Current and projected workforce of spinal cord injury medicine board-certified physicians through 2040.

Care delivered by physicians experienced and trained in spinal cord injury medicine (SCIM) offers benefit to individuals with spinal cord injury (SCI). The American Board of Physical Medicine and Rehabilitation (ABPMR) offers board certification (BC) to physicians who have met eligibility requirements. Enough individuals must earn and maintain BC in order to maintain a SCIM specialty-trained workforce. This study used demographic data of physicians with SCIM BC obtained from the ABPMR, American Board of Internal Medicine, American Board of Medical Specialties, and National Resident Matching Program. Since the SCIM Examination was first offered, 723 physicians received initial certification, and 464 physicians held BC in 2020. Peak workforce size is estimated to have occurred in 2007, and SCIM fellowship trained-BC physicians began to make up the majority of all current SCIM board-certified physicians in 2019. Models for best fit were developed with known data. Projections suggest a continued decrease in total SCIM board-certified physicians until 2034, then only a slight increase until steady state is reached with 376 SCIM board-certified physicians. If the number of individuals receiving SCIM BC remains unchanged, there will be reductions in SCIM board-certified physicians for another 15 years. Whether this supply meets demand is unknown.

Impact of traumatic brain injury on amyotrophic lateral sclerosis: from bedside to bench.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the loss of upper and lower motor neurons, which manifests clinically as progressive weakness. Although several epidemiological studies have found an association between traumatic brain injury (TBI) and ALS, there is not a consensus on whether TBI is an ALS risk factor. It may be that it can cause ALS in a subset of susceptible patients, based on a history of repetitive mild TBI and genetic predisposition. This cannot be determined based on clinical observational studies alone. Better preclinical models are necessary to evaluate the effects of TBI on ALS onset and progression. To date, only a small number of preclinical studies have been performed, mainly in the superoxide dismutase 1 transgenic rodents, which, taken together, have mixed results and notable methodological limitations. The more recent incorporation of additional animal models such as Drosophila flies, as well as patient-induced pluripotent stem cell-derived neurons, should facilitate a better understanding of a potential functional interaction between TBI and ALS.

Regular physical activity prevents chronic pain by altering resident muscle macrophage phenotype and increasing interleukin-10 in mice.

Regular physical activity in healthy individuals prevents development of chronic musculoskeletal pain; however, the mechanisms underlying this exercise-induced analgesia are not well understood. Interleukin-10 (IL-10), an antiinflammatory cytokine that can reduce nociceptor sensitization, increases during regular physical activity. Since macrophages play a major role in cytokine production and are present in muscle tissue, we propose that physical activity alters macrophage phenotype to increase IL-10 and prevent chronic pain. Physical activity was induced by allowing C57BL/6J mice free access to running wheels for 8 weeks and compared to sedentary mice with no running wheels. Using immunohistochemical staining of the gastrocnemius muscle to label regulatory (M2, secretes antiinflammatory cytokines) and classical (M1, secretes proinflammatory cytokines) macrophages, the percentage of M2-macrophages increased significantly in physically active mice (68.5% ± 4.6% of total) compared with sedentary mice (45.8% ± 7.1% of total). Repeated acid injections into the muscle enhanced mechanical sensitivity of the muscle and paw in sedentary animals, which does not occur in physically active mice; no sex differences occur in either sedentary or physically active mice. Blockade of IL-10 systemically or locally prevented the analgesia in physically active mice, ie, mice developed hyperalgesia. Conversely, sedentary mice pretreated systemically or locally with IL-10 had reduced hyperalgesia after repeated acid injections. Thus, these results suggest that regular physical activity increases the percentage of regulatory macrophages in muscle and that IL-10 is an essential mediator in the analgesia produced by regular physical activity.