Background: The management and treatment of major depressive disorder are major public health challenges, the lifetime prevalence of this illness being 4.4%-20% in the general population. Major depressive disorder and treatment resistant depression appear to be, in part, related to a dysfunction of the immune response. Among the treatments for depression ECT occupies an important place. The underlying cerebral mechanisms of ECT remain unclear.
Objectives/hypothesis: The aim of this review is to survey the potential actions of ECT on the immuno-inflammatory cascade activated during depression.
Methods: A systematic search of the literature was carried out, using the bibliographic search engines PubMed and Embase. The search covered articles published up until october 2017. The following MESH terms were used: Electroconvulsive therapy AND (inflammation OR immune OR immunology).
Results: Our review shows that there is an acute immuno-inflammatory response immediately following an ECT session. There is an acute stress reaction. Studies show an increase in the plasma levels of cortisol and of interleukins 1 and 6. However, at the end of the course of treatment, ECT produces, in the long term, a fall in the plasma level of cortisol, a reduction in the levels of TNF alpha and interleukin 6.
Limitations: One of the limitations of this review is that a large number of studies are relatively old, with small sample sizes and methodological bias.
Conclusion: Advances in knowledge of the immuno-inflammatory component of depression seem to be paving the way towards models to explain the mechanism of action of ECT.
Keywords: Cortisol; Depressive disorder; ECT; Immune; Inflammation.
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