Electroconvulsive therapy increases temporarily plasma vascular endothelial growth factor in patients with major depressive disorder.

OBJECTIVES: Vascular endothelial growth factor (VEGF) has been related to the etiology of major depressive disorder (MDD). The findings involving the effects of electroconvulsive therapy (ECT) on the VEGF levels have been conflicting. The aim was to examine the possible changes in the VEGF levels and their associations with clinical outcome in patients with MDD during ECT. METHODS: The study comprised 30 patients suffering from MDD. Their plasma VEGF levels were measured at baseline and 2 and 4 hr after the first, fifth, and last ECT session. The severity of depression was quantified by the Montgomery-Asberg Depression Rating Scale (MADRS). RESULTS: The VEGF levels increased between the 2-hr and 4-hr measurements during the first (p = .003) and the fifth (p = .017) sessions. The baseline VEGF levels between individual ECT sessions remained unchanged during the ECT series. No correlations were found between the increased VEGF levels and the clinical outcome. CONCLUSIONS: Electroconvulsive therapy increased the VEGF levels repeatedly at the same time point in two different ECT sessions. These increases had no association with the response to ECT. Consequently, VEGF may act as a mediator in the mechanism of action of ECT.

Effect of electroconvulsive therapy on brain-derived neurotrophic factor levels in patients with major depressive disorder.

OBJECTIVES: Brain-derived neurotrophic factor (BDNF) has been associated with depression and its treatment response. The aim of the present study was to explore the effect of electroconvulsive therapy (ECT) on serum and plasma BDNF levels and change of Montgomery-Asberg Depression Rating Scale (MADRS) and their associations in patients with major depressive disorder (MDD). METHODS: The study included thirty patients suffering from MDD. Their serum and plasma BDNF levels were examined before ECT (baseline) and after the first, fifth, and last ECT session. The severity of the depression and the response to ECT were measured with MADRS. RESULTS: Electroconvulsive therapy caused no significant changes in serum BDNF levels. Plasma BDNF levels decreased during the fifth ECT session between the baseline and the 2-hr samples (p = 0.019). No associations were found between serum or plasma BDNF levels and remission. The correlations between plasma and serum BDNF levels in each measurement varied between 0.187 and 0.636. CONCLUSIONS: Neither serum nor plasma BDNF levels were systematically associated with the clinical remission. However, the plasma BDNF levels somewhat varied during the ECT series. Therefore, the predictive value of BDNF for effects of ECT appears to be at least modest.

Low tumor necrosis factor-α levels predict symptom reduction during electroconvulsive therapy in major depressive disorder.

Objective: Changes in the tumor necrosis factor-α (TNFα) have been associated with major depressive disorder (MDD). Findings concerning the effects of electroconvulsive therapy (ECT) on the TNFα level have been contradictory. The aim was to examine the immediate and long-term changes in the TNFα level and their associations with symptom reduction in patients with MDD during ECT. Method: The study included 30 patients with MDD. Their TNFα levels were measured at baseline and 2 and 4 hr after the first, fifth and last ECT session. Depressive symptoms were assessed with the Montgomery-Asberg Depression Rating Scale (MADRS). Results: The TNFα level decreased from baseline to the 2- and 4-hr measurements. There was a correlation between the first ECT session TNFα levels and the relative symptom reduction according to the MADRS score after the ECT series. Both the first (baseline) ECT and 4-hr TNFα levels were lower in responders than in nonresponders. Conclusion: ECT consistently induced a decrease in the TNFα level after each studied session. A low TNFα level at the first ECT appeared to predict a symptom reduction. These findings suggest that TNFα might have a role in the pathogenesis in MDD and in the mechanism of action of ECT.

Effects of S-ketamine as an anesthetic adjuvant to propofol on treatment response to electroconvulsive therapy in treatment-resistant depression: a randomized pilot study.

OBJECTIVE: Ketamine in electroconvulsive therapy (ECT) anesthesia has been reported to be associated with better seizure quality and longer duration compared with methohexital anesthesia. Furthermore, ketamine may enhance the efficacy of ECT while having rapid independent antidepressant properties itself. However, data on the effects of ketamine with ECT are inconsistent, and there are no reports of S-ketamine. The aim of the present pilot study was to explore the effects of S-ketamine as an adjuvant to propofol on the efficacy, seizure duration, and quality of electroencephalography in patients with treatment-resistant depression. METHODS: Thirty-two patients with a recurrent severe or psychotic major depressive disorder with treatment resistance to antidepressants were included in the study. For induction of anesthesia, the patients were randomized into 2 study groups. The S-ketamine group first received S-ketamine (0.4 mg/kg) as a bolus and then propofol. The treatment-as-usual group first received saline and then propofol. RESULTS: A statistically significant and clinically relevant reduction in the depression symptom scores was found in both study groups during ECT. There was no difference in the magnitude or speed of response between the study groups, nor was there any difference in the numbers of ECT treatments, seizure thresholds, seizure durations, and the electrical doses either. The patients recovered from anesthesia equally, but the degree of posttreatment disorientation and restlessness was more marked in the S-ketamine group. CONCLUSIONS: In conclusion, a subanesthetic adjuvant dose of S-ketamine with propofol may not increase the effects of ECT in patients with treatment-resistant depression. However, S-ketamine was associated with increased posttreatment disorientation and restlessness.

One-year follow-up after discontinuing maintenance electroconvulsive therapy.

OBJECTIVES: Electroconvulsive therapy (ECT) has been established as an effective method in the treatment of severe depressive or psychotic disorders. Its efficacy is greatest in severe major depressive disorder (MDD) with or without psychotic symptoms. However, maintaining remission after a successful course of short-term ECT is often difficult owing to resistance to medication in these patients. Therefore, the relapse rate after short-term ECT is high; 40% to 60% of patients relapse even with adequate antidepressant continuation therapy. The risk of relapse is greatest during the first months after discontinuation of short-term ECT. Continuation/maintenance (c/m) ECT is an option in maintaining remission, but systematic data and clinical guidelines are lacking. The point at which to discontinue this treatment has not been adequately established. METHODS: Altogether 45 consecutive patients treated with c/mECT after short-term ECT to prevent relapse were followed up 1 year after discontinuation of this treatment. RESULTS: Twenty (44%) of 45 patients relapsed during follow-up, all within the first 8 months. Patients having a diagnosis other than MDD (bipolar disorder, depressive episode type I, schizophrenia, and schizoaffective disorder) were more likely to relapse than MDD patients. CONCLUSIONS: Almost half of the patients relapsed in 1 year after discontinuation of c/mECT, most of these within the first 3 months and all within the first 8 months. The risk of relapse is greater in the patients with diagnoses other than MDD. When discontinuing c/mECT, patients should be carefully followed up; and for those at risk of relapse, even permanent mECT should be considered. To the best of our knowledge, the present study is the first to report the prognosis of patients after discontinuing c/mECT.