慢性酒精中毒对脑血流动力学和代谢的影响。

J Lotfi, J S Meyer
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引用次数: 0

摘要

神经系统特别容易受到酒精的有害影响。其中包括Wernicke-Korsakoff综合征,这与慢性酒精滥用继发的硫胺素缺乏有关。酒精对认知障碍的其他神经毒性影响包括震颤谵妄、酒精性癫痫或“朗姆酒发作”,以及酒精性神经病。近年来,人们已经认识到,即使在没有营养缺乏的情况下,酒精及其代谢物也会直接损害神经系统。脑血流量(CBF)测量提供了一种无创的脑代谢活动的间接监测。结论表明,用133Xe吸入法测量的CBF在慢性酒精中毒中下降,与酒精摄入量密切相关。戒断后,如果慢性酒精中毒的神经毒性作用是最近开始的,CBF恢复到正常水平。临床和病理研究表明,即使在年轻的“社交”饮酒者中,酒精滥用后也会导致脑容量显著减少并伴有心室扩张。酒精的这种毒性作用伴随着不同程度的认知障碍,从轻微的记忆丧失到坦率的痴呆。无论是否伴有营养缺乏,脑容量的减少和认知障碍在很大程度上都可以通过节制和营养补充来逆转。酒精似乎会加速与年龄相关的CBF下降,而营养缺乏则会增强酒精的神经毒性作用。吸入稳定的氙气作为对比剂,结合连续的大脑计算机断层成像,可以利用三维方法测量大脑深部结构(包括下丘脑、丘脑、前脑核和边缘系统)的局部CBF (LCBF)和分区系数(L lambda)。在慢性酗酒者中,皮层和皮层下灰质CBF有显著的弥漫性减少,尤其是在下丘脑和nominata中,其中包括Meynert基底核,这是新皮层和海马胆碱能输入的主要来源。在有或没有Wernicke-Korsakoff综合征的认知障碍患者中,LCBF的减少是可测量的。CBF包括白质减少,在Wernicke-Korsakoff综合征患者中更为严重。这两种类型的脑病都会随着治疗而改善,但如果没有营养缺乏,恢复通常会更快更彻底。酒精似乎也是中风的一个危险因素,可能是通过消耗神经元储备和不利地影响心血管风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cerebral hemodynamic and metabolic effects of chronic alcoholism.

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.

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