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酒精对大脑的神经生理和神经化学影响与当前基于证据的梦游模型不一致。

The neurophysiological and neurochemical effects of alcohol on the brain are inconsistent with current evidence based models of sleepwalking.

机构信息

Sleep Medicine Services, Lankenau Medical Center, Wynnewood, PA, USA; Lankenau Institute for Medical Research, Wynnewood, PA, USA; Department of Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA; Charles Widger School of Law, Villanova University, Villanova, PA, USA.

出版信息

Sleep Med Rev. 2019 Feb;43:92-95. doi: 10.1016/j.smrv.2018.10.003. Epub 2018 Nov 10.

DOI:10.1016/j.smrv.2018.10.003
PMID:30537569
Abstract

The DSM-5 and ICSD-3 have removed alcohol from the list of potential triggers for sleepwalking due to the lack of empirical evidence. Recent imaging and EEG based studies of sleepwalking and confusional arousals have provided a more data-based method of examining if alcohol is compatible with what is known about the neurophysiology and neurochemistry of sleepwalking. These studies have demonstrated a deactivation of the frontal areas of the brain, while the cingulate or motor cortex remains active and characterized activation in the form of beta EEG. This increase in activation is attributed to a decrease in the inhibitory activity the neurotransmitter GABAA. This cerebral excitability of the cingulate cortex of sleepwalkers is also present in the brains of sleepwalkers during wakefulness compared to normal controls. Alcohol is well established to have an inhibitory effect on the brain and specifically on the motor areas via the inhibitory effects of increased GABAA activity. Thus, the empirical data show sleepwalking is characterized by a decrease in the inhibitory activity of GABAA - permitting or facilitating motor activity while alcohol has the opposite effect of increasing GABAA and inhibiting motor activity. This is inconsistent with theories that alcohol is somehow a trigger or facilitator for sleepwalking.

摘要

DSM-5 和 ICSD-3 已经将酒精从梦游的潜在触发因素列表中删除,因为缺乏经验证据。最近对梦游和意识模糊性觉醒的影像学和 EEG 研究提供了一种更基于数据的方法来检查酒精是否与已知的梦游的神经生理学和神经化学相容。这些研究表明大脑额叶区域失活,而扣带回或运动皮层仍然活跃,并以β脑电的形式表现出特征性激活。这种激活的增加归因于神经递质 GABA-A 的抑制活性的降低。与正常对照相比,梦游者在清醒时的扣带回皮层的这种大脑兴奋性也存在于梦游者的大脑中。酒精通过增加 GABA-A 活性的抑制作用,对大脑特别是运动区域具有抑制作用。因此,经验数据表明,梦游的特征是 GABA-A 的抑制活性降低,从而允许或促进运动活动,而酒精则通过增加 GABA-A 和抑制运动活动产生相反的效果。这与酒精以某种方式是梦游的触发因素或促进因素的理论不一致。

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