TY - JOUR
T1 - Neuronal network mechanisms associated with depressive symptom improvement following electroconvulsive therapy
AU - Takamiya, Akihiro
AU - Kishimoto, Taishiro
AU - Hirano, Jinichi
AU - Nishikata, Shiro
AU - Sawada, Kyosuke
AU - Kurokawa, Shunya
AU - Yamagata, Bun
AU - Kikuchi, Toshiaki
AU - Mimura, Masaru
N1 - Publisher Copyright:
Copyright © The Author(s) 2020. Published by Cambridge University Press.
PY - 2021/12/1
Y1 - 2021/12/1
N2 - Background Electroconvulsive therapy (ECT) is the most effective antidepressant treatment for severe depression. Although recent structural magnetic resonance imaging (MRI) studies have consistently reported ECT-induced hippocampal volume increases, most studies did not find the association of the hippocampal volume changes with clinical improvement. To understand the underlying mechanisms of ECT action, we aimed to identify the longitudinal effects of ECT on hippocampal functional connectivity (FC) and their associations with clinical improvement. Methods Resting-state functional MRI was acquired before and after bilateral ECT in 27 depressed individuals. A priori hippocampal seed-based FC analysis and a data-driven multivoxel pattern analysis (MVPA) were conducted to investigate FC changes associated with clinical improvement. The statistical threshold was set at cluster-level false discovery rate-corrected p < 0.05. Results Depressive symptom improvement after ECT was positively associated with the change in the right hippocampus-ventromedial prefrontal cortex FC, and negatively associated with the right hippocampus-superior frontal gyrus FC. MVPA confirmed the results of hippocampal seed-based analyses and identified the following additional clusters associated with clinical improvement following ECT: the thalamus, the sensorimotor cortex, and the precuneus. Conclusions ECT-induced change in the right frontotemporal connectivity and thalamocortical connectivity, and changes in the nodes of the default mode network were associated with clinical improvement. Modulation of these networks may explain the underlying mechanisms by which ECT exert its potent and rapid antidepressant effect.
AB - Background Electroconvulsive therapy (ECT) is the most effective antidepressant treatment for severe depression. Although recent structural magnetic resonance imaging (MRI) studies have consistently reported ECT-induced hippocampal volume increases, most studies did not find the association of the hippocampal volume changes with clinical improvement. To understand the underlying mechanisms of ECT action, we aimed to identify the longitudinal effects of ECT on hippocampal functional connectivity (FC) and their associations with clinical improvement. Methods Resting-state functional MRI was acquired before and after bilateral ECT in 27 depressed individuals. A priori hippocampal seed-based FC analysis and a data-driven multivoxel pattern analysis (MVPA) were conducted to investigate FC changes associated with clinical improvement. The statistical threshold was set at cluster-level false discovery rate-corrected p < 0.05. Results Depressive symptom improvement after ECT was positively associated with the change in the right hippocampus-ventromedial prefrontal cortex FC, and negatively associated with the right hippocampus-superior frontal gyrus FC. MVPA confirmed the results of hippocampal seed-based analyses and identified the following additional clusters associated with clinical improvement following ECT: the thalamus, the sensorimotor cortex, and the precuneus. Conclusions ECT-induced change in the right frontotemporal connectivity and thalamocortical connectivity, and changes in the nodes of the default mode network were associated with clinical improvement. Modulation of these networks may explain the underlying mechanisms by which ECT exert its potent and rapid antidepressant effect.
KW - electroconvulsive therapy
KW - functional connectivity
KW - functional magnetic resonance imaging
KW - hippocampus
KW - multivoxel pattern analysis
UR - http://www.scopus.com/inward/record.url?scp=85085740933&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85085740933&partnerID=8YFLogxK
U2 - 10.1017/S0033291720001518
DO - 10.1017/S0033291720001518
M3 - Article
C2 - 32476629
AN - SCOPUS:85085740933
SN - 0033-2917
VL - 51
SP - 2856
EP - 2863
JO - Psychological Medicine
JF - Psychological Medicine
IS - 16
ER -