Journal of neurotrauma
-
Journal of neurotrauma · Jun 2015
Facility characteristics and in-hospital pediatric mortality following severe traumatic brain injury.
More than 500,000 children sustain a traumatic brain injury (TBI) each year. Previous studies have described significant variation in inhospital mortality after pediatric TBI. The aim of this study was to identify facility-level characteristics independently associated with 30-day inhospital mortality after pediatric severe TBI. ⋯ Other facility-level characteristics were not found to be significant. To our knowledge, this is one of the largest investigations to identify regional variation in inhospital mortality after pediatric severe TBI in a national sample after accounting for individual and other facility-level characteristics. Further investigations to help explain this variation are needed to inform evidence-based decision-making for pediatric severe TBI care across different settings.
-
Journal of neurotrauma · Jun 2015
Long-lasting suppression of acoustic startle response following mild traumatic brain injury.
Acoustic startle response (ASR) is a defensive reflex that is largely ignored unless greatly exaggerated. ASR is suppressed after moderate and severe traumatic brain injury (TBI), but the effect of mild TBI (mTBI) on ASR has not been investigated. Because the neural circuitry for ASR resides in the pons in all mammals, ASR may be a good measure of brainstem function after mTBI. ⋯ In contrast to the suppression of ASR, working memory impairment was transient; memory was impaired 1 and 7 days after injury, but recovered by 21 days. The long-lasting suppression of ASR suggests long-term dysfunction of brainstem neural circuits at a time when forebrain neural circuits responsible for spatial working memory have recovered. These results have important implications for return-to-activity decisions because recovery of cognitive impairments plays an important role in these decisions.
-
Journal of neurotrauma · Jun 2015
Wallerian degeneration in the optic nerve stretch-injury model of TBI: a stereological analysis.
Patients with chronic traumatic encephalopathy (CTE) show loss of central white matter, central gray matter, and cortical gray matter with increasing post-traumatic survival. The majority of experimental studies using animals have, however, discussed only the ultrastructural pathophysiology of injured central white matter leading to secondary axotomy and the formation of axonal terminal bulbs. Using the stretch-injured optic nerve model in adult guinea pigs, the present study provides novel quantitative data concerning Wallerian degeneration of disconnected axonal fragments following secondary axotomy out to 12 weeks after injury to an optic nerve. ⋯ This data suggests that some nerve fibers initiate Wallerian degeneration days and weeks after the initial time of mechanical injury to an optic nerve. The number of intact nerve fibers continues to fall over at least three months after injury in the stretch-injury model of traumatic axonal injury. It is suggested that these novel findings relate to the mechanism(s) whereby central white matter volume decreases over months and years in CTE patients.
-
Journal of neurotrauma · Jun 2015
Decompressive craniectomy reduces white matter injury following controlled cortical impact in mice.
Reduction and avoidance of increases in intracranial pressure (ICP) after severe traumatic brain injury (TBI) continue to be the mainstays of treatment. Traumatic axonal injury is a major contributor to morbidity after TBI, but it remains unclear whether elevations in ICP influence axonal injury. Here we tested the hypothesis that reduction in elevations in ICP after experimental TBI would result in decreased axonal injury and white matter atrophy in mice. ⋯ At 4 weeks post-injury, Open animals had an 18% reduction in white matter volume compared with 34% in Closed animals (p<0.01). Thus, our results indicate that CCI with decompressive craniectomy was associated with reductions in ICP and reduced pericontusional axonal injury and white matter atrophy. If similar in humans, therapeutic interventions that ameliorate intracranial hypertension may positively influence white matter injury severity.
-
Journal of neurotrauma · Jun 2015
Retraction Of PublicationRetractions of DOI: 10.1089/neu.2008.0707 and 10.1089/neu.2011.1842.