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睡眠剥夺作为原发性酗酒者稳态睡眠调节的一种探究手段。

Sleep deprivation as a probe of homeostatic sleep regulation in primary alcoholics.

作者信息

Irwin Michael, Gillin J Christian, Dang Jeff, Weissman Jeffrey, Phillips Evie, Ehlers Cindy L

机构信息

Cousins Center for Psychoneuroimmunology, Department of Psychiatry and Biobehavioral Sciences, University of California, 300 UCLA Medical Plaza, Los Angeles, CA 90095, USA.

出版信息

Biol Psychiatry. 2002 Apr 15;51(8):632-41. doi: 10.1016/s0006-3223(01)01304-x.

DOI:10.1016/s0006-3223(01)01304-x
PMID:11955463
Abstract

BACKGROUND

Alcoholic patients show prominent disturbances of sleep electroencephalograms (EEGs) with a marked loss of slow wave sleep that is even more profound in African American alcoholics as compared to European Americans. Using partial sleep deprivation, this study examined the extent to which abnormal sleep is reversible in alcoholic subjects.

METHODS

In a sample stratified on ethnicity, polysomnographic and spectral sleep EEG measures were compared in male primary alcoholic in patients (n=46) and age-matched comparison controls (n=32) at baseline-and recovery sleep following a night of partial sleep deprivation.

RESULTS

As compared to controls, alcoholic patients showed a loss of slow wave sleep and more spectral power in beta frequencies. Following sleep deprivation, slow wave sleep and delta power differentially changed between the groups. European American controls showed increases of slow wave sleep that were more robust than responses found in African American controls, whereas both alcoholic groups failed to show increases of slow wave sleep from baseline to recovery. Spectral EEG analyses revealed similar results; sleep deprivation induced significant increases of delta power during NREM-1 in the controls, but not in the alcoholics.

CONCLUSIONS

Alcohol dependence compromises the augmentation of slow wave sleep and delta power seen in healthy adults following sleep deprivation. The differential effect of alcoholism on sleep stage physiology suggests a defect in the regulation or plasticity of slow wave sleep with implications for theories linking sleep depth to morbidity and outcome in alcoholics.

摘要

背景

酒精性患者的睡眠脑电图(EEG)显示出明显紊乱,慢波睡眠显著减少,与欧裔美国人相比,非裔美国酒精性患者的慢波睡眠减少更为严重。本研究采用部分睡眠剥夺法,探讨酒精性受试者异常睡眠的可逆程度。

方法

在一个按种族分层的样本中,对46名男性原发性酒精性住院患者和32名年龄匹配的对照者在基线时以及部分睡眠剥夺一夜后的恢复睡眠时进行多导睡眠图和频谱睡眠EEG测量,并进行比较。

结果

与对照组相比,酒精性患者慢波睡眠减少,β频率的频谱功率增加。睡眠剥夺后,两组之间慢波睡眠和δ功率有不同变化。欧裔美国对照组慢波睡眠增加,比非裔美国对照组的反应更强烈,而两个酒精性组从基线到恢复睡眠均未显示慢波睡眠增加。EEG频谱分析得出类似结果;睡眠剥夺导致对照组在NREM-1期间δ功率显著增加,但酒精性患者未出现此情况。

结论

酒精依赖会损害健康成年人在睡眠剥夺后出现的慢波睡眠和δ功率增加。酒精中毒对睡眠阶段生理的不同影响表明慢波睡眠的调节或可塑性存在缺陷,这对将睡眠深度与酒精性患者的发病率和预后联系起来的理论具有启示意义。

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