Background: Clinical research into the Clinical High Risk state for Psychosis (CHR-P) has allowed primary indicated prevention in psychiatry to improve outcomes of psychotic disorders. The strategic component of this approach is the implementation of clinical services to detect and take care of CHR-P individuals, which are recommended by several guidelines. The actual level of implementation of CHR-P services worldwide is not completely clear. Aim: To assess the global geographical distribution, core characteristics relating to the level of implementation of CHR-P services; to overview of the main barriers that limit their implementation at scale. Methods: CHR-P services worldwide were invited to complete an online survey. The survey addressed the geographical distribution, general implementation characteristics and implementation barriers. Results: The survey was completed by 47 CHR-P services offering care to 22 248 CHR-P individuals: Western Europe (51.1%), North America (17.0%), East Asia (17.0%), Australia (6.4%), South America (6.4%) and Africa (2.1%). Their implementation characteristics included heterogeneous clinical settings, assessment instruments and length of care offered. Most CHR-P patients were recruited through mental or physical health services. Preventive interventions included clinical monitoring and crisis management (80.1%), supportive therapy (70.2%) or structured psychotherapy (61.7%), in combination with pharmacological treatment (in 74.5%). Core implementation barriers were staffing and financial constraints, and the recruitment of CHR-P individuals. The dynamic map of CHR-P services has been implemented on the IEPA website: https://iepa.org.au/list-a-service/. Conclusions: Worldwide primary indicated prevention of psychosis in CHR-P individuals is possible, but the implementation of CHR-P services is heterogeneous and constrained by pragmatic challenges.
GH-deficient TBI patients are depressed and have cognitive impairment. GH therapy induced reduction of depression, social dysfunction, and certain cognitive domains. Our preliminary data support the necessity of conducting randomized placebo-controlled trials on the effects of GH therapy on neuropsychological and psychiatric status in GHD TBI patients.
Aims
Psychosis spectrum disorder has a complex pathoetiology characterised by interacting environmental and genetic vulnerabilities. The present study aims to investigate the role of gene–environment interaction using aggregate scores of genetic (polygenic risk score for schizophrenia (PRS-SCZ)) and environment liability for schizophrenia (exposome score for schizophrenia (ES-SCZ)) across the psychosis continuum.
Methods
The sample consisted of 1699 patients, 1753 unaffected siblings, and 1542 healthy comparison participants. The Structured Interview for Schizotypy-Revised (SIS-R) was administered to analyse scores of total, positive, and negative schizotypy in siblings and healthy comparison participants. The PRS-SCZ was trained using the Psychiatric Genomics Consortiums results and the ES-SCZ was calculated guided by the approach validated in a previous report in the current data set. Regression models were applied to test the independent and joint effects of PRS-SCZ and ES-SCZ (adjusted for age, sex, and ancestry using 10 principal components).
Results
Both genetic and environmental vulnerability were associated with case-control status. Furthermore, there was evidence for additive interaction between binary modes of PRS-SCZ and ES-SCZ (above 75% of the control distribution) increasing the odds for schizophrenia spectrum diagnosis (relative excess risk due to interaction = 6.79, [95% confidential interval (CI) 3.32, 10.26], p < 0.001). Sensitivity analyses using continuous PRS-SCZ and ES-SCZ confirmed gene–environment interaction (relative excess risk due to interaction = 1.80 [95% CI 1.01, 3.32], p = 0.004). In siblings and healthy comparison participants, PRS-SCZ and ES-SCZ were associated with all SIS-R dimensions and evidence was found for an interaction between PRS-SCZ and ES-SCZ on the total (B = 0.006 [95% CI 0.003, 0.009], p < 0.001), positive (B = 0.006 [95% CI, 0.002, 0.009], p = 0.002), and negative (B = 0.006, [95% CI 0.004, 0.009], p < 0.001) schizotypy dimensions.
Conclusions
The interplay between exposome load and schizophrenia genetic liability contributing to psychosis across the spectrum of expression provide further empirical support to the notion of aetiological continuity underlying an extended psychosis phenotype.
Increasing levels of depressive symptoms in elderly hip fracture patients influence short-term functional outcome. We strongly support the introduction of routine assessment of this baseline comorbidity, especially in female patients. Failure to identify such patients is a missed opportunity for possible improvement of early functional outcome after hip fracture in elderly.
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