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The reactivity of cerebral blood vessels to changes in PaCO2 in areas of the cerebral cortex with or without diaschisis was investigated in 13 patients in a subacute or chronic stage after a small capsular infarct. A focal area of hypoperfusion (area of diaschisis) was detected in the ipsilateral sensorimotor cortex in each patient. Hyperventilation caused a significant reduction of regional cerebral blood flow in the area without diaschisis and only a tendency for regional cerebral blood flow to decrease in the area with diaschisis; CO2 inhalation induced a slight increase in regional cerebral blood flow in the area without diaschisis and a significant increase in regional cerebral blood flow in the area with diaschisis. Regional cerebral blood flow reactivity to hypocapnia was significantly less in the area with diaschisis than in the area without, whereas the hypercapnic response was more marked in the area with diaschisis than in the area without. Our results suggest that in the area with diaschisis, the arterioles may be abnormally vasoconstricted at rest such that they cannot constrict further in response to hypocapnia but can dilate more during hypercapnia than in the area without diaschisis. This excessive resting vasoconstriction may result from decreased tissue elaboration of CO2 due to local decrease of metabolic function.

Vascular response to carbon dioxide in areas with and without diaschisis in patients with small, deep hemispheric infarction.