Brain, Vol. 116, No. 6, 1509-1525, 1993
© 1993 Guarantors of Brain
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The case of aphasia or neglect after striatocapsular infarction
1Department of Neurology, University of Essen Germany 2Department of Neurology Germany 3Department of Nuclear Medicine Germany 4Department of Neuroradiology, RWTH Aachen Germany
Correspondence to:
Correspondence to: Dr med Cornelius Weiller, Neurologische Klinik und Poliklinik, Hufelandstrasse 55, D-45147 Essen, Germany.
The occurrence of aphasia or neglect was related to anatomo-structural (CT/MRI), functional [regional cerebral blood flow (rCBF)] and pathogenetic features [duration of middle cerebral artery (MCA) occlusion and degree of cortical leptomeningeal anastomoses] in 57 cases (26 with and 31 without aphasia or neglect) with strictly subcortical infarcts of one defined type, i.e. striatocapsular infarcts. No distinct pattern of language disturbances was found. Aphasic syndromes did not differ in the amount of involvement of the putamen, pallidum, head of caudate nucleus and white matter. Patients with aphasia or neglect had larger infarcts than those without. However, there was no specific involvement of the basal ganglia, the internal capsule or the deep white matter in patients with aphasia or neglect. Patients with aphasia or neglect had a significantly longer duration of MCA occlusion and mostly poor leptomeningeal collaterals. The cortical rCBF was significantly decreased in the cortical MCA territory in the patients with aphasia or neglect only. The rCBF remained low at follow-up after 1 year and corresponded to focal cortical atrophy on MRI, although neglect had subsided completely in all patients and aphasia had improved considerably in almost 75% of the cases. Aphasia or neglect after striatocapsular infarcts are most likely due to selective neuronal loss of the cerebral cortex due to prolonged MCA occlusion and insufficient collateral blood flow. Individual differences in recovery from aphasia after striatocapsular infarction can be explained in terms of the number of surviving cortical neurons.
Received March 22, 1993. Revised June 15, 1993. Accepted July 31, 1993.
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