We used single-photon emission computed tomography to measure cerebral blood flow, cerebral blood volume, and cerebral perfusion reserve and transcranial Doppler sonography with CO, stimulation to assess hemispheric vasomotor reactivity in 37 patients and in normal controls. Computed tomography and magnetic resonance imaging were performed to differentiate morphologically low-flow infarcts (n=17) from territorial infarcts (n=20). In patients with either type of infarct, blood flow was decreased and blood volume was increased in the infarcted areas compared with the same areas in the controls. Perfusion reserve and vasomotor reactivity were significantly reduced in patients with territorial infarcts and carotid artery occlusions (n=12) and even more reduced in patients with low-flow infarcts (p< 0.001). Both parameters were normal in patients with cardiac embolic territorial infarcts (n=8). In patients with territorial infarcts, blood flow and perfusion reserve changes were restricted to the infarcted areas, whereas in patients with low-flow infarcts, regions of decreased perfusion reserve considerably exceeded the area of the infarct Low-flow infarcts are related to the hemodynamic effects of severe extracranial carotid artery disease. (Stroke 1991^2:1117-1123)

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.

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CD and PD carotid artery stenosis measurements are highly reproducible, and in our hands provided accuracy equal to PSF.