For many patients with neuropsychiatric illnesses, standard psychiatric treatments with mono or combination pharmacotherapy, psychotherapy, and transcranial magnetic stimulation are ineffective. For these patients with treatment-resistant neuropsychiatric illnesses, a main therapeutic option is electroconvulsive therapy (ECT). Decades of research have found ECT to be highly effective; however, it can also result in adverse neurocognitive effects. Specifically, ECT results in disorientation after each session, anterograde amnesia for recently learned information, and retrograde amnesia for previously learned information. Unfortunately, the neurocognitive effects and underlying mechanisms of action of ECT remain poorly understood. The purpose of this paper was to synthesize the multiple moderating and mediating factors that are thought to underlie the neurocognitive effects of ECT into a coherent model. Such factors include demographic and neuropsychological characteristics, neuropsychiatric symptoms, ECT technical parameters, and ECT-associated neurophysiological changes. Future research is warranted to evaluate and test this model, so that these findings may support the development of more refined clinical seizure therapy delivery approaches and efficacious cognitive remediation strategies to improve the use of this important and widely used intervention tool for neuropsychiatric diseases.
From the *Division of Brain Stimulation and Neurophysiology, Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC; †Department of Psychology and Neuroscience, Duke University, Durham, NC; ‡Department of Psychiatry, UT Southwestern Medical Center, Dallas, TX and §Department of Psychiatry, New York State Psychiatric Institute, Columbia University Medical Center, New York, NY.
Received for publication February 18, 2014; accepted March 17, 2014.
Reprints: Shawn M. McClintock, PhD, MSCS, Division of Brain Stimulation and Neurophysiology, Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, 200 Trent Dr, Durham, NC (e-mail: Shawn.email@example.com).
This manuscript was supported in part by grants from the National Institutes of Health/National Institute of Mental Health (K23 MH087739 and K23 MH086755).
Drs. McClintock and Choi report research support from the National Institutes of Health (NIH). Dr. Krystal reports having received grants or research support from NIH, Teva/Cephalon, Pfizer, Sunovion/Sepracor, Transcept, Phillips-Respironics, Astellas, Abbott, Neosync, and Brainsway. He has served as a consultant to Abbott, Astellas, AstraZeneca, BMS, Teva/Cephalon, Eisai, Eli Lilly, GlaxoSmithKline, Jazz, Johnson and Johnson, Merck, Neurocrine, Novartis, Ortho-McNeil-Janssen, Respironics, Roche, Sanofi-Aventis, Somnus, Sunovion/Sepracor, Somaxon, Takeda, Transcept, and Kingsdown Inc. Dr. Lisanby reports having served as a principal investigator on industry-sponsored research grants to Columbia/RFMH or Duke (Neuronetics [past], Brainsway, ANS/St Jude Medical, Cyberonics [past], and NeoSync); equipment loans to Columbia or Duke (Magstim and MagVenture). She is a coinventor on a patent application on TMS/MST technology; is supported by grants from NIH (R01MH091083-01, 5U01MH084241-02, and 5R01MH060884-09), Stanley Medical Research Institute, and Brain & Behavior Research Foundation/NARSAD; and has no consultancies, speakers bureau memberships, board affiliations, or equity holdings in related device industries. Drs. Deng and Appelbaum have no conflicts of interest or financial disclosures to report.