Halliday G, Ellis J, Harper C
Department of Pathology, University of Sydney, NSW, Australia.
Brain Res. 1992 Dec 11;598(1-2):33-7. doi: 10.1016/0006-8993(92)90164-5.
The loss of noradrenergic locus coeruleus neurons has been identified as the possible critical lesion inducing amnesia in alcoholic patients with the Wernicke-Korsakoff syndrome. The present study aims to test this hypothesis by quantifying the number of pigmented locus coeruleus neurons in 4 alcoholics with the Wernicke-Korsakoff syndrome, 5 alcoholics with Wernicke's encephalopathy alone but no amnesia, and 1 alcoholic and 5 age-matched controls with no neurological disorders. Apart from an increased vascularity in the locus coeruleus of alcoholics, no significant differences in the number, morphology or distribution of pigmented locus coeruleus neurons was noted between any of the groups analysed. There was a significant correlation between the number of locus coeruleus neurons and brain weight. These data demonstrate that neither alcohol neurotoxicity nor thiamine deficiency result in a reduction in the number of pigmented cells in the locus coeruleus and refute the hypothesis that locus coeruleus cell loss is critical for the amnesia in the Wernicke-Korsakoff syndrome.
去甲肾上腺素能蓝斑神经元的丧失已被确定为导致韦尼克-科尔萨科夫综合征酒精中毒患者失忆的可能关键病变。本研究旨在通过量化4例患有韦尼克-科尔萨科夫综合征的酗酒者、5例仅患有韦尼克脑病但无失忆的酗酒者、1例酗酒者以及5例无神经疾病的年龄匹配对照者的蓝斑色素神经元数量来验证这一假设。除了酗酒者蓝斑血管增多外，在所分析的任何组之间，蓝斑色素神经元的数量、形态或分布均未发现显著差异。蓝斑神经元数量与脑重量之间存在显著相关性。这些数据表明，酒精神经毒性和硫胺素缺乏均不会导致蓝斑色素细胞数量减少，并反驳了蓝斑细胞丧失对韦尼克-科尔萨科夫综合征失忆至关重要的假设。
