Riemann D, Schnitzler M, Hohagen F, Berger M
Psychiatrische Klinik, Universität Freiburg.
Fortschr Neurol Psychiatr. 1994 Dec;62(12):458-78. doi: 10.1055/s-2007-1002303.
Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a Major Depressive Disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous subtype of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison to other psychopathological groups is also challenged. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state-markers or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.
快速眼动(REM)睡眠异常,即REM潜伏期缩短、首个REM期时长延长以及REM密度增加,在重度抑郁症(MDD)患者中经常观察到,这已引起了相当大的关注。最初希望这些异常的睡眠模式构成抑郁症原发性/内源性亚型的特异性标志物,但这一希望并未实现。与其他精神病理学群体相比,REM睡眠抑制对抑郁症的特异性也受到了挑战。年龄和性别等人口统计学变量对睡眠生理有很大影响,在寻找抑郁睡眠的特异性标志物时必须加以控制。睡眠异常是抑郁症的状态标志物还是特质标志物,仍然是一个悬而未决的问题。除了基线研究外,胆碱能REM诱导试验(CRIT)表明,与健康对照组和其他精神病理学群体相比,抑郁症患者的REM睡眠系统对胆碱能刺激的反应性增强,但精神分裂症患者除外。大多数抗抑郁药具有众所周知的REM睡眠抑制作用,这支持了REM睡眠在抑郁症中具有特殊作用的观点。通过唤醒进行选择性REM剥夺的抗抑郁作用强调了REM睡眠调节机制对于理解抑郁症病理生理学的重要性。此外,全睡眠剥夺对抑郁情绪的积极作用可被白天小睡逆转,这进一步强调了睡眠与抑郁症之间的关系。上述实验证据催生了几种理论,如REM剥夺假说、双过程模型和非REM-REM睡眠调节的相互作用模型,以解释抑郁症患者异常的睡眠模式。将参照该领域收集的实证数据对不同模型进行讨论。