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October 1990

The Large Striatocapsular Infarct: A Clinical and Pathophysiological Entity

Author Affiliations

From the Departments of Neurology (Drs Weiller and Ringelstein), Neuroradiology (Dr Thron), and Nuclear Medicine (Drs Reiche and Buell), Klinikum Rheinisch-Westfaelische Technische Hochshule, Aachen, West Germany. Dr Weiller is now a Feodor Lynen research fellow of the Alexander von Humboldt Foundation with the Medical Research Council Cyclotron Unit, Hammersmith Hospital, London, England.

Arch Neurol. 1990;47(10):1085-1091. doi:10.1001/archneur.1990.00530100051013

• We examined 29 patients with strictly subcortical large striatocapsular infarctions. Eight of them had aphasia or neglect. All patients underwent transcranial Doppler ultrasonography or selective carotid angiography, magnetic resonance imaging, and single photon emission tomography for assessment of cerebral blood flow, blood volume, and cerebral perfusion reserve. The signs were compatible with cortical territorial infarctions rather than lacunes. On both magnetic resonance imaging and computed tomographic scans, the lesions corresponded to the territories of the medial and lateral group of the lenticulostriate arteries, Heubner's artery, or the anterior choroidal artery. The infarctions were either due to cerebral embolization into the M1 segment of the middle cerebral artery or due to stenosis at the same site, ie, lesions that acutely and simultaneously occluded the orifices of the lenticulostriate or neighboring arteries. Persistent occlusion of the middle cerebral arteries and a decrease of cortical regional cerebral blood flow were only found in patients with aphasia or neglect. All patients without aphasia or neglect showed a rapid recanalization of the middle cerebral artery occlusion or a stenosis of the M1 segment and no cortical regional cerebral blood flow decrease. Large striatocapsular infarctions occur due to occlusive disease of the middle cerebral artery (large-vessel disease) and not due to a disseminated in situ occlusion of the long penetrating arteries (small-vessel disease), as in lacunes. Neuropsychological deficits can be explained by decreased cortical blood flow due to a persistent occlusive lesion of the middle cerebral artery.