Having acknowledged these valuable contributors, the authors remain fully and solely responsible for the report and its contents.Please address comments and correspondence concerning this report to info@rickhanseninsti tute.org, with "Incidence and Prevalence Report" in the subject line. D e c e m b e r 2 0 1 0This report may be reproduced in whole or in part with appropriate acknowledgement of the source. U R B A N F U T U R E SS S t t r r a a t t e e g g i i c c R R e e s s e e a a r r c c h h t t o o M M a a n n a a g g e e C C h h a a n n g g e e P a g e i December 2010 The Incidence and Prevalence of Spinal Cord Injury in Canada U R B A N F U T U R E SS S t t r r a a t t e e g g i i c c R R e e s s e e a a r r c c h h t t o o M M a a n n a a g g e e C C h h a a n n g g e e P a g e i i December 2010 The Incidence and Prevalence of Spinal Cord Injury in CanadaThis page intentionally left blank. U R B A N F U T U R E SS S t t r r a a t t e e g g i i c c R R e e s s e e a a r r c c h h t t o o M M a a n n a a g g e e C C h h a a n n g g e Executive SummaryThis report was prepared to provide a review of the current measures of the incidence and prevalence of spinal cord injury (SCI) in Canada. It is to be considered within the context of a strategic discussion concerning the need for, and directi on of, further formal research into the extent of spinal cord injury in the country. The report commences with considerati on of defi niti ons relati ng to spinal cord injury, followed by a review of methodology used in the measurement of its incidence (annual number of new cases) and prevalence (total number of people living with SCI, the cumulati ve net result of past SCI), and of the major Canadian publicati ons, and selected internati onal ones, that are concerned with this measurement. On this basis, esti mates of the current levels of incidence and prevalence of spinal cord injury in Canada are presented, before concluding with recommendati ons concerning these esti mates and possible directi ons for further research.The terms of reference for this research were to produce esti mates of the incidence and prevalence of spinal cord injury in Canada based on currently published evidence. It is important to note that no such measures currently exist: very litt le has been published about the extent of spinal cord injury in Canada, and what has is limited to the incidence of traumati c spinal cord injury, with the literature silent on its prevalence, and most strikingly, on both the incidence and prevalence of non-traumati c spinal cord injury. The absence of esti mates of incidence and prevalence is of signifi cant concern, as it limits a wide range of research and policy, ranging from the determinati on of the most eff ecti ve preventi on strategies through the delivery of health and medical care to the considerati on of the fi nancial impact of SCI and funding of preventi on and care programmes.Given the informati on provided in the reviewed publicati ons, and data on the current and historical demography of Canad...

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Receptor-mediated activation of heterotrimeric guanine nucleotide-binding proteins (G proteins) results in the dissociation of alpha from beta gamma subunits, thereby allowing both to regulate effectors. Little is known about the regions of effectors required for recognition of G beta gamma. A peptide encoding residues 956 to 982 of adenylyl cyclase 2 specifically blocked G beta gamma stimulation of adenylyl cyclase 2, phospholipase C-beta 3, potassium channels, and beta-adrenergic receptor kinase as well as inhibition of calmodulin-stimulated adenylyl cyclases, but had no effect on interactions between G beta gamma and G alpha o. Substitutions in this peptide identified a functionally important motif, Gln-X-X-Glu-Arg, that is also conserved in regions of potassium channels and beta-adrenergic receptor kinases that participate in G beta gamma interactions. Thus, the region defined by residues 956 to 982 of adenylyl cyclase 2 may contain determinants important for receiving signals from G beta gamma.

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Study design: Survey of expert opinion, feedback, and development of final consensus. Objective: Present the background, purpose, development process, and results for the International Spinal Cord Injury (SCI) Core Data Set. Setting: International. Methods: A committee of experts was established to select and define data elements to be included in an International SCI Core Data Set. A draft core data set was developed and disseminated to appropriate organisations for comment. All suggested revisions were considered, and a final version of the core data set was disseminated again for approval and adoption. Results: The core data set consists of 24 variables, including basic demographic characteristics, dates of admission and discharge from initial acute and rehabilitation care, cause of injury, place of discharge, presence of vertebral fractures and associated injuries, occurrence of spinal surgery, and measures of neurological and ventilator status. Conclusion: Collection of the core data set should be a basic ingredient of all future studies of SCI to facilitate accurate description of patient populations and comparison of results across published studies from around the world.

Acute spinal cord injury (SCI) causes systemic immunosuppression and life-threatening infections, thought to result from noradrenergic overactivation and excess glucocorticoid release via hypothalamus-pituitary-adrenal axis stimulation. Instead of consecutive hypothalamus-pituitary-adrenal axis activation, we report that acute SCI in mice induced suppression of serum norepinephrine and concomitant increase in cortisol, despite suppressed adrenocorticotropic hormone, indicating primary (adrenal) hypercortisolism. This neurogenic effect was more pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared with low-thoracic level (Th9) SCI. Prophylactic adrenalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depletion but did not prevent pneumonia. When adrenalectomized mice were transplanted with denervated adrenal glands to restore physiologic glucocorticoid levels, the animals were completely protected from pneumonia. These findings identify a maladaptive sympathetic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, implying that therapeutic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strategy to prevent detrimental infections.

Pneumonia is the leading cause of death after acute spinal cord injury and is associated with poor neurological outcome. In contrast to the current understanding, attributing enhanced infection susceptibility solely to the patient's environment and motor dysfunction, we investigate whether a secondary functional neurogenic immune deficiency (spinal cord injury-induced immune deficiency syndrome, SCI-IDS) may account for the enhanced infection susceptibility. We applied a clinically relevant model of experimental induced pneumonia to investigate whether the systemic SCI-IDS is functional sufficient to cause pneumonia dependent on spinal cord injury lesion level and investigated whether findings are mirrored in a large prospective cohort study after human spinal cord injury. In a mouse model of inducible pneumonia, high thoracic lesions that interrupt sympathetic innervation to major immune organs, but not low thoracic lesions, significantly increased bacterial load in lungs. The ability to clear the bacterial load from the lung remained preserved in sham animals. Propagated immune susceptibility depended on injury of central pre-ganglionic but not peripheral postganglionic sympathetic innervation to the spleen. Thoracic spinal cord injury level was confirmed as an independent increased risk factor of pneumonia in patients after motor complete spinal cord injury (odds ratio = 1.35, P < 0.001) independently from mechanical ventilation and preserved sensory function by multiple regression analysis. We present evidence that spinal cord injury directly causes increased risk for bacterial infection in mice as well as in patients. Besides obvious motor and sensory paralysis, spinal cord injury also induces a functional SCI-IDS ('immune paralysis'), sufficient to propagate clinically relevant infection in an injury level dependent manner.