Journal of neurotrauma
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Journal of neurotrauma · Jun 2014
Methylene Blue is Neuroprotective against mild Traumatic Brain Injury.
Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Methylene blue (MB) has known energy-enhancing and antioxidant properties. This study tested the hypothesis that MB treatment reduces lesion volume and behavioral deficits in a rat model of mild TBI. ⋯ Smaller numbers of dark-stained Nissl cells and Fluoro-Jade(®) positive cells were observed in the MB-treated group than in vehicle-treated animals 14 days post-TBI. In conclusion, MB treatment minimized lesion volume, behavioral deficits, and neuronal degeneration following mild TBI. MB is already approved by the United States Food and Drug Administration (FDA) to treat a number of indications, likely expediting future clinical trials in TBI.
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Journal of neurotrauma · May 2014
Agreement on and predictors of long term psychosocial development 16 years post childhood traumatic brain injury.
Childhood traumatic brain injury (CTBI) is one of the most common causes of childhood mortality and morbidity, with psychosocial impairment being among the most debilitating persisting consequences. Child and adolescent survivors of CTBI have fewer friends and lower self-esteem with a higher risk of developing a psychiatric disorder. In most research to date, findings in the psychosocial domain have been based on parent reports, with the child or adolescent only consulted infrequently. ⋯ On the scales with poor agreement, there was no consistent contribution identified for any injury or preinjury factors. Preinjury adaptive behavior partly predicted withdrawn and overall internalizing symptoms, with a trend to also partly predict anxious/depressed and rule-breaking behavior reported by the significant other. Because young adults and significant others had poor agreement on the less-overt symptoms, these young adults may be at a higher risk of developing more-severe symptoms or disorders if it is not identified in time.
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Journal of neurotrauma · May 2014
Prehospital Heart Rate and Blood Pressure Increase the Positive Predictive Value of the Glasgow Coma Scale for High-Mortality Traumatic Brain Injury.
We hypothesized that vital signs could be used to improve the association between a trauma patient's prehospital Glasgow Coma Scale (GCS) score and his or her clinical condition. Previously, abnormally low and high blood pressures have both been associated with higher mortality for patients with traumatic brain injury (TBI). We undertook a retrospective analysis of 1384 adult prehospital trauma patients. ⋯ When the GCS was <15, ROC AUCs were significantly higher for a multi-variate regression model (GCS, SBP, and HR) versus GCS alone. In particular, patients with abnormalities in all parameters (GCS, SBP, and HR) were significantly more likely to have high-mortality TBI versus those with abnormalities in GCS alone. This could be useful for mobilizing resources (e.g., neurosurgeons and operating rooms at the receiving hospital) and might enable new prehospital management protocols where therapies are selected based on TBI mortality risk.
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Journal of neurotrauma · May 2014
Diffusion tensor imaging reveals white matter injury in a rat model of repetitive blast-induced traumatic brain injury.
Blast-induced traumatic brain injury (bTBI) is one of the most common combat-related injuries seen in U. S. military personnel, yet relatively little is known about the underlying mechanisms of injury. In particular, the effects of the primary blast pressure wave are poorly understood. ⋯ Computational statistical methods such as voxelwise analysis have shown promise in localizing and quantifying bTBI throughout the brain. In this study, we use voxelwise analysis of DTI to quantify white matter injury in a rat model of repetitive primary blast exposure. Our results show a significant increase in microstructural damage with a second blast exposure, suggesting that primary bTBI may sensitize the brain to subsequent injury.
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Journal of neurotrauma · May 2014
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is neuroprotective in experimental traumatic brain injury.
Traumatic brain injury (TBI) is an international health concern with a complex pathogenesis resulting in major long-term neurological, neurocognitive, and neuropsychiatric outcomes. Although neuroinflammation has been identified as an important pathophysiological process resulting from TBI, the function of specific inflammatory mediators in the aftermath of TBI remains poorly understood. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is an inflammatory cytokine that has been reported to have neuroprotective effects in various animal models of neurodegenerative disease that share pathological similarities with TBI. ⋯ All mice given a LFP injury displayed significant brain atrophy and behavioral impairments compared with those given sham-injuries; however, this was significantly worse in the GM-CSF(-/-) mice compared with the WT mice. GM-CSF(-/-) mice given LFP injury also had reduced astrogliosis compared with their WT counterparts. These novel findings indicate that the inflammatory mediator, GM-CSF, may have significant protective properties in the chronic sequelae of experimental TBI and suggest that further research investigating GM-CSF and its potential benefits in the injured brain is warranted.