Relation of Cerebral Blood Flow to Motor and Cognitive Functions in Chronic Stroke Patients

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Background and Purpose

The aim of this study was to examine the levels of cerebral blood flow in relation to motor and cognitive functions in 300 chronic unilateral stroke patients (age, 64 $$ 12 years; mean $$ SD).


Cerebral blood flow was measured by the 133Xe inhalation method, adjusted for age, sex, and Pco2 level. Motor function was scored according to Brunnstrom hemiplegic staging and cognitive function according to the Hasegawa dementia rating scale tested in Japanese.


Asymmetries of blood flow between affected and nonaffected hemispheres increased with lesion size and were highest in 11 embolic strokes (20 $$ 9%) and higher in 80 nonembolic cortical infarctions (11 $$ 11%) and 76 hemorrhages (9 $$7%) than in the group of 133 subcortical infarctions (2$$6%) or 16 control subjects (1$$2%). Severity of hemipare-sis correlated with decreased cerebral blood flow in the affected hemisphere (P<.01) and increased hemispheric asymmetries of blood flow (P<.001). Cognitive impairments, after adjusting for age, correlated with decreased cerebral blood flow in the nonaffected hemisphere (P<.0001), left hemispheric lesions (p><.0005), and embolic stroke (P<.005) but not with asymmetries of blood flow. Among 67 patients having bilateral reductions of cerebral blood flow, 25 patients with left hemispheric lesions showed more severe cognitive impairments than among 42 patients with right hemispheric lesions (P<.05).


We confirmed that severity of hemiparesis correlated with the degree of asymmetries of cerebral blood flow, reflecting the extent and location of the lesions. Bilateral reductions of cerebral blood flow in patients with left hemispheric lesions may in part contribute to cognitive impairments, indicating reductions of global neuronal activities in the contralateral hemisphere or diffuse cerebrovascular changes. Further studies of cerebral metabolism and follow-up of cerebral circulation are required to reveal the pathophysiology and clinical consequences. (Stroke. 1994;25:309-317.)

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