Lundsgaard Christoffer Cramer, Mathiassen André Beyer, Wiberg Larsson Henrik Bo, Videbech Poul, Gbyl Krzysztof, Vestergaard Mark Bitsch
Center for Neuropsychiatric Depression Research, Mental Health Center Glostrup, Copenhagen University Hospital - Mental Health Services CPH, Denmark; Department of Clinical Medicine, University of Copenhagen, Denmark.
Center for Neuropsychiatric Depression Research, Mental Health Center Glostrup, Copenhagen University Hospital - Mental Health Services CPH, Denmark; Department of Clinical Medicine, University of Copenhagen, Denmark.
Brain Stimul. 2025 Sep-Oct;18(5):1470-1478. doi: 10.1016/j.brs.2025.07.005. Epub 2025 Jul 8.
Neurobiological understanding of the antidepressant mechanisms of electroconvulsive therapy (ECT) is important to advance the treatment. ECT may work by improving depression-related alterations in the cerebral oxygen metabolism.
21 in-patients with depression treated with an ECT series were examined 1) within two days before, and 2) a few days (median = 4 days) after the last ECT session. Depression severity was assessed by the six-item Hamilton Depression Rating Scale (HDRS-6). Magnetic resonance imaging (MRI) was used to measure 1) global cerebral blood flow (CBF) by phase contrast mapping technique and 2) global cerebral metabolic rate of oxygen (CMRO) by measuring cerebral extraction of oxygen (A-V.O) using susceptibility-based oximetry. Statistical analyses were performed using multiple linear regression, adjusting for age and gender.
ECT relieved depressive symptoms from HDRS-6 = 13.9 to 5.2 (p < 0.001), as expected. A larger increase in CMRO after ECT was correlated with a better treatment effect (0.5 % reduction in HDRS-6 per 1 % increase in CMRO, adjusted R = 0.24, p = 0.026). The effect was driven by both higher A-V.O and increased CBF. Before ECT, an abnormal decoupling between CMRO and CBF was observed, which was normalized after the treatment (adjusted R = 0.17, p = 0.03).
The treatment effect of ECT for depression was associated with increased CMRO. Furthermore, ECT restored the normal coupling between CBF and CMRO. The results suggest that the cerebral oxygen metabolism may be abnormally altered in patients with depression and ECT restores such dysfunction.
从神经生物学角度理解电休克治疗(ECT)的抗抑郁机制对于改进该治疗方法至关重要。ECT可能通过改善与抑郁相关的脑氧代谢改变来发挥作用。
对21例接受系列ECT治疗的抑郁症住院患者进行了检查,1)在最后一次ECT治疗前2天内,以及2)在最后一次ECT治疗后几天(中位数 = 4天)。采用6项汉密尔顿抑郁评定量表(HDRS-6)评估抑郁严重程度。磁共振成像(MRI)用于测量:1)通过相位对比映射技术测量全脑血流量(CBF),以及2)通过基于磁化率的血氧测定法测量脑氧摄取率(A-V.O)来计算全脑氧代谢率(CMRO)。使用多元线性回归进行统计分析,并对年龄和性别进行校正。
正如预期的那样,ECT使抑郁症状从HDRS-6 = 13.9缓解至5.2(p < 0.001)。ECT后CMRO的更大增加与更好的治疗效果相关(CMRO每增加1%,HDRS-6降低0.5%,校正R = 0.24,p = 0.026)。这种效应是由较高的A-V.O和增加的CBF共同驱动的。在ECT治疗前,观察到CMRO和CBF之间存在异常解耦,治疗后这种情况恢复正常(校正R = 0.17,p = 0.03)。
ECT治疗抑郁症的效果与CMRO增加有关。此外,ECT恢复了CBF和CMRO之间的正常耦合。结果表明,抑郁症患者的脑氧代谢可能发生异常改变,而ECT可恢复这种功能障碍。