Notes

Tasks of miR-204 throughout retinal development and also routine maintenance.
Spinal cord injury (SCI) substantially increases the risk of neurogenic obesity, diabetes, and metabolic syndrome. Much like in the general population, a discussion of these syndromes in SCI would be incomplete without acknowledging the association of SCI with sleep-disordered breathing (SDB). This article will outline the interplay between obesity and obstructive sleep apnea (OSA), discussing the pathophysiology of obesity in OSA both for the general population and SCI population. The role of insulin resistance in SDB and SCI will also be examined. The epidemiology and pathophysiology of OSA and central sleep apnea in SCI are discussed through an examination of current evidence, followed by a review of central sleep apnea in SCI. Principles of diagnosis and management of SDB will also be discussed. Because sleep deprivation in itself can be a risk factor for developing obesity, the significance of comorbid insomnia in SCI is explored. Ultimately, a thorough sleep history, testing, and treatment are key to improving the sleep of individuals with SCI and to potentially reducing the impact of neurogenic obesity and metabolic syndrome.The prevalence of obesity and of neuropathic pain are both estimated at above 50% in the population of people with chronic spinal cord injury (SCI). These secondary consequences of SCI have significant negative impact on physical functioning, activities of daily living, and quality of life. Investigations of relationships between weight or body composition and chronic neuropathic pain in people with SCI are lacking, but investigations in non-SCI cohorts suggest an association between obesity and the presence and severity of neuropathic pain conditions. In the present article, we present a review of the literature linking obesity and neuropathic pain and summarize findings suggesting that metabolic syndrome and chronic, systemic inflammation due to excess adiposity increase the risk for neuropathic pain after an SCI.Persons with spinal cord injury (SCI) are at high risk for developing neurogenic obesity due to muscle paralysis and obligatory sarcopenia, sympathetic blunting, anabolic deficiency, and blunted satiety. Persons with SCI are also at high risk for shoulder, elbow, wrist, and hand injuries, including neuromusculoskeletal pathologies and nociceptive pain, as human upper extremities are poorly designed to facilitate chronic weight-bearing activities, including manual wheelchair propulsion, transfers, self-care, and day-to-day activities. This article reviews current literature on the relationship between obesity and increased body weight with upper extremity overuse injuries, detailing pathology at the shoulders, elbows, and wrists that elicit pain and functional decline and stressing the importance of weight management to preserve function.Spinal cord injury (SCI) results in dramatic changes in body composition, with lean mass decreasing and fat mass increasing in specific regions that have important cardiometabolic implications. Accordingly, the recent Consortium for Spinal Cord Medicine (CSCM) released clinical practice guidelines for cardiometabolic disease (CMD) in SCI recommending the use of compartmental modeling of body composition to determine obesity in adults with SCI. This recommendation is guided by the fact that fat depots impact metabolic health differently, and in SCI adiposity increases around the viscera, skeletal muscle, and bone marrow. The contribution of skeletal muscle atrophy to decreased lean mass is self-evident, but the profound loss of bone is often less appreciated due to methodological considerations. General-population protocols for dual-energy x-ray absorptiometry (DXA) disregard assessment of the sites of greatest bone loss in SCI, but the International Society for Clinical Densitometry (ISCD) recently released an official position on the use of DXA to diagnose skeletal pathology in SCI. In this review, we discuss the recent guidelines regarding the evaluation and monitoring of obesity and bone loss in SCI. Then we consider the possible interactions of obesity and bone, including emerging evidence suggesting the possible influence of metabolic, autonomic, and endocrine function on bone health in SCI.The population with SCI is at a significant risk for both insulin resistance and type 2 diabetes mellitus (T2DM) secondary to neurogenic obesity. find more The prevalence of insulin resistance and T2DM in persons with SCI suggests that disorders of carbohydrate metabolism are at epidemic proportions within the population. However, the true frequency of such disorders may be underestimated because biomarkers of insulin resistance and T2DM used from the population without SCI remain nonspecific and may in fact fail to identify true cases that would benefit from intervention. Furthermore, diet and exercise have been used to help mitigate neurogenic obesity, but results on disorders of carbohydrate metabolism remain inconsistent, likely because of the various ways carbohydrate metabolism is assessed. The objective of this article is to review current literature on the prevalence and likely mechanisms driving insulin resistance and T2DM in persons with SCI. This article also explores the various assessments and diagnostic criteria used for insulin resistance and T2DM and briefly discusses the effects of exercise and/or diet to mitigate disorders of carbohydrate metabolism brought on by neurogenic obesity.Over two-thirds of persons with spinal cord injury (SCI) experience neurogenic obesity-induced cardiometabolic syndrome (CMS) and other chronic comorbidities. Obesity is likely to impede social and recreational activities, impact quality of life, and impose additional socioeconomic burdens on persons with SCI. Advances in imaging technology facilitate the mapping of adiposity and its association with the cardiometabolic profile after SCI. Central adiposity or central obesity is characterized by increased waist (WC) and abdominal circumferences (AC) as well as visceral adipose tissue (VAT). A number of studies, while relying on expensive imaging techniques, have reported direct associations of both central obesity and VAT in imposing significant health risks after SCI. The mechanistic role of central obesity on cardiometabolic heath in persons with SCI has yet to be identified, despite the knowledge that it has been designated as an independent risk factor for cardiometabolic dysfunction and premature mortality in other clinical populations.
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