Objectives: Electroconvulsive therapy (ECT) is a non-pharmacological treatment that is effective in treating severe and treatment-resistant depression. Although the efficacy of ECT has been demonstrated to treat major depressive disorder (MDD), the brain mechanisms underlying this process remain unclear. Structural–functional changes occur with the use of ECT as a treatment for depression based on magnetic resonance imaging (MRI). For this reason, we have tried to identify the changes that were identified by MRI to try to clarify some operating mechanisms of ECT. We focus to brain changes on MRI [structural MRI (sMRI), functional MRI (fMRI) and diffusion tensor imging (DTI)] after ECT.Methods: A systematic search of the international literature was performed using the bibliographic search engines PubMed and Embase. The research focused on papers published up to 30 September 2015. The following Medical Subject Headings (MESH) terms were used: electroconvulsive therapy AND (MRI OR fMRI OR DTI). Papers published in English were included. Four authors searched the database using a predefined strategy to identify potentially eligible studies.Results: There were structural changes according to the sMRI performed before and after ECT treatment. These changes do not seem to be entirely due to oedema. This investigation assessed the functional network connectivity associated with the ECT response in MDD. ECT response reverses the relationship from negative to positive between the two pairs of networks.Conclusion: We found structural–functional changes in MRI post-ECT. Because of the currently limited MRI data on ECT in the literature, it is necessary to conduct further investigations using other MRI technology.
Introduction: The hippocampus plays a key role in depressive disorder, and the amygdala is involved in depressive disorder through the key role that it plays in emotional regulation. Electroconvulsive therapy (ECT) may alter the microstructure of these two regions. Since mean diffusivity (MD), is known to be an indirect marker of microstructural integrity and can be derived from diffusion tensor imaging (DTI) scans, we aim to test the hypothesis that treatment-resistant depression (TRD) patients undergoing bilateral (BL) ECT exhibit a decrease of MD in their hippocampus and amygdala. Methods: Patients, between 50 and 70 years of age, diagnosed with TRD were recruited from the University Hospital of Toulouse and assessed clinically (Hamilton Depression Rating Scale, HAM-D) and by DTI scans at three time points: baseline, V2 (during treatment), and V3 within 1 week of completing ECT. Results: We included 15 patients, who were all responders. The left and right hippocampi and the left amygdala showed a significant decrease in MD at V3, compared to baseline [respectively: β = −2.78, t = −1.97, p = 0.04; β = −2.56, t = −2, p = 0.04; β = −2.5, t = −2.3, p = 0.04, false discovery rate (FDR) corrected]. MD did not decrease in the right amygdala. Only the left amygdala was significantly associated with a reduction in HAM-D (ρ = 0.55, p = 0.049, FDR corrected). Conclusion: MD is an indirect microstructural integrity marker, which decreases in the hippocampus and the left amygdala, during BL ECT in TRD populations. This could be interpreted as a normalization of microstructural integrity in these structures.