P50 Suppression and Its Neural Generators in Antipsychotic-Na?ve First-Episode Schizophrenia Before and After 6 Months of Quetiapine Treatment

Background: Numerous studies have demonstrated sensory gating deficits in schizophrenia. However, only a few longitudinal studies report on the effects of antipsychotic treatment on sensory gating deficits and their results are inconsistent. In the present study, P50 suppression and its neural generators were investigated in antipsychotic-naïve first-episode patients with schizophrenia before and after 6 months of treatment with quetiapine. Methods: Thirty-four antipsychotic-naïve first-episode schizophrenia patients and age and gender matched healthy controls were tested in an auditory sensory gating paradigm at baseline and after 6 months. During this period, the patients were treated with quetiapine, while controls received no treatment. Sixteen patients completed the study. Results: Patients showed significant reduced P50 suppression compared with controls at baseline but not at follow-up. Furthermore, a significant positive correlation between baseline P50 suppression and dose of quetiapine at follow-up was found. P50 suppression in patients receiving above median dosages of quetiapine increased significantly from baseline to follow-up. At baseline, a frontocentral source was significantly more active in patients than in controls at the time of the testing stimulus. Conclusions: The present findings suggest that P50 suppression deficits are already present at an early stage of schizophrenia. Furthermore, particularly those patients with more severe gating deficits appeared to need higher dosages of quetiapine, although their clinical symptoms did not seem to indicate this. Quetiapine treatment significantly improved these gating deficits. Furthermore, a frontocentral source in the brain appeared to be involved in the deficient P50 gating of the patients.     

Psykiatriska synspunkter på problemet dold kriminalitet och anonyma brottslingar,med särskild hänsyn till exhibitionism

Background: Electroconvulsive therapy, ECT, is an effective acute treatment for severe depression. Today ECT is usually discontinued when the patient's depressive symptoms abate, although relapse is common. Some studies suggest that continuation ECT (cECT) may prevent relapse of depression, but there are few studies available. Aims: The aim of this study was to describe the need for inpatient care before, during and after cECT. Methods: A retrospective chart review was conducted of all patients (n=27) treated with cECT between 2005 and 2007 at Örebro University Hospital, Sweden. All patients were severely depressed at the initiation of index ECT. The DSM-IV diagnoses were major depression (n=19), bipolar depression (n=5) or schizoaffective depression (n=3). Results: The hospital day quotient was lower (HDQ=15) during cECT (mean duration±standard deviation=104±74 days) than during the 3 years prior to cECT (HDQ=26). The rehospitalization rate was 43% within 6 months and 58% within 2 years after the initiation of cECT. Seven patients were rehospitalized while on cECT. Conclusion: The need for inpatient care was reduced during cECT. However, rehospitalization was common. At the initiation of the cECT, the patients were improved by the index ECT. Also cECT was often terminated after rehospitalization, which contributed to the lowered hospital day quotient during cECT. Randomized clinical trials are needed to establish the efficacy of cECT. Clinical implications: Relapses and recurrences in depressed patients are common after ECT treatment. The results indicate that continuation ECT combined with pharmacotherapy might be an alternative treatment strategy.     

病人健康问卷抑郁自评量表（PHQ-9）的临床应用

病人健康问卷（Patient Health Questionnaire-9,PHQ-9）是一个简便、有效的抑郁障碍自评量表,在抑郁症诊断的辅助和症状严重程度评估方面,均具有良好的信度和效度.在基于评估的治疗策略中,PHQ-9可以作为制订治疗方案的参考,以及治疗过程中对疗效的评估工具.PHQ-9的衍生版本PHQ-8,PHQ-2和他评量表PHQ-9-OV,针对不同研究对象,有着相应的临床应用效果.现就PHQ-9在临床的应用及优势进行论述.     

Intervenir précocement dans les stades débutants du trouble bipolaire : pourquoi,quand et comment

ObjectivesBipolar disorder (BD) is a chronic and severe psychiatric disease. There are often significant delays prior to diagnosis, and only 30 to 40 % of patients will experience complete remission. Since BD occurs most often at a young age, the disorder can seriously obstruct future socio-professional development and integration. Vulnerability-stress model of BD is considered to be the result of an interaction between vulnerability genes and environmental risk factors, which leads to the onset of the disorder most often in late adolescence or early adulthood. The clinical “staging” model of BD situates the subject in a clinical continuum of varying degrees of severity (at-risk status, first episode, full-blown BD). Given the demonstrated effectiveness of early intervention in the early stages of psychotic disorder, we posit that early intervention for early stages of BD (i.e. at-risk status and first episode mania or hypomania) would reduce the duration of untreated illness and optimize the chances of therapeutic response and recovery.MethodsWe conducted a narrative review of the literature to gather updated data on: (1) features of early stages: risk factors, at-risk symptoms, clinical specificities of the first manic episode; (2) early screening: targeted populations and psychometric tools; (3) early treatment: settings and therapeutic approaches for the early stages of BD.Results(1) Features of early stages: among genetic risk factors, we highlighted the diagnosis of BD in relatives and affective temperament including as cyclothymic, depressive, anxious and dysphoric. Regarding prenatal environmental risk, we identified peripartum factors such as maternal stress, smoking and viral infections, prematurity and cesarean delivery. Later in the neurodevelopmental course, stressful events and child psychiatric disorders are recognized as increasing the risk of developing BD in adolescence. At-risk symptoms could be classified as “distal” with early but aspecific expressions including anxiety, depression, sleep disturbance, decreased cognitive performance, and more specific “proximal” symptoms which correspond to subsyndromic hypomanic symptoms that increase in intensity as the first episode of BD approaches. Specific clinical expressions have been described to assess the risk of BD in individuals with depression. Irritability, mixed and psychotic features are often observed in the first manic episode. (2) Early screening: some individuals with higher risk need special attention for screening, such as children of people with BD. Indeed, it is shown that children with at least one parent with BD have around 50 % risk of developing BD during adolescence or early adulthood. Groups of individuals presenting other risk factors, experiencing an early stage of psychosis or depressive disorders should also be considered as targeted populations for BD screening. Three questionnaires have been validated to screen for the presence of at-risk symptoms of BD: the Hypomanic Personality Scale, the Child Behavior Checklist-Paediatric Bipolar Disorder, and the General Behavior Inventory. In parallel, ultra-high risk criteria for bipolar affective disorder (“bipolar at-risk”) distinguishing three categories of at-risk states for BD have been developed. (3) Early treatment: clinical overlap between first psychotic and manic episode and the various trajectories of the at-risk status have led early intervention services (EIS) for psychosis to reach out for people with an early stage of BD. EIS offers complete biopsychosocial evaluations involving a psychiatric examination, semi-structured interviews, neuropsychological assessments and complementary biological and neuroimaging investigations. Key components of EIS are a youth-friendly approach, specialized and intensive care and client-centered case management model. Pharmaceutical treatments for at-risk individuals are essentially symptomatic, while guidelines recommend the use of a non-antipsychotic mood stabilizer as first-line monotherapy for the first manic or hypomanic episode. Non-pharmacological approaches including psychoeducation, psychotherapy and rehabilitation have proven efficacy and should be considered for both at-risk and first episode of BD.ConclusionsEIS for psychosis might consider developing and implementing screening and treatment approaches for individuals experiencing an early stage of BD. Several opportunities for progress on early intervention in the early stages of BD can be drawn. Training first-line practitioners to identify at-risk subjects would be relevant to optimize screening of this population. Biomarkers including functional and structural imaging measures of specific cortical regions and inflammation proteins including IL-6 rates constitute promising leads for predicting the risk of transition to full-blown BD. From a therapeutic perspective, the use of neuroprotective agents such as folic acid has shown particularly encouraging results in delaying the emergence of BD. Large-scale studies and long-term follow-up are still needed to achieve consensus in the use of screening and treatment tools. The development of specific recommendations for the early stages of BD is warranted.