Journal of neurotrauma
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Journal of neurotrauma · Mar 2017
2015 ParaPan American Games: Autonomic function, but not physical activity, is associated with vascular-cognitive impairment in spinal cord injury.
Autonomic dysfunction and diminished capacity for physical exercise are commonly implicated in the 3- to 4-fold increased risk of cerebrovascular disease after spinal cord injury (SCI). We assessed cerebrovascular function (transcranial Doppler; neurovascular coupling [NVC], and cerebral pressure-flow regulation) in elite national level wheelchair rugby players (n = 23), normally active SCI individuals (n = 12), and able-bodied controls (n = 13). Cognitive (Stroop test) and autonomic function (postural change) also were evaluated. ⋯ Autonomic dysfunction but not physical activity was related to impaired NVC and cerebral pressure-flow regulation after SCI. Routine upper-body exercise, as utilized by elite wheelchair rugby athletes, may not elicit beneficial cerebrovascular effects. On the other hand, autonomic dysfunction needs to be considered a key culprit in cerebrovascular diseases after SCI.
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Journal of neurotrauma · Mar 2017
Evaluation of whole-brain resting-state functional connectivity in spinal cord injury - a large-scale network analysis using network based statistic.
Large-scale network analysis characterizes the brain as a complex network of nodes and edges to evaluate functional connectivity patterns. The utility of graph-based techniques has been demonstrated in an increasing number of resting-state functional MRI (rs-fMRI) studies in the normal and diseased brain. However, to our knowledge, graph theory has not been used to study the reorganization pattern of resting-state brain networks in patients with traumatic complete spinal cord injury (SCI). ⋯ Upon further examination, increased connectivity was observed in a subnetwork of the sensorimotor cortex and cerebellum network in SCI. In conclusion, our findings emphasize the applicability of NBS to study functional connectivity architecture in diseased brain states. Further, we show reorganization of large-scale resting-state brain networks in traumatic SCI, with potential prognostic and therapeutic implications.
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Journal of neurotrauma · Mar 2017
Activation of KCNQ channels suppresses spontaneous activity in DRG neurons and reduces chronic pain after spinal cord injury.
A majority of people who have sustained spinal cord injury (SCI) experience chronic pain after injury, and this pain is highly resistant to available treatments. Contusive SCI in rats at T10 results in hyperexcitability of primary sensory neurons, which contributes to chronic pain. KCNQ channels are widely expressed in nociceptive dorsal root ganglion (DRG) neurons, are important for controlling their excitability, and their activation has proven effective in reducing pain in peripheral nerve injury and inflammation models. ⋯ These results encourage the further exploration of U. S. Food and Drug Administration-approved KCNQ activators for treating SCI pain, as well as efforts to develop a new generation of KCNQ activators that lack central side effects.
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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
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.