Posterior Circulation Stroke

Posterior circulation strokes involve the vertebrobasilar arterial system supplying the brainstem, cerebellum, thalamus, and occipital lobes, and account for approximately 20% of all ischemic strokes. The vertebral arteries join to form the basilar artery, which gives rise to the posterior cerebral arteries; occlusion at various levels produces distinct clinical syndromes. Basilar artery occlusion (the most devastating) can cause locked-in syndrome, coma, or death. Cerebellar infarction causes vertigo, ataxia, nystagmus, and headache, with risk of posterior fossa edema causing brainstem compression and obstructive hydrocephalus. Posterior cerebral artery occlusion causes contralateral homonymous hemianopia from occipital cortex ischemia and may affect the thalamus (causing contralateral sensory loss and thalamic pain syndrome). The nurse recognizes that posterior circulation strokes are frequently missed initially because they may present with non-specific symptoms (dizziness, nausea, headache, diplopia) rather than classic hemiparesis, performs serial neurological assessments including cerebellar function (finger-to-nose, heel-to-shin, rapid alternating movements), monitors for signs of cerebellar edema and brainstem compression (declining consciousness, irregular respirations, new cranial nerve deficits), monitors swallowing function (dysphagia is common), and escalates clinical deterioration immediately for possible surgical decompression.