ABSTRACT
On the basis of the scientific state of knowledge it is outlined that psychotherapy is an important part of an efficacious and guideline-compliant treatment of schizophrenia. Firstly, aspects of the methodologically sound British National Institute for Health and Clinical Excellence (NICE) guidelines regarding the field of psychosis psychotherapy are presented in which cognitive behavioral therapy and family interventions are recommended without restrictions. Afterwards, empirically substantiated starting points for psychosis psychotherapy are described, taking particular account of the cognitive model of delusions. Furthermore, disorder-specific strategies of building the therapeutic relationship are identified, which take account of symptoms, such as mistrust or affective flattening. Finally, the evidence-based therapeutic strategies for relapse prevention and symptom reduction are delineated. In conclusion, psychosis psychotherapy does not have an evidence problem but an implementation problem.
Subject(s)
Evidence-Based Medicine , Practice Guidelines as Topic , Psychotherapy/standards , Psychotic Disorders/therapy , Schizophrenia/therapy , Humans , Psychotherapy/trends , Psychotic Disorders/complications , Psychotic Disorders/diagnosis , Schizophrenia/complications , Schizophrenia/diagnosisABSTRACT
OBJECTIVE: There is little work demonstrating the effectiveness of cognitive behaviourally oriented interventions in routine service settings. This pragmatic trial is designed to test the impact of a group treatment service on relapse rates under the conditions of routine health care. METHOD: A total of 169 schizophrenia patients were randomly allocated either to a comprehensive cognitive behaviourally oriented service (CBOS) or to treatment as usual (TAU). The primary outcome is the time until the first relapse after discharge from hospital. Relapse was defined as an increase in positive or negative symptoms as assessed with the Positive and Negative Syndrome Scale. Survival analysis has been conducted up to the 6-month assessment. RESULTS: The mean time to relapse after discharge from hospital in the CBOS group was significantly longer than in the TAU group (log rank test, P = 0.033). This was due to less exacerbations regarding negative symptoms in the CBOS condition (log rank test, P = 0.014). The number of social contacts was improved in the CBOS group only. CONCLUSION: The CBOS intervention appears to be beneficial in reducing early negative symptom exacerbations.
Subject(s)
Cognitive Behavioral Therapy , Psychotic Disorders/rehabilitation , Schizophrenia/rehabilitation , Schizophrenic Psychology , Adult , Antipsychotic Agents/administration & dosage , Combined Modality Therapy , Dose-Response Relationship, Drug , Female , Germany , Hospitals, Psychiatric , Humans , Male , Middle Aged , Psychiatric Status Rating Scales , Psychotic Disorders/psychology , Secondary Prevention , Treatment Outcome , Young AdultABSTRACT
Alzheimer's disease (AD) is characterized by cognitive decline and loss of neurons in specific brain regions. Recent findings have suggested an involvement of brain-derived neurotrophic factor (BDNF) in the pathogenesis of AD. BDNF is an endogenous protein involved in the maintenance of neuronal function, synaptic plasticity and structural integrity in the adult brain. To our knowledge, the present pilot study assessed for the first time BDNF serum and CSF concentrations in 30 patients with different stages of AD in comparison to 10 age-matched non-demendet controls. AD patients were divided in two groups according to their MMSE score: Group 1 (n = 15) in early stages with MMSE scores >or=21 (mean of 25.5) and Group 2 (n = 15) with more severe stages of dementia with MMSE scores <21 (mean of 13.3). As main results, we found in patients with early stages of probable AD significantly increased BDNF serum concentrations as compared to more severe stages of AD (p < 0.0001) and age-matched healthy controls (p = 0.028). BDNF serum values in all AD patients correlated significantly with MMSE scores (r = 0.486; p < 0.0001). Levels of BDNF were below the detection limit of the assay in unconcentrated CSF samples of AD patients and non-demendet controls.In summary, BDNF serum values are increased in early stages of Alzheimer's disease, which may reflect a compensatory repair mechanism in early neurodegeneration and could also contribute to increased degradation of beta-amyloid (Abeta). During the course of the disease, BDNF is decreasing, which correlates with the severity of dementia. The decrease of BDNF may constitute a lack of trophic support with an increase of Abeta accumulation and thus contribute to progressive degeneration of specific regions in the AD-affected brain. BDNF should be further evaluated as a candidate marker for clinical diagnosis and therapeutic monitoring in Alzheimer's disease.
