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What Does the Electroencephalogram Tell Us About the Mechanisms of Action of ECT in Major Depressive Disorders?

Farzan, Faranak PhD*; Boutros, Nash N. MD; Blumberger, Daniel M. MD, MSc, FRCPC*; Daskalakis, Zafiris J. MD, PhD, FRCP(C)*

doi: 10.1097/YCT.0000000000000144
Invited Reviews

Electroconvulsive therapy (ECT) remains to be one of the most effective treatment options in treatment-resistant major depressive disorder (MDD). From the early days, researchers have embarked on extracting information from electroencephalography (EEG) recordings before, during, and after ECT to identify neurophysiological targets of ECT and discover EEG predictors of response to ECT in patients with MDD. In this article, we provide an overview of visually detected and quantitative EEG features that could help in furthering our understanding of the mechanisms of action of ECT in MDD. We further discuss the EEG findings in the context of postulated hypotheses of ECT therapeutic pathways. We introduce an alternative and unifying hypothesis suggesting that ECT may exert its therapeutic efficacy through resetting the aberrant functional connectivity and promoting the generation of new and healthy connections in brain regions implicated in MDD pathophysiology, a mechanism that may be in part mediated by the ECT-induced activation of inhibitory and neuroplasticity mechanisms. We further discuss the added value of EEG markers in the larger context of ECT research and as complementary to neuroimaging and genetic markers. We conclude by drawing attention to the need for longitudinal studies in large cohort of patients and the need for standardization and validation of EEG algorithms of functional connectivity across studies to facilitate the translation of EEG correlates of ECT response in routine clinical practice.

From the *Centre for Addiction and Mental Health, Temerty Centre for Therapeutic Brain Intervention, Department of Psychiatry, University of Toronto, Ontario, Canada and †Department of Psychiatry and Neurosciences, University of Missouri, Kansas City, MO.

Received for publication January 31, 2014; accepted March 20, 2014.

Reprints: Faranak Farzan, PhD, Centre for Addiction and Mental Health, Temerty Centre for Therapeutic Brain Intervention, University of Toronto, 1001 Queen St, Unit 4-118A, Toronto, Ontario, Canada (e-mail:

Conflict of Interest: DMB receives research support from CIHR, Brain and Behaviour Research Foundation (formerly NARSAD), the Temerty Family through the CAMH Foundation and the Campbell Research Institute; and equipment support-in-kind for an investigator-initiated study from MagVenture/Tonika and research and in-kind equipment support for an investigator-initiated study from Brainsway Ltd. In the past 5 years, ZJD received research and equipment in-kind support for an investigator-initiated study through Brainsway Inc and a travel allowance through Merck. ZJD has also received speaker funding through Sepracor Inc and AstraZeneca, served on the advisory board for Hoffmann-La Roche Limited and Merck, and received speaker support from Eli Lilly. This work was supported by the Ontario Mental Health Foundation (OMHF), CIHR, the Brain and Behaviour Research Foundation, the Temerty Family, and the Grant Family and through the Centre for Addiction and Mental Health (CAMH) Foundation and the Campbell Institute. FF and NNB have no conflict of interest to disclose.

© 2014 by Lippincott Williams & Wilkins