Objective: Past neuroimaging work has suggested that increased activation to cognitive and emotional tasks and decreased connectivity in frontal regions are related to cognitive inefficiency in depression; normalization of these relationships has been associated with successful treatment. The present study investigated brain function before and after electroconvulsive therapy (ECT) in patients with major depressive disorder (MDD) and demonstrated the effect of treatment on cortical activation patterns.
Methods: Six ECT-naive patients with depression (mean ± SD age, 39.0 ± 5.4 years) were treated with ECT. Within 1 week before and 1 to 3 weeks after ECT, the patients underwent a magnetic resonance imaging session with functional magnetic resonance image scanning during working memory and affective tasks and during rest. Changes in voxelwise statistical maps of brain response to each task in regions identified to be relevant from past studies of depression were compared with changes in depression severity as measured by the Hamilton Depression Rating Score. Changes in functional connectivity between brain regions were also compared with changes in depression severity.
Results: Activation during both tasks was generally found to be decreased after ECT. Remission of depression was significantly associated with reduced affective deactivation after ECT in the orbitofrontal cortex (P = 0.03). Whole-brain functional connectivity of the anterior cingulate cortex showed a consistent increase in connectivity to the right dorsolateral prefrontal cortex and posterior cingulate cortex after ECT.
Conclusions: These results suggest that successful ECT for MDD is associated with decreased activation to cognitive and emotional tasks and an increase in resting connectivity.
From the *Imaging Institute, and †Neurological Institute, Cleveland Clinic, Cleveland, OH; and ‡Neurosciences Therapeutic Resource Center, Medco Health Solutions, Inc, Fort Worth, TX.
Received for publication August 31, 2011; accepted May 9, 2012.
Reprints: Erik B. Beall, PhD, Cleveland Clinic, 9500 Euclid Ave, U-15, Cleveland, OH 44195 (e-mail: firstname.lastname@example.org).
Conflicts of Interest and Source of Funding: DAM has received fees for being on the speakers’ bureau for Bristol-Myers Squibb and Lilly and research funding from Medtronic. RMD has received fees for being on the speakers’ bureau for AstraZeneca. DJM has received no funding from outside sources since becoming an employee and shareholder at Medco Health Solutions, Inc in December 2009. Before December 2009, DJM received honoraria for being on the speakers’ bureau and for advisory board activities for AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Pfizer, and Wyeth and received research funding from Abbott Labs, Lilly, Pfizer, GlaxoSmithKline, and Repligen Corp. MJL has received fees for participation in a medical advisory board for EMD Serono and has received research funding from Medtronic. For the remaining authors, no interests were declared. This work was supported by internal funding from the Research Program Committee of the Cleveland Clinic Lerner College of Medicine (RPC #2010-1007).
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