Stroke, Vol 21, 519-524, Copyright © 1990 by American Heart Association
S Pappata, B Mazoyer, S Tran Dinh, H Cambon, M Levasseur and JC Baron
We used positron emission tomography to study the cortical and cerebellar
metabolic rates in 21 strictly selected patients with pure internal
capsular infarct (n = 8), thalamocapsular hemorrhage (n = 6), or pure
thalamic stroke (n = 7). Significant diffuse ipsilateral cortical
hypometabolism relative to 62 controls free of cerebrovascular risk factors
was frequently, although not consistently, found in the 13 patients with
thalamocapsular or thalamic lesions and neuropsychological impairment but
was absent from the eight patients with pure internal capsule infarct and
free of neuropsychological deficit. These data suggest that damage to the
thalamus or the thalamocortical projections is important in the development
of ipsilateral cortical hypometabolism and that the latter may underlie the
associated neuropsychological impairment. Significant contralateral
cerebellar hypometabolism relative to 49 controls was found in three of six
patients with pure internal capsule infarct, suggesting a pathogenetic role
for the corticopontocerebellar system. However, the occurrence of
hypometabolism in two of six patients with thalamic lesions indicates that
this phenomenon may also result either from damage to the ascending
cerebellothalamocortical system or indirectly from hypofunction of the
cerebral cortex. No systematic association was observed between crossed
cerebellar hypometabolism and ipsilateral ataxia.
ARTICLES
Effects of capsular or thalamic stroke on metabolism in the cortex and cerebellum: a positron tomography study
Service Hospitalier Frederic Joliot, Departement de Biologie, Commissariat a l'Energie Atomique, Orsay, France.
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