Increased Plasma Concentration of Brain-Derived Neurotrophic Factor With Electroconvulsive Therapy: A Pilot Study in Patients With Major Depression

Christopher M. Marano, M.D.; Pornima Phatak, Ph.D.; Ugandhar Rao Vemulapalli, M.D.; Amritpal Sasan, M.B.B.S.; Maria R. Nalbandyan; Sailakshmi Ramanujam, M.D.; Surjo Soekadar, M.D.; Maria Demosthenous, D.O.; and William T. Regenold, M.D.C.M.

Objective: The therapeutic mechanism of electroconvulsive therapy (ECT) is unknown. Animal research supports a neurotrophic effect of ECT. To investigate a neurotrophic effect in humans, we examined whether plasma concentration of brain-derived neurotrophic factor (BDNF) increases in patients receiving ECT for major depression.

Method: We conducted a prospective, self-controlled study of 15 patients with a DSM-IV diagnosis of major depressive episode who were referred for ECT at the University of Maryland Medical Center (Baltimore, Md.) between January 2004 and September 2005. Plasma BDNF concentration was measured by enzyme-linked immunosorbent assay before and during an acute course of ECT. Depression severity was measured using the 21-item Hamilton Rating Scale for Depression (HAM-D).

Results: ECT resulted in a significant increase in plasma BDNF (Z = 2.897, p = .004) from a pre-ECT median of 84.9 pg/mL to a post-ECT median of 141.2 pg/mL. This change was accompanied by a significant decrease in HAM-D score (Z = 3.411, p = .001) from a pre-ECT median of 30.0 to a post-ECT median of 9.0. BDNF increased in 13 (86.7%) of 15 subjects.

Conclusion: This is the first report of an increase in plasma BDNF concentration in patients receiving ECT. These preliminary results encourage further investigation of a neurotrophic mechanism for the antidepressant effect of ECT.

(J Clin Psychiatry 2007;68:512-517)

Received April 27, 2006; accepted Aug. 17, 2006. From the Department of Psychiatry, University of Maryland School of Medicine, Division of Geriatric Psychiatry (all authors); and VA Maryland Healthcare System (Drs. Marano, Phatak, Vemulapalli, Demosthenous, and Regenold), Baltimore, Md.

Data presented in part in poster form at the American Association for Geriatric Psychiatry annual meeting, March 2005, San Diego, Calif.

The authors report no financial or other relationship relevant to the subject of this article.

Corresponding author and reprints: William T. Regenold, M.D.C.M., Department of Psychiatry, Division of Geriatric Psychiatry, University of Maryland Medical Center, Box #351 Room S12A09, 22 South Greene St., Baltimore, MD 21201 (e-mail: wregenol@psych.umaryland.edu).