Journal of neurotrauma
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Journal of neurotrauma · Mar 2013
Randomized Controlled TrialDivergent modulation of clinical measures of volitional and reflexive motor behaviors following serotonergic medications in human incomplete spinal cord injury.
Incomplete spinal cord injury (SCI) can result in profound impairments in volitional strength and reflex excitability, which contribute to loss of function. Human and animal models suggest that disruption of endogenous monoaminergic input, particularly serotonin (5-HT), from supraspinal centers contributes to this impaired motor function following SCI. In the present study, we investigated the effects of 5-HT medications on motor function in individuals with chronic (>1 year) SCI. ⋯ Results indicated that 5-HT medications modulated both volitional and reflexive behaviors with little change in walking performance; 5-HT antagonist medications depressed clinical measures of strength and spasticity/spasms, whereas SSRIs augmented both strength and spasticity/spasms. These changes are consistent with the dysregulation of 5-HT sensitive spinal neurons following SCI. This understanding may augment clinicians' awareness of the motor consequences of 5-HT medications.
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Journal of neurotrauma · Mar 2013
B-cell maturation antigen, a proliferation-inducing ligand, and B-cell activating factor are candidate mediators of spinal cord injury-induced autoimmunity.
Autoimmunity is thought to contribute to poor neurological outcomes after spinal cord injury (SCI). There are few mechanism-based therapies, however, designed to reduce tissue damage and neurotoxicity after SCI because the molecular and cellular bases for SCI-induced autoimmunity are not completely understood. Recent groundbreaking studies in rodents indicate that B cells are responsible for SCI-induced autoimmunity. ⋯ Real-time polymerase chain reaction analysis from ribonucleic acid samples confirmed upregulation of these three genes in SCI. To our knowledge, this is the first report that peripheral blood mononuclear cells produce increased levels of BAFF and APRIL in chronic SCI. This finding provides evidence of systemic regulation of SCI-autoimmunity via APRIL and BAFF mediated activation of B cells through BMCA and points toward these molecules as potential targets of therapies designed to reduce neuroinflammation after SCI.
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Journal of neurotrauma · Mar 2013
Process benchmarking appraisal of surgical decompression of spinal cord following traumatic cervical spinal cord injury: opportunities to reduce delays in surgical management.
Prior pre-clinical and clinical studies indicate that early decompression of the spinal cord (≤ 24 h post-trauma) may have benefits regarding clinical outcomes and neurological recovery after spinal cord injury (SCI). This study examines the benchmarking of management of patients with acute traumatic cervical SCI in order to determine the potential barriers and ideal timelines for each step to early surgical decompression. We reviewed patient charts and the Surgical Trial in Acute Spinal Cord Injury Study (STASCIS) forms regarding the time and reasons for delay of each step in the management of patients with SCI. ⋯ Our benchmarking analysis suggests that health-related factors are key determinants of the timing from SCI to spinal cord decompression. Time in the general hospital and time of waiting for a surgical decision were the most important causes of delay of surgical spinal cord decompression. Early surgery is possible in the vast majority of the cases.
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Journal of neurotrauma · Mar 2013
The effect of cigarette smoke exposure on spinal cord injury in rats.
In this study, we examined whether cigarette smoke has neuroprotective or toxic effects on spinal cord injury (SCI). Male Sprague-Dawley rats were included in the study and received either cigarette smoke exposure or fresh air exposure. Twenty-four hours after the last cigarette smoke or fresh air exposure, all rats were injured at thoracic level 12 (T12), using an established static compression model. ⋯ These results suggested that cigarette smoke can reinforce the oxidative stress injury via HIF-1α and AQP4 in the early stage after SCI. It is possible that cigarette smoke exposure does not affect SCI recovery in the long term; however, it can aggravate the edema and deteriorate BSCB disruption via HIF-1α and AQP4 in the early stage after SCI. More studies will be essential to consider this hypothesis and elucidate the mechanisms involved.
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Traumatic brain injury (TBI) is a major cause of seizures in the general population. Several studies have shown an increased risk of epilepsy after traumatic brain injury, depending on risk factors, such as severity and time post trauma. The aim of our study was to evaluate the appearance of late seizures after a very mild head trauma or whiplash injury. ⋯ Three patients (0.1%) out of the whole study group developed seizures: 2 (0.18%) in the head trauma group and 1 (0.1%) in the control group. The conclusion of the study was that post trauma seizure incidence is not significantly different in patients with very mild head or spine trauma and is similar respective to subjects with no non-head or cervical spine injury. This may have medico-legal repercussions.