Morphological correlates to cognitive dysfunction in schizophrenia as studied with Bayesian regression

BACKGROUND: Relationships between cognitive deficits and brain morphological changes observed in schizophrenia are alternately explained by less gray matter in the brain cerebral cortex, by alterations in neural circuitry involving the basal ganglia, and by alteration in cerebellar structures and related neural circuitry. This work explored a model encompassing all of these possibilities to identify the strongest morphological relationships to cognitive skill in schizophrenia. METHODS: Seventy-one patients with schizophrenia and sixty-five healthy control subjects were characterized by neuropsychological tests covering six functional domains. Measures of sixteen brain morphological structures were taken using semi-automatic and fully manual tracing of MRI images, with the full set of measures completed on thirty of the patients and twenty controls. Group differences were calculated. A Bayesian decision-theoretic method identified those morphological features, which best explained neuropsychological test scores in the context of a multivariate response linear model with interactions. RESULTS: Patients performed significantly worse on all neuropsychological tests except some regarding executive function. The most prominent morphological observations were enlarged ventricles, reduced posterior superior vermis gray matter volumes, and increased putamen gray matter volumes in the patients. The Bayesian method associated putamen volumes with verbal learning, vigilance, and (to a lesser extent) executive function, while caudate volumes were associated with working memory. Vermis regions were associated with vigilance, executive function, and, less strongly, visuo-motor speed. Ventricular volume was strongly associated with visuo-motor speed, vocabulary, and executive function. Those neuropsychological tests, which were strongly associated to ventricular volume, showed only weak association to diagnosis, possibly because ventricular volume was regarded a proxy for diagnosis. Diagnosis was strongly associated with the other neuropsychological tests, implying that the morphological associations for these tasks reflected morphological effects and not merely group volumetric differences. Interaction effects were rarely associated, indicating that volumetric relationships to neuropsychological performance were similar for both patients and controls. CONCLUSION: The association of subcortical and cerebellar structures to verbal learning, vigilance, and working memory supports the importance of neural connectivity to these functions. The finding that a morphological indicator of diagnosis (ventricular volume) provided more explanatory power than diagnosis itself for visuo-motor speed, vocabulary, and executive function suggests that volumetric abnormalities in the disease are more important for cognition than non-morphological features

Cerebral cortical thickness and a history of obstetric complications in schizophrenia

Introduction: Magnetic resonance imaging (MRI) studies have demonstrated that patients with schizophrenia have thinner brain cortices compared with healthy control subjects. Neurodevelopment is vulnerable to obstetric complications (OCs) such as hypoxia and birth trauma, factors that are also related to increased risk of developing schizophrenia. With the hypothesis that OCs might explain the thinner cortices found in schizophrenia, we studied patients with schizophrenia and healthy controls subjects for association between number and severity of OCs and variation in cortical thickness. Methods: MRI scans of 54 adults with schizophrenia or schizoaffective disorder and 54 healthy controls were acquired at Karolinska Institutet, Stockholm, Sweden. Measures of brain cortical thickness were obtained using automated computer processing (FreeSurfer). OCs were assessed from obstetric records and scored blindly according to the McNeil-Sjostrom scale. At numerous cortical locations, putative effects of OCs on cortical thickness variation were tested for each trimester, for labour, for composite OC scores, severe OC scores, and hypoxia scores among patients and controls separately. Results: Number and severity of OCs varied among both patient and control subjects but were not associated with cortical thickness in either of the groups. Patients demonstrated thinner brain cortices but there were no significant differences in number and severity of OC scores across groups. Conclusion: In the present study, number and severity of obstetric complications were not associated with brain cortical thickness, in patients with schizophrenia or in healthy control subjects. The thinner brain cortices found in patients with schizophrenia were not explained by a history of OCs. (C) 2009 Elsevier Ltd. All rights reserved

Risk stratification for short‐term mortality at hospital admission for acute exacerbations of COPD

Background and objective Exacerbations of chronic obstructive pulmonary disease (ECOPD) are associated with increased in-hospital and short-term mortality. Developing an easy-to-use model to predict adverse outcomes will be useful in daily clinical practice and will facilitate management decisions. We aimed to assess mortality rates and potential predictors for short-term mortality after severe ECOPD. Classification and Regression Tree (CART) model was used to identify predictors of adverse outcome. Methods A retrospective observational cohort study, including all patients admitted to Maastricht University Medical Center with ECOPD between June 2011 and December 2014 was performed. The last admission was taken into account, and its demographic, clinical and biochemical data were recorded. Results A total of 364 hospitalized patients were enrolled. Mean (SD) age was 70.5 (10.2) years, 54.4% were male and mean FEV1 45.2% (17.7) of predicted. The in-hospital and 90-day mortality were, respectively, 8.5 and 16.2%. Independent risk factors for 90-day mortality were: PaC0(2) (odds ratio (OR): 1.31; 95% confidence interval (CI): 1.00-0.35), age (OR: 1.09; CI: 0.06-0.11), body mass index (BMI) = 9.1 kPa, age > 80 years, BMI <18.5 kg/m(2) and previous admission for ECOPD as the most discriminatory factors. Conclusion According CART analysis, high PaCO2 and age, low BMI and previous admission for ECOPD in last 2 years were the strongest predictors of 90-day mortality in patients with severe ECOPD. In absence of any of these factors, no patients died, suggesting that this model indeed enables risk stratification

Risk stratification for short-term mortality at hospital admission for acute exacerbations of COPD

Background and objective Exacerbations of chronic obstructive pulmonary disease (ECOPD) are associated with increased in-hospital and short-term mortality. Developing an easy-to-use model to predict adverse outcomes will be useful in daily clinical practice and will facilitate management decisions. We aimed to assess mortality rates and potential predictors for short-term mortality after severe ECOPD. Classification and Regression Tree (CART) model was used to identify predictors of adverse outcome. Methods A retrospective observational cohort study, including all patients admitted to Maastricht University Medical Center with ECOPD between June 2011 and December 2014 was performed. The last admission was taken into account, and its demographic, clinical and biochemical data were recorded. Results A total of 364 hospitalized patients were enrolled. Mean (SD) age was 70.5 (10.2) years, 54.4% were male and mean FEV1 45.2% (17.7) of predicted. The in-hospital and 90-day mortality were, respectively, 8.5 and 16.2%. Independent risk factors for 90-day mortality were: PaC0(2) (odds ratio (OR): 1.31; 95% confidence interval (CI): 1.00-0.35), age (OR: 1.09; CI: 0.06-0.11), body mass index (BMI) = 9.1 kPa, age > 80 years, BMI <18.5 kg/m(2) and previous admission for ECOPD as the most discriminatory factors. Conclusion According CART analysis, high PaCO2 and age, low BMI and previous admission for ECOPD in last 2 years were the strongest predictors of 90-day mortality in patients with severe ECOPD. In absence of any of these factors, no patients died, suggesting that this model indeed enables risk stratification

The global spread of HIV-1 subtype B epidemic

Human immunodeficiency virus type 1 (HIV-1) was discovered in the early 1980s when the virus had already established a pandemic. For at least three decades the epidemic in the Western World has been dominated by subtype B infections, as part of a sub-epidemic that traveled from Africa through Haiti to United States. However, the pattern of the subsequent spread still remains poorly understood. Here we analyze a large dataset of globally representative HIV-1 subtype B strains to map their spread around the world over the last 50 years and describe significant spread patterns. We show that subtype B travelled from North America to Western Europe in different occasions, while Central/Eastern Europe remained isolated for the most part of the early epidemic. Looking with more detail in European countries we see that the United Kingdom, France and Switzerland exchanged viral isolates with non-European countries than with European ones. The observed pattern is likely to mirror geopolitical landmarks in the post-World War II era, namely the rise and the fall of the Iron Curtain and the European colonialism. In conclusion, HIV-1 spread through specific migration routes which are consistent with geopolitical factors that affected human activities during the last 50 years, such as migration, tourism and trade. Our findings support the argument that epidemic control policies should be global and incorporate political and socioeconomic factors

The global spread of HIV-1 subtype B epidemic

Human immunodeficiency virus type 1 (HIV-1) was discovered in the early 1980s when the virus had already established a pandemic. For at least three decades the epidemic in the Western World has been dominated by subtype B infections, as part of a sub-epidemic that traveled from Africa through Haiti to United States. However, the pattern of the subsequent spread still remains poorly understood. Here we analyze a large dataset of globally representative HIV-1 subtype B strains to map their spread around the world over the last 50 years and describe significant spread patterns. We show that subtype B travelled from North America to Western Europe in different occasions, while Central/Eastern Europe remained isolated for the most part of the early epidemic. Looking with more detail in European countries we see that the United Kingdom, France and Switzerland exchanged viral isolates with non-European countries than with European ones. The observed pattern is likely to mirror geopolitical landmarks in the post-World War II era, namely the rise and the fall of the Iron Curtain and the European colonialism. In conclusion, HIV-1 spread through specific migration routes which are consistent with geopolitical factors that affected human activities during the last 50 years, such as migration, tourism and trade. Our findings support the argument that epidemic control policies should be global and incorporate political and socioeconomic factors

The global spread of HIV-1 subtype B epidemic

Human immunodeficiency virus type 1 (HIV-1) was discovered in the early 1980s when the virus had already established a pandemic. For at least three decades the epidemic in the Western World has been dominated by subtype B infections, as part of a sub-epidemic that traveled from Africa through Haiti to United States. However, the pattern of the subsequent spread still remains poorly understood. Here we analyze a large dataset of globally representative HIV-1 subtype B strains to map their spread around the world over the last 50years and describe significant spread patterns. We show that subtype B travelled from North America to Western Europe in different occasions, while Central/Eastern Europe remained isolated for the most part of the early epidemic. Looking with more detail in European countries we see that the United Kingdom, France and Switzerland exchanged viral isolates with non-European countries than with European ones. The observed pattern is likely to mirror geopolitical landmarks in the post-World War II era, namely the rise and the fall of the Iron Curtain and the European colonialism. In conclusion, HIV-1 spread through specific migration routes which are consistent with geopolitical factors that affected human activities during the last 50years, such as migration, tourism and trade. Our findings support the argument that epidemic control policies should be global and incorporate political and socioeconomic factors.publisher: Elsevier articletitle: The global spread of HIV-1 subtype B epidemic journaltitle: Infection, Genetics and Evolution articlelink: http://dx.doi.org/10.1016/j.meegid.2016.05.041 content_type: article copyright: © 2016 The Authors. Published by Elsevier B.V.status: publishe