Course: Understanding the Mechanisms of Action of Electroconvulsive Therapy: Revisiting Neuroinflammatory and Neuroplasticity Hypotheses
CME Credits: 1.00
Released: 2023-04-19
Electroconvulsive therapy (ECT) has been effectively used for almost a century, but its mechanisms of action remain poorly understood. Two primary hypotheses have been postulated: the structural neuroplasticity and the neuroinflammatory models. Structural neuroplasticity, which embraces different biological processes, including neurogenesis, synaptogenesis (eg, dendritic arborization), and supporting mechanisms like angiogenesis and gliogenesis, has been traditionally favored over ECT-induced neuroinflammation. Inflammation is generally considered a pathological process, one that is involved in the pathophysiology of depression, so it may be counterintuitive to formulate it as a therapeutic mechanism. But inflammation is also a mechanism of repair and recovery, and parallel neuroinflammatory routes coexist; while systemic inflammatory processes modulating the hypothalamic-pituitary adrenal axis and neurotransmitter systems are associated with the pathophysiology of depression, local and transient neuroinflammatory mechanisms, often cell-mediated involving glial activation, may account for repair mechanisms linked to the antidepressant therapeutic action of ECT.
To identify the key insights or developments described in this article
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