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Updated: Aug 14, 2025

Neuroimaging-Guided TMS–EEG for Real-Time Cortical Network Mapping
Published on: June 13, 2025
Distinct and shared patterns of brain plasticity during electroconvulsive therapy and treatment as usual in
Tobias Bracht1,2, Sebastian Walther3,4, Sigrid Breit3,4
1Translational Research Center, University Hospital of Psychiatry and Psychotherapy, University of Bern, Bern, Switzerland. tobias.bracht@upd.unibe.ch.
Abstract:
Electroconvulsive therapy (ECT) is a highly effective treatment for depression. Previous studies point to ECT-induced volume increase in the hippocampi and amygdalae, and to increase in cortical thickness. However, it is unclear if these neuroplastic changes are associated with treatment response. This observational study aimed to address this research question by comparing neuroplasticity between patients with depression receiving ECT and patients with depression that respond to treatment as usual (TAU-responders). Twenty ECT-patients (16 major depressive disorder (MDD), 4 depressed bipolar disorder), 20 TAU-responders (20 MDD) and 20 healthy controls (HC) were scanned twice with multimodal magnetic resonance imaging (structure: MP2RAGE; perfusion: arterial spin labeling). ECT-patients were scanned before and after an ECT-index series (ECT-group). TAU-responders were scanned during a depressive episode and following remission or treatment response. Volumes and cerebral blood flow (CBF) of the hippocampi and amygdalae, and global mean cortical thickness were compared between groups. There was a significant group × time interaction for hippocampal and amygdalar volumes, CBF in the hippocampi and global mean cortical thickness. Hippocampal and amygdalar enlargements and CBF increase in the hippocampi were observed in the ECT-group but neither in TAU-responders nor in HC. Increase in global mean cortical thickness was observed in the ECT-group and in TAU-responders but not in HC. The co-occurrence of increase in global mean cortical thickness in both TAU-responders and in ECT-patients may point to a shared mechanism of antidepressant response. This was not the case for subcortical volume and CBF increase.
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