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Widespread Functional Effects of Discrete Thalamic Infarction
Brigitte Szelies, MD;
Kare Herholz, MD;
Gunther Pawlik, MD;
Hans Karbe, MD;
Ira Hebold, MD;
Wolf-Dieter Heiss, MD
Arch Neurol. 1991;48(2):178-182.
Abstract
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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.
Author Affiliations
From the Clinic and Policlinic for Neurology and Psychiatry and the Max Planck Institute for Neurological Research, Cologne, Federal Republic of Germany.
Footnotes
Accepted for publication June 15, 1990.
Reprint requests to Klinik und Poliklinik für Neurologie und Psychiatrie, Max Planck Institut für Neurologische Forschung, Joseph Stelzmann Str 9,5000 Köln 41, Federal Republic of Germany (Dr Heiss).
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