Introduction Despite evidence that central nervous system (CNS) trauma, including traumatic brain injury and spinal cord injury, can cause sustained neurocognitive impairment, it remains unclear whether trauma-related variables are associated with incident dementia independently of other known risk factors. Methods All adults without dementia entering the health-care system with diagnoses of CNS trauma were examined for occurrence of dementia. All trauma-related variables were examined as predictors in sex-specific Cox regression models, controlling for other known risk factors. Results Over a median follow-up of 52 months, 32,834 of 712,708 patients (4.6%) developed dementia. Traumatic brain injury severity and spinal cord injury interacted with age to influence dementia onset; women were at a greater risk of developing dementia earlier than men, all other factors being equal. Discussion Risk stratification of patients with CNS trauma by sex is vital in identifying those most likely to develop dementia and in understanding the course and modifying factors.

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Ethical approval and informed consentApproval: The study protocol was approved by the ethics committees at the clinical (Toronto Rehabilitation Institute-University Health Network) and academic (Institute for Clinical Evaluative Sciences) institutions. All methods were carried out in accordance with the relevant guidelines and regulations. Informed consent: This research utilised encrypted administrative health data with no access to personal information. Availability of materials and dataThe datasets generated during and/or analysed during the current study are available in the ICES repository, [www.ices.on.ca/ DAS

Objective To understand how pre-injury health status present five-years preceding traumatic brain injury (TBI) affects direct medical cost two years post-injury. Methods Patients age �19 years in the emergency department (ED) or acute care for a TBI between April 1, 2007 and March 31, 2014 in Ontario, Canada (N = 55,669) were identified from population-based health administrative data. Forty-three factors of pre-injury health status (i.e., comorbidities and personal, social, and environmental factors) that were internally validated for the TBI population were assessed in this study. The outcome of interest was direct medical cost within two years of discharge. Sex-specific multivariable linear regressions were conducted to understand the associations between direct medical cost within two years of discharge and pre-injury health status.

Introduction Evidence of the effect of comorbid spinal cord injury (SCI) on cognitive outcomes in persons undergoing rehabilitation following newly diagnosed traumatic brain injury (TBI) is limited. We conducted a population‐based study to investigate this effect. Objective To compare cognitive outcomes in patients with TBI with and without a comorbid SCI. Setting/Participants Adult patients diagnosed with TBI were identified and followed for 1 year through provincial health administrative data; those who entered inpatient rehabilitation were studied. Design A retrospective matched cohort study using the National Rehabilitation Reporting System data of all acute care and freestanding rehabilitation hospitals in Ontario, Canada. Main Measures The exposure was a comorbid SCI in patients with diagnosed TBI. Exposed patients were matched to unexposed (TBI‐only) on sex, age, injury severity, and income, in a ratio of one to two. Gain differences in the cognitive subscale of the Functional Independence Measure were compared between exposed and unexposed patients using multivariable mixed linear model, controlling for comorbidity propensity score, gains in motor function, and rehabilitation care indicators. Results Over the first year post injury, 12 750 (0.84%) of all TBI patients entered inpatient rehabilitation, of whom 1359 (10.66%) had a comorbid SCI. A total of 1195 exposed patients (65.4% male, mean age 50.9 ± 20.6 for male and 61.8 ± 21.8 for female patients) were matched to 2390 unexposed patients. Controlling for confounding, exposed patients had lower cognitive gain (beta −0.43; 95% CI −0.72, −0.15), for both male (beta −0.39; 95% CI −0.75, −0.03) and female (beta −0.51; 95% CI −0.97, −0.05) patients. The adverse effects of comorbid SCI were driven largely by lower gains in problem solving and comprehension. Conclusions Adult patients with TBI and comorbid SCI showed a lower cognitive domain response to inpatient rehabilitation than patients with TBI alone. Identifying patients at risk for worse cognitive outcomes may facilitate the development of targeted strategies that improve cognitive outcomes.

Background Premature mortality is an important population health indicator used to assess health system functioning and to identify areas in need of health system intervention. Predicting the future incidence of premature mortality in the population can facilitate initiatives that promote equitable health policies and effective delivery of public health services. This study protocol proposes the development and validation of the Premature Mortality Risk Prediction Tool (PreMPoRT) that will predict the incidence of premature mortality using large population-based community health surveys and multivariable modeling approaches. Methods PreMPoRT will be developed and validated using various training, validation, and test data sets generated from the six cycles of the Canadian Community Health Survey (CCHS) linked to the Canadian Vital Statistics Database from 2000 to 2017. Population-level risk factor information on demographic characteristics, health behaviors, area level measures, and other health-related factors will be used to develop PreMPoRT and to predict the incidence of premature mortality, defined as death prior to age 75, over a 5-year period. Sex-specific Weibull accelerated failure time models will be developed using a Canadian provincial derivation cohort consisting of approximately 500,000 individuals, with approximately equal proportion of males and females, and about 12,000 events of premature mortality. External validation will be performed using separate linked files (CCHS cycles 2007–2008, 2009–2010, and 2011–2012) from the development cohort (CCHS cycles 2000–2001, 2003–2004, and 2005–2006) to check the robustness of the prediction model. Measures of overall predictive performance (e.g., Nagelkerke’s R2), calibration (e.g., calibration plots), and discrimination (e.g., Harrell’s concordance statistic) will be assessed, including calibration within defined subgroups of importance to knowledge users and policymakers. Discussion Using routinely collected risk factor information, we anticipate that PreMPoRT will produce population-based estimates of premature mortality and will be used to inform population strategies for prevention.

ObjectiveTo understand how pre-injury health status present five-years preceding traumatic brain injury (TBI) affects direct medical cost two years post-injury. MethodsPatients age �19 years in the emergency department (ED) or acute care for a TBI between April 1, 2007 and March 31, 2014 in Ontario, Canada (N = 55,669) were identified from population-based health administrative data. Forty-three factors of pre-injury health status (i.e., comorbidities and personal, social, and environmental factors) that were internally validated for the TBI population were assessed in this study. The outcome of interest was direct medical cost within two years of discharge. Sex-specific multivariable linear regressions were conducted to understand the associations between direct medical cost within two years of discharge and pre-injury health status.

Introduction We aimed to examine the association between sleep disorders and dementia risk in a population-based cohort of adult male and female patients with traumatic brain injury (TBI). Methods We studied a province-wide retrospective cohort of all adult patients (≥ 18 years) free of dementia at the admission to the emergency department or acute care hospital with diagnoses of TBI between May 2003 and April 2013. All patients were followed through until May 2016. The primary exposure was a sleep disorder, and the primary outcome was dementia, both defined by the International Classification of Diseases, tenth revision diagnosis. Associations of sleep disorders with dementia were analyzed in multivariate Cox Proportional Hazard modeling. Results In total, 712,708 patients with TBI of all severities were included in this study. Their median age was 44 years, 59% were males. Over a median follow-up of 52 months (interquartile range, 19–86 months), 32,834 (4.6%) developed dementia. Controlling for age, sex, income level, injury severity, and known comorbidity risks, diagnosed sleep disorder was a significant predictor of incident dementia: hazard ratio (HR), 1.250 [95% CI, 1.146–1.363]. When results were stratified by sex, the association of sleep disorder with dementia remained significant in male: HR 1.255 [95% CI, 1.112–1.415] and in female patients: HR 1.234 [95% CI, 1.088–1.400]. Sensitivity analyses on Alzheimer’s disease case definition and using Fine and Gray competing risk models confirmed the association between sleep disorder and dementia in both sexes. Conclusion In both sexes, sleep disorders were independently associated with dementia onset (adjusted HRs>1.2). Thus, screening for sleep disorders should be part of regular care for TBI patients, as with the steady increase of TBI survivorship and life expectancy, undiagnosed sleep disorders can initiate a new cascade of cognitive deficits independent from TBI. Support (if any) This work was supported by the postdoctoral research grant from the Alzheimer’s Association (AARF-16-442937) to T.Mollayeva. The authors were also supported by the Eunice Kennedy Shriver National Institute of Child Health & Human Development of the National Institutes of Health under Award Number R21HD089106 and the Canadian Institutes for Health Research Grant–Institute for Gender and Health (#CGW-126580).