Journal of neurotrauma
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Explosive blast traumatic brain injury (TBI) is one of the more serious wounds suffered by United States service members injured in the current conflicts in Iraq and Afghanistan. Some military medical treatments for blast TBI that have been introduced successfully in the war theater include decompressive craniectomy, cerebral angiography, transcranial Doppler, hypertonic resuscitation fluids, among others. Stateside neurosurgery, neuro-critical care, and rehabilitation for these patients have similarly progressed. ⋯ Rigorous study at the basic science and clinical levels, including detailed biomechanical analysis, is needed to improve understanding of this disease. A comprehensive epidemiological study is also warranted to determine the prevalence of this disease and the factors that contribute most to the risk of developing it. Sadly, this military-specific disease has significant potential to become a civilian one as well.
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Journal of neurotrauma · Jun 2009
ReviewBlast-induced brain injury and posttraumatic hypotension and hypoxemia.
Explosive munitions account for more than 50% of all wounds sustained in military combat, and the proportion of civilian casualties due to explosives is increasing as well. But there has been only limited research on the pathophysiology of blast-induced brain injury, and the contributions of alterations in cerebral blood flow (CBF) or cerebral vascular reactivity to blast-induced brain injury have not been investigated. Although secondary hypotension and hypoxemia are associated with increased mortality and morbidity after closed head injury, the effects of secondary insults on outcome after blast injury are unknown. ⋯ Superoxide radicals combine with nitric oxide (NO), another ROS produced by blast injury as well as other types of TBI, to form peroxynitrite, a powerful oxidant that impairs cerebral vascular responses to reduced intravascular pressure and other cerebral vascular responses. While current research suggests that blast injury impairs cerebral vascular compensatory responses, thereby leaving the brain vulnerable to secondary insults, the effects of blast injury on the cerebral vascular reactivity have not been investigated. It is clear that further research is necessary to address these critical concerns.
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Journal of neurotrauma · Jun 2009
Combination therapies for traumatic brain injury: prospective considerations.
Traumatic brain injury (TBI) initiates a cascade of numerous pathophysiological events that evolve over time. Despite the complexity of TBI, research aimed at therapy development has almost exclusively focused on single therapies, all of which have failed in multicenter clinical trials. Therefore, in February 2008 the National Institute of Neurological Disorders and Stroke, with support from the National Institute of Child Health and Development, the National Heart, Lung, and Blood Institute, and the Department of Veterans Affairs, convened a workshop to discuss the opportunities and challenges of testing combination therapies for TBI. ⋯ Food and Drug Administration be included in early discussions of experimental design. Furthermore, it was agreed that an efficient and validated screening platform for candidate therapeutics, sensitive and clinically relevant biomarkers and outcome measures, and standardization and data sharing across centers would greatly facilitate the development of successful combination therapies for TBI. Overall there was great enthusiasm for working collaboratively to act on these recommendations.
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Journal of neurotrauma · Jun 2009
Hemorrhagic shock after experimental traumatic brain injury in mice: effect on neuronal death.
Traumatic brain injury (TBI) from blast injury is often complicated by hemorrhagic shock (HS) in victims of terrorist attacks. Most studies of HS after experimental TBI have focused on intracranial pressure; few have explored the effect of HS on neuronal death after TBI, and none have been done in mice. We hypothesized that neuronal death in CA1 hippocampus would be exacerbated by HS after experimental TBI. ⋯ CA3 neuron counts did not differ between groups. Fluorojade C staining confirmed neurodegeneration in CA1 in the 90-min CCI+HS group. Our data suggest a critical time window for exacerbation of neuronal death by HS after CCI and may have implications for blast injury victims in austere environments where definitive management is delayed.