Synopsis
Recognise vertebrobasilar stroke beyond FAST, localise brainstem, cerebellar and occipital syndromes, and obtain urgent vascular and tissue imaging for reperfusion and swelling management.
- 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.
Key red flags
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.
Investigation priorities
Exclude intracranial haemorrhage and detect a large established posterior infarct, hydrocephalus or another structural lesion.
Management branches
New continuous vertigo, nausea, nystagmus and gait unsteadiness persist for hours rather than brief positional spells.
- Check glucose and observations and examine pupils, ocular alignment and movement, nystagmus, cranial nerves, speech, limbs, coordination and ability to sit or stand safely.
- Use HINTS only if trained and the patient meets its intended syndrome; any central sign or unresolved high-risk presentation needs urgent stroke assessment.
- Obtain brain and head-and-neck vascular imaging, recognising that early CT and occasionally early MRI may miss small posterior infarction.
- Admit or arrange specialist follow-up according to objective findings and diagnostic certainty, with explicit return advice if a peripheral diagnosis is made.
The posterior circulation infarct is stable after acute reperfusion and complication decisions.
- Review vertebral and basilar anatomy, dissection clues, cardiac rhythm and conventional vascular risk factors to define the most likely mechanism.
- Choose antiplatelet or anticoagulant secondary prevention according to that mechanism and begin high-intensity lipid and blood-pressure management.
- Assess swallowing, speech, vision, vestibular symptoms, gait and falls and provide targeted multidisciplinary rehabilitation.