A CONTROLLED STUDY OF THE ANTIDEPRESSANT EFFICACY OF SLEEP DEPRIVATION

而大约60%的抑郁症患者经历了 睡眠剥夺(SD)后的抗抑郁反应 这种干预的效用受到这样一个事实的限制，即大多数 经过一夜的恢复睡眠后，患者会复发。这些活动的目的是 研究旨在测试SD的两种可能的临床应用：(1)其 有能力加速抗抑郁药物的起效，以及 (2)其增强抗抑郁药物作用的能力 部分有反应的病人。 因为病人不能无视这样一个事实，他们正在 睡眠不足，很难设计出适当的控制条件 对于SD。文献表明，下半夜的SD (晚期SD，或LSD)是一种比上半年SD更有效的治疗方法 夜晚(早期的SD，或ESD)。因此，这些实验也测试了 使用ESD作为LSD的控制条件的效用。两种情况下的患者 方案被随机分配给ESD或LSD，并遵循 连续两个晚上连续两个晚上的SD时间表 几周。对情绪和行为进行了广泛、系统的监测 在SD之前，以及在最后一次SD之后的三周。 在第一个方案中，患者在治疗开始时是不用药的 研究开始前四天开始服用氟西汀20 mg，每日一次。 SD的第一个晚上。24名患者完成了治疗方案，其中11名 其中13人处于LSD状态，13人处于ESD状态。没有 ESD组与LSD组之间存在显著差异 他们对氟西汀的反应过程。因此，在患者病情好转的同时 值得注意的是，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。在这一点上没有 表明SD可用于加速行动的开始 氟西汀。 接受第二方案的所有患者都在接受稳定的方案 服用抗抑郁药物至少8周，而且他们 在整个研究过程中继续使用这种养生法。26名患者 完成了这一方案，14人处于ESD状态，12人处于 迷幻药状态。两组的反应无显著差异。 这两组人，所以ESD似乎不是一个足够的控制 在这一人群中出现LSD的情况。然而，SD治疗确实做到了 似乎显著降低了受试者的汉密尔顿抑郁评分 刻度分数。这种影响仍然显著，即使在患者 进入这项研究(所谓的安慰剂)后，分数下降了30%或更多 应答者“)被排除。因此，SD似乎可能会增强 抗抑郁药物的疗效。催乳素、皮质醇、促甲状腺激素和 FT3级别在上午8：00绘制在基线和SD之后的早晨 在研究过程中变化很大，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.