Okuda B, Tanaka H, Tachibana H, Kawabata K, Sugita M
Fifth Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Stroke. 1994 Jul;25(7):1495-9. doi: 10.1161/01.str.25.7.1495.
Global aphasia after subcortical stroke is very rare, and its pathophysiology remains unsolved. To clarify the mechanism underlying subcortical global aphasia, we investigated lesion sites and cerebral blood flow in patients with subcortical global aphasia and nonaphasic patients with subcortical stroke.
We examined four patients with global aphasia and four nonaphasic patients. Language testing was performed more than 4 weeks after the onset. Measurement of cerebral blood flow was done between 35 and 75 days after stroke by using single-photon emission computed tomography (SPECT) with N-isopropyl-p[123I]iodoamphetamine as a tracer and three-dimensional surface display generated from SPECT.
All aphasic patients had subcortical lesions in the putamen, posterior internal capsule, temporal isthmus, and periventricular white matter in the left hemisphere. No cortical lesions were found on either magnetic resonance imaging or computed tomographic scanning. The nonaphasic patients had smaller periventricular white matter lesions and no temporal isthmus lesions. All aphasic patients showed cortical hypoperfusion mainly in the perisylvian areas, including Broca's and Wernicke's areas. In contrast, cortical cerebral blood flow of the nonaphasic patients was decreased in smaller areas and spared the perisylvian language areas.
These results suggest that cortical hypoperfusion in the perisylvian language areas, presumably due to undercutting of the white matter, is crucial for the development of subcortical global aphasia.
