A CONTROLLED STUDY OF THE ANTIDEPRESSANT EFFICACY OF SLEEP DEPRIVATION

虽然大约60%的抑郁症患者使用抗抑郁药， 睡眠剥夺（SD）后的反应，这种临床效用 由于大多数患者在治疗后复发， 一夜的恢复睡眠 本研究的目的是测试两个 SD可能的临床应用：（1）其加速发病的能力 抗抑郁药物的作用，以及（2）它的能力， 增强抗抑郁药物在部分反应中的作用 患者 因为病人不能忽视他们正在睡觉的事实 因此，很难为SD设计一个适当的控制条件。 有文献表明，睡眠不足的下半年， 睡眠剥夺（late sleep deprivation，LSD）是一种更积极的治疗方法。 比前半夜的睡眠剥夺（早睡） 或ESD）。 因此，除了上述目标外， 实验还测试了使用ESD作为控制条件的效用， SD研究中的LSD 两种方案中的患者被随机分配至 ESD或LSD，并按照SD的时间表连续两晚， 连续两个星期。 有广泛、系统的监测， 情绪和行为之前的SD，并为三个星期后，最后SD。 在第一个方案中，患者在治疗开始时是无药物的。 研究，并开始氟西汀20毫克前四天，他们的第一次 SD的夜晚 21名患者完成了方案，11名患者在 LSD状态和ESD状态下的13。 初步分析 的数据表明，没有显着差异， ESD组和LSD组对氟西汀的反应过程。 因此，在这一点上，没有迹象表明SD可以用于 加速氟西汀的起效。 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 完成了方案，14个处于ESD条件，12个处于LSD条件 条件 似乎没有显着差异， 两组的反应，所以ESD似乎不是一个足够的 该人群中LSD的控制条件。 然而，SD治疗 确实明显降低了受试者的汉密尔顿抑郁症 评定量表评分。 这种影响即使在患者 他们的分数在进入研究时下降了30%或更多（所谓的 “安慰剂应答者”）。 因此，SD可能 增强抗抑郁药物的疗效。 在SD的夜晚之前和之后，抽血以监测TSH的水平， 三碘甲状腺原氨酸皮质醇催乳素。 目前正在分析这些数据。

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 this study is to test two possible clinical applications of SD: (1) its ability to hasten the onset of the 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. There is literature to indicate that sleep deprivation in the second half of the night (late sleep deprivation, or LSD) is a more active treatment than sleep deprivation in the first half of the night (early sleep deprivation, or ESD). Thus, in addition to the goals noted above, these experiments also test the utility of using ESD as a control condition for LSD in SD research. Patients in both protocols are randomly assigned to ESD or LSD, and follow that schedule of SD for two nights in a row during each of two successive weeks. There is extensive, systematic monitoring of mood and behavior prior to the SD, and for three weeks after the last SD. In the first protocol, patients are drug-free at the beginning of the study, and are started on fluoxetine 20 mg four days before their first night of SD. Twenty-one patients have completed the protocol, eleven in the LSD condition and thirteen in the ESD condition. Preliminary analyses of the data indicate that there are no significant differences between the ESD group and the LSD group in the course of their response to fluoxetine. Therefore, at this point there is no indication that SD can be used to hasten the onset of the action of fluoxetine. All patients accepted in the second protocol have been on a stable regimen of antidepressant medication for at least eight weeks, and they are continued on this regimen throughout the study. Twenty-six patients have completed the protocol, fourteen in the ESD condition and twelve in the LSD condition. There do not appear to be 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 does appear to decrease significantly the subjects' Hamilton Depression Rating Scale scores. This effect remains significant even after patients whose scores dropped 30% or more upon entry into the study (so-called "placebo responders") are excluded. Therefore, it appears that SD may potentiate the efficacy of antidepressant medications. Before and after the nights of SD, blood is drawn to monitor levels of TSH, T-3, cortisol, and prolactin. These data are currently being analyzed.