Autor: |
Szelies, Brigitte, Herholz, Kare, Pawlik, Gunther, Karbe, Hans, Hebold, Ira, Heiss, Wolf-Dieter |
Zdroj: |
Archives of Neurology; February 1991, Vol. 48 Issue: 2 p178-182, 5p |
Abstrakt: |
• In order to investigate functional effects of various thalamic structures on metabolism in remote, morphologically intact cerebral regions, we used positron emission tomography of (18F)-2-fluoro-2-deoxy-D-glucose to study regional cerebral metabolic rates of glucose (rCMRGIu) in 11 patients with chronic unilateral or bilateral infarcts strictly confined to the thalamus. Patients were grouped according to computed tomographic scans showing anterior (three), medial (four), or posterior (four) lesions. Compared with a matched group of 11 healthy subjects (hemispheric CMRGIu 35.2 ± 3.49 μmol/100 g per minute), glucose metabolism was significantly lower in the hemisphere ipsilateral to the infarction (31.2 ± 2.97 μmol/100 g per minute). Patients with bilateral infarcts had lower hemispheric CMRGIu (29.9 ± 2.74 μmol/100 g per minute) than those with unilateral lesions (32.2 ± 2.97 μmol/100 g per minute). Depending on infarct location within the thalamus, there was differential depression of rCMRGIu, with the largest effects on frontal and occipital areas in medial infarctions. Except for ipsilateral thalamic deactivation, metabolic patterns with anterior thalamic infarcts were close to normal, while posterior infarcts mostly depressed rCMRGIu in the visual and in the inferior limbic cortex. Cerebellar metabolic rates were within normal limits in most cases. These patterns of regional cerebral deactivation may be related to categories of thalamic projections—intrathalamic, to limbic system and basal ganglia, diffuse to most cortical areas, and specific to defined neocortical areas. Even small brain lesions may have widespread functional sequelae, potentially demonstrable by positron emission tomography. |
Databáze: |
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