Paramedian thalamic structures and part of the upper midbrain are frequently supplied by posterior thalamoperforating arteries originating from one common trunk. Local impairment of flow entails a bilateral more or less symmetric thalamic infarction with varying involvement of the midbrain. Diagnosis usually can neither be firmly established on clinical grounds nor by angiography alone. In the present series of four patients the two cases observed before the CT era were diagnosed correctly only at autopsy. Only one patient presented the classical syndrome of hypersomnia, thalamic dementia, and oculomotor nerve paralysis, while in the others clinical signs were probably masked by serious impairment of consciousness. In two cases X-ray computed tomography and magnetic resonance tomography (one case) afforded precise definition of infarct localization and size. Infarction in the described terminal vascular supply territory may be detected more often by these modern diagnostic techniques than anticipated from previous clinico-pathological experience as the underlying cause of coma in the elderly-a group of patients at particular risk for low-flow states. Positron emission tomography repeat studies with 18F-2-fluorodeoxyglucose (one case) revealed complex disturbances of brain energy metabolism; correlative analysis of clinical function and metabolic patterns during the course of the disease may not only advance individual prognostication but also contribute to the understanding and localization of brain function.

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