Journal of neurotrauma
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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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Spinal Cord Injury (SCI) is an acute trauma to the neural elements resulting in temporary or permanent sensory and motor deficit. Studies have indicated that although 66% of SCI occur in Caucasians, there are a growing number of other racial groups affected by SCI. Furthermore, there has been a lack of research concerning racial disparities in outcomes following SCI. ⋯ For disposition status, African Americans (OR 0.844, CI 0.730-0.976) and Asians (OR 0.475, CI 0.297-0.760) were much less likely than Caucasians or Hispanic populations to be discharged to an acute rehabilitation program. The results from this large-scale study (n=18,671) demonstrate a number of racial disparities following SCI at the national level, including rate of complications, length of stay, and disposition to acute rehabilitation centers. This should raise awareness to cultural differences but also serve as an opportunity to reduce gaps in care across ethnicities for this universally life-altering condition.
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Journal of neurotrauma · Mar 2013
Delayed post-injury administration of riluzole is neuroprotective in a preclinical rodent model of cervical spinal cord injury.
Riluzole, a sodium/glutamate antagonist has shown promise as a neuroprotective agent. It is licensed for amyotrophic lateral sclerosis and is in clinical trial development for spinal cord injury (SCI). This study investigated the therapeutic time-window and pharmacokinetics of riluzole in a rodent model of cervical SCI. ⋯ Riluzole penetrates the spinal cord in 15 min, and SCI slowed elimination of riluzole from the spinal cord, resulting in a longer half-life and higher drug concentration in spinal cord and plasma. Initiation of riluzole treatment 1 and 3 hours post-SCI led to functional, histological, and molecular benefits. While extrapolation of post-injury time windows from rat to man is challenging, evidence from SCI-related biomarker studies would suggest that the post-injury time window is likely to be at least 12 hours in man.
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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
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.