Electroconvulsive therapy (ECT) and aerobic exercise training (AET) increased plasma BDNF and ameliorated depressive symptoms in patients suffering from major depressive disorder

BackgroundTo treat patients suffering from major depressive disorder (MDD), research has focused on electroconvulsive therapy (ECT) and aerobic exercise training (AET). Brain derived neurotrophic factor (BDNF) seems to be key in MDD. The aims of the present study were therefore two-fold, to investigate in a three-arm interventional study the differential effects of ECT, ECT plus AET, and AET alone in patients suffering from TR-MDD on 1. depressive symptoms and 2. plasma BDNF (pBDNF).Methods60 patients with MDD (mean age: 31 years; 31.6% female patients) were randomly assigned either to the ECT, ECT + AET, or AET condition. The AET condition consisted of treadmill exercise for 45 min, three times a week. Both depression severity and pBDNF levels were assessed at baseline and 4 weeks later. All patients were further treated with an SSRI standard medication.ResultspBDNF levels increased over time in all three study conditions, though, highest increase was observed in the ECT + EAT condition, and lowest increase was observed in the AET condition. Depressive symptoms decreased in all three conditions over time, though, strongest decrease was observed in the ECT + AET condition. The combination of ECT + AET led to significantly greater remission rates than in either the ECT or AET alone conditions. BDNF levels were not associated with symptoms of depression.ConclusionsThe pattern of results suggests that ECT, AET and particularly their combination are promising directions for the treatment of patients suffering from MDD, and that it remains unclear to what extent pBDNF is key and a reliable biomarker for MDD.     

Acute and subsequent continuation electroconvulsive therapy elevates serum BDNF levels in patients with major depression

IntroductionThe induction of brain-derived neurotrophic factor (BDNF) release and subsequent restoration of neuroplastic homeostasis may underlie the effects of electroconvulsive therapy (ECT).ObjectivesWe aimed to assess serum and plasma BDNF levels during the course of acute ECT, as well as before and after subsequent continuation ECT, in patients with depression.MethodsWe included 24 patients with major depressive disorder (mean age ± SD: 54.5 ± 13.7; f/m: 17/7; baseline 17-item Hamilton Depression Rating Scale score of 26.79 ± 4.01). Serum and plasma BDNF (sBDNF, pBDNF) levels were assessed at nine time-points before, during, and after acute ECT series. Data were analysed using linear regression and linear mixed models, which were adjusted for multiple comparisons via Bonferroni correction. Five patients received continuation ECT subsequent to the acute ECT series. In these patients, BDNF levels were assessed before and after each two continuation ECT sessions using Wilcoxon signed-rank tests.ResultsRelative to baseline (mean ng/ml ±SD: 24.68 ± 14.40), sBDNF levels were significantly higher 1 day (33.04 ± 14.11, p = 0.013, corrected), 1 week (37.03 ± 10.29, p < 0.001, corrected), and 1 month (41.05 ± 10.67, p = 0.008, corrected) after the final ECT session, while pBDNF levels did not significantly differ (p > 0.1). Furthermore, our results indicated that sBDNF levels increased after each continuation ECT session. There was no significant association between sBDNF levels and clinical parameters or treatment response.ConclusionThe absence of an association between changes in sBDNF levels and depressive symptoms challenges the proposed concept of sBDNF/pBDNF as key markers of the effects of ECT.     

BDNF blood levels after electroconvulsive therapy in patients with mood disorders: A systematic review and meta-analysis

Objectives. To evaluate whether electroconvulsive therapy (ECT), a very effective non-pharmacological treatment for mood disorders, induces neurotrophic effects, indexed by the measurement of peripheral brain-derived neurotrophic factor (BDNF) levels. Methods. Systematic review and meta-analysis of clinical trials published in PubMed/Medline from the first date available to October 2013. We included studies measuring pre- and post-BDNF blood levels under ECT in patients with mood disorders in the acute depressive episode. Results. Eleven studies (n = 221 subjects) were eligible. These studies enrolled subjects with unipolar, bipolar and psychotic depression and varied regarding electrode placement (unipolar vs. bipolar) and previous use of pharmacotherapy. Nonetheless, BDNF significantly increased after ECT (Hedges’ g pooled, random-effects model of 0.354; 95% CI = 0.162–0.546). The results were robust according to sensitivity analysis and Begg's funnel plot did not suggest publication bias. Meta-regression results did not show association of the outcome with any clinical and demographic variable, including depression improvement. Conclusions. Our meta-analysis indicates that, similar to pharmacological interventions, peripheral BDNF increases after ECT treatment. The lack of correlation between BDNF increasing and depression improvement suggests that ECT induces neurotrophic effects regardless of clinical response in depression.     

Brain-derived neurotrophic factor (BDNF) polymorphisms G196A and C270T are not associated with response to electroconvulsive therapy in major depressive disorder

The aim of the present study was to examine an association of brain-derived neurotrophic factor (BDNF) polymorphisms G196A and C270T and the response to electroconvulsive therapy (ECT) in major depressive disorder (MDD). The study group consisted of 119 patients consecutively admitted for ECT in the Department of Psychiatry, Tampere University Hospital. All patients fulfilled the diagnostic criteria of DSM-IV for MDD. ECT was administered three times a week with a brief pulse constant current device. The Montgomery and Asberg Depression Rating Scale (MADRS) was used as an outcome measure of depression. Genotyping was performed using fluorescent allele-specific TaqMan probes. No association between either G196A or C270T and the response to ECT was found in the whole population. There were no significant differences in responses between men and women or between psychotic and non-psychotic patients. However, within subgroups such as in psychotic and in late-onset depression CC genotype of C270T may predict good response. BDNF may not be associated with response to ECT in general, but some association in subgroups may exist.     

Brain functional effects of electroconvulsive therapy during emotional processing in major depressive disorder

BackgroundIn treatment-resistant major depressive disorder (MDD), electroconvulsive therapy (ECT) is a treatment with high efficacy. While knowledge regarding changes in brain structure following ECT is growing, the effects of ECT on brain function during emotional processing are largely unknown.ObjectiveWe investigated the effects of ECT on the activity of the anterior cingulate cortex (ACC) and amygdala during negative emotional stimuli processing and its association with clinical response.MethodsIn this non-randomized longitudinal study, patients with MDD (n = 37) were assessed before and after treatment with ECT. Healthy controls (n = 37) were matched regarding age and gender. Functional magnetic resonance imaging (fMRI) was obtained twice, at baseline and after six weeks using a supraliminal face-matching paradigm. In order to evaluate effects of clinical response, additional post-hoc analyses were performed comparing responders to non-responders.ResultsAfter ECT, patients with MDD showed a statistically significant increase in ACC activity during processing of negative emotional stimuli (p_FWE = .039). This effect was driven by responders (p_FWE = .023), while non-responders showed no increase. Responders also had lower pre-treatment ACC activity compared to non-responders (p_FWE = .025). No significant effects in the amygdala could be observed.ConclusionsECT leads to brain functional changes in the ACC, a relevant region for emotional regulation during processing of negative stimuli. Furthermore, baseline ACC activity might serve as a biomarker for treatment response. Findings are in accordance with recent studies highlighting properties of pre-treatment ACC to be associated with general antidepressive treatment response.     

Pre-treatment peripheral biomarkers associated with treatment response in panic symptoms in patients with major depressive disorder and panic disorder: A 12-week follow-up study

ObjectivePeripheral biomarkers have been studied to predict treatment response of panic symptoms. We hypothesized that depressive disorder (MDD) vs. panic disorder (PD) would exhibit different peripheral biomarkers, and their correlation with severity of panic attacks (PA) would also differ.MethodsForty-one MDD patients, 52 PD patients, and 59 healthy controls were followed for 12 weeks. We measured peripheral biomarkers along with the Panic Disorder Severity Scale (PDSS) at each visit—pre-treatment, 2, 4, 8, and 12 weeks on a regular schedule. Peripheral biomarkers including serum cytokines, plasma and serum brain-derived neurotrophic factor (BDNF), leptin, adiponectin, and C-reactive protein (CRP) were quantified using enzyme-linked immunosorbent assay (ELISA).ResultsPatients with MDD and PD demonstrated significantly higher levels of pre-treatment IL-6 compared to controls, but no differences were seen in plasma and serum BDNF, leptin, adiponectin, and CRP. Pre-treatment leptin showed a significant clinical correlation with reduction of panic symptoms in MDD patients at visit 5 (p = 0.011), whereas pre-treatment IL-6 showed a negative correlation with panic symptom reduction in PD patients (p = 0.022). An improvement in three panic-related items was observed to be positively correlated with pre-treatment leptin in MDD patients: distress during PA, anticipatory anxiety, and occupational interference.ConclusionHigher pre-treatment leptin was associated with better response to treatment regarding panic symptoms in patients with MDD, while higher IL-6 was associated with worse response regarding panic symptoms in PD patients. Different predictive peripheral biomarkers observed in MDD and PD suggest the need for establishing individualized predictive biomarkers, even in cases of similar symptoms observed in different disorders.     

Reduced platelet BDNF level in patients with major depression

Serum and plasma brain-derived neurotrophic factor (BDNF) levels as well as brain BDNF have previously been shown to be decreased in patients with major depressive disorder (MDD). We explored whether platelet BDNF levels, circulating stored BDNF, would be lower in MDD patients than in normal controls. BDNF levels were examined in platelet-rich plasma (PRP) and platelet-poor plasma (PPP) in 20 hospitalized non-suicidal MDD patients, 20 recent-suicidal MDD patients, and 20 normal controls. Platelet BDNF content was calculated by subtracting PPP BDNF level from PRP BDNF level, and dividing the result by the total platelet count, and it was expressed as pg/10⁶ platelets. Individuals were evaluated using a Structured Clinical Interview for DSM-IV and a Hamilton Depression Rating Scale. Platelet BDNF contents were significantly lower in non-suicidal patients (3.09 ± 2.53 pg/10⁶ platelets) and recent-suicidal MDD patients (3.16 ± 1.99 pg/10⁶ platelets) than in healthy controls (6.17 ± 2.64 pg/10⁶ platelets) (p < 0.01). However, platelet BDNF contents had no significant differences between non-suicidal and recent-suicidal patients. PRP BDNF levels were also significantly lower in non-suicidal and suicidal MDD patients than in healthy controls (p = 0.029), while PPP BDNF had no significant difference between 3 groups (p = 0.971). Our findings suggest that there is a decrease in the platelet BDNF of patients with major depression. Reduced platelet BDNF contents as circulating stored BDNF could be associated with lower serum BDNF level in patients with major depression.     

Comparison of the efficacy and safety of melatonin and memantine in the alleviation of cognitive impairments induced by electroconvulsive therapy: A randomized clinical trial

The purpose of this study was to assess and compare the efficacy and safety of melatonin and memantine in the alleviation of cognitive disorders in patients diagnosed with major depressive disorder (MDD) undergoing electroconvulsive therapy (ECT). Patients undergoing ECT for treatment of MDD were randomly allocated to the melatonin (3 mg/d) or memantine (5 mg/d) groups. The participants received either melatonin or memantine (tablet) through the ECT therapy, which was started at beginning the first day of ECT and continued to the sixth session. The Modified Mental State Examination (MMSE) was used to evaluate cognitive function before and after the intervention. Frothy eligible patients (22 females and 18 males) were studied. There was no significant difference between two groups in terms of demographic characteristics, hemodynamic parameters and baseline MMSE and item 3 MMSE. The Memantine group scored significantly higher at the end of the ECT sessions either by MMSE or item 3MMSE than the baseline (P = 0.04 and P = 0.03, respectively). In the melatonin group, both MMSE and item 3MMSE scores were decreased significantly than the baseline (p = 0.03 and p = 0.02, respectively). No withdrawal was observed due to the drugs' adverse effects. It seems that memantine (5 mg/d) is more effective than melatonin (3 mg/d), to alleviate cognitive disorders induced by ECT.     

Differences in sleep functioning between individuals with seasonal affective disorder and major depressive disorder in Finland

BackgroundSleep problems are commonly reported in seasonal affective disorder (SAD) and major depressive disorder (MDD). However, the specific characteristics of sleep difficulties differ. Frequent sleep problems in MDD are insomnia and night awakenings, whereas SAD patients complain of hypersomnia and daytime sleepiness. No previous studies have reported differences in sleep functioning between these two disorders.MethodsWe interviewed 4554 subjects from the Health 2011 survey and included 4153 individuals in this study. We selected participants who fulfilled the criteria for SAD (n = 223), nonseasonal-MDD (n = 238), SAD + MDD (n = 65), and controls (n = 3627). They completed the World Health Organization Composite International Diagnostic Interview, Munich version (M-CIDI), the Seasonal Pattern Assessment Questionnaire (SPAQ), The Beck Depression Inventory (BDI), the EuroQoL (EQ-5), the Alcohol Use Disorders Identification Test (AUDIT) and several questions about sleeping, based on the Basic Nordic Sleep Questionnaire (BNSQ).ResultsWe found Significant differences between groups for “enough sleep”, “breathing interruptions during sleep”, “tiredness during the day”, and “sleeping difficulties”. Controls reported better functioning in all sleep variables. SAD + MDD individuals showed more problems in “enough sleep” than SAD, more “breathing interruptions during sleep” than SAD and nonseasonal-MDD, felt more “tired during the day” than SAD and nonseasonal-MDD, and reported more “sleeping difficulties” than SAD and nonseasonal-MDD. Finally, nonseasonal-MDD individuals felt more “tired during the day” than SAD.ConclusionIndividuals with SAD + MDD show generalized sleeping problems. However, when SAD and nonseasonal-MDD appear separately, similar sleep functioning is observed. Nonseasonal-MDD subjects report to be more tired during the day than SAD.     

Association between serum brain-derived neurotrophic factor and plasma interleukin-6 in major depressive disorder with melancholic features

Inflammatory processes as well as attenuation of brain-derived neurotrophic factor (BDNF) availability are involved in the pathophysiology of major depressive disorder (MDD). Although it is generally presumed that these two systems interact negatively in the brain, preclinical and human in vitro studies have shown synergistic rather than antagonistic interactions in the periphery. We therefore examined the association between serum levels of BDNF and plasma levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in patients with MDD (n = 1070) and non-depressed controls (n = 379) from the Netherlands Study of Depression and Anxiety. We used multiple regression analyses with serum BDNF as the dependent variable and we specifically tested the presence of BDNF–cytokine associations in DSM-IV-assigned melancholic MDD patients, identified by the Inventory of Depressive Symptomatology. After adjustment for sociodemographics, sampling variability, lifestyle indicators, somatic diseases and medication use, BDNF levels were predicted by the interaction between MDD diagnosis and IL-6 (p-interaction = .006). Stratified analyses showed that BDNF levels are indeed positively associated with IL-6 levels in MDD patients (β = .07, p = .02), but not in non-depressed controls (β = −.07, p = .23). When further stratified for melancholic and non-melancholic MDD (p-interaction = .005), IL-6 emerged as a robust positive predictor of BDNF only in the melancholic sample (β = .21, p = .01), wherein serum BDNF levels were accordingly enhanced. Post-hoc exploratory analyses verified an accentuated positive association of BDNF levels with leucocyte counts in melancholia. No significant associations emerged between BDNF and TNF-α. Overall, our cross-sectional approach may have disclosed an allostatic, BDNF-inducing component of peripheral immunity and/or an immunotrophic function of peripheral BDNF. Both scenarios may warrant further exploration, as they could inform new research concepts towards immune-based antidepressive treatment strategies.     

Factors causing a relapse of major depressive disorders following successful electroconvulsive therapy: A retrospective cohort study

BACKGROUNDElectroconvulsive therapy (ECT) is used to treat major depressive disorder (MDD). Relapse is often observed even after successful ECT, followed by adequate pharmaceutical treatment for MDD. AIMTo investigate the diagnostic factors and treatment strategies associated with depression relapse.METHODSWe analyzed the relationships between relapse, the diagnostic change from MDD to bipolar disorder (BP), and treatment after the initial ECT. We performed a 3-year retrospective study of the prognoses of 85 patients of the Shiga University of Medical Science Hospital. The relative risk of relapse of depressive symptoms was calculated based on the diagnostic change from MDD to BP. A receiver operating characteristic (ROC) curve was generated to evaluate the predictive accuracy of diagnostic changes from MDD to BP based on the duration between the first course of ECT and the relapse of depressive symptoms.RESULTSEighty-five patients initially diagnosed with MDD and successfully treated with ECT were enrolled in the study. Compared with the MDD participants, more BP patients experienced relapses and required continuation and/or maintenance ECT to maintain remission (65.6% vs 15.1%, P < 0.001; relative risk = 4.35, 95%CI: 2.19-8.63, P < 0.001). Twenty-nine patients experienced relapses during the three-year follow-up. In 21 (72.4%, 21/29) patients with relapse, the diagnosis was changed from MDD to BP. The duration from the first course of ECT to relapse was shorter for the BP patients than for the MDD patients (9.63 ± 10.4 mo vs 3.38 ± 3.77 mo, P = 0.022); for most patients, the interval was less than one month. The relative risk of depressive symptoms based on diagnostic changes was 4.35 (95% confidence interval: 2.19–8.63, P < 0.001), and the area under the ROC curve for detecting diagnostic changes based on relapse duration was 0.756 (95%CI: 0.562-0.895, P = 0.007).CONCLUSIONIt may be beneficial to suspect BP and change the treatment strategy from MDD to BP for patients experiencing an early relapse.     

Val66Met polymorphism association with serum BDNF and inflammatory biomarkers in major depression

Objectives: Current evidence supports participation of neurotrophic and inflammatory factors in the pathogenesis of major depressive disorder (MDD). Some studies reported an association between the Val66Met polymorphism (rs6265) of brain-derived neurotrophic factor (BDNF) gene with MDD and peripheral BDNF levels. However, no previous studies have examined the association of this polymorphism with inflammation. The present study assessed the association of the Val66Met polymorphism with serum levels of BDNF and inflammatory markers among depressed outpatients.

Methods: All participants (n?=?73) met DSM-IV criteria for a unipolar depressive episode. The serum levels of BDNF and inflammatory biomarkers (IL-2, IL-4, IL-6, IL-10, TNF-α and IFN-γ) were compared between individuals presenting with at least one Met allele (Met-carriers) and those homozygous for the Val allele.

Results: In our sample (84.9% female, mean age 52.4?±?10.3 years), 24.7% (n?=?18) were Met-carriers. After Bonferroni correction, the Met allele was significantly associated with higher BDNF and lower TNF-α. These associations persisted after adjusting for potential confounders.

Conclusions: The pattern of low BDNF and high inflammation in MDD may be influenced by the Val66Met polymorphism. The association of a polymorphism in the BDNF gene with inflammatory markers in addition to BDNF levels suggests an interaction between these systems.     

Brain-derived neurotrophic factor and electroconvulsive therapy in a schizophrenic patient with treatment-resistant paranoid-hallucinatory symptoms

It has been proposed that deficits in the production and the utilization of brain-derived neurotrophic factor (BDNF) may contribute to the pathogenesis of schizophrenia. At the same time, electroconvulsive shock, an experimental model of electroconvulsive therapy (ECT), has been shown to induce an increase of BDNF protein in brains of animal models. These findings suggest that one putative mechanism of action of ECT is the regulation of BDNF and/or related neurotrophins. In this case report, a 54-year-old man with severe treatment-resistant schizophrenic symptoms was treated with ECT. To evaluate the effect of ECT on BDNF serum levels, we collected a blood sample before each ECT session. During the course of ECT treatment, the paranoid and hallucinatory symptoms gradually improved, whereas BDNF levels increased over time. In addition, there was a general improvement of its positive and negative schizophrenic symptoms and depressive state. In conclusion, this case report further validates the therapeutic efficacy of ECT in schizophrenic patients with inadequate or poor response to traditional treatments. Moreover, ECT therapeutic effect is associated with an increase in BDNF serum levels. Further studies are needed to characterize the relationship between BDNF and ECT in schizophrenic patients.     

Serum brain-derived neurotrophic factor levels in conversion disorder: Comparative study with depression

The aim of the present study was to compare serum brain-derived neurotrophic factor (BDNF) levels of patients with major depressive disorder (MDD) and conversion disorder (CD). Serum BDNF levels were measured in the following three groups: 15 CD patients without any comorbid diagnosis of psychiatric disorder, 24 patients with MDD, and 26 healthy subjects without any psychiatric diagnosis or psychiatric treatment. The serum BDNF level of the healthy control group (31.4 +/- 8.8 ng/mL) was statistically higher than the level of the MDD group (21.2 +/- 11.3 ng/mL) and the CD group (24.3 +/- 9.0 ng/mL; P = 0.008). This suggests that BDNF level may play a similar role in the pathophysiology of MDD and CD.     

团体归因治疗与选择性5-羟色胺回收抑制剂对血浆脑源性神经营养因子的作用

目的:比较团体归因治疗(ARGT)与选择性5-羟色胺回收抑制剂(SSRI)对抑郁症、焦虑症、强迫症患者血浆脑源性神经营养因子(BDNF)的作用.方法:采用ARGT与SSRI对照的前瞻性干预研究设计,根据就诊顺序将129例门诊患者(其中抑郁症45例、焦虑症45例、强迫症39例)分至ARGT组63例(其中抑郁症21例、焦虑...     

Rapid decrease in depressive symptoms with an N-methyl-d-aspartate antagonist in ECT-resistant major depression

Background

Ketamine rapidly improves depressive symptoms in patients with treatment-resistant major depressive disorder (MDD) who do not respond to multiple standard antidepressants. However, it remains unknown whether ketamine is equally effective in patients with MDD who previously also did not respond to electroconvulsive therapy (ECT).

Methods

This study compared 17 patients with treatment-resistant MDD who previously did not respond to ECT and 23 patients with treatment-resistant MDD who had not previously received ECT. All subjects received a single open-label infusion of ketamine (0.5 mg/kg). Patients were evaluated using the Montgomery-Asberg Depression Rating Scale (MADRS) at baseline (60 min before the infusion), as well as at 40, 80, 120, and 230 min after infusion.

Results

Depressive symptoms were significantly improved in the ECT-resistant group at 230 minutes with a moderate effect size (p < .001, d = 0.50, 95% C.I.: 0.21-0.80). At 230 minutes, the non-ECT exposed group showed significant improvement with a large effect size (p < .001, d = 1.00, 95% C.I.: 0.71-1.29).

Conclusion

Ketamine appears to improve depressive symptoms in patients with MDD who had previously not responded to ECT. These preliminary results encourage further investigation with a larger sample size to determine effectiveness compared to other treatment-resistant patients with MDD.     

Correlation of serum BDNF levels with hippocampal volumes in first episode, medication-free depressed patients

The hippocampus seems to be affected in MDD, and brain-derived neurotrophic factor (BDNF) has positive effects on neurogenesis within the hippocampus. Although there are inconsistencies among study results, a smaller hippocampal volume in depressed patients is thought to be related to the pathophysiology of the disease. We looked at the correlation between serum BDNF (sBDNF) levels and hippocampal volumes (HCV) of first-episode MDD patients (18 female, 7 male; mean age = 32.1 ± 9.3) and healthy controls (17 female, 5 male; mean age = 29.7 ± 6.4). Region of interest analysis was conducted on the images acquired via MRI. sBDNF levels and HCV correlated only in the MDD group (right: r = 0.46, P = 0.02; left: r = 0.47, P = 0.02); however, HCV did not differ between MDD patients and healthy controls (right: F = 2.45, df = 1.46, P > 0.05; left: F = 0.05, df = 1.46, P > 0.05). BDNF may be a factor underlying HCV differences between MDD and healthy control subjects, which become apparent as severe and multiple episodes are experienced.     

Double-blind randomized controlled study showing symptomatic and cognitive superiority of bifrontal over bitemporal electrode placement during electroconvulsive therapy for schizophrenia

BackgroundSeveral studies show that bifrontal electrode placement produces relatively fewer cognitive adverse effects than bitemporal placement during electroconvulsive therapy (ECT) in depression. There are no reports comparing these electrode placements in schizophrenia.ObjectivesThis study compared the clinical and cognitive effects of bifrontal and bitemporal electrode placements in schizophrenia patients referred for electroconvulsive therapy (ECT).Methods122 schizophrenia patients who were prescribed ECT were randomized to receive ECT with either bifrontal (BFECT; n = 62) or bitemporal (BTECT; n = 60) placement. Their concomitant anti-psychotic medications and the number of ECT sessions were not controlled. Psychopathology was assessed using the Brief Psychiatric Rating Scale (BPRS), Bush-Francis Catatonia Rating Scale (BFCRS), and the Nurse Observation Scale for Inpatient Evaluation (NOSIE). Cognitive functions were assessed 24-h after the final ECT using a battery of tests. Clinical improvement was compared using chi-square test, repeated measures ANOVA and analysis of covariance (ANCOVA). Cognitive adverse effects were compared using t-test.ResultsAt the end of 2 weeks (after 6 ECT sessions) 63% and 13.2% of BFECT and BTECT patients respectively had met the response criterion for BPRS (40% reduction in total score; OR = 20.8; 95% CI = 3.61–34.33). BFECT patients showed significantly faster clinical response on BPRS (Time × Group interaction effect: P = 0.001), BFCRS (P < 0.001) and the NOSIE total assets score (P = 0.003). ANCOVA using baseline scores as covariates and treatment-resistance status as between-subject factor showed that BFECT patients had significantly greater improvement in all measures. BFECT patients had significantly higher PGI-memory-scale total score than BTECT patients (t = 5.16; P < 0.001). They also showed superior performance in other cognitive measures.ConclusionsBFECT results in superior clinical and cognitive outcomes than BTECT in schizophrenia patients referred for ECT.     

Mismatch negativity in patients with major depressive disorder: A meta-analysis

ObjectiveDeficits of mismatch negativity (MMN), a general index of echoic memory function, have been documented in patients with schizophrenia. However, it remains controversial whether patients with major depressive disorder (MDD) demonstrate MMN defects compared with healthy controls (HC).MethodsAfter screening 41 potential studies identified in PubMed and Medline, 13 studies consisting of 343 HC and 339 patients with MDD were included in the present meta-analysis. The effect sizes (Hedges’s g) with a random-effect and inverse-variance weighted model were estimated for the MMN amplitudes and latencies. The effects of different deviant types (i.e., frequency and duration) and of different illness stages (i.e., acute and chronic) on MMN were also examined.ResultsWe found that 1) MMN amplitudes (g = 1.273, p < 0.001) and latencies (g = 0.303, p = 0.027) to duration, but not frequency deviants, were significantly impaired in patients with MDD compared to HC; 2), acute patients exhibited lower MMN amplitudes (g = 1.735, p < 0.001) and prolonged MMN latencies (g = 0.461, p = 0.007) for the duration deviants compared to HC. Only the attenuated duration MMN amplitudes were detected in patients with chronic MDD (g = 0.822, p = 0.027); and 3) depressive symptoms did not significantly correlate with MMN responses.ConclusionsPatients with MDD demonstrated abnormal MMN responses to duration deviants compared to HC.SignificanceDuration MMN may constitute an electrophysiological indicator to differentiate HC from patients with MDD, particularly those in the acute stage.     

Higher serum tropomyosin-related kinase B protein level in major depression

Accumulating evidence suggests that the brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are molecules involved in the pathophysiology of major depressive disorder and response of antidepressants. To examine both BDNF and TrkB protein levels and their relationship with psychopathology in patients with major depressive disorder, 55 physically healthy patients with major depressive disorder were compared with 53 healthy controls. The severity of major depression was assessed by the 17-item Hamilton Depression Rating Scale (HDRS). Serum BDNF and TrkB protein levels were measured with Enzyme-linked immunosorbent assay (ELISA) kits. After using the analysis of covariance (ANCOVA) with age adjustment, the results of this work showed that BDNF presented no significant difference (F_(1,107) = 0.149, p = 0.701) but the TrkB protein level was significantly higher in depressive patients than in healthy controls (F_(1,107) = 4.043, p = 0.047). These findings suggest that the serum TrkB protein level may play an important role in the psychopathology of major depression.