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 charcoal on the absorption and elimination of the antiepileptic drugs lamotrigine and oxcarbazepine.

OBJECTIVE: The effects of single and repeated doses of oral activated charcoal (OAC) on the absorption and elimination of the antiepileptic drugs, lamotrigine (CAS 84057-84-1, LTG, Lamictal) and oxcarbazepine (CAS 28721-07-5, OXC, Trileptal) were studied in healthy volunteers to assess the therapeutic potential of OAC in the treatment of LTG and OXC overdose. METHODS: In three open, randomized, cross-over sessions with > or = 14 days washout, LTG 100 mg and OXC 600 mg were given orally, each to 6 subjects. In one session the drugs were given alone, and in two others with single (50 g) or repeated (20 g) doses of OAC as water suspension. The single OAC dose was given 30 min after the drugs, and repeated doses 6-72 h after LTG and 12-48 h after OXC. Serum concentrations of the parent drugs as well as those of the pharmacolocigally active metabolite of OXC, 10,11-dihydro-10-hydroxy-carbamazepine (MHD), were measured with reverse-phase high-performance liquid chromatography. Pharmacokinetic variables were calculated by non-compartmental analysis. RESULTS: Single OAC dose decreased AUC0-infinity of LTG, OXC and MHD to 58%, 2.8% and 4.2% of the respective variables without OAC. Also Tmax of OXC and MHD decreased to 4.4% and 8.1%, respectively. Repeated OAC doses after LTG decreased its AUC from 6 h to infinity (AUC6-infinity) to 39% and t1/21beta to 44%. Repeated OAC doses after a single dose of OXC decreased the AUC12-infinity and t/12beta of MHD to 46% and 45% of the respective variables without OAC. CONCLUSION: OAC greatly reduces gastrointestinal absorption of LTG and especially that of OXC, and it accelerates the elimination of LTG and MHD. The use of OAC is hence strongly favoured in the treatment of overdose with these drugs.