Halliday G, Cullen K, Harding A
Department of Pathology, University of Sydney, Australia.
Alcohol Alcohol Suppl. 1994;2:245-51.
The Wernicke-Korsakoff syndrome is a neuropathological term which encompasses two clinical syndromes in thiamine-deficient alcoholics, Wernicke's encephalopathy and Korsakoff's psychosis. Wernicke's encephalopathy is characterised by eye and gait disorders and mental confusion, and can lead to the profound and permanent amnesia known as Korsakoff's psychosis. Despite this specific difference, both conditions appear to have identical neuropathology with haemorrhages and other lesions around the ventricular system. The memory deficit has been attributed to a number of brain lesions, including a recent suggestion that brain pathways utilising particular neurotransmitters are specifically damaged. To examine this, the number of chemically identified neurons in particular brain regions was quantified in patients with Wernicke's encephalopathy alone or in combination with Korsakoff's psychosis and compared with age- and sex-matched controls. Noradrenaline, a neurotransmitter thought to be involved in the process of selective attention, is localised in pathways projecting to the cortex. Our patients with either Wernicke's encephalopathy or additional Korsakoff's psychosis do not differ from controls in the distribution and number of these cells. Serotonin is another neurotransmitter that has been linked with alcohol dependency. Both patient groups have a profound loss of serotonin-containing neurons compared with controls. The loss of forebrain neurons containing acetylcholine in patients with Alzheimer's disease has implicated this neurotransmitter in the maintenance of memory functions. There was a large variation in the number of these forebrain neurons in thiamine-deficient alcoholics compared with controls. Cholinergic cell loss reflected the severity of cognitive dysfunction, but was not exclusive to patients with amnesia. Two thalamic nuclei are involved in relaying memories for storage and retrieval, the anterior and mediodorsal thalamic nuclei. While patients with Wernicke's encephalopathy often had neuronal loss in the mediodorsal nucleus, only patients with Korsakoff's psychosis had cell loss in both medial thalamic nuclei. The results suggest that cumulative lesions contribute to the amnesia seen in thiamine-deficient alcoholics, including deficits in serotonergic, cholinergic and medial thalamic pathways.
韦尼克 - 科尔萨科夫综合征是一个神经病理学术语，涵盖了硫胺缺乏的酗酒者中的两种临床综合征，即韦尼克脑病和科尔萨科夫精神病。韦尼克脑病的特征是眼部和步态障碍以及精神错乱，并可导致被称为科尔萨科夫精神病的严重且永久性失忆。尽管存在这种特定差异，但两种病症似乎具有相同的神经病理学特征，即脑室系统周围出现出血和其他病变。记忆缺陷归因于多种脑损伤，包括最近有人提出利用特定神经递质的脑通路受到特异性损伤。为了对此进行研究，对仅患有韦尼克脑病或合并科尔萨科夫精神病的患者特定脑区中化学鉴定的神经元数量进行了量化，并与年龄和性别匹配的对照组进行比较。去甲肾上腺素是一种被认为参与选择性注意过程的神经递质，定位于投射到皮层的通路中。我们患有韦尼克脑病或合并科尔萨科夫精神病的患者在这些细胞的分布和数量上与对照组没有差异。血清素是另一种与酒精依赖有关的神经递质。与对照组相比，两组患者含血清素的神经元均有严重缺失。阿尔茨海默病患者前脑含乙酰胆碱的神经元缺失表明这种神经递质与记忆功能的维持有关。与对照组相比，硫胺缺乏的酗酒者中这些前脑神经元的数量存在很大差异。胆碱能细胞损失反映了认知功能障碍的严重程度，但并非失忆患者所特有。两个丘脑核参与记忆的中继存储和检索，即丘脑前核和丘脑背内侧核。虽然韦尼克脑病患者的丘脑背内侧核经常出现神经元损失，但只有科尔萨科夫精神病患者的两个内侧丘脑核都有细胞损失。结果表明，累积性损伤导致了硫胺缺乏的酗酒者出现失忆，包括血清素能、胆碱能和内侧丘脑通路的缺陷。
