RESUMEN
We aimed to find agreement between diagnoses obtained through standardized (SDI) and non-standardized diagnostic interviews (NSDI) for schizophrenia and Bipolar Affective Disorder (BD). METHODS: A systematic review with meta-analysis was conducted. Publications from 2007 to 2020 comparing SDI and NSDI diagnoses in adults without neurological disorders were screened in MEDLINE, ISI Web of Science, and SCOPUS, following PROSPERO registration CRD42020187157, PRISMA guidelines, and quality assessment using QUADAS-2. RESULTS: From 54231 entries, 22 studies were analyzed, and 13 were included in the final meta-analysis of kappa agreement using a mixed-effects meta-regression model. A mean kappa of 0.41 (Fair agreement, 95% CI: 0.34 to 0.47) but high heterogeneity (Î2 = 92%) were calculated. Gender, mean age, NSDI setting (Inpatient vs. Outpatient; University vs. Non-university), and SDI informant (Self vs. Professional) were tested as predictors in meta-regression. Only SDI informant was relevant for the explanatory model, leaving 79% unexplained heterogeneity. Egger's test did not indicate significant bias, and QUADAS-2 resulted in "average" data quality. CONCLUSIONS: Most studies using SDIs do not report the original sample size, only the SDI-diagnosed patients. Kappa comparison resulted in high heterogeneity, which may reflect the influence of non-systematic bias in diagnostic processes. Although results were highly heterogeneous, we measured a fair agreement kappa between SDI and NSDI, implying clinicians might operate in scenarios not equivalent to psychiatry trials, where samples are filtered, and there may be more emphasis on maintaining reliability. The present study received no funding.
RESUMEN
Generalized anxiety disorder (GAD) is highly prevalent and incapacitating. Here we used the Carioca High-Conditioned Freezing (CHF) rats, a previously validated animal model for GAD, to identify biomarkers and structural changes in the hippocampus that could be part of the underlying mechanisms of their high-anxiety profile. Spatial and fear memory was assessed in the Morris water maze and passive avoidance test. Serum corticosterone levels, immunofluorescence for glucocorticoid receptors (GR) in the dentate gyrus (DG), and western blotting for hippocampal brain derived neurotrophic factor (BDNF) were performed. Immunohistochemistry for markers of cell proliferation (bromodeoxiuridine/Ki-67), neuroblasts (doublecortin), and cell survival were undertaken in the DG, along with spine staining (Golgi) and dendritic arborization tracing. Hippocampal GABA release was assessed by neurochemical assay. Fear memory was higher among CHF rats whilst spatial learning was preserved. Serum corticosterone levels were increased, with decreased GR expression. No differences were observed in hippocampal cell proliferation/survival, but the number of newborn neurons was decreased, along with their number and length of tertiary dendrites. Increased expression of proBDNF and dendritic spines was observed; lower ratio of GABA release in the hippocampus was also verified. These findings suggest that generalized anxiety/fear could be associated with different hippocampal biomarkers, such as increased spine density, possibly as a compensatory mechanism for the decreased hippocampal number of neuroblasts and dendritic arborization triggered by high corticosterone. Disruption of GABAergic signaling and BDNF impairment are also proposed as part of the hippocampal mechanisms possibly underlying the anxious phenotype of this model.
