Effects of capsular or thalamic stroke on metabolism in the cortex and cerebellum: a positron tomography study.

Abstract

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. (Stroke 1990^21:519-524)

Mesial temporal cortex hypoperfusion is associated with depression in subcortical stroke.

“…Normalized CBF values in the mesial ). Counts in ROIs belonging to the same anatomicofunctional area were averaged, obtaining 11 regions, as follows: basal temporal (T) region (1); basal frontal (F) region (2); lateral temporal cortex (3,7,14); mesial temporal cortex (4); prefrontal region (5,12,16); motor areas (6,13,17,20); parietal (P) cortex (18,21); occipital (O) cortex (8,15,19); caudate nucleus (9); lenticular nucleus (10); and thalamus (11).…”

Brain stem infarction and diaschisis. A SPECT cerebral perfusion study.

“…Yet a positron emission tomography study on capsular and thalamic strokes suggests that the thalamocortical projections must sustain damage before hypometabolism of the overlying cortical mantle develops. 19 The authors of the same study speculate that cortical hypoactivity per se might suffice to cause a contralateral cerebellar diaschisis. The inverse could have been observed by us; ie, cerebellar deactivation after upper pontine stroke may have back-projected to cortical areas through intact cerebellocerebral connections.…”

Crossed hemispheric diaschisis in unilateral cerebellar lesions.

“…23 ' 6 Interruption of the corticopontocerebellar tracts was, indeed, proposed as an explanation of this remote effect. 1 Nonetheless, the fact that reduced cerebellar metabolism or low flow can be found in strictly thalamic lesions 512 - 13 suggested that a retrograde mechanism or cortical hypometabolism may also play a part. 6 The reduction in hemispheric CBF that we observed had a number of particular features that should be emphasized.…”