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.
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.
Authors: Alexandra Kleimann; Alexandra Kotsiari; Wolfgang Sperling; Michael Gröschl; Annemarie Heberlein; Kai G Kahl; Thomas Hillemacher; Stefan Bleich; Johannes Kornhuber; Helge Frieling Journal: J Neural Transm (Vienna) Date: 2014-11-12 Impact factor: 3.575
Authors: John Strauss; Stuart McGregor; Natalie Freeman; Arun Tiwari; Charles J George; Maria Kovacs; James L Kennedy Journal: Psychiatry Res Date: 2012-03-27 Impact factor: 3.222
Authors: Mohamed R Mughal; Akanksha Baharani; Srinivasulu Chigurupati; Tae Gen Son; Edmund Chen; Peter Yang; Eitan Okun; Thiruma Arumugam; Sic L Chan; Mark P Mattson Journal: Hum Mol Genet Date: 2010-11-24 Impact factor: 6.150
Authors: André R Brunoni; Rodrigo Machado-Vieira; Carlos A Zarate; Erica L M Vieira; Marie-Anne Vanderhasselt; Michael A Nitsche; Leandro Valiengo; Isabela M Benseñor; Paulo A Lotufo; Wagner F Gattaz; Antonio L Teixeira Journal: Eur Neuropsychopharmacol Date: 2014-03-27 Impact factor: 4.600