Department of Psychiatry and Psychotherapy, Medical University of Vienna, 1090, Vienna, Waehringerstr 18-20, Austria.
Department of Psychiatry and Psychotherapy, Medical University of Vienna, 1090, Vienna, Waehringerstr 18-20, Austria; Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hung Hom, M1504, Li Ka Shing Tower, Hong Kong; The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, 5 Sassoon R., Pokfulam, Hong Kong.
Brain Stimul. 2019 Jul-Aug;12(4):1041-1050. doi: 10.1016/j.brs.2019.02.015. Epub 2019 Feb 26.
The induction of brain-derived neurotrophic factor (BDNF) release and subsequent restoration of neuroplastic homeostasis may underlie the effects of electroconvulsive therapy (ECT).
We aimed to assess serum and plasma BDNF levels during the course of acute ECT, as well as before and after subsequent continuation ECT, in patients with depression.
We included 24 patients with major depressive disorder (mean age ± SD: 54.5 ± 13.7; f/m: 17/7; baseline 17-item Hamilton Depression Rating Scale score of 26.79 ± 4.01). Serum and plasma BDNF (sBDNF, pBDNF) levels were assessed at nine time-points before, during, and after acute ECT series. Data were analysed using linear regression and linear mixed models, which were adjusted for multiple comparisons via Bonferroni correction. Five patients received continuation ECT subsequent to the acute ECT series. In these patients, BDNF levels were assessed before and after each two continuation ECT sessions using Wilcoxon signed-rank tests.
Relative to baseline (mean ng/ml ±SD: 24.68 ± 14.40), sBDNF levels were significantly higher 1 day (33.04 ± 14.11, p = 0.013, corrected), 1 week (37.03 ± 10.29, p < 0.001, corrected), and 1 month (41.05 ± 10.67, p = 0.008, corrected) after the final ECT session, while pBDNF levels did not significantly differ (p > 0.1). Furthermore, our results indicated that sBDNF levels increased after each continuation ECT session. There was no significant association between sBDNF levels and clinical parameters or treatment response.
The absence of an association between changes in sBDNF levels and depressive symptoms challenges the proposed concept of sBDNF/pBDNF as key markers of the effects of ECT.
脑源性神经营养因子(BDNF)的释放诱导和随后的神经可塑性动态平衡的恢复可能是电抽搐治疗(ECT)作用的基础。
我们旨在评估抑郁症患者在急性 ECT 过程中以及随后继续 ECT 前后的血清和血浆 BDNF 水平。
我们纳入了 24 名患有重性抑郁症的患者(平均年龄±标准差:54.5±13.7;男女比例:17/7;基线 17 项汉密尔顿抑郁量表评分为 26.79±4.01)。在急性 ECT 系列之前、期间和之后的九个时间点评估血清和血浆 BDNF(sBDNF,pBDNF)水平。使用线性回归和线性混合模型分析数据,并通过 Bonferroni 校正进行多次比较调整。五名患者在急性 ECT 系列后接受了继续 ECT。在这些患者中,使用 Wilcoxon 符号秩检验在每次两次继续 ECT 治疗前后评估 BDNF 水平。
与基线相比(平均 ng/ml ±标准差:24.68±14.40),sBDNF 水平在最后一次 ECT 治疗后 1 天(33.04±14.11,p=0.013,校正)、1 周(37.03±10.29,p<0.001,校正)和 1 个月(41.05±10.67,p=0.008,校正)时显著升高,而 pBDNF 水平无显著差异(p>0.1)。此外,我们的结果表明 sBDNF 水平在每次继续 ECT 治疗后增加。sBDNF 水平与临床参数或治疗反应之间没有显著关联。
sBDNF 水平变化与抑郁症状之间缺乏关联,这对 sBDNF/pBDNF 作为 ECT 效果关键标志物的观点提出了挑战。