Journal of neurotrauma
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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.
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Journal of neurotrauma · Mar 2017
NorBNI blocks the adverse effects of morphine following spinal cord injury.
Opioids are frequently used for the treatment of pain following spinal cord injury (SCI). Unfortunately, we have shown that morphine administered in the acute phase of SCI results in significant, adverse secondary consequences including compromised locomotor and sensory recovery. Similarly, we showed that selective activation of the κ-opioid receptor (KOR), even at a dose 32-fold lower than morphine, is sufficient to attenuate recovery of locomotor function. ⋯ This suggests that activation of the KOR system plays a significant role in the morphine-induced attenuation of recovery. Our research suggests that morphine, and other opioid analgesics, may be contraindicated for the SCI population. Blocking KOR activity may be a viable strategy for improving the safety of clinical opioid use.
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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.