Neuronal network mechanisms associated with depressive symptom improvement following electroconvulsive therapy.

electroconvulsive therapy functional connectivity functional magnetic resonance imaging hippocampus multivoxel pattern analysis

Journal

Psychological medicine
ISSN: 1469-8978
Titre abrégé: Psychol Med
Pays: England
ID NLM: 1254142

Informations de publication

Date de publication:
12 2021
Historique:
pubmed: 2 6 2020
medline: 25 11 2022
entrez: 2 6 2020
Statut: ppublish

Résumé

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. Resting-state functional MRI was acquired before and after bilateral ECT in 27 depressed individuals. 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. 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.

Sections du résumé

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.
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.

Identifiants

pubmed: 32476629
doi: 10.1017/S0033291720001518
pii: S0033291720001518
pmc: PMC8640363
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2856-2863

Auteurs

Akihiro Takamiya (A)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.
Center for Psychiatry and Behavioral Science, Tokyo193-8505, Japan.

Taishiro Kishimoto (T)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

Jinichi Hirano (J)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

Shiro Nishikata (S)

Center for Psychiatry and Behavioral Science, Tokyo193-8505, Japan.

Kyosuke Sawada (K)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

Shunya Kurokawa (S)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

Bun Yamagata (B)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

Toshiaki Kikuchi (T)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

Masaru Mimura (M)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo160-8582, Japan.

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