View clinical trials related to Depressive Disorder, Major.
Filter by:Objective There is growing evidence showing a relation between depression, metabolic syndrome, diabetes, cardiovascular disease (1), serum lipid profile (2,3) and body weight (4), as well as the effects of some of the antidepressant medications on these various conditions and profiles. The aim of the study is to examine the influence of antidepressant medications on the metabolic profiles (5) of patients suffering from Major Depressive Disorder (MDD). Group of patients: 30 Patients aged 18-65, who were diagnosed with MDD according to the DSM-IV criteria. Research Design and Methods: Research duration will be 8 weeks. Patients meeting the inclusion criteria will be recruited after being diagnosed with MDD and having undertaken the HDRS. A follow-up HDRS will be taken at weeks 4 and 8. The psychiatric evaluation will be held by a resident in psychiatry. The following metabolic parameters will be examined at base-line and at the end of the 8 weeks: Weight, height, waist circumference, body mass index (BMI: (Weight in Kg/(Height in meters)2), sitting blood pressure (after 3 minutes of sitting). Serum lipid profile (performed in Ziv hospital's chemistry lab): Low density lipoprotein cholesterol, High density Lipoprotein cholesterol, Triglycerides, Total cholesterol, Apolipoprotein level (Apo AI, Apo B, Apo E, Apo AII). Fasting glucose and insulin blood levels, in order to evaluate insulin-release and resistance, according to the following formulas: Insulin Resistance: HOMA IR=Fasting glucose (mg/dL)x Fasting insulin (mmol/L)/405 Insulin Release: HOMA-β={360xfasting insulin (mmol/L)}/{glucose(mg/dL)-63} Serum oxidative stress parameters according to the F2-Isoprostane kit will be measured. Malonylaialdehyde (MDA) content in serum will be analyzed by the thiobarbituric acid reactive substances assay, which measures malondialdehyde equivalent (13). Conjugated dienes will be measured at 234nm (14, 15).
Major depression is accompanied by cognitive changes as well as alterations in multiple physical functions. The inflammatory system is altered generally toward a pro-inflammatory state. Antidepressants are associated with a decrease in this proinflammatory state. This study aims to generate pilot data concerning a possible link between cognition, inflammation and response to treatment. The cognitive function of subjects with major depression will be tested before and after treatment with duloxetine. Inflammatory markers will be measured at both time points.
Current methods of choosing treatment for major depressive disorder (MDD) are inefficient. The Strategic Treatment to Achieve Remission of Depression (STAR*D) Trial revealed that only about 1/3 of patients treated with antidepressant drugs will go into remission with the first medication chosen. We hypothesize that pattern recognition software using Machine Learning methods can accurately predict response to a variety of antidepressant medications (ADM) or cognitive behavior therapy (CBT) after training using pre-treatment demographic, clinical, laboratory or electroencephalographic (EEG) data. These algorithms might assist the clinician to chose, for any given patient, an antidepressant treatment option with greater probability of favourable response than is achievable using current best practise methods.
Recently, there are increasing data about intensity dependent amplitude change (IDAP: N100 amplitude slope) of auditory evoked Event Related Potential (ERP) components for its role on surrogate marker of central serotonergic activity. A high N100 amplitude slope reflects low serotonergic neurotransmission and vice versa. There are a couple of studies reporting associations of N1 amplitude slope with response to Citalopram (positive correlation) and Reboxetine (negative correlation) treatment in major depressive disorder patients (2,3). The investigator also published a case series about SSRI super-sensitivity and SSRI induced mania in patients with aberrantly high N100 slope (4). And serotonin transporter gene polymorphism was studied for its role about pathophysiology of bipolar disorder (5, 6, 7). Serotonin promoter gene was known to have significant relationship with N100 amplitude slope (8). Furthermore previous study showed that N100 amplitude slope was well correlated with hypomanic and hyperthymic personality (9). Conclusively from above results, the investigator hypothesized that if depressive patients show aberrant high or low N100 amplitude slope (N100 response outliers), they will not response well to SSRI medication. They will response better to quetiapine XR adjunctive therapy. In this study, the investigator will confirm it by comparing treatment effect between SSRI monotherapy and quetiapine XR adjunctive in aberrant N100 responder. Hypothesis First visit depressive patients might have monopolar or bipolar depression. If depressive patients show aberrantly high or low N100 amplitude slope, they will not response to SSRI medication. Patients who have aberrantly high or low N100 amplitude slope will response better to quetiapine XR adjunctive therapy.
Electroconvulsive therapy (ECT), is considered the most effective treatment for severe treatment resistant major depressive disorder (MDD), but it requires about 3 weeks of treatments and can cause considerable acute deficits in memory. It would be a major advance in treatment if ECT could work faster with fewer treatments and result in decrease incidence of memory problems. Ketamine is an excellent candidate for augmentation of ECT because of its acute effects on depression, its short half-life, and its safety profile when given at low doses. Ketamine is given as an infusion and could easily be incorporated into the routine management of patients undergoing ECT, but has never been evaluated prospectively in this context. The investigators propose to assess the efficacy, feasibility, tolerability and safety of N-methyl-D-aspartate antagonist augmentation of ECT using ketamine.
The purpose of this study is to determine whether an oxytocin ad-on, or oxytocin and tibolone ad-on can induce a response to antidepressants in patients with treatment resistant depression.
The purpose of this study is to establish the clinical effectiveness of antidepressants by pharmacogenomic approach, and to determine the levels of inflammatory factors between the baseline and the end point of the study in Taiwanese major depressive disorder (MDD) patients.
The objective of this study is to investigate the antidepressant efficacy of rTMS, and to assess cortical metabolism before and after rTMS sessions in patients with major depression. We also aimed to investigate differences between the responders and nonresponders to rTMS and what would predict clinical response to rTMS.
Background: According to the WHO, major depressive disorder is the second largest healthcare problem worldwide in terms of disability caused by illness. It afflicts an estimated 17% of individuals during their lifetimes at tremendous costs. A number of depressive patients are treated with antidepressant medication. The efficacy of antidepressant medication has been studied in a number of systematic reviews, and in recent years some of these reviews have shown that the efficacy is questionable for many patients. So are there other effective treatments for this serious illness? Cognitive- and psychodynamic therapies are probably both significantly more effective for depression than no treatment, but only limited comparisons have been made between the two interventions. A Cochrane review shows that cognitive therapy has a preventive effect against recurrent depression, and that this effect may surpass the preventive effect of antidepressant medication. Mindfulness training may be an effective technique in preventing relapse in patients who have had at least 3 previous depressive episodes. But efficacy in treating currently depressed patients has not been studied. Objective To perform a randomised clinical trial with blinded assessment of efficacy variables in order to study the effects of mindfulness based behavioral therapy (cognitive therapy and mindfulness) versus psychodynamic therapy in depressive patients. Methods A randomised clinical trial of 84 consecutive patients diagnosed with major depressive disorder, referred to the day clinic, Roskilde psychiatric services. The patients will be randomised to one of two interventions: 1. MIBT (mindfulness-based behavioural therapy) 2. PT (psychodynamic therapy)
Neuropattern is a first translational tool in stress medicine. Neuropattern is a diagnostic tool, which can be applied by in- and outpatients and physicians to detect dysregulation in the stress response network. The physician provides anamnestic and anthropometric data, while the patient takes other measures at home, e.g. psychological, symptomatic, and biological data. Among the biological data are ECG measures for analyses of heart rate variability, and salivary cortisol measures before and after a dexamethasone challenge test. All data are analyzed in a central laboratory, which generates a written report for the physician, including a disease model, from which personalized recommendations for pharmacological and psychological treatments are derived. Neuropattern additionally offers individualized internet modules to inform the patient about the disease model and to teach him/her what he/she can do to improve his/her medical conditions. The current study applies Neuropattern in 2000 patients of family doctors, suffering from major depression, depressive episodes, adjustment disorders, and somatoform disorders. The patients receive either unspecific or individualized internet modules in a randomized order.