Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Jul 2014
Using the Olfactory System as an in vivo Model to Study Traumatic Brain Injury and Repair.
Loss of olfactory function is an early indicator of traumatic brain injury (TBI). The regenerative capacity and well-defined neural maps of the mammalian olfactory system enable investigations into the degeneration and recovery of neural circuits after injury. Here, we introduce a unique olfactory-based model of TBI that reproduces many hallmarks associated with human brain trauma. ⋯ Behavioral experiments measured 4 days after impact also demonstrated loss of olfactory function, yet following a 30-day recovery period, we observed a significant improvement in olfactory function and partial recovery of olfactory circuitry, despite the persistence of TBI markers. Interestingly, by using the M71-IRES-tauLacZ reporter line to track OSN organization, we further determined that inducing neural activity during the recovery period with intense odor conditioning did not enhance the recovery process. Together, these data establish the mouse olfactory system as a new model to study TBI, serving as a platform to understand neural disruption and the potential for circuit restoration.
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Journal of neurotrauma · Jul 2014
Transport mode to level I and II trauma centers and survival of pediatric patients with traumatic brain injury.
The use of helicopter emergency medical services (EMS) for pediatric trauma patients is an issue of debate. We investigated the association of helicopter transport with survival of pediatric patients with traumatic brain injury (TBI). We conducted a retrospective cohort study of pediatric patients with TBI who were transported to level I and II trauma centers and were registered in the National Trauma Data Bank (NTDB) between 2009 and 2011. ⋯ Multivariable logistic regression analysis demonstrated an association of helicopter transport with increased survival (OR, 2.35; 95% CI, 1.30-4.25; ARR 5.36%). This again persisted after propensity score matching (OR 2.56; 95% CI 1.28-5.11; ARR 6.14). Pediatric patients with TBI transported to level I and II trauma centers had improved survival in comparison with similar patients transported via ground EMS.
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Journal of neurotrauma · Jul 2014
Sleep problems and their relationship to cognitive and behavioral outcomes in young children with traumatic brain injury.
This study examined the effect of traumatic brain injury (TBI) in young children on sleep problems and the relationship of sleep problems to neuropsychological and psychosocial functioning. Participants were drawn from an ongoing longitudinal study of injury in young children recruited from 3 to 6 years of age. They constituted three groups: orthopedic injury (OI; n=92), complicated mild/moderate TBI (mTBI; n=55); and severe TBI (sTBI; n=20). ⋯ In contrast, sleep problems were generally not related to neuropsychological test performance. The results suggest that young children with TBI demonstrate more sleep problems than children with injuries not involving the head. Sleep problems, in turn, significantly increase the risk of poor psychosocial outcomes across time, but are not associated with worse neuropsychological test performance.
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Traumatic brain injury (TBI) causes deleterious critical-illness-related-corticosteroid-insufficiency (CIRCI), leading to high mortality and morbidity. However, the incidence of CIRCI following different TBI severities is not fully defined. This study was designed to investigate mechanistically the effects of injury severity on corticosteroid response and the development of CIRCI in a rat model of experimentally controlled TBI. ⋯ Second, TBI-induced CIRCI is closely correlated with injury severity. As the injury severity rises both the incidence of CIRCI and mortality surge; Third, increased level of injury severity reduces the expression of endothelial tight junction protein, aggravate BBB permeability and exacerbate the ensuing neural apoptosis in the PVN of hypothalamus. These findings indicate that increased severity of TBI aggravate the incidence of CIRCI by causing damage to tight junctions of vascular endothelial cells and increasing neuronal apoptosis in the PVN of hypothalamus.
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Following traumatic brain injury (TBI) SUR1-regulated NCCa-ATP (SUR1/TRPM4) channels are transcriptionally up-regulated in ischemic astrocytes, neurons, and capillaries. ATP depletion results in depolarization and opening of the channel leading to cytotoxic edema. Glibenclamide is an inhibitor of SUR-1 and, thus, might prevent cytotoxic edema and secondary brain damage following TBI. ⋯ An effect on acute parameters, however, could not be detected, most likely because of the up-regulation of the channel within 3-6h after injury. Furthermore, there was no significant effect on motor function assessed by the beam-walking test throughout 7days. In accordance to these results and the available literature, glibenclamide seems to have promising potency in the treatment of TBI.