Objective: To evaluate the association between cardiovascular disease (CVD) and spinal cord injury (SCI) in a large representative sample.Methods: Data were compiled from more than 60,000 individuals from the 2010 cycle of the cross-sectional Canadian Community Health Survey (CCHS). Multivariable logistic regression analysis was conducted to examine this relationship, adjusting for confounders and using probability weighting to account for the CCHS sampling method.Results: After adjusting for age and sex, SCI was associated with a significant increased odds of heart disease (adjusted odds ratio [OR] 5 2.72, 95% confidence interval [CI] 1.94-3.82) and stroke (adjusted OR 5 3.72, 95% CI 2.22-6.23).Conclusions: These remarkably heightened odds highlight the exigent need for targeted interventions and prevention strategies addressing modifiable risk factors for CVD in individuals with SCI. Over the last decade, there have been marked changes in the trends of morbidity and mortality among individuals with spinal cord injury (SCI). With advances in acute care and in the management of septicemia, renal failure, and pneumonia, cardiovascular complications are now a leading cause of death in those with SCI. 1 Moreover, several risk factors for cardiovascular disease (CVD) are amplified in individuals with SCI compared with able-bodied individuals, including physical inactivity, dyslipidemia, blood pressure irregularities, chronic inflammation, and abnormal glycemic control. 2-22While most of the literature with respect to CVD and SCI has shown a higher prevalence of risk factors for CVD, 2-22 relatively few studies have examined the prevalence of CVD itself and corresponding risk estimates. [23][24][25][26] None of these studies has provided direct comparisons of risk estimates for multiple CVD outcomes in the SCI population compared to a non-SCI population, with appropriate adjustment for confounding, in a large representative sample.It thus remains unknown whether there is excess risk of both heart disease and stroke (after adjustment for potential confounders) in individuals with SCI. The current study addresses this knowledge gap by utilizing the national Canadian Community Health Survey (CCHS), which is comprised of comprehensive, up-to-date, cross-sectional data. Our aim was to estimate the prevalence of heart disease and stroke outcomes in the SCI population, to compare their risk with a non-SCI population, and to investigate this relationship after controlling for confounders.

Parkinson's disease is a heterogeneous disorder with multiple factors contributing to disease initiation and progression. Using serial, multi-tracer positron emission tomography imaging, we studied a cohort of 78 subjects with sporadic Parkinson's disease to understand the disease course better. Subjects were scanned with radiotracers of presynaptic dopaminergic integrity at baseline and again after 4 and 8 years of follow-up. Non-linear multivariate regression analyses, using random effects, of the form BP(ND)(t) or K(occ)(t) = a*e((-)(bt)(-d)(A) + c, where BP(ND) = tracer binding potential (nondispaceable), K(OCC) = tracer uptake constant a, b, c and d are regression parameters, t is the symptom duration and A is the age at onset, were utilized to model the longitudinal progression of radiotracer binding/uptake. We found that the initial tracer binding/uptake was significantly different in anterior versus posterior striatal subregions, indicating that the degree of denervation at disease onset was different between regions. However, the relative rate of decline in tracer binding/uptake was similar between the striatal subregions. While an antero-posterior gradient of severity was maintained for dopamine synthesis, storage and reuptake, the asymmetry between the more and less affected striatum became less prominent over the disease course. Our study suggests that the mechanisms underlying Parkinson's disease initiation and progression are probably different. Whereas factors responsible for disease initiation affect striatal subregions differently, those factors contributing to disease progression affect all striatal subregions to a similar degree and may therefore reflect non-specific mechanisms such as oxidative stress, inflammation or excitotoxicity.

Our results suggest that, compared to older patients, younger PD patients progress more slowly and are able to endure more damage to the dopaminergic system before the first motor symptoms appear. These observations suggest that younger PD patients have more efficient compensatory mechanisms.