title: [Hemodynamic and metabolic changes in crossed cerebellar hypoperfusion--similarity to the early stage of olivo-ponto-cerebellar atrophy].
abstract: Using positron emission tomography in twenty-four unilateral supratentorial stroke patients, we evaluated regional blood flow, metabolic rate of oxygen, oxygen extraction fraction, and blood volume in the cerebellar cortex and pons. Sixteen patients with a significant cerebellar blood flow asymmetry, which lay beyond the upper ninety-five percent confidence limits defined in eight normal subjects, were selected as the group with crossed cerebellar hypoperfusion. In these patients, cerebellar metabolic rate of oxygen was also significantly decreased in the cerebellar cortex contralateral to the supratentorial stroke, compared with the ipsilateral cerebellar cortex, although to a lesser degree than the cerebellar blood flow. The degrees of cerebellar asymmetry in these two parameters were negatively correlated with the metabolic rate of oxygen in the pons. Oxygen extraction fraction was slightly, but significantly, increased in the cerebellar cortex contralateral to the stroke. In contrast to the ischemic state, cerebellar blood volume was decreased, with no difference in the ratio of cerebellar blood flow to blood volume. These findings suggest 1) interruption of the cortico-ponto-cerebellar tract as the mechanism of crossed cerebellar hypoperfusion and 2) mild elevation in the oxygen extraction fraction in this state, with a mechanism distinct from primary hypoperfusion. We also studied six patients with sporadic olivo-ponto-cerebellar atrophy who were in the incipient stage of the disease with slight cerebellar atrophy on magnetic resonance images. The cerebellar cortex in these patients showed the same hemodynamic and metabolic changes as in crossed cerebellar hypoperfusion, suggesting the cerebellar metabolic depression by transneuronal mechanism in the early stage of olivo-ponto-cerebellar atrophy.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University.
authors.forename: H
authors.initials: H
authors.lastname: Yamauchi
authors.forename: H
authors.initials: H
authors.lastname: Fukuyama
authors.forename: K
authors.initials: K
authors.lastname: Harada
authors.forename: S
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: J
authors.initials: J
authors.lastname: Kimura
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism*; D002531:Cerebellum / Q000098:blood supply*; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009849:Olivopontocerebellar Atrophies / Q000378:metabolism / Q000503:physiopathology*; D010100:Oxygen / Q000378:metabolism
chemical_list: D010100:Oxygen