BACKGROUND AND PURPOSE: The clinical significance of the periventricular hyperintensity incidentally found on magnetic resonance images of the brain is questionable. We evaluated resting cerebral blood flow and cerebrovascular dilatory capacity of subjects with asymptomatic periventricular hyperintensities to study their cerebral hemodynamics. METHODS: Magnetic resonance imaging of the brain was performed in 28 asymptomatic subjects with cerebrovascular risk factors to determine the severity of periventricular hyperintensity. Mean gray matter flow was computed by a 133Xe-clearance technique in subjects at rest and after the administration of 1 g acetazolamide. Flow values were correlated with the scores for periventricular hyperintensity. RESULTS: Resting gray matter flow was not significantly correlated with the severity of periventricular hyperintensity for the whole brain (rs = -.364), whereas flow after acetazolamide loading (rs = -.783, P < .001) and the absolute value of increased flow (rs = -.567, P < .01) were significantly and negatively correlated with the severity of periventricular hyperintensity. CONCLUSIONS: A decrease in vasodilatory capacity and compensatory vasodilation occur in the cerebral cortex of subjects with asymptomatic periventricular lesions and maintain cerebral blood flow.
BACKGROUND AND PURPOSE: The clinical significance of the periventricular hyperintensity incidentally found on magnetic resonance images of the brain is questionable. We evaluated resting cerebral blood flow and cerebrovascular dilatory capacity of subjects with asymptomatic periventricular hyperintensities to study their cerebral hemodynamics. METHODS: Magnetic resonance imaging of the brain was performed in 28 asymptomatic subjects with cerebrovascular risk factors to determine the severity of periventricular hyperintensity. Mean gray matter flow was computed by a 133Xe-clearance technique in subjects at rest and after the administration of 1 g acetazolamide. Flow values were correlated with the scores for periventricular hyperintensity. RESULTS: Resting gray matter flow was not significantly correlated with the severity of periventricular hyperintensity for the whole brain (rs = -.364), whereas flow after acetazolamide loading (rs = -.783, P < .001) and the absolute value of increased flow (rs = -.567, P < .01) were significantly and negatively correlated with the severity of periventricular hyperintensity. CONCLUSIONS: A decrease in vasodilatory capacity and compensatory vasodilation occur in the cerebral cortex of subjects with asymptomatic periventricular lesions and maintain cerebral blood flow.
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