Electroconvulsive therapy reduces frontal cortical connectivity in severe depressive disorder
- Jennifer S. Perrina,1,
- Susanne Merzb,
- Daniel M. Bennetta,
- James Curriea,
- Douglas J. Steelec,
- Ian C. Reida, and
- Christian Schwarzbauerb
+ Author Affiliations
aApplied Health Sciences (Mental Health), University of Aberdeen, Royal Cornhill Hospital, Aberdeen AB25 2ZH, United Kingdom;
bAberdeen Biomedical Imaging Centre, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, United Kingdom; and
cDivision of Neuroscience, Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom
Edited by Marcus E. Raichle, Washington University in St. Louis, St. Louis, MO, and approved February 14, 2012 (received for review October 18, 2011)
To date, electroconvulsive therapy (ECT) is the most potent treatment in severe depression. Although ECT has been successfully applied in clinical practice for over 70 years, the underlying mechanisms of action remain unclear. We used functional MRI and a unique data-driven analysis approach to examine functional connectivity in the brain before and after ECT treatment. Our results show that ECT has lasting effects on the functional architecture of the brain. A comparison of pre- and posttreatment functional connectivity data in a group of nine patients revealed a significant cluster of voxels in and around the left dorsolateral prefrontal cortical region (Brodmann areas 44, 45, and 46), where the average global functional connectivity was considerably decreased after ECT treatment (P < 0.05, family-wise error-corrected). This decrease in functional connectivity was accompanied by a significant improvement (P < 0.001) in depressive symptoms; the patients’ mean scores on the Montgomery Asberg Depression Rating Scale pre- and posttreatment were 36.4 (SD = 4.9) and 10.7 (SD = 9.6), respectively. The findings reported here add weight to the emerging “hyperconnectivity hypothesis” in depression and support the proposal that increased connectivity may constitute both a biomarker for mood disorder and a potential therapeutic target.
Author contributions: J.S.P., D.M.B., D.J.S., and I.C.R. designed research; J.S.P., D.M.B., J.C., and I.C.R. performed research; S.M. and C.S. contributed new analytic tools; J.S.P., S.M., I.C.R., and C.S. analyzed data; and J.S.P., S.M., I.C.R., and C.S. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
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