Experimental Therapeutics and Pathophysiology Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA.
Department of Statistics, University of Haifa, Haifa, Israel.
Transl Psychiatry. 2024 Jun 4;14(1):238. doi: 10.1038/s41398-024-02956-2.
The glutamatergic modulator ketamine is associated with changes in sleep, depression, and suicidal ideation (SI). This study sought to evaluate differences in arousal-related sleep metrics between 36 individuals with treatment-resistant major depression (TRD) and 25 healthy volunteers (HVs). It also sought to determine whether ketamine normalizes arousal in individuals with TRD and whether ketamine's effects on arousal mediate its antidepressant and anti-SI effects. This was a secondary analysis of a biomarker-focused, randomized, double-blind, crossover trial of ketamine (0.5 mg/kg) compared to saline placebo. Polysomnography (PSG) studies were conducted one day before and one day after ketamine/placebo infusions. Sleep arousal was measured using spectral power functions over time including alpha (quiet wakefulness), beta (alert wakefulness), and delta (deep sleep) power, as well as macroarchitecture variables, including wakefulness after sleep onset (WASO), total sleep time (TST), rapid eye movement (REM) latency, and Post-Sleep Onset Sleep Efficiency (PSOSE). At baseline, diagnostic differences in sleep macroarchitecture included lower TST (p = 0.006) and shorter REM latency (p = 0.04) in the TRD versus HV group. Ketamine's temporal dynamic effects (relative to placebo) in TRD included increased delta power earlier in the night and increased alpha and delta power later in the night. However, there were no significant diagnostic differences in temporal patterns of alpha, beta, or delta power, no ketamine effects on sleep macroarchitecture arousal metrics, and no mediation effects of sleep variables on ketamine's antidepressant or anti-SI effects. These results highlight the role of sleep-related variables as part of the systemic neurobiological changes initiated after ketamine administration. Clinical Trials Identifier: NCT00088699.
谷氨酸调节剂氯胺酮与睡眠、抑郁和自杀意念 (SI) 的变化有关。本研究旨在评估 36 名治疗抵抗性重度抑郁症 (TRD) 患者和 25 名健康志愿者 (HV) 之间与觉醒相关的睡眠指标的差异。还试图确定氯胺酮是否能使 TRD 患者的觉醒正常化,以及氯胺酮对觉醒的影响是否介导其抗抑郁和抗 SI 作用。这是一项针对氯胺酮(0.5mg/kg)与生理盐水安慰剂的生物标志物为重点的、随机、双盲、交叉试验的二次分析。在氯胺酮/安慰剂输注前一天和后一天进行多导睡眠图 (PSG) 研究。使用时间上的频谱功率函数来测量睡眠觉醒,包括 alpha(安静觉醒)、beta(警觉觉醒)和 delta(深度睡眠)功率,以及宏观结构变量,包括睡眠后觉醒时间 (WASO)、总睡眠时间 (TST)、快速眼动 (REM) 潜伏期和睡眠后觉醒睡眠效率 (PSOSE)。在基线时,睡眠宏观结构的诊断差异包括 TRD 组的 TST 较低(p=0.006)和 REM 潜伏期较短(p=0.04)。与安慰剂相比,氯胺酮在 TRD 中的时间动态效应包括夜间早期 delta 功率增加和夜间后期 alpha 和 delta 功率增加。然而,在 alpha、beta 或 delta 功率的时间模式方面没有显著的诊断差异,氯胺酮对睡眠宏观结构觉醒指标没有影响,睡眠变量也没有对氯胺酮的抗抑郁或抗 SI 作用产生中介作用。这些结果强调了睡眠相关变量作为氯胺酮给药后启动的系统神经生物学变化的一部分的作用。临床试验标识符:NCT00088699。