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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Brain glucose metabolism in postanoxic syndrome. Positron emission tomographic study.

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.[1]


  1. Brain glucose metabolism in postanoxic syndrome. Positron emission tomographic study. DeVolder, A.G., Goffinet, A.M., Bol, A., Michel, C., de Barsy, T., Laterre, C. Arch. Neurol. (1990) [Pubmed]
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