Electroconvulsive Therapy Changes Peripheral Blood Neurotrophic and Inflammatory Markers in Depressed Patients

Electroconvulsive therapy (ECT) is one of the most effective treatments for treatment-resistant depression, yet its precise mechanisms of action remain to be further elucidated. Among other effects, ECT induces an acute inflammatory immune response that might reinforce the expression of neurotrophins such as brain-derived neurotrophic factor (BDNF). The aim of this study is to unveil the potentially beneficial role of inflammation observed during ECT.

Within a repeated measures design study of 6 weeks, 9 patients diagnosed with depressive disorder received 3 ECT sessions per week. We tracked the clinical progress using the Hamilton Depression rating scale (HAMD-21) and Beck's depression inventory. By collecting peripheral blood samples before and throughout the entire course of ECT, we investigated week-by-week changes in inflammation markers such as IL-6, IL-1β, TNF-α, and IL-4, serum BDNF, and cortisol levels.

Seven out of 9 patients successfully responded to ECT according to HAMD-21 scores. Serum BDNF levels progressively increased during the ECT series, and negatively correlated with HAMD-21 scores. TNF-α levels increased until week 4 and decreased after the end of the therapy. Moreover, we found altered expression of the anti-inflammatory cytokine IL-4, while serum cortisol levels did not change during ECT.

The initial activation of the immune-inflammatory response observed during ECT may be beneficial for therapeutic effects, as it is related to a long-term stimulation of BDNF, which enhances neuronal plasticity. The downregulation of proinflammatory markers after the end of the ECT series may be associated with clinical improvement.