Articles: traumatic-brain-injuries.
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Nociceptive and neuropathic pain occurs as part of the disease process after traumatic brain injury (TBI) in humans. Central and peripheral inflammation, a major secondary injury process initiated by the traumatic brain injury event, has been implicated in the potentiation of peripheral nociceptive pain. We hypothesized that the inflammatory response to diffuse traumatic brain injury potentiates persistent pain through prolonged immune dysregulation. ⋯ We conclude that traumatic brain injury increased the inflammatory pain associated with cutaneous inflammation by contributing to systemic immune dysregulation. Regulatory T cells are immune suppressors and failure of T cells to differentiate into regulatory T cells leads to unregulated cytokine production which may contribute to the potentiation of peripheral pain through the excitation of peripheral sensory neurons. In addition, regulatory T cells are identified as a potential target for therapeutic rebalancing of peripheral immune homeostasis to improve functional outcome and decrease the incidence of peripheral inflammatory pain following traumatic brain injury.
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Since 2002, France has been strengthening legislation on road traffic. This study is intended to evaluate the changes in Traumatic Brain Injury (TBI) incidence and mortality resulting from Road Traffic Collision (RTC) in the two 6-year periods before and after 2002. ⋯ The greater reductions in the incidence, severity and mortality of TBI when compared with the reduction of casualty incidence have mainly affected car users. These results should be attributable to the improvements in standards of care, primary safety of the car fleet and general road architecture safety. However, the increased reduction in the TBI epidemics in France, when compared to those observed in other developed countries for the same periods, suggests that the effects should be strongly attributable to changes in road user behaviour induced by law enforcement. The at-risk groups for TBI after RTC are now two-wheel users (motorized or not) and individuals over 60 years of age.
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Head injuries are common in pediatrics, and headaches are the most common complaint following mild head trauma. Although moderate and severe traumatic brain injuries occur less frequently, headaches can complicate recovery. ⋯ While there are few studies on the treatment of posttraumatic headache, proper evaluation and management of posttraumatic headaches is essential to prevent further injury and to promote recovery. In this article, we will review the current definitions and epidemiology of pediatric posttraumatic headache and discuss current recommendations for the evaluation and management of this syndrome in children and adolescents.
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Brain injury : [BI] · Jan 2016
Protective effect of rhEPO on tight junctions of cerebral microvascular endothelial cells early following traumatic brain injury in rats.
The goal of this study was to investigate the protective effect of recombinant human EPO(rhEPO) on cerebral microvascular endothelial cells and the mechanisms by which rhEPO interacts with TJs proteins, claudin-5, Occludin and ZO-1 during the early period following traumatic brain injury. ⋯ It was found that administration of rhEPO protected cerebral microvascular endothelial cells and reduced permeability of BBB and the mechanisms may be due to increasing the expression of TJs proteins.
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Successful therapy for TBI disabilities awaits refinement in the understanding of TBI neurobiology, quantitative measurement of treatment-induced incremental changes in recovery trajectories, and effective translation to human TBI using quantitative methods and protocols that were effective to monitor recovery in preclinical models. Details of the specific neurobiology that underlies these injuries and effective quantitation of treatment-induced changes are beginning to emerge utilizing a variety of preclinical and clinical models (for reviews see (Morales et al., Neuroscience 136:971-989, 2005; Fujimoto et al., Neurosci Biobehav Rev 28:365-378, 2004; Cernak, NeuroRx 2:410-422, 2005; Smith et al., J Neurotrauma 22:1485-1502, 2005; Bose et al., J Neurotrauma 30:1177-1191, 2013; Xiong et al., Nat Rev Neurosci 14:128-142, 2013; Xiong et al., Expert Opin Emerg Drugs 14:67-84, 2009; Johnson et al., Handb Clin Neurol 127:115-128, 2015; Bose et al., Brain neurotrauma: molecular, neuropsychological, and rehabilitation aspects, CRC Press/Taylor & Francis, Boca Raton, 2015)). Preclinical models of TBI, essential for the efficient study of TBI neurobiology, benefit from the setting of controlled injury and optimal opportunities for biometric quantitation of injury and treatment-induced changes in the trajectories of disability. ⋯ Accordingly, use of this preclinical model offers an opportunity for (a) gaining a greater understanding of the relationships of TBI induced diffuse axonal injuries and associated long term disabilities, and (b) to provide a platform for quantitative assessment of treatment interactions upon the trajectories of TBI-induced disabilities. Using the impact acceleration closed head TBI model to induce mild/moderate injuries in the rat, we have observed and quantitated multiple morbidities commonly observed following TBI in humans (Bose et al., J Neurotrauma 30:1177-1191, 2013). This chapter describes methods and protocols used for TBI-induced multiple morbidity involving cognitive dysfunction, balance instability, spasticity and gait, and anxiety-like disorder.