电休克治疗后抑郁症及认知缺陷的临床改善
Clinical Improvement in Depression and Cognitive Deficit Following Electroconvulsive Therapy.
作者信息
Ahmad Hariza Ahmad Mus'ab, Mohd Yunus Mohd Heikal, Murthy Jaya Kumar, Wahab Suzaily
机构信息
Department of Physiology, Faculty of Medicine, UKM Medical Centre, Jalan Yaacob Latiff, Bandar Tun Razak, Kuala Lumpur 56000, Malaysia.
Department of Psychiatry, Faculty of Medicine, UKM Medical Centre, Jalan Yaacob Latiff, Bandar Tun Razak, Kuala Lumpur 56000, Malaysia.
出版信息
Diagnostics (Basel). 2023 Apr 28;13(9):1585. doi: 10.3390/diagnostics13091585.
Electroconvulsive therapy (ECT) is a long-standing treatment choice for disorders such as depression when pharmacological treatments have failed. However, a major drawback of ECT is its cognitive side effects. While numerous studies have investigated the therapeutic effects of ECT and its mechanism, much less research has been conducted regarding the mechanism behind the cognitive side effects of ECT. As both clinical remission and cognitive deficits occur after ECT, it is possible that both may share a common mechanism. This review highlights studies related to ECT as well as those investigating the mechanism of its outcomes. The process underlying these effects may lie within BDNF and NMDA signaling. Edema in the astrocytes may also be responsible for the adverse cognitive effects and is mediated by metabotropic glutamate receptor 5 and the protein Homer1a.
当药物治疗无效时，电休克疗法（ECT）是治疗抑郁症等疾病的一种长期选择。然而，ECT的一个主要缺点是其认知副作用。虽然许多研究已经调查了ECT的治疗效果及其机制，但关于ECT认知副作用背后机制的研究却少得多。由于ECT后既出现临床缓解又出现认知缺陷，两者可能存在共同机制。本综述重点介绍了与ECT相关的研究以及那些探究其治疗结果机制的研究。这些效应背后的过程可能存在于脑源性神经营养因子（BDNF）和N-甲基-D-天冬氨酸（NMDA）信号传导中。星形胶质细胞水肿也可能是认知不良影响的原因，并且由代谢型谷氨酸受体5和蛋白质Homer1a介导。
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