A CONTROLLED STUDY OF THE ANTIDEPRESSANT EFFICACY OF SLEEP DEPRIVATION

虽然大约60%的抑郁症患者会经历 睡眠剥夺（SD）后的抗抑郁反应，临床 这种干预措施的效用受到限制，因为大多数 病人经过一夜的恢复睡眠后复发。 施行本 研究旨在测试SD的两种可能的临床应用：（1）其 加速抗抑郁药物起效的能力，以及 (2)它能够增强抗抑郁药物的作用， 部分有反应的患者。 因为病人不能忽视他们正在被 睡眠剥夺，很难设计出一个足够的控制条件 对于SD。 文献表明，下半夜的SD (late SD，或LSD）是一种比上半年的SD更有效的治疗方法 夜间（早期SD或ESD）。 因此，这些实验也测试了 使用ESD作为LSD的控制条件的实用性。 鼻饲病人 协议被随机分配到ESD或LSD，然后， 连续两个晚上的SD时间表， 周对情绪和行为进行了广泛而系统的监测 SD前和末次SD后3周。 在第一个方案中，患者在治疗开始时没有药物。 研究，并开始氟西汀20毫克qd前四天， SD的第一天 24名患者完成了方案，11名 在迷幻药状态和13在ESD状态。 没有 ESD组和LSD组之间在 他们对氟西汀的反应过程。 因此，当患者改善 在研究过程中，不可能 区分氟西汀、SD和患者的相对贡献 对这一临床变化的期望。 目前，没有 表明SD可用于加速 氟西汀。 第二个方案中接受的所有患者都接受了稳定的治疗方案 服用抗抑郁药至少八周， 在整个研究中继续这种方案。 26名患者 完成本方案，14人处于ESD条件，12人处于 迷幻药中毒。 在反应中没有显著差异， 这两组，所以ESD似乎不是一个足够的控制 LSD在这一人群中的作用 然而，SD治疗确实 似乎显著降低受试者的汉密尔顿抑郁评分 量表评分。 这种效果仍然显着，即使在患者， 在进入研究时，分数下降30%或更多（所谓的"安慰剂 ”反应者被排除。 因此，SD似乎可以增强 抗抑郁药物的疗效。 催乳素、皮质醇、TSH和 基线时8：00 a.m.和SD后早晨采集的fT3水平 在研究过程中变化显著，但与 临床反应。

While approximately 60% of depressed patients experience an antidepressant response after sleep deprivation (SD), the clinical utility of this intervention has been limited by the fact that most patients relapse after a night of recovery sleep. The purpose of these studies was to test two possible clinical applications of SD: (1) its ability to hasten the onset of action of antidepressant medication, and (2) its ability to potentiate the action of antidepressant medication in partially-responsive patients. Because patients cannot be blind to the fact that they are being sleep-deprived, it is difficult to design an adequate control condition for SD. The literature indicates that SD in the second half of the night (late SD, or LSD) is a more effective treatment than SD in the first half of the night (early SD, or ESD). Thus, these experiments also tested the utility of using ESD as a control condition for LSD. Patients in both protocols were randomly assigned to ESD or LSD, and followed that schedule of SD for two nights in a row during each of two successive weeks. There was extensive, systematic monitoring of mood and behavior prior to the SD, and for three weeks after the last SD. In the first protocol, patients were drug-free at the beginning of the study, and were started on fluoxetine 20mg qd four days before their first night of SD. Twenty-four patients completed the protocol, eleven in the LSD condition and thirteen in the ESD condition. There are no significant differences between the ESD group and the LSD group in the course of their response to fluoxetine. Thus, while patients improved significantly over the course of the study, it was impossible to distinguish the relative contributions of fluoxetine, SD, and patient expectations to this clinical change. At this point there is no indication that SD can be used to hasten the onset of action of fluoxetine. All patients accepted in the second protocol had been on a stable regimen of antidepressant medication for at least eight weeks, and they were continued on this regimen throughout the study. Twenty-six patients completed this protocol, fourteen in the ESD condition and twelve in the LSD condition. There were no significant differences in the response of the two groups, so ESD does not appear to be an adequate control condition for LSD in this population. However, the SD treatment did appear to decrease significantly the subjects' Hamilton Depression Rating Scale scores. This effect remained significant even after patients whose scores dropped 30% or more upon entry into the study (so-called "placebo responders") were excluded. Therefore, it appears that SD may potentiate the efficacy of antidepressant medications. Prolactin, cortisol, TSH and fT3 levels drawn at 8:00 a.m. at baseline and on the mornings after SD varied significantly over the course of the study but were not related to clinical response.