Journal of neurotrauma
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Journal of neurotrauma · Jan 2017
Multicenter StudyPredicting blunt cerebrovascular injury in pediatric trauma: Validation of the "Utah Score".
Risk factors for blunt cerebrovascular injury (BCVI) may differ between children and adults, suggesting that children at low risk for BCVI after trauma receive unnecessary computed tomography angiography (CTA) and high-dose radiation. We previously developed a score for predicting pediatric BCVI based on retrospective cohort analysis. Our objective is to externally validate this prediction score with a retrospective multi-institutional cohort. ⋯ The Utah Score misclassified 16.6% of patients in the validation cohort. The Utah Score for predicting BCVI in pediatric trauma patients was validated with a low misclassification rate using a large, independent, multicenter cohort. Its implementation in the clinical setting may reduce the use of CTA in low-risk patients.
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Journal of neurotrauma · Jan 2017
Comparative StudyLongitudinal assessment of clinical signs of recovery in patients with unresponsive wakefulness syndrome after traumatic or nontraumatic brain injury.
Although clinical examination is the gold standard for differential diagnosis between unresponsive wakefulness syndrome (UWS) and minimally conscious state (MCS), clinical signs denoting the first occurrence of conscious behavior in patients with UWS have not been clarified. In this prospective single-center cohort study, 31 consecutive patients with UWS after traumatic brain injury (TBI) (17 patients) or non-TBI were assessed with the Coma Recovery Scale Revised (CRS-R) at admission to a rehabilitation department and after 1, 2, 3, 6, and 12 months. Of the 21 patients who recovered consciousness during the study, 90.5% recovered consciousness within the first 3 months. ⋯ The remaining patients showed conscious behaviors on more than two CRS-R subscales. In conclusion, visual fixation and visual pursuit are the commonest early clinical signs denoting MCS. When emerging from UWS, patients with TBI often showed more signs of consciousness and had higher CRS-R scores than patients with non-TBI.
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Journal of neurotrauma · Jan 2017
ReviewGlutamate neurotransmission in rodent models of traumatic brain injury.
Traumatic brain injury (TBI) is a leading cause of death and disability in people younger than 45 and is a significant public health concern. In addition to primary mechanical damage to cells and tissue, TBI involves additional molecular mechanisms of injury, termed secondary injury, that continue to evolve over hours, days, weeks, and beyond. The trajectory of recovery after TBI is highly unpredictable and in many cases results in chronic cognitive and behavioral changes. ⋯ Diffusion of glutamate outside the synapse due to impaired uptake may lead to increased extrasynaptic glutamate signaling, secondary injury through activation of cell death pathways, and loss of fidelity and specificity of synaptic transmission. Coordination of glutamate release and uptake is critical to regulating synaptic strength, long-term potentiation and depression, and cognitive processes. In this review, we will discuss dysregulation of extracellular glutamate and glutamate uptake in the acute stage of TBI and how failure to resolve acute disruptions in glutamate homeostatic mechanisms may play a causal role in chronic cognitive symptoms after TBI.
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Journal of neurotrauma · Jan 2017
The Effect of Underwater Blast on Aggregating Brain Cell Cultures.
Although the deleterious effects of primary blast on gas-filled organs are well accepted, the effect of blast-induced shock waves on the brain is less clear because of factors that complicate the interpretation of clinical and experimental data. Brain cell aggregate cultures are comprised of multiple differentiated brain cell types and were used to examine the effects of underwater blast. Suspensions of these cultures encased in dialysis tubing were exposed to explosive-generated underwater blasts of low (∼300 kPa), medium (∼2,700 kPa), or high (∼14,000 kPa) intensities and harvested at 1-28 days post-exposure. ⋯ The free-floating nature of the aggregates during blast wave exposure, coupled with their highly hydrolyzed dialysis tubing containment, results in minimized boundary effects, thus enabling accurate assessment of brain cell response to a simplified shock-induced stress wave. This work shows that, at its simplest, blast-induced shock waves produce subtle changes in brain tissue. This study has mechanistic implications for the study of primary blast-induced traumatic brain injury and supports the thesis that underwater blast may cause subtle changes in the brains of submerged individuals.
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Journal of neurotrauma · Jan 2017
Striatal Mitochondrial Disruption Following Severe Traumatic Brain Injury.
Traumatic brain injury (TBI) results in oxidative stress and calcium dysregulation in mitochondria. However, little work has examined perturbations of mitochondrial homeostasis in peri-injury tissue. We examined mitochondrial homeostasis after a unilateral controlled cortical impact over the sensorimotor cortex in adult male rats. ⋯ We detected an acute increase in superoxide dismutase 2 mRNA expression, as well as an induction of microRNA (miR)-21 and miR-155, which have been previously demonstrated to disrupt mitochondrial homeostasis. Behaviorally, rats with TBI exhibited marked error rates in contrainjury forelimb performance on the ladder test. These findings reveal that there may be differential susceptibilities of various peri-injury brain structures to mitochondrial dysfunction and associated behavioral deficits, and that molecular pathways demonstrated to interfere with mitochondrial homeostasis and function are activated subacutely post-TBI.