Abstract

ObjectivesBrain‐derived neurotrophic factor (BDNF) has been associated with depression and its treatment response. The aim of the present study was to explore the effect of electroconvulsive therapy (ECT) on serum and plasma BDNF levels and change of Montgomery–Asberg Depression Rating Scale (MADRS) and their associations in patients with major depressive disorder (MDD).MethodsThe study included thirty patients suffering from MDD. Their serum and plasma BDNF levels were examined before ECT (baseline) and after the first, fifth, and last ECT session. The severity of the depression and the response to ECT were measured with MADRS.ResultsElectroconvulsive therapy caused no significant changes in serum BDNF levels. Plasma BDNF levels decreased during the fifth ECT session between the baseline and the 2‐hr samples (p = 0.019). No associations were found between serum or plasma BDNF levels and remission. The correlations between plasma and serum BDNF levels in each measurement varied between 0.187 and 0.636.ConclusionsNeither serum nor plasma BDNF levels were systematically associated with the clinical remission. However, the plasma BDNF levels somewhat varied during the ECT series. Therefore, the predictive value of BDNF for effects of ECT appears to be at least modest.

Highlights

  • Electroconvulsive therapy (ECT) is considered to be the most ef‐ fective therapy for severe major depressive disorder (MDD) with reported effectiveness rates between 80% and 90% (UK ECT Review Group, 2003)

  • Serum Brain‐derived neurotrophic factor (BDNF) levels were not influenced by ECT

  • The BDNF levels decreased during the fifth ECT session between the baseline and the 2‐hr samples (p = 0.019)

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Summary

Introduction

Electroconvulsive therapy (ECT) is considered to be the most ef‐ fective therapy for severe major depressive disorder (MDD) with reported effectiveness rates between 80% and 90% (UK ECT Review Group, 2003). Indication of ECT as the first‐line treatment is a need for rapid, definitive response because of the severity of the psychotic or suicidal symptoms as well as a favorable prior re‐ sponse to ECT. Treatment resistance is a secondary indication for ECT (American Psychiatric Association, 2001). Molecules in several brain areas are affected by ECT includ‐ ing neurotransmitters, neuropeptides, and neurotrophic factors. ECT is well toler‐ ated; for example, it does not cause long‐term cognitive impair‐ ment (Haghighi et al, 2016; Haghighi, Bajoghli, et al, 2013).

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