改良电休克治疗（modified electroconvulsive therapy，MECT）与重复经颅磁刺激治疗（repetitive transcranial magnetic stimulation，rTMS）是治疗抑郁障碍（major depressive disorder，MDD）的有效物理手段，但二者对认知功能的影响明显不同。MECT 起效迅速却常伴记忆与执行功能损害，rTMS 则在改善情绪的同时保护乃至增强认知功能。本文从突触可塑性、脑源性神经营养因子（brain-derived neurotrophic factor，BDNF）信号、神经炎 症及神经发生4个维度，系统梳理并比较了2种治疗的核心机制。MECT 的认知功能损伤源于全面性惊厥触发的N-甲基-D-天冬氨酸（N-methyl-D-aspartate，NMDA）受体过度激活、BDNF失调性释放及神经炎症级联反应；而rTMS的认知功能保护机制源于对BDNF-原肌球蛋白相关激酶B（tropomyosin receptor kinase B，TrkB）信号的生理性活化，并通过诱导有序的长时程增强样效应，实现对突触可塑性的精准、良性调控。本文讨论2种治疗在关键分子节点上的交汇与分歧，提出从“认知悖论”走向“协同对话”的机制框架，并为MDD的临床参数优化、联合治疗方案设计及个体化治疗决策提供了理论依据与未来研究方向。

Modified electroconvulsive therapy (MECT) and repetitive transcranial magnetic stimulation (rTMS) are effective physical interventions for major depressive disorder (MDD); however, they exert opposing effects on cognitive function. MECT acts rapidly but is frequently accompanied by impairments in memory and executive function, whereas rTMS not only alleviates mood symptoms but also preserves and even enhances cognition. This review systematically delineates and compares the core mechanisms of these two treatments across four dimensions: synaptic plasticity, brain-derived neurotrophic factor (BDNF) signaling, neuroinflammation, and neurogenesis. The cognitive costs of MECT arise from generalized seizure-induced overactivation of N-methyl-D-aspartate (NMDA) receptors, dysregulated BDNF release, and a downstream neuroinflammatory cascade. In contrast, the cognitive protective mechanism of rTMS is rooted in the physiological activation of BDNF-tropomyosin receptor kinase B (TrkB) signaling and the induction of orderly long-term potentiation (LTP)-like effects, thereby achieving precise and benign modulation of synaptic plasticity. This article further dissects the intersections and divergences of these two modalities at key molecular nodes, proposes a mechanistic framework that transitions from a “cognitive paradox” to a “synergistic dialogue,” and provides a theoretical basis and future research directions for optimizing clinical parameters, designing combination treatment regimens, and guiding individualized treatment decisions in MDD.