Articles: traumatic-brain-injuries.
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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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This is the first socioeconomic study on traumatic brain injury (TBI) undertaken to determine the sociodemographic factors implicated in the occurrence of TBI and to assess the value of the direct cost of the management of TBI at the initial phase in the Hubert Koutoukou Maga National Teaching Hospital of Cotonou. ⋯ The organization of Benin's health system did not allow for the optimum management of TBI. It seems imperative to develop an insurance system that will allow a proper and effective support for victims of traffic accidents.
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Retrospective studies of TBI have found a neuroendocrine dysfunction following traumatic brain injury in 23 to 60% of adults and 15 to 21% of children. Our aims were to determine the prevalence of hypothalamo-hypophyseal dysfunction in children following brain injury, assess its relationship to the type of injury and the course of the acute post-traumatic phase. ⋯ Within a year after injury, a hormonal disorder was found in 17.6% of the patients. Neuroendocrine dysfunction as a late consequence of craniocerebral trauma in children and adolescents was less frequent than in adults. Risk factors for its development are the gravity of the injury, brain scan pathology, and possibly the development of DI, SIADH, or CSWS in the acute post-traumatic phase.
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To validate the proxy version of the Quality of Life after Brain Injury (QOLIBRI) questionnaire to utilize caregivers for comparison and to evaluate the correspondence between patients' self-perceived and caregivers' perception of patients' Health-Related Quality of Life (HRQoL). Ninety-two patients with severe TBI and their main caregivers were enrolled. Patients' and caregivers' HRQoL was assessed by the Patient-QOLIBRI (Pt-QOLIBRI) and the Proxy-QOLIBRI (Pro-QOLIBRI), respectively. ⋯ There was also positive correlation between the level of satisfaction measured by Pro-QOLIBRI but not by Pt-QOLIBRI, and the disability severity and social integration of the patients. The comparison between the Pt-QOLIBRI and Pro-QOLIBRI confirmed the usefulness of the Pro-QOLIBRI, especially the caregiver-centered version, to predict the social reintegration of survivors. To our knowledge this is the first study that correlates the HRQoL of survivors, as self-perceived and as perceived by the caregivers with social reintegration.
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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.