Hashioka Sadayuki
Department of Psychiatry, Asahikawa Medical University, 2-1-1-1 Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
CNS Neurol Disord Drug Targets. 2025;24(1):2-6. doi: 10.2174/0118715273319405240707164638.
Although electroconvulsive therapy (ECT) has immediate and profound effects on severe psychiatric disorders compared to pharmacotherapy, the mechanisms underlying its therapeutic effects remain elusive. Increasing evidence indicates that glial activation is a common pathogenetic factor in both major depression and schizophrenia, raising the question of whether ECT can inhibit glial activation. This article summarizes the findings from both clinical and experimental studies addressing this key question. Based on the findings, it is proposed that the suppression of glial activation associated with neuroinflammation may be involved in the mechanism by which ECT restores brain homeostasis and exerts its therapeutic effects.
尽管与药物治疗相比,电休克疗法(ECT)对严重精神障碍有直接且显著的效果,但其治疗效果背后的机制仍不清楚。越来越多的证据表明,胶质细胞激活是重度抑郁症和精神分裂症共同的致病因素,这就引出了ECT是否能抑制胶质细胞激活的问题。本文总结了针对这一关键问题的临床和实验研究结果。基于这些发现,有人提出,与神经炎症相关的胶质细胞激活的抑制可能参与了ECT恢复脑内稳态并发挥其治疗作用的机制。