Electroconvulsive therapy or clozapine for adolescents with treatment-resistant schizophrenia: an explorative analysis on symptom dimensions.

OBJECTIVE: This study sought to compare pre-intervention patient characteristics and post-intervention outcomes in a naturalistic sample of adolescent inpatients with treatment-resistant psychotic symptoms who received either electroconvulsive therapy (ECT) or clozapine. METHODS: Data of adolescents with schizophrenia/schizoaffective disorder receiving ECT or clozapine were retrospectively collected from two tertiary-care psychiatry-teaching university hospitals. Subscale scores of the Positive and Negative Symptom Scale (PANSS) factors were calculated according to the five-factor solution. Baseline demographics, illness characteristics, and post-intervention outcomes were compared. RESULTS: There was no significant difference between patients receiving ECT (n = 13) and clozapine (n = 66) in terms of age, sex, and the duration of hospital stay. The ECT group more commonly had higher overall illness and aggression severity. Smoking was less frequent in the clozapine group. Baseline resistance/excitement symptom severity was significantly higher in the ECT group, while positive, negative, affect, disorganisation, and total symptom scores were not. Both interventions provided a significant reduction in PANSS scores with large effect sizes. CONCLUSION: Both ECT and clozapine yielded high effectiveness rates in adolescents with treatment-resistant schizophrenia/schizoaffective disorder. Youth receiving ECT were generally more activated than those who received clozapine.

A Systematic Review of the Literature Regarding the Relationship Between Oxidative Stress and Electroconvulsive Therapy.

Objective: Brain's aerobic energy metabolism, abundance of the fatty acids and unsaturated lipids, generation of Reactive Oxygen Species (ROS) by hormones, physiological roles of transition metals (i.e., iron and copper), and free radicals in the nervous system may cause inclination to oxidative stress in psychiatric disorders. Electroconvulsive therapy (ECT) may cause oxidative stress by the electrical field or by the induced seizure. It was aimed to review the literature in terms of the influence of ECT on levels of oxidant and antioxidant compounds. Methods: The literature search was performed with the keywords that were oxidative stress or "DNA damage" or "RNA damage" or "lipid peroxidase" or "superoxide dismutase" or "catalase" or "glutathione" or "nitrite" or "nitric oxide" and "electroconvulsive therapy" or "electroconvulsive shock" or "electroconvulsive seizure". Twenty of 1480 records were included. Results: Eleven studies were performed in human subjects, whereas 9 studies were performed in rats. Human studies are conducted with serum, plasma, or urine samples; rat studies include brain tissues from various sites. In rats, four independent studies showed increased levels of lipid oxidation markers, and four independent studies reported increased levels of oxidative stress markers in brain samples. In human studies, studies were performed with circulating blood samples and the results were more inconsistent. Conclusion: Although some markers like superoxide dismutase or thioredoxin imply that ECT may increase the balance for oxidative stress, this notion is not supported by other markers of ECT. The current literature does not clearly suggest that the ECT is associated with oxidative stress in psychiatric disorders. Further studies with similar methods should be performed in big samples.

Electroconvulsive Therapy and Extracellular Matrix Glycoproteins in Patients with Depressive Episodes.

Background: The brain extracellular matrix (ECM) is composed of glycoproteins deriving from the cell membrane and joining into nets called perineuronal nets (PNNs). The ECM glycoproteins limit neuroplasticity, cell proliferation, and differentiation. Electroconvulsive therapy (ECT) is provided by electrical currents that may alter several cascades and biophysical effects. ECM conformation might be influenced by the effects of ECT. Methods: Patients with depressive disorders (n = 23) and healthy control subjects (n = 21) were enrolled. Serum levels of the ECM glycoproteins versican, brevican, neurocan, phosphocan and tenascin C were measured with enzyme-linked immunosorbent assay. Serum samples were collected from the patients in the patient group at 3 time points: before ECT, 30 min after the first session, and 30 min after the seventh session. Results: There was a significant difference in tenascin C levels (P = .001) between the groups. No other significant difference was observed. Serum levels of the measured ECM glycoproteins and prolidase activity did not differ in the depression group after the administration of ECT. Conclusions: Our results did not support the claim suggesting a possible mechanism for modulation of ECM glycoproteins by ECT. Serum levels may not necessarily reflect conformational changes in the ECM. Further studies are needed to investigate the effects of ECT on ECM glycoproteins. Modulation of the ECM may provide a new window suggesting improvement in treatments.