McGirr Alexander, Berlim Marcelo T, Bond David J, Neufeld Nicholas H, Chan Peter Y, Yatham Lakshmi N, Lam Raymond W
Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada.
Neuromodulation Research Clinic, Douglas Mental Health University Institute and McGill University, Montréal, Québec, Canada; Depressive Disorders Program, Douglas Mental Health University Institute and McGill University, Montréal, Québec, Canada.
J Psychiatr Res. 2015 Mar;62:23-30. doi: 10.1016/j.jpsychires.2015.01.003. Epub 2015 Jan 26.
Electroconvulsive therapy (ECT) remains one of the most effective tools in the psychiatric treatment armamentarium, particularly for refractory depression. Yet, there remains a subset of patients who do not respond to ECT or for whom clinically adequate seizures cannot be elicited, for whom ketamine has emerged as a putative augmentation agent.
We searched EMBASE, PsycINFO, CENTRAL, and MEDLINE from 1962 to April 2014 to identify randomized controlled trials evaluating ketamine in ECT (PROSPERO #CRD42014009035). Clinical remission, response, and change in depressive symptom scores were extracted by two independent raters. Adverse events were recorded. Drop-outs were assessed as a proxy for acceptability. Meta-analyses employed a random effects model.
Data were synthesized from 5 RCTs, representing a total of 182 patients with major depressive episodes (n = 165 Major Depressive Disorder, n = 17 Bipolar Disorder). ECT with ketamine augmentation was not associated with higher rates of clinical remission (Risk Difference (RD) = 0.00; 95%CI = -0.08 to 0.10), response (RD = -0.01; 95%CI = -0.11 to 0.08), or improvements in depressive symptoms (SMD = 0.38; 95%CI = -0.41 to 1.17). Ketamine augmentation was associated with higher rates of confusion/disorientation/prolonged delirium (OR = 6.59, 95%CI: 1.28-33.82, NNH = 3), but not agitation, hypertension or affective switches.
Our meta-analysis of randomized controlled trials of ketamine augmentation in the ECT setting suggests a lack of clinical efficacy, and an increased likelihood of confusion. Individuals for whom adequate seizures or therapeutic response cannot be obtained have not been studied using randomized controlled designs. Additional research is required to address the role of ketamine in this population.
电休克疗法（ECT）仍然是精神科治疗手段中最有效的工具之一，尤其对于难治性抑郁症。然而，仍有一部分患者对ECT无反应或无法诱发临床上足够的癫痫发作，对于这些患者，氯胺酮已成为一种假定的增效剂。
我们检索了1962年至2014年4月期间的EMBASE、PsycINFO、CENTRAL和MEDLINE，以识别评估氯胺酮在ECT中应用的随机对照试验（PROSPERO #CRD42014009035）。临床缓解、反应以及抑郁症状评分的变化由两名独立评估者提取。记录不良事件。将退出情况作为可接受性的一个指标进行评估。荟萃分析采用随机效应模型。
数据来自5项随机对照试验，共纳入182例重度抑郁发作患者（n = 165例重度抑郁症，n = 17例双相情感障碍）。ECT联合氯胺酮增效与更高的临床缓解率（风险差异（RD）= 0.00；95%置信区间 = -0.08至0.10）、反应率（RD = -0.01；95%置信区间 = -0.11至0.08）或抑郁症状改善（标准化均数差 = 0.38；95%置信区间 = -0.41至1.17）无关。氯胺酮增效与更高的困惑/定向障碍/谵妄延长发生率相关（比值比 = 6.59，95%置信区间：1.28 - 33.82，需治疗人数 = 3），但与激越、高血压或情感转换无关。
我们对ECT中氯胺酮增效的随机对照试验进行的荟萃分析表明，其缺乏临床疗效，且困惑的可能性增加。对于无法获得足够癫痫发作或治疗反应的个体，尚未采用随机对照设计进行研究。需要进一步的研究来探讨氯胺酮在这一人群中的作用。
