Abstract
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.