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Brain Glucose Metabolism in Postanoxic SyndromePositron Emission Tomographic Study
Anne G. DeVolder, MD;
André M. Goffinet, MD, PhD;
Anne Bol, PhD;
Christian Michel, PhD;
Thierry de Barsy, MD, PhD;
Christian Laterre, MD, PhD
Arch Neurol. 1990;47(2):197-204.
Abstract
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Thirteen positron emission tomographic studies of cerebral glucose utilization were carried out in 12 patients with postanoxic syndrome due to cardiac arrest. Seven subjects were in a persistent vegetative state. The 5 other subjects were normally conscious, but disclosed focal neurological signs. When compared with normal values, mean cerebral glucose metabolism was drastically decreased (±50%) in vegetative subjects, and to a lesser degree (±25%) in conscious patients. The most consistent regional alterations were found in the parieto-occipital cortex (9 cases), the frontier between vertebral and carotid arterial territories, followed by the frontomesial junction (5 cases), the striatum (3 cases with dystonia), thalamus (2 cases), and visual cortex (2 cases with cortical blindness). These data suggest that brain anoxia can result in global brain hypometabolism, which appears related to the vigilance state, as well as in regional alterations preferentially located in arterial border zones.
Author Affiliations
From the Positron Tomography Laboratory, University of Louvain (Belgium) (Drs DeVolder, Goffinet, Bol, and Michel), and the Neurology Service, Cliniques Universitaires St Luc, Louvain-en-Woluwe, Belgium (Drs Laterre and de Barsy).
Footnotes
Accepted for publication July 11, 1989.
Reprint requests to Positron Tomography Laboratory, University of Louvain, 2 Chemin du Cyclotron, B-1348 Louvain-la-Neuve, Belgium (Dr DeVolder).
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