Journal of neurotrauma
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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.
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Journal of neurotrauma · Jun 2015
Endogenous nutritive support following traumatic brain injury: peripheral lactate production for glucose supply via gluconeogenesis.
We evaluated the hypothesis that nutritive needs of injured brains are supported by large and coordinated increases in lactate shuttling throughout the body. To that end, we used dual isotope tracer ([6,6-(2)H2]glucose, i.e., D2-glucose, and [3-(13)C]lactate) techniques involving central venous tracer infusion along with cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Patients with traumatic brain injury (TBI) who had nonpenetrating head injuries (n=12, all male) were entered into the study after consent of patients' legal representatives. ⋯ This previously unrecognized mobilization of lactate subserves hepatic and renal gluconeogenesis. As such, a lactate shuttle mechanism indirectly makes substrate available for the body and its essential organs, including the brain, after trauma. In addition, when elevations in arterial lactate concentration occur after TBI, lactate shuttling may provide substrate directly to vital organs of the body, including the injured brain.
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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.
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Journal of neurotrauma · Jun 2015
Subjective and Objective Assessment of Sleep in Adolescents with Mild Traumatic Brain Injury.
There is increased recognition that sleep problems may develop in children and adolescents after mild traumatic brain injury (mTBI). However, few studies have utilized both subjective and objective measures to comprehensively assess sleep problems in the pediatric population following the acute post-TBI period. The aims of this study were to compare sleep in adolescents with mTBI to healthy adolescents using subjective and objective measures, and to identify the clinical correlates associated with sleep problems. ⋯ Our findings suggest that adolescents may experience subjective and objective sleep disturbances up to one year following mTBI. These findings require further replication in larger samples. Additionally, research is needed to identify possible mechanisms for poor sleep in youth with mTBI.
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Journal of neurotrauma · Jun 2015
Retraction Of PublicationRetractions of DOI: 10.1089/neu.2008.0707 and 10.1089/neu.2011.1842.