awareness and vertical eye movements remain, making careful communication crucial.

Cerebellar swelling is delayed

Initial stability does not remove risk because oedema can build over several days within the restricted posterior fossa.

11Common pitfallsFrequent interpretation and management errors.

01
Do not exclude stroke because FAST is negative, limb power is normal or the NIHSS is low.
02
Do not label continuous severe vertigo as benign positional vertigo without defining triggers, nystagmus and gait.
03
Do not use HINTS outside its intended syndrome or when the examiner is not trained to elicit and interpret the signs.
04
Do not let a normal early CT, or even one early negative MRI, overrule persistent objective brainstem or cerebellar findings.
05
Do not postpone CTA in fluctuating bilateral brainstem symptoms, because basilar occlusion can deteriorate catastrophically.
06
Do not give oral water or tablets to a dysarthric or bulbar patient before swallowing screening.
07
Do not wait for profound coma before discussing a swelling cerebellar infarct with neurosurgery.