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
Cognitive impairment and mood states following spinal cord injury.
Spinal cord injury (SCI) is believed to be associated with high rates of cognitive impairment, which can result in complications in recovery. This study concerned two groups of adults with SCI. The first sample involved 150 participants with SCI who were assessed once for cognitive capacity with comparisons made with 45 able-bodied adults. ⋯ Results from Sample 2 revealed that the development of negative mood states was a significant problem in those with cognitive impairment after they transitioned into the community, a time when personal resources are severely challenged. Findings suggest all adults with SCI admitted to rehabilitation should receive a cognitive screen, and that rehabilitation strategies should then be guided by the cognitive performance of the person. Special attention should also be given to improving skills of those with cognitive impairment before they transition into the community, so as to reduce risk of comorbid mental health problems.
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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.
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Journal of neurotrauma · Mar 2017
High-intensity locomotor exercise increases brain-derived neurotrophic factor in individuals with incomplete spinal cord injury.
High-intensity locomotor exercise is suggested to contribute to improved recovery of locomotor function after neurological injury. This may be secondary to exercise-intensity-dependent increases in neurotrophin expression demonstrated previously in control subjects. However, rigorous examination of intensity-dependent changes in neurotrophin levels is lacking in individuals with motor incomplete spinal cord injury (SCI). ⋯ Significant correlations were observed between changes in BDNF and specific indicators of exercise intensity (e.g., rating of perceived exertion; R = 0.43; p = 0.02). Additionally, the data suggest that Val66Met SNP carriers may not exhibit intensity-dependent changes in serum BDNF concentration. Given the known role of BDNF in experience-dependent neuroplasticity, these preliminary results suggest that exercise intensity modulates serum BDNF concentrations and may be an important parameter of physical rehabilitation interventions after neurological injury.