ArticleBrain, behavior, & immunity - health2025
Trajectory of peripheral inflammation during index ECT in association with clinical outcomes in treatment-resistant depression.
Article in Brain, behavior, & immunity - health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- New insights into the mechanisms of electroconvulsive therapy in treatment-resistant depression.Frontiers in psychiatry · 2025Review
- Immune-inflammatory, neuroplastic, and epigenetic effects of electroconvulsive therapy in mood disorders: an overview of recent studies.Frontiers in psychiatry · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
Background: Electroconvulsive therapy (ECT) is a highly efficacious intervention for severe and intractable depression. Evidence suggests ECT provokes an initial acute inflammatory response that subsequently decreases with repeated administration. However, relationships between inflammatory changes and clinical effects are unclear. Improved understanding of these processes may provide critical insight into effective intervention for treatment-resistant depression (TRD). Methods: Plasma inflammatory markers were assessed at pre-treatment (T1), after the second ECT session (T2), and after ECT index series completion (post-treatment/T3) in TRD (n = 40). Changes were examined over time and in association with post-treatment Responder/Non-responder status (≥50% reduction in global depression severity) and percent change in affective, cognitive and neurovegetative depressive symptom domains. Results: C-reactive protein (CRP) and interleukin-6 (IL-6) increased from pre-treatment to T2, and decreased from T2 to post-treatment. Neither early (%T2-T1) nor total (%T1-T3) change in inflammation predicted clinical outcomes, however, the interaction between early/acute inflammatory response and post-treatment inflammation (relative to baseline) was associated with clinical outcomes. Larger initial increases in IL-6 predicted greater reductions in both affective and cognitive symptoms in subjects with higher post-treatment IL-6; those with lower post-treatment IL-6 trended toward the opposite. The same was found between changes in CRP and neurovegetative symptoms. Conclusions: Though preliminary, these results demonstrate how processes involved in the acute inflammatory response to ECT may differentially influence clinical outcomes depending on overall trajectory of inflammation following ECT. Findings also highlight the importance of examining symptom-specific changes in depression when studying treatment mechanisms, rather than relying solely on global measures of severity.
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