Viot-Blanc V
SHU, Service des Prs H. Loo et J.P. Olie, Hopital Sainte-Anne, Paris.
Encephale. 1995 Dec;21 Spec No 7:35-40.
The relationship between insomnia and depression cannot be summarized as a symptom/disease relationship. It is well admitted now that sleep deprivation has an antidepressant effect on depressed patients. The effect is immediate, global but transient : the relapse occurs after subsequent sleep, diurnal nap or recovery night. On an other hand, sleep architecture is impaired in depressed patients, some of these alterations, especially in REM sleep, might have been considered specific of depressive disease. Antidepressant drugs exert an effect on sleep architecture which is different. This effect varies over time and generally tend to correct sleep impairment. This has led some authors to propose the hypothesis that sleep himself might be involved in the causal process of depression. Three main hypotheses will be considered, excluding those involving circadian rhythm impairment, according to their strong and weak points. For G. Vogel, an excess of REM sleep is the causal process in depression. As a matter of fact, he did show that selective REM sleep deprivation exerts an antidepressant effect following the same temporal profile as antidepressant drugs. An other argument is that the shortening of REM latency and the increased amount of REM sleep in the first half of the night are evidences of the excess of REM sleep and at last, most antidepressant drugs are REM suppressors and may act through REM sleep suppression. The second hypothesis is the process S deficiency proposed by Alexander Borbely, according to his two process model of sleep homeostasis. The impairment of process S, which is reflected by slow wave activity, is responsible for depression. This explain disruptions and shortening of sleep in depressed patients, REM sleep abnormalities being only secondary to the slow wave sleep reduction. More recently, D. Beersma and R. van den Hoofdakker proposed that non REM sleep might be depressogenic after an experiment of selective REM sleep deprivation in normals which showed that non REM sleep deprivation was also largely reduced. REM suppression effects might therefore also be attributed to non REM suppression. All these hypothesis must explain the effect of antidepressant drugs on sleep. There is a large heterogeneity of effects on slow wave, non REM and even REM sleep, hardly compatible with a causal role of sleep, REM or non REM.
失眠与抑郁之间的关系不能简单概括为症状/疾病关系。目前人们普遍承认，睡眠剥夺对抑郁症患者具有抗抑郁作用。这种作用是即时、全面但短暂的：随后的睡眠、日间小睡或恢复性夜间睡眠后会出现复发。另一方面，抑郁症患者的睡眠结构受损，其中一些改变，尤其是快速眼动睡眠（REM睡眠）方面的改变，可能曾被认为是抑郁症的特异性表现。抗抑郁药物对睡眠结构产生的影响则有所不同。这种影响会随时间变化，总体上倾向于纠正睡眠障碍。这使得一些作者提出假说，认为睡眠本身可能参与了抑郁症的病因过程。根据其优缺点，将考虑三个主要假说，不包括那些涉及昼夜节律受损的假说。对于G. 沃格尔来说，快速眼动睡眠过多是抑郁症的病因过程。事实上，他确实表明选择性快速眼动睡眠剥夺会产生与抗抑郁药物相同时间模式的抗抑郁作用。另一个论据是，快速眼动睡眠潜伏期缩短以及夜间前半段快速眼动睡眠量增加是快速眼动睡眠过多的证据，最后，大多数抗抑郁药物都是快速眼动睡眠抑制剂，可能通过抑制快速眼动睡眠起作用。第二个假说是亚历山大·博尔贝利根据他的睡眠稳态双过程模型提出的S过程缺陷。S过程的受损由慢波活动反映出来，是抑郁症的病因。这解释了抑郁症患者睡眠的中断和缩短，快速眼动睡眠异常只是慢波睡眠减少的次要表现。最近，D. 贝尔斯马和R. 范登霍夫达克在对正常人进行选择性快速眼动睡眠剥夺实验后提出，非快速眼动睡眠可能具有致抑郁作用，该实验表明非快速眼动睡眠剥夺也大幅减少。因此，快速眼动睡眠抑制作用也可能归因于非快速眼动睡眠抑制。所有这些假说都必须解释抗抑郁药物对睡眠的影响。这些药物对慢波睡眠、非快速眼动睡眠甚至快速眼动睡眠的影响存在很大异质性，这很难与睡眠、快速眼动睡眠或非快速眼动睡眠的因果作用相契合。
