Infarctions in the territory of the posterior cerebral artery (PCA) occur in about 5-10% of all ischemic strokes. The PCA can be divided into 'deep' (P1 and P2 segments) and 'superficial' (P3 and P4) segments. Occlusion of paramedian perforating arteries arising from P1 causes rostral midbrain infarction with or without thalamic lesion. The classical clinical triad after thalamomesencephalic infarcts is hypersomnolence, cognitive deficits and vertical oculomotor paresis. Two main arterial groups arise from P2: infarction in the territory of the thalamogeniculate arteries causes severe contralateral hypesthesia and ataxia, whereas infarction in the territory of the posterior choroidal arteries results in sectoranopia with involvement of the lateral geniculate body. After superficial PCA infarcts, visual field defects and somatosensory deficits are the most frequent signs. Additionally, disorders of reading may be seen after unilateral left infarction and disorientation for place and visual neglect after right lesion. After bilateral PCA infarcts, amnesia, cortical blindness (the patient cannot see but pretend he can) may occur. Acute thrombolysis is as useful after PCA infarctions as after anterior circulation strokes. Mortality after PCA strokes is low, but long-term behavioral and cognitive deficits are underestimated.