CENTRAL AND PERIPHERAL NERVOUS SYSTEM FUNCTION IN ABSTINENT ALCOHOLICS

酗酒者的行为缺陷已经被概念化， 两种神经病理学上不同的综合征：酒精性痴呆 和科萨科夫精神病（酒精遗忘症）。 酒精 痴呆的特征是弥漫性皮质损伤， 与酒精的神经毒性有关;科萨科夫精神病是 与营养（硫胺素）引起的皮质下病变相关 缺陷 严重记忆障碍， 其他智力功能与科萨科夫的精神病 酒精性痴呆（临床上可能无法区分 从最常见的痴呆症的原因，阿尔茨海默氏病）。 我们 最近发现科尔萨科夫病患者的睡眠 与正常人相比， 志愿者，而阿尔茨海默病患者有正常的乳酸。 此外，阿尔茨海默病患者的δ睡眠减少，但 在科萨科夫患者中是正常的 我们还证明了减少 褪黑激素的主要尿代谢物的每日排泄， 羟褪黑激素治疗科萨科夫精神病 这 提示松果体功能受损。 遗传 硫胺素代谢的差异可能使患者 发展成科萨科夫精神病 大多数科萨科夫病患者 我们研究过的精神病患者曾服用过转酮酶 降低对焦磷酸硫胺素的亲和力。 大多数 有认知障碍的酗酒者表现出 这两种症状的特征。 药理学调节 神经递质系统可能是有效的治疗 皮质下综合征，而酒精性痴呆可能需要 治疗策略类似于阿尔茨海默病。 这 方案旨在利用临床，神经放射学， 生理学和神经药理学测试来区分 这两个病理实体，遵循纵向过程， 将治疗方案中的变量与结果联系起来。

Behavioral deficits in alcoholics have been-conceptualized in terms of two neuropathologically distinct syndromes: alcoholic dementia and Korsakoff's psychosis (alcohol amnestic disorder). Alcoholic dementia is characterized by diffuse cortical damage primarily related to the neurotoxicity of alcohol; Korsakoff's psychosis is associated with subcortical lesions due to nutritional (thiamine) deficiency. Severe memory impairment with relative sparing of other intellectual functions distinguishes Korsakoff's psychosis from alcoholic dementia (which may be clinically indistinguishable from the most common cause of dementia, Alzheimer's disease). We have recently found that sleep in Korsakoff patients is characterized by a reduced REM latency compared to normal volunteers, whereas Alzheimer patients have normal latencies. Furthermore, delta sleep is reduced in Alzheimer's disease, but is normal in Korsakoff patients. We have also demonstrated reduced daily excretion of the major urinary metabolite of melatonin, hydroxymelatonin, in patients with Korsakoff's psychosis. This finding is suggestive of impaired pineal function. Genetic differences in thiamine metabolism may predispose patients to develop Korsakoff's psychosis. Most patients with Korsakoff's Psychosis whom we have studied have had a transketolase with reduced affinity for thiamine pyrophosphate. The majority of alcoholics with cognitive impairment demonstrate features characteristic of both syndromes. Pharmacologic modulation of neurotransmitter systems may be effective in treatment of the subcortical syndrome, whereas alcoholic dementia may require treatment strategies similar to those in Alzheimer's disease. This protocol is intended to utilize clinical, neuroradiological, physiological, and neuropharmacological tests to differentiate these two pathologic entities, to follow a longitudinal course, and to relate variables in treatment protocols to outcome.