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.