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Objectives. To determine the effects of neurotrophin-secreting transplants combined with exercise and serotonergic drug challenges on recovery of hindlimb function in rats with midthoracic spinal cord transection injuries. Methods. Spinalized [...]

In the USA, substantial geographic variation in health care utilization exists in the Department of Veterans Affairs (VA) health care system. Utilization of health care services is especially important for veterans with spinal cord injuries and disorders (SCI&D) who are often at high risk for secondary complications related to their SCI&D. Due to impaired mobility, access to health care for veterans with SCI&D may be even more challenging. The goal of this cross-sectional study was to describe health care utilization relative to SCI&D veteran residential geographic proximity to VA health care facilities. A negative binomial regression model was used to examine VA outpatient utilization. Veterans with SCI&D utilized outpatient services less frequently when VA facilities were farther away from their residences (p Keywords: Spinal cord injury: Veterans; Health care access/utilization; USA

Recruitment of inflammatory leukocytes to the injured spinal cord is a physiological response that is associated with the production of cytokines and proteinases that are involved in host defense and wound repair. Cells in the spinal cord are mainly post-mitotic and tissue regeneration is poor; thus, these inflammatory mediators can exacerbate the damage to spared tissue and thereby impair spontaneous functional recovery. Although several aspects of immune function might benefit the CNS, experimental studies indicate that acute neuroinflammation aggravates tissue injury. Until the timing and nature of the molecular signals that govern leukocyte recruitment and activation after spinal injury are defined, clinical therapies designed to boost immune cell function should be avoided.

Inflammation is thought to exacerbate the outcome of spinal cord injury. However, our findings have led us to view inflammation as a healing response that needs the help of a systemic immune response mediated by T helper 1 (Th1) cells that are specific to the abundant antigens residing in the lesion site. Strains differ in their ability to manifest, at the right time and intensity, a spontaneous T-cell response to antigens at the lesion site and therefore in their ability to generate a local inflammatory response whose outcome is beneficial (maintenance and repair). All strains, however, can benefit from immune intervention that boosts and regulates the inflammatory response. Because recovery comprises multi-step processes, pharmacological intervention will be less effective than well-synchronized, self-healing immune activity. Risk-free neuroprotective intervention might be achieved by post-traumatic vaccination with a weak, non-pathogenic, auto-antigen, causing autoimmune T cells to home to the lesion site where they become activated and therefore activate local phagocytic cells to remove hostile elements and provide growth factors.

CM101, an antiangiogenic polysaccharide derived from group B streptococcus, was administered by i.v. injection 1 hr post-spinal-cord crush injury in an effort to prevent inflammatory angiogenesis and gliosis (scarring) in a mouse model. We postulated that gliosis would sterically prevent the reestablishment of neuronal connectivity; thus, treatment with CM101 was repeated every other day for five more infusions for the purpose of facilitating regeneration of neuronal function. Twenty-five of 26 mice treated with CM101 survived 28 days after surgery, and 24 of 26 recovered walking ability within 2-12 days. Only 6 of 14 mice in the control groups survived 24 hr after spinal cord injury, and none recovered function in paralyzed limbs. MRI analysis of injured untreated and treated animals showed that CM101 reduced the area of damage at the site of spinal cord compression, which was corroborated by histological analysis of spinal cord sections from treated and control animals. Electrophysiologic measurements on isolated central nervous system and neurons in culture showed that CM101 protected axons from Wallerian degeneration; reversed [Gamma]-aminobutyrate-mediated depolarization occurring in traumatized neurons; and improved recovery of neuronal conductivity of isolated central nervous system in culture.