@article{b9160ec2e3454604bd2e61833d4e3b51,
title = "Depressive Symptom Dimensions in Treatment-Resistant Major Depression and Their Modulation with Electroconvulsive Therapy",
abstract = "Objective Symptom heterogeneity in major depressive disorder obscures diagnostic and treatment-responsive biomarker identification. Whether symptom constellations are differentially changed by electroconvulsive therapy (ECT) remains unknown. We investigate the clustering of depressive symptoms over the ECT index and whether ECT differentially influences symptom clusters. Methods The 17-item Hamilton Depression Rating Scale (HDRS-17) was collected from 111 patients with current depressive episode before and after ECT from 4 independent participating sites of the Global ECT-MRI Research Collaboration. Exploratory factor analysis of HDRS-17 items pre-and post-ECT treatment identified depressive symptom dimensions before and after ECT. A 2-way analysis of covariance was used to determine whether baseline symptom clusters were differentially changed by ECT between treatment remitters (defined as patients with posttreatment HDRS-17 total score ≤8) and nonremitters while controlling for pulse width, titration method, concurrent antidepressant treatment, use of benzodiazepine, and demographic variables. Results A 3-factor solution grouped pretreatment HDRS-17 items into core mood/anhedonia, somatic, and insomnia dimensions. A 2-factor solution best described the symptoms at posttreatment despite poorer separation of items. Among remitters, core mood/anhedonia symptoms were significantly more reduced than somatic and insomnia dimensions. No differences in symptom dimension trajectories were observed among nonremitting patients. Conclusions Electroconvulsive therapy targets the underlying source of depressive symptomatology and may confer differential degrees of improvement in certain core depressive symptoms. Our findings of differential trajectories of symptom clusters over the ECT index might help related predictive biomarker studies to refine their approaches by identifying predictors of change along each latent symptom dimension.",
keywords = "Hamilton Depression Rating Scale, electroconvulsive therapy, factor analysis, major depressive disorder, symptom heterogeneity",
author = "Wade, {Benjamin S.C.} and Gerhard Hellemann and Espinoza, {Randall T.} and Woods, {Roger P.} and Joshi, {Shantanu H.} and Ronny Redlich and Anders J{\o}rgensen and Abbott, {Christopher C.} and Oedegaard, {Ketil J.} and McClintock, {Shawn M.} and Leif Oltedal and Narr, {Katherine L.}",
note = "Funding Information: Objective: Symptom heterogeneity in major depressive disorder obscures diagnostic and treatment-responsive biomarker identification. Whether symptom constellations are differentially changed by electroconvulsive therapy (ECT) remains unknown. We investigate the clustering of depressive symptoms over the ECT index and whether ECT differentially influences symptom clusters. Methods: The 17-item Hamilton Depression Rating Scale (HDRS-17) was collected from 111 patients with current depressive episode before and after ECT from 4 independent participating sites of the Global ECT-MRI Research Collaboration. Exploratory factor analysis of HDRS-17 items pre-and post-ECT treatment identified depressive symptom dimensions before and after ECT. A 2-way analysis of covariance was used to determine whether baseline symptom clusters were differentially changed by ECT between treatment remitters (defined as patients with posttreatment HDRS-17 total score ≤8) and nonremitters while controlling for pulse width, titration method, concurrent antidepressant treatment, use of benzodiazepine, and demographic variables. Results: A 3-factor solution grouped pretreatment HDRS-17 items into core mood/anhedonia, somatic, and insomnia dimensions. A 2-factor From the *Department of Neurology, University of California Los Angles (UCLA), Ahmanson-Lovelace Brain Mapping Center; †Department of Psychiatry and Biobehavioral Sciences, Semel Institute; ‡Department of Psychiatry and Biobehavioral Sciences, UCLA, Los Angeles, CA; §Department of Psychiatry, University of M{\"u}nster, M{\"u}nster, Germany; ||Psychiatric Center Copenhagen, Copenhagen, Denmark; ¶Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque, NM; #Department of Clinical Medicine, University of Bergen, Bergen, Norway; **Department of Psychiatry, UT Southwestern Medical Center, Dallas, TX; and ††Mohn Medical Imaging and Visualization Centre, Department of Radiology, Haukeland University Hospital, Bergen, Norway. Received for publication February 21, 2019; accepted June 26, 2019. Reprints: Katherine L. Narr, Department of Neurology, UCLA, Ahmanson-Lovelace Brain Mapping Center, 635 Charles Young Drive, South Los Angeles, CA 90095 (e‐mail: narr@ucla.edu). This work is supported in part by the National Institute of Mental Health (MH092301, MH110008, and MH102743 to the UCLA investigators). This study is supported by the Western Norway Regional Health Authority, Haukeland University Hospital, and the University of Bergen, Norway. In addition, individual sites acknowledge support from the Muriel Harris Chair in Geriatric Psychiatry (R. T. E.); the M{\"u}nster Cohort, funded by the German Research Foundation (DFG; grant FOR2107, 1151/5-1 to R. R.) and Innovative Medizinische Forschung (IMF; RE111604 to R. R.); Centers of Biomedical Research Excellence (2P20GM103472-01 to C. C. A.); for UCLA, funding was obtained through award numbers R01MH092301 and K24MH102743 from the National Institute of Mental Health. B. S. C. W. is supported by a NARSAD Young Investigator Grant (#27786). All other authors have no conflicts of interest or financial disclosures to report. Supplemental digital contents are available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal{\textquoteright}s Web site (www.ectjournal.com). Copyright {\textcopyright} 2019 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/YCT.0000000000000623 solution best described the symptoms at posttreatment despite poorer separation of items. Among remitters, core mood/anhedonia symptoms were significantly more reduced than somatic and insomnia dimensions. No differences in symptom dimension trajectories were observed among nonremitting patients. Conclusions: Electroconvulsive therapy targets the underlying source of depressive symptomatology and may confer differential degrees of improvement in certain core depressive symptoms. Our findings of differential trajectories of symptom clusters over the ECT index might help related predictive biomarker studies to refine their approaches by identifying predictors of change along each latent symptom dimension.",
year = "2020",
month = jun,
day = "1",
doi = "10.1097/YCT.0000000000000623",
language = "English (US)",
volume = "36",
pages = "123--129",
journal = "Journal of ECT",
issn = "1095-0680",
publisher = "Lippincott Williams and Wilkins",
number = "2",
}