McMillan Rebecca, Sumner Rachael, Forsyth Anna, Campbell Doug, Malpas Gemma, Maxwell Elizabeth, Deng Carolyn, Hay John, Ponton Rhys, Sundram Frederick, Muthukumaraswamy Suresh
School of Pharmacy, University of Auckland, New Zealand.
School of Pharmacy, University of Auckland, New Zealand.
Prog Neuropsychopharmacol Biol Psychiatry. 2020 Apr 20;99:109838. doi: 10.1016/j.pnpbp.2019.109838. Epub 2019 Dec 13.
A single subanaesthetic dose of ketamine rapidly alleviates the symptoms of major depressive disorder (MDD). However, few studies have investigated the acute effects of ketamine on the BOLD pharmacological magnetic resonance imaging (phMRI) response and EEG spectra. In a randomised, double-blind, active placebo-controlled crossover trial, resting-state simultaneous EEG/fMRI was collected during infusion of ketamine or active placebo (remifentanil) in 30 participants with MDD. Montgomery-Asberg depression rating scale scores showed a significant antidepressant effect of ketamine compared to placebo (69% response rate). phMRI analyses showed BOLD signal increases in the anterior cingulate and medial prefrontal cortices and sensitivity of the decrease in subgenual anterior cingulate cortex (sgACC) BOLD signal to noise correction. EEG spectral analysis showed increased theta, high beta, low and high gamma power, and decreased delta, alpha, and low beta power with differing time-courses. Low beta and high gamma power time courses explained significant variance in the BOLD signal. Interestingly, the variance explained by high gamma power was significantly associated with non-response to ketamine, but significant associations were not found for other neurophysiological markers when noise correction was implemented. The results suggest that the decrease in sgACC BOLD signal is potentially noise and unrelated to ketamine's antidepressant effect, highlighting the importance of noise correction and multiple temporal regressors for phMRI analyses. The lack of effects significantly associated with antidepressant response suggests the phMRI methodology employed was unable to detect such effects, the effect sizes are relatively small, or that other processes, e.g. neural plasticity, underlie ketamine's antidepressant effect.
单次亚麻醉剂量的氯胺酮可迅速缓解重度抑郁症(MDD)的症状。然而,很少有研究调查氯胺酮对血氧水平依赖性功能磁共振成像(BOLD-phMRI)反应和脑电图频谱的急性影响。在一项随机、双盲、活性安慰剂对照的交叉试验中,对30名患有MDD的参与者在输注氯胺酮或活性安慰剂(瑞芬太尼)期间进行静息状态下同步脑电图/功能磁共振成像检查。蒙哥马利-阿斯伯格抑郁评定量表评分显示,与安慰剂相比,氯胺酮具有显著的抗抑郁作用(反应率69%)。BOLD-phMRI分析显示,前扣带回和内侧前额叶皮质的BOLD信号增加,以及膝下前扣带回皮质(sgACC)BOLD信号下降对噪声校正的敏感性。脑电图频谱分析显示,θ波、高β波、低γ波和高γ波功率增加,δ波、α波和低β波功率在不同时间进程中下降。低β波和高γ波功率时间进程解释了BOLD信号的显著差异。有趣的是,高γ波功率解释的差异与对氯胺酮无反应显著相关,但在进行噪声校正时,未发现其他神经生理标记物有显著关联。结果表明,sgACC的BOLD信号下降可能是噪声,与氯胺酮的抗抑郁作用无关,突出了噪声校正和多个时间回归器对BOLD-phMRI分析的重要性。与抗抑郁反应缺乏显著关联的结果表明,所采用的BOLD-phMRI方法无法检测到此类效应,效应大小相对较小,或者其他过程(如神经可塑性)是氯胺酮抗抑郁作用的基础。