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首页> 外文期刊>Addiction biology >Neurological, nutritional and alcohol consumption factors underlie cognitive and motor deficits in chronic alcoholism
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Neurological, nutritional and alcohol consumption factors underlie cognitive and motor deficits in chronic alcoholism

机译：神经系统，营养和饮酒因子在慢性酗酒中的认知和电机缺陷

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摘要

Variations in pattern and extent of cognitive and motor impairment occur in alcoholism (ALC). Causes of such heterogeneity are elusive and inconsistently accounted for by demographic or alcohol consumption differences. We examined neurological and nutritional factors as possible contributors to heterogeneity in impairment. Participants with ALC (n = 96) and a normal comparison group (n = 41) were examined on six cognitive and motor domains. Signs of historically determined subclinical Wernicke's encephalopathy were detected using the Caine et al. criteria, which were based on postmortem examination and chart review of antemortem data of alcoholic cases with postmortem evidence for Wernicke's encephalopathy. Herein, four Caine criteria provided quantification of dietary deficiency, cerebellar dysfunction, low general cognitive functioning and oculomotor abnormalities in 86 of the 96 ALC participants. Subgroups based on Caine criteria yielded a graded effect, where those meeting more criteria exhibited greater impairment than those meeting no to fewer criteria. These results could not be accounted for by history of drug dependence. Multiple regression indicated that compromised performance on ataxia, indicative of cerebellar dysfunction, predicted non-mnemonic and upper motor deficits, whereas low whole blood thiamine level, consistent with limbic circuit dysfunction, predicted mnemonic deficits. This double dissociation indicates biological markers that contribute to heterogeneity in expression of functional impairment in ALC. That non-mnemonic and mnemonic deficits are subserved by the dissociable neural systems of frontocerebellar and limbic circuitry, both commonly disrupted in ALC, suggests neural mechanisms that can differentially affect selective functions, thereby contributing to heterogeneity in pattern and extent of dysfunction in ALC.
机译：酗酒（ALC）发生认知和电机损伤模式和程度的变化。这种异质性的原因是难以捉摸的，并且通过人口或酒精消费差异不一致地占据。我们认为神经系统和营养因素作为可能的损伤异质性可能的贡献者。在六个认知和电动机域上检查ALC（n = 96）和正常比较组（n = 41）的参与者。使用Caine等人检测到历史上确定的亚临床脑脊质的脑病的迹象。标准，基于淘汰妇女患者患者患者脑病脑病的后期审查和图表审查。在此，四个CAINE标准提供了量化膳食缺乏，小脑功能障碍，低一般认知功能和96 ALC参与者86中的通用认知功能和动血管异常。基于CAINE标准的亚组产生了分级效应，其中满足更多标准的人表现出比满足更少标准的人更大的减值。这些结果无法通过药物依赖的历史来占据。多元回归表明，损害了患者的性能，指示小脑功能障碍，预测的非助记符和上部电机缺陷，而全血硫胺水平低，与肢体电路功能障碍一致，预测的助记符。这种双重解离表明在ALC中表达功能损伤的异质性有助于异质性。非助记符和助记符缺陷由可解离的前脑和肢体电路的神经系统所携带，这两者都在ALC中突破，表明可以差异地影响选择性功能的神经机制，从而有助于ALC功能障碍的模式和程度的异质性。

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