THE CASE OF APHASIA OR NEGLECT AFTER STRIATOCAPSULAR INFARCTION

Citation
C. Weiller et al., THE CASE OF APHASIA OR NEGLECT AFTER STRIATOCAPSULAR INFARCTION, Brain, 116, 1993, pp. 1509-1525
Citations number
66
Categorie Soggetti
Neurosciences
Journal title
BrainACNP
ISSN journal
00068950
Volume
116
Year of publication
1993
Part
6
Pages
1509 - 1525
Database
ISI
SICI code
0006-8950(1993)116:<1509:TCOAON>2.0.ZU;2-Y
Abstract
The occurrence of aphasia or neglect was related to anatomo-structural (CT/MRI), functional [regional cerebral blood flow (rCBF)] and pathog enetic features [duration of middle cerebral artery (MCA) occlusion an d 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 patter n of language disturbances was found. Aphasic syndromes did not differ in the amount of involvement of the putamen, pallidum, head of caudat e nucleus and white matter. Patients with aphasia or neglect had large r infarcts than those without. However, there was no specific involvem ent of the basal ganglia, the internal capsule or the deep white matte r in patients with aphasia or neglect. Patients with aphasia or neglec t had a significantly longer duration of MCA occlusion and mostly poor leptomeningeal collaterals. The cortical rCBF was significantly decre ased in the cortical MCA territory in the patients with aphasia or neg lect only. The rCBF remained low at follow-up after 1 year and corresp onded to focal cortical atrophy on MRI, although neglect had subsided completely in all patients and aphasia had improved considerably in al most 75% of the cases. Aphasia or neglect after striatocapsular infarc ts are most likely due to selective neuronal loss of the cerebral cort ex due to prolonged MCA occlusion and insufficient collateral blood fl ow. Individual differences in recovery from aphasia after striatocapsu lar infarction can be explained in terms of the number of surviving co rtical neurons.