Eighty-eight patients were admitted to the acute ward of a catchment area suffering from the following functional psychoses: schizophrenia (S; n = 41), affective disorder (AD; n = 22), other disorders (OD; n = 25). Follow-up data were obtained for 97%. Ten patients were dead at follow-up, 8 due to suicide. Sixty-five were personally interviewed. While nearly all the patients had only brief periods of rehospitalization, most had used neuroleptics during the follow-up period. Compared to other samples, functioning at follow-up was fairly good for the AD and OD patients, but rather poor for the S patients.
The reorganization in 1981 of a general hospital psychiatric ward in Oslo, Norway, to achieve a more suitable treatment milieu for patients with schizophrenia resulted in a change in patients' perceptions of the ward atmosphere. Reduced group participation and increased individualized support from staff led patients to perceive of the ward as having a low level of anger and aggression and a high level of order and organization. This study examined whether the reorganization was associated with improved treatment outcome.
Psychiatrists retrospectively examined the charts of all patients with a DSM-III-R diagnosis of schizophrenia or schizophreniform disorder who were admitted to the ward the year before and the second year after the reorganization. Multiple regression analyses were used to examine treatment outcomes for both groups. Outcome was measured indirectly by length of stay, level of functioning at discharge, and whether the patient was rehospitalized during the following seven years.
Patients treated after the reorganization had significantly shorter stays with no reductions in either level of functioning at discharge or length of community tenure after discharge. Differences in demographic characteristics, illness history, or psychopharmacological treatment could not account for differences in outcome.
The results supported the hypothesis that the organization and milieu of brief-stay wards influence the short-term outcome of inpatient treatment of patients with schizophrenia.
Several studies have reported structural brain abnormalities, decreased myelination and oligodendrocyte dysfunction in schizophrenia. In the central nervous system, glia-derived de novo synthesized cholesterol is essential for both myelination and synaptogenesis. Previously, we demonstrated in glial cell lines that antipsychotic drugs induce the expression of genes involved in cholesterol and fatty acids biosynthesis through activation of the sterol regulatory element binding protein (SREBP) transcription factors, encoded by the sterol regulatory element binding transcription factor 1 (SREBF1) and sterol regulatory element binding transcription factor 2 (SREBF2) genes. Considering the importance of these factors in the lipid biosynthesis and their possible involvement in antipsychotic drug effects, we hypothesized that genetic variants of SREBF1 and/or SREBF2 could affect schizophrenia susceptibility. We therefore conducted a HapMap-based association study in a large German sample, and identified association between schizophrenia and five markers in SREBF1 and five markers in SREBF2. Follow-up studies in two independent samples of Danish and Norwegian origin (part of the Scandinavian collaboration of psychiatric etiology study, SCOPE) replicated the association for the five SREBF1 markers and for two markers in SREBF2. A combined analysis of all samples resulted in highly significant genotypic P-values of 9 x 10(-4) for SREBF1 (rs11868035, odd ration (OR)=1.26, 95% confidence interval (CI) (1.09-1.45)) and 4 x 10(-5) for SREBF2 (rs1057217, OR=1.39, 95% CI (1.19-1.63)). This finding strengthens the hypothesis that SREBP-controlled cholesterol biosynthesis is involved in the etiology of schizophrenia.