Electroconvulsive therapy disrupts functional connectivity between hippocampus and posterior default mode network

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Background
The mechanisms underlying memory deficits after electroconvulsive therapy (ECT) remain unclear but altered functional interactions between hippocampus and neocortex may play a role.

Objectives
To test whether ECT reduces functional connectivity between hippocampus and posterior regions of the default mode network (DMN) and to examine whether altered hippocampal-neocortical functional connectivity correlates with memory impairment. A secondary aim was to explore if these connectivity changes are present 6 months after ECT.

Methods
In-patients with severe depression (n = 35) received bitemporal ECT. Functional connectivity of the hippocampus was probed with resting-state fMRI before the first ECT-session, after the end of ECT, and at a six-month follow-up. Memory was assessed with the Verbal Learning Test – Delayed Recall. Seed-based connectivity analyses established connectivity of four hippocampal seeds, covering the anterior and posterior parts of the right and left hippocampus.

Results
Compared to baseline, three of four hippocampal seeds became less connected to the core nodes of the posterior DMN in the week after ECT with Cohen's d ranging from −0.9 to −1.1. At the group level, patients showed post-ECT memory impairment, but individual changes in delayed recall were not correlated with the reduction in hippocampus-DMN connectivity. At six-month follow-up, no significant hippocampus-DMN reductions in connectivity were evident relative to pre-ECT, and memory scores had returned to baseline.

Conclusion
ECT leads to a temporary disruption of functional hippocampus-DMN connectivity in patients with severe depression, but the change in connectivity strength is not related to the individual memory impairment.
OriginalsprogEngelsk
Artikelnummer110981
TidsskriftProgress in Neuro-Psychopharmacology and Biological Psychiatry
Vol/bind132
Antal sider11
ISSN0278-5846
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
First of all, we thank all patients who participated in the study. We are also thankful to all funders: Augustinusfonden, Axel Muusfeldts Fond, Beckett-Fonden, A.P. Møller Fonden: Fonden til Lægevidenskabens Fremme, Sundhedsstyrelsen (the Danish Ministry of Health), Helsefonden, Ivan Nielsens Fond for personer med specielle sindslidelser, Jascha Fonden, Læge Gerhard Linds Legat, Lundbeckfonden, Psykiatrisk Forskningsfond af 1967, and Region Hovedstaden Fond. Hartwig R. Siebner and Poul Videbech are supported by a Grand Solutions grant “Precision Brain-Circuit Therapy - Precision-BCT)” from Innovation Fund Denmark (grant nr. 9068-00025B). Hartwig R. Siebner was supported by a collaborative project grant “ADAptive and Precise Targeting of cortex-basal ganglia circuits in Parkinson's Disease - ADAPT-PD” from Lundbeckfonden (grant nr. R336-2020-1035). Finally, the clinicians that referred the patients to the study should also be acknowledged.

Funding Information:
First of all, we thank all patients who participated in the study. We are also thankful to all funders: Augustinusfonden, Axel Muusfeldts Fond, Beckett-Fonden, A.P. Møller Fonden: Fonden til Lægevidenskabens Fremme, Sundhedsstyrelsen (the Danish Ministry of Health), Helsefonden, Ivan Nielsens Fond for personer med specielle sindslidelser, Jascha Fonden, Læge Gerhard Linds Legat, Lundbeckfonden, Psykiatrisk Forskningsfond af 1967, and Region Hovedstaden Fond. Hartwig R. Siebner and Poul Videbech are supported by a Grand Solutions grant “Precision Brain-Circuit Therapy - Precision-BCT)” from Innovation Fund Denmark (grant nr. 9068-00025B ). Hartwig R. Siebner was supported by a collaborative project grant “ADAptive and Precise Targeting of cortex-basal ganglia circuits in Parkinson's Disease - ADAPT-PD” from Lundbeckfonden (grant nr. R336-2020-1035 ). Finally, the clinicians that referred the patients to the study should also be acknowledged.

Publisher Copyright:
© 2024 The Authors

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