Active clinical trials for "Psychotic Disorders"

This study aims to evaluate the presence of lung function impairment in a sample of patients diagnosed with non-affective psychosis.

REKO-A is a randomized controlled intervention study that addressed women and men on sick leave in Uppsala County. Participants which are on sick leave due to mental illness.

The investigators would like to know the association of gene polymorphisms and metabolic adversities in clozapine-treated patients with schizophrenia in Taiwan.

This prospective study examines the differences among several measures of adherence to antipsychotic medications in outpatients with schizophrenia. Adherence is assessed by using self-report, physician report, pill count and electronic monitoring. The rates of adherence/non-adherence with various tools will be manifested. The association between antipsychotic adherence/non-adherence and various clinical status, including psychotic symptoms, depressive symptoms, side effects, neurocognitive function and insight are analyzed. Participants are assessed at baseline during a visit to their outpatient clinic and followed up for 8 weeks.

The aim of this study is to identify specifics of pre-ECT assessments and ECT application in European psychiatric services. We will engage European centres that provide ECT for psychiatric patients and for psychiatric indications. It could bring better insights on current standards and possibly give some further improvements in the field of European ECT practices.

A burgeoning body of research has pointed to increased efficacy of clozapine (CLZ) over other antipsychotics in schizophrenia (SCZ). On the other hand, safety concerns likely cause underutilization across a range of European and other nations. The lack of data available to predict efficacy and adverse drug reactions (ADRs) of CLZ further contributes to underprescription rates in these countries. Here, we hypothesize that (epi)genetic and non-genetic factors aid to help predict treatment outcome (efficacy + ADRs) to CLZ. We furthermore posit that such prediction will result in enhanced quality of life of both patients and family members. Our primary objective is to predict CLZ treatment outcome based on phenotypic and genetic data obtained through the current design. The first secondary objective is to investigate which methylation levels/patterns are correlated with CLZ treatment outcome. The second secondary objective is to aid in the further elucidation of the genetic architecture of SCZ and any possible differences between 'regular' SCZ patients and those on CLZ, who are generally more severely ill. We thus intend to cover two currently unmet needs using a precision medicine approach: the lack of knowledge about determinants of treatment response to CLZ and the lack of insight into neurobiological differences between 'regular' SCZ and relatively treatment resistant subjects (CLZ users). The prime analysis will be a common variant hypothesis-generating genotyping endeavor investigating treatment response to CLZ. Additional analyses include whole-genome methylation and gene expression analyses and analyses of non-genetic determinants of response. We will include 2,500 CLZ treated patients for our discovery cohort, which is in line with previous whole-genome pharmacogenomics studies and our power calculations. We will replicate any genome-wide loci using our prospectively collected cohort of new users (N=59). Potential yields include a publicly available prediction tool to help identify patients responsive to CLZ in early disease stages and prevent harmful effects. In addition, common variant analyses compounded by pathway analyses may help elucidate the mechanisms of action of CLZ. We ask for broad informed consent from participants ensuring rich, longitudinal phenotypic and genotypic data resources for both currently planned and future analyses, allowing e.g. next-generation sequencing focused on both CLZ and SCZ disease genetics (e.g. in large consortia). We plan to also generate polygenic risk scores (PRS) of CLZ efficacy and use those to identify other diseases or patients for which CLZ may be helpful, e.g. schizoaffective disorder patients who are sometimes first treated with mood stabilizers. Last, evidence hints that disparaging genetic loci influence efficacy to different antipsychotics. Adding genetic data from our cohort to existing datasets of response to other antipsychotics may help identify such loci. Finally, comparison studies with non-CLZ using patients suffering from SCZ may deepen the understanding of biological mechanisms underlying treatment resistance (or: a relatively severe course of illness).The results of this genetic part of the study will be combined with the results from our other research protocol 'Phenomics and genomic of clozapine pharmacotherapy - New Users'.The overarching goal of both projects is to create a prediction model for clozapine outcome (response (and side effects). This model includes genetic, epigenetic and clinical data.

Schizophrenia is a chronic brain disease that is still understood as a condition that limits the development of a normal life for the patient who suffers it and their families. The idea that only one third of patients have a good outcome is still in force, despite the lack of clinical and epidemiological longitudinal studies that have addressed this issue rigorously. Most studies that have established the poor prognosis of the disease have followed a cross-sectional design and are based on samples of patients undergoing treatment in healthcare devices and therefore represents an important bias. Based on clinical, cognitive, functional outcome and biomarkers studies (brain imaging) to medium term (3 years) we can establish that the particular idea of poor prognosis should be reconsidered. The development of longitudinal studies of first-episode patients in representative samples of a population and long-term it is of high value to shed light on the clinical course of the disease. The belief that there are factors determining the disease progression beyond the initial three years brings us to publish this study. Given this background, our project's main objective is to know the evolution at 10 years of patients followed in the First Episode Psychosis Clinical Program (PAFIP). Our hypothesis is that a higher percentage of expected patients have a favorable outcome of the disease. Factors such as enhancing treatment completion, abstinence from drug use, return to work, the reduction of expressed emotion in families during the early years of the disease (at least 3 years of intensive intervention PAFIP) will have a positive impact on the evolution of patients on long-term (10 years). Our hypothesis defends the existence of certain factors as independent risk factors for poor clinical and functional outcome of patients who should be known for establishing intervention strategies that attempt to mitigate their impact on the quality of life of patients and their families.

There is growing evidence of high rates of substance use disorders among individuals with psychotic disorders especially in young people with predisposition for psychosis. There is some genetic evidence that carriers of the valine158 allele of the catechol-O-methyltransferase (COMT) gene had increased risk to exhibit psychotic symptoms and to develop schizophrenia if they used cannabis by the age of 18. It was also shown that carriers of the COMT val/val genotype were most sensitive to THC-induced psychotic experiences but this was conditional on pre-existing susceptibility to psychosis. The investigators propose to use brain-imaging and molecular genetics to investigate whether genetic factors may contribute to the THC-induced dopamine release and possibly to cannabis- induced psychosis.

The purpose of this study is to evaluate the efficacy of repetitive transcranial magnetic stimulation in the prevention of relapse of the symptoms of schizoaffective disorder. Primary Outcome Measures:Time between subject randomization to treatment and the first occurrence of a relapse during the Relapse Prevention Period. Secondary Outcome Measures: Symptom change as measured by the Positive and Negative Syndrome Scale (PANSS) total and PANSS factor scores; Illness severity change as measured by Clinical Global Impression of Severity for depression (CGI-S-DEP); Change in subject functioning using the Personal and Social Performance Scale; Change in subject medication satisfaction using the Medication Satisfaction Questionnaire (MSQ).

Environmental risk factors for the development of schizophrenia include infections during the perinatal period or later in life with Toxoplasma gondii (TG) being one of the candidate agents. A recent review (Torrey and Yolken, 2003) on TG in schizophrenia and other serious mental disorder reported higher antibodies to TG in patients compared to controls in 18 of 19 studies, one having been conducted by the investigators group. In a second, independent study on first-episode schizophrenia (n=56) and control subjects (n=32), sera were sampled and standard instruments used to assess diagnoses and psychopathology, respectively to screening controls. For the total sample, contacts with animals during pregnancy and age emerged as a non-significant predictors of TG IgG titers. Means of patients' and controls' TG IgG titers did not differ significantly but variances did; a subgroup of patients' titers reached much higher levels than those of controls. Patients in the high TG IgG subgroup were older (p=0.001), also they were older when psychiatric symptoms appeared, more individuals had regular animal contacts during pregnancy, or rural upbringing including regular animal contact, more consumption of raw meat, and a higher absolute treatment response (all trend levels). Regarding the short term course of patients, the investigators detected decreasing IgG titers in several individuals A power analysis demonstrated that results fell short of significance due to lack of statistical power. Based on the power analysis, the investigators propose an opel label, multicenter study at three regionally different sites within Germany (Halle, Hamm, Heidelberg). The investigators intent to study 173 first-episode patients with schizophrenia, schizoaffective, and schizophreniform disorder and 173 matched controls. The investigators hypothesize that - according to the heterogeneity of the illness - a subgroup of patients will exhibit higher TG IgG titers compared to the remaining patients and to controls; that this subgroup will have had regular contact with animals during pregnancy and early life as well as developmental delays; and that clinical improvement, response to treatment, and subjective well-being will run parallel with TG IgG decrease. Patients shall be assessed on admission to hospital, at discharge and at 6- and 12-month-follow-up with respect to TG antibody titers, symptomatology, neuropsychology, predictors of outcome, quality of life, and neurological soft signs. In controls two assessments shall be performed, 12 months apart. All foreseen assessments will be performed using standard measurement instruments with sound reliability and validity such as the SCID and the PANSS. Exposure to cats, other warm-blooded life-stock, and raw meat will be assessed using a special questionnaire.