Articles: traumatic-brain-injuries.
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Arch Clin Neuropsychol · Mar 2017
Consistency of Self-Reported Neurocognitive Symptoms, Post-Traumatic Stress Disorder Symptoms, and Concussive Events From End of First Deployment to Veteran Health Administration Comprehensive Traumatic Brain Injury Evaluation by Operations Enduring Freedom/Iraqi Freedom/New Dawn Veterans.
This study examined the consistency of self-reported symptoms and concussive events in combat veterans who reported experiencing concussive events. ⋯ These findings raise questions regarding the accuracy of veteran self-report of both near and distant traumatic events, and argue for the inclusion of contemporaneous Department of Defense (DOD) records in veteran assessment and treatment planning.
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Impaired hemostasis represents a major risk factor for increased morbidity and mortality in patients with traumatic intracranial hemorrhage. In cases of polytrauma with major bleeding, hyperfibrinolysis may develop and this may result in excessive coagulopathy. ⋯ The basic principles of the pathophysiology and effects of coagulation impairment in this patient population are reviewed. Furthermore, the use of specific coagulation tests and the administration of hemostatic substances are discussed.
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Experimental neurology · Mar 2017
Neuropathology and neurobehavioral alterations in a rat model of traumatic brain injury to occupants of vehicles targeted by underbody blasts.
Many victims of blast-induced traumatic brain injury are occupants of military vehicles targeted by land mines. Recently improved vehicle designs protect these individuals against blast overpressure, leaving acceleration as the main force potentially responsible for brain injury. We recently developed a unique rat model of under-vehicle blast-induced hyperacceleration where exposure to acceleration as low as 50G force results in histopathological evidence of diffuse axonal injury and astrocyte activation, with no evidence of neuronal cell death. ⋯ All rats exposed to 2400G acceleration survived and exhibited transient deficits in working memory and long-term anxiety like behaviors, while those exposed to 1200 acceleration G force only demonstrated increased anxiety. Behavioral deficits were associated with acute microglia/macrophage activation, increased hippocampal neuronal death, and reduced levels of tight junction- and synapse- associated proteins. Taken together, these results suggest that exposure of rats to high underbody blast-induced G forces results in neurologic injury accompanied by neuronal apoptosis, neuroinflammation and evidence for neurosynaptic alterations.
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Traumatic brain injury (TBI) is extremely common across the lifespan and is an established risk factor for dementia. The cognitive profile of the large and growing population of older adults with prior TBI who do not have a diagnosis of dementia, however, has not been well described. Our aim was to describe the cognitive profile associated with prior TBI exposure among community-dwelling older adults without dementia-an understudied but potentially vulnerable population. ⋯ In this population-based study of community-dwelling older adults without dementia, those with prior TBI with LOC were more likely to report subjective memory impairment compared to those without TBI even after adjustment for demographics, medical comorbidities, and active depression. Lack of greater objective cognitive impairment among those with versus without TBI may be due to poor sensitivity of the cognitive battery or survival bias, or may suggest that post-TBI cognitive impairment primarily affects executive function and processing speed, which were not rigorously assessed in this study. Our findings show that among community-dwelling non-demented older adults, history of TBI is common but may not preferentially impact cognitive domains of episodic memory, attention, working memory, verbal semantic fluency, or calculation.