作者: J.J Kril , G.M Halliday , M.D Svoboda , H Cartwright
DOI: 10.1016/S0306-4522(97)00083-3
关键词: White matter 、 Cerebral cortex 、 Psychosis 、 Wernicke's encephalopathy 、 Endocrinology 、 Wernicke Encephalopathy 、 Neuroscience 、 Temporal lobe 、 Frontal lobe 、 Internal medicine 、 Psychology 、 Brain size 、 General Neuroscience
摘要: There is some controversy in the literature concerning whether chronic alcohol consumption damages cerebral cortex. While decreased neuronal density specific cortical regions well described alcoholics, a recent study by Badsberg Jensen and Pakkenberg using unbiased stereological methods questions neurodegeneration occurs. In order to assess selective cortex of regional volumes estimates number (including identification with calcium-binding proteins) were calculated for 14 alcoholics 21 controls. Cases carefully screened exclude any interfering pathologies. Lifetime maximum daily was determined, homogeneous groups identified (four Wernicke's encephalopathy Korsakoff's psychosis, four alone, six without or controls). Brain volume analysis revealed that discrete significantly smaller compared As previously shown, white matter (particularly frontal lobe) most reduced volume. Alcoholics (either alone combination psychosis) had than controls these complications. Medial temporal lobe thalamus also Regression analyses both negatively correlated consumption. Consistent interpretation previous studies, loss found superior association while no occurred from motor The parvalbumin-, calbindin- calretinin-immunoreactive neurons be unaltered suggesting confined non-GABAergic pyramidal neurons. observed all alcoholic groups, damage not restricted amnesia psychosis. These results are consistent notion associated vulnerability. focus atrophy supported neuropsychological, blood flow, magnetic resonance imaging studies dysfunction may correlate abnormalities working memory.