Journal of neurotrauma
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Journal of neurotrauma · Mar 2017
Pain Input Impairs Recovery After Spinal Cord Injury: Treatment With Lidocaine.
More than 90% of spinal cord injuries are caused by traumatic accidents and are often associated with other tissue damage (polytrauma) that can provide a source of continued pain input during recovery. In a clinically relevant spinal cord contusion injury model, prior work has shown that noxious stimulation at an intensity that engages pain (C) fibers soon after injury augments secondary injury and impairs functional recovery. Noxious input increases the expression of pro-inflammatory cytokines (interleukin 1β and 18), cellular signals associated with cell death (caspase 3 and 8), and physiological signs of hemorrhage. ⋯ Contused rats that received nociceptive stimulation soon after injury exhibited poor locomotor recovery, less weight gain, and greater tissue loss at the site of injury. Prophylactic application of lidocaine blocked the adverse effect of nociceptive stimulation on behavioral recovery and reduced tissue loss from secondary injury. The results suggest that quieting neural excitability using lidocaine can reduce the adverse effect of pain input (from polytrauma or surgery) after SCI.
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Journal of neurotrauma · Mar 2017
Changes in gene expression and metabolism in the testes of the rat following spinal cord injury.
Spinal cord injury (SCI) results in devastating changes to almost all aspects of a patient's life. In addition to a permanent loss of sensory and motor function, males also will frequently exhibit a profound loss of fertility through poorly understood mechanisms. We demonstrate that SCI causes measureable pathology in the testis both acutely (24 h) and chronically up to 1.5 years post-injury, leading to loss in sperm motility and viability. ⋯ At 1.5 years post-SCI, there is a chronic low level immune response as evidenced by an elevation in T cells. These data suggest that SCI elicits a wide range of pathological processes within the testes, the actions of which are not restricted to the acute phase of injury but rather extend chronically, potentially through the lifetime of the subject. The multiplicity of these pathological events suggest a single therapeutic intervention is unlikely to be successful.
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Journal of neurotrauma · Mar 2017
3D quantification of microarchitecture and vessel regeneration by synchrotron radiation μCT in a rat model of spinal cord injury.
A full understanding of the mechanisms behind spinal cord injury (SCI) processes requires reliable three-dimensional (3D) imaging tools for a thorough analysis of changes in angiospatial architecture. We aimed to use synchrotron radiation μCT (SRμCT) to characterize 3D temporal-spatial changes in microvasculature post-SCI. Morphometrical measurements revealed a significant decrease in vascular volume fraction, vascular bifurcation density, vascular segment density, and vascular connectivity density 1 day post-injury, followed by a gradual increase at 3, 7, and 14 days. ⋯ We describe a methodology for 3D analysis of vascular repair in SCI and reveal that endogenous revascularization occurs during the healing process. The spinal cord microvasculature configuration undergoes 3D remodeling and modification during the post-injury repair process. Examination of these processes might contribute to a full understanding of the compensatory vascular mechanisms after injury and aid in the development of novel and effective treatment for SCI.
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Journal of neurotrauma · Mar 2017
Increased Central Arterial Stiffness after Spinal Cord Injury: Contributing Factors, Implications and Possible Interventions.
Individuals with spinal cord injury (SCI) experience life-threatening cardiovascular events and various autonomic consequences in addition to the well-appreciated motor and neurological impairments. As a result, cardiovascular disease is a major cause of death after SCI, corresponding to a two-to-fourfold increased risk of cardiovascular events. A combination of neuroanatomical changes, unstable blood pressure, and rapid deconditioning as a result of decreased physical activity likely contributes to accelerated cardiovascular disease progression after SCI. ⋯ The potential factors contributing to increased central arterial stiffness are also reviewed in light of the available literature, including autonomic disruptions, blood pressure instability, metabolic changes, and physical inactivity. Further, measurement techniques, risk factors, cardiac dysfunction, and differences in arterial stiffness from able-bodied populations are discussed. Finally, potential therapeutic interventions for preventing or improving central arterial stiffening are also explored, including dietary, physical activity, and pharmacological strategies.
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Journal of neurotrauma · Mar 2017
Characterization of the antibody response after cervical spinal cord injury.
The immune system plays a critical and complex role in the pathobiology of spinal cord injury (SCI), exerting both beneficial and detrimental effects. Increasing evidence suggests that there are injury level-dependent differences in the immune response to SCI. Patients with traumatic SCI have elevated levels of circulating autoantibodies against components of the central nervous system, but the role of these antibodies in SCI outcomes remains unknown. ⋯ Further, increased levels of secreted IgG antibodies and enhanced proliferation of T-cells in splenocyte cultures from injured rats were found. These findings suggest the potential development of autoantibody responses following cSCI in the rat. The impact of the post-traumatic antibody responses on functional outcomes of cSCI is a critical topic that requires further investigation.