Journal of neurotrauma
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Journal of neurotrauma · Feb 2017
Risk of Dementia in Patients with Spinal Cord Injury: A Nationwide Population-Based Cohort Study.
Spinal cord injury (SCI) can cause physical disability and psychological distress; however, whether SCI is a risk factor for dementia is unclear. This study evaluated the incidence of dementia in patients with SCI. Study participants were recruited from a nationwide cohort during 2004-2007 and categorized into SCI (patients diagnosed with SCI; n = 941) and non-SCI (age- and sex-matched controls; n = 5060) cohorts. ⋯ Patients with SCI had a significantly higher risk of dementia than did those without SCI (crude hazard ratio [HR] = 2.14, 95% confidence interval [CI], 1.57-2.92, p < 0.001 vs. adjusted HR = 1.95, 95% CI, 1.43-2.67, p < 0.001). Further analysis found that there is no statistical significance of higher risk for developing Alzheimer's disease among SCI patients, but that SCI patients were at higher risk of developing other types of dementia than the control cohort (crude HR = 1.88, 95% CI, 1.33-2.63, p < 0.001 vs. adjusted HR = 1.90, 95% CI, 1.35-2.68, p < 0.001). In conclusion, patients with SCI are at high risk of dementia, and effective dementia prevention strategies are recommended for comprehensive SCI care.
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Journal of neurotrauma · Feb 2017
A Morphological and Molecular Characterization of the Spinal Cord Following Ventral Root Avulsion or Distal Peripheral Nerve Axotomy Injuries in Adult Rats.
Retrograde cell death in sensory dorsal root ganglion cells following peripheral nerve injury is well established. However, available data regarding the underlying mechanism behind injury induced motoneuron death are conflicting. By comparing morphological and molecular changes in spinal motoneurons after L4-L5 ventral root avulsion (VRA) and distal peripheral nerve axotomy (PNA) 7 and 14 days postoperatively, we aimed to gain more insight about the mechanism behind injury-induced motoneuron degeneration. ⋯ Moreover, the altered gene expression correlated with protein changes. These results show that the spinal motoneurons reacted in a similar fashion with respect to morphological changes after both proximal and distal injury. However, the increased expression of caspase-3, caspase-8, and related death receptors after VRA suggest that injury- induced motoneuron degeneration is mediated through an apoptotic mechanism, which might involve both the intrinsic and the extrinsic pathways.
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Journal of neurotrauma · Feb 2017
Disruption of locomotion in response to hindlimb muscle stretch at acute and chronic time points after a spinal cord injury in rats.
After spinal cord injury (SCI) muscle contractures develop in the plegic limbs of many patients. Physical therapists commonly use stretching as an approach to avoid contractures and to maintain the extensibility of soft tissues. We found previously that a daily stretching protocol has a negative effect on locomotor recovery in rats with mild thoracic SCI. ⋯ The current study extends our observations of the stretching phenomenon to a more clinically relevant moderately severe SCI animal model. The results are in agreement with our previous findings and further demonstrate that spinal cord locomotor circuitry is especially vulnerable to the negative effects of stretching at chronic time points. While the clinical relevance of this phenomenon remains unknown, we speculate that stretching may contribute to the lack of locomotor recovery in some patients.
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Opioids and non-steroidal anti-inflammatory drugs are used commonly to manage pain in the early phase of spinal cord injury (SCI). Despite its analgesic efficacy, however, our studies suggest that intrathecal morphine undermines locomotor recovery and increases lesion size in a rodent model of SCI. Similarly, intravenous (IV) morphine attenuates locomotor recovery. ⋯ These data suggest that morphine use is contraindicated in the acute phase of a spinal injury. Faced with a lifetime of intractable pain, however, simply removing any effective analgesic for the management of SCI pain is not an ideal option. Instead, these data underscore the critical need for further understanding of the molecular pathways engaged by conventional medications within the pathophysiological context of an injury.
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Journal of neurotrauma · Feb 2017
High thoracic contusion model for the investigation of cardiovascular function post spinal cord injury.
Cardiovascular disease is the leading cause of death for individuals with spinal cord injury (SCI). Because of a lack of a standardized and accessible animal model for cardiovascular disease after SCI, few laboratories have conducted pre-clinical trials aimed at reinstating descending cardiovascular control. Here, we utilized common contusion methodology applied to the midline of the upper-thoracic cord of adult Wistar rats accompanied with telemetric blood pressure monitoring and FluoroGold retrograde neuronal tracing, as well as lesion site and lumbrosacral afferent immunohistochemistry. ⋯ Further, we provide a description of the neuroanatomical changes that accompany cardiovascular abnormalities. Specifically, we describe 1) the injury site including white matter sparing as well as lesion volume, and their correlations to cardiovascular as well as motor outcomes; 2) the severity of injury-dependent changes in sympathoexcitatory medullary neuron spinal connectivity, as measured using FluoroGold tracing; and 3) the extent of aberrant afferent plasticity within the lumbosacral region of the spinal cord, which has been linked to the development of autonomic dysreflexia. We believe that this model, which utilizes equipment common to numerous SCI laboratories, can serve as a research standard for studies specifically aimed at investigating autonomic neuroprotective and regenerative strategies following SCI.