effects-blast-induced-neurotrauma-on-pressurized-rodent-middle

Effects of Blast-induced Neurotrauma on Pressurized Rodent Middle Cerebral Arteries

Though there have been studies on the histopathological and behavioral effects of blast exposure, fewer have been dedicated to blast&#39;s cerebral ...

University of Texas Medical Branch

university of texas medical branch

In terms of human suffering, medical expenses, and lost productivity, head injury is one of the major health care problems in the United States, and inadequate cerebral blood flow is an important contributor to mortality and morbidity after traumatic brain injury. Despite the importance of cerebral vascular dysfunction in the pathophysiology of traumatic brain injury, the effects of trauma on the cerebral circulation have been less well studied than the effects of trauma on the brain. Recent research has led to a better understanding of the physiologic, cellular, and molecular components and causes of traumatic cerebral vascular injury. A more thorough understanding of the direct and indirect effects of trauma on the cerebral vasculature will lead to improvements in current treatments of brain trauma as well as to the development of novel and, hopefully, more effective therapeutic strategies.

Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature.

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. Hemorrhage accounted for approximately 50% of combat deaths, and the lungs are one of the primary organs damaged by blast overpressure. Thus, it is likely that blast-induced lung injury and/or hemorrhage leads to hypotensive and hypoxemic secondary injury in a significant number of combatants exposed to blast overpressure injury. Although the effects of blast injury on CBF and cerebral vascular reactivity are unknown, blast injury may be associated with impaired cerebral vascular function. Reactive oxygen species (ROS) such as the superoxide anion radical and other ROS, likely major contributors to traumatic cerebral vascular injury, are produced by traumatic brain injury (TBI). 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.

Blast-induced brain injury and posttraumatic hypotension and hypoxemia.

Traumatic brain injury (TBI) is one of the most frequent causes of combat casualties in Operations Iraqi Freedom (OIF), Enduring Freedom (OEF), and New Dawn (OND). Although less common than combat-related blast exposure, there have been significant numbers of blast injuries in civilian populations in the United States. Current United States Department of Defense (DoD) ICD-9 derived diagnoses of TBI in the DoD Health Care System show that, for 2016, severe and moderate TBIs accounted for just 0.7% and 12.9%, respectively, of the total of 13,634 brain injuries, while mild TBIs (mTBIs) accounted for 86% of the total. Although there is a report that there are differences in the frequency of long-term complications in mTBI between blast and non-blast TBIs, clinical presentation is classified by severity score rather than mechanism because severity scoring is associated with prognosis in clinical practice. Blast TBI (bTBI) is unique in its pathology and mechanism, but there is no treatment specific for bTBIs-these patients are treated similarly to TBIs in general and therapy is tailored on an individual basis. Currently there is no neuroprotective drug recommended by the clinical guidelines based on evidence.

Article	Year
Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature. Journal of neurotrauma\| PubMed ID: 14577860	2003
Blast-induced brain injury and posttraumatic hypotension and hypoxemia. Journal of neurotrauma\| PubMed ID: 18447627	2009
Impact & Blast Traumatic Brain Injury: Implications for Therapy. Molecules (Basel, Switzerland)\| PubMed ID: 29373501	2018

Douglas S. DeWitt

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