engleski

ECT IN TREATMENT-RESISTANT SCHIZOPHRENIA: CURRENT PRACTICE AND FUTURE PERSPECTIVES

Treatment resistance continues to represent the greatest unmet need in schizophrenia care, despite the ever growing number of antipsychotics. However, about one third of patients do not show sufficient improvement with antipsychotics. About half of those patients with treatment-resistant schizophrenia (TRS) have a poor response to clozapine. The pathophysiology of TRS is highly heterogeneous and includes dopaminergic, glutamatergic, and GABAergic dysfunction. Although electroconvulsive therapy (ECT) is primarily utilized to treat patients with severe depression, it can effectively reduce the symptoms of TRS, although some patients do not respond to this treatment. ECT produces changes in different brain regions/networks, that are supposed to correlate with the pathological findings in schizophrenia. In preclinical models, ECT had both acute and chronic effects on neurogenesis, while chronic ECT reduced neuroinflammation. However, the data on peripheral markers on inflammation and growth factors in patients are often heterogeneous, and studies were carried out mostly on patients with depression, while the data in schizophrenia are scarce. The mechanism of efficacy of ECT in TRS is not known. While preclinical trials suggest it may normalize dopamine supersensitivity state, clinical data are missing. Such effects may be important for patients who were not initially resistant. Other patients may be resistant from the illness onset, which could have unaltered dopamine synthesis capacity, but show NMDA receptor dysfunction on GABA interneurons. Chronic overactivation of the immune system can also be present from the illness onset. Establishing clinical and biological markers of TRS, as well as predictors of response to ECT, is a priority. Such markers would distinguish patients who will benefit from ECT, and provide this treatment early in the disease course, which may improve the long-term outcome

ECT - treatment-resistant schizophrenia - dopamine supersensitivity - neuroinflammation

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