Electroconvulsive therapy and biomarkers of neuronal injury and plasticity: Serum levels of neuron-specific enolase and S-100b protein

Abstract Electroconvulsive therapy (ECT) is considered an effective and safe treatment in major depressive disorders. However, the possibility that it may induce cognitive adverse effects observed in selected patients has raised a concern that ECT may induce neuronal damage. The biomarkers of brain damage, neuron-specific enolase (NSE) and S-100b protein (S-100b), were measured in serum before and after ECT to determine whether this treatment induces neuronal injury or glial activation. ECT was administered to 10 patients with major depressive disorder. The serum samples were analyzed before (baseline) and after ECT at 1 h, 2 h, 6 h, 24 h and 48 h. The severity of depression was scored with the Montgomery-Asberg Depression Rating Scale (MADRS) and Beck Depression Inventory (BDI) pre-to-post ECT. There were no statistically significant changes in the median concentrations of NSE or S-100b at various time points before or after ECT. However, there were substantial elevations in the levels of S-100b in four patients. High levels of S-100 at 2 and 6 h correlated with the response to the treatment. These results suggest that ECT does not produce neuronal injury. The transient increase in the levels of S-100b reflecting activation of glial cells may play a part in mediating the antidepressant effects of ECT.