Articles: brain-injuries.
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Traumatic brain injury is a leading cause of death from injury in the United States. This article reviews nursing interventions to prevent and minimize secondary brain injuries and improve patient outcomes.
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Traumatic brain injury (TBI) is an epigenetic risk factor for Alzheimer's disease (AD). To test the hypothesis that TBI contributes to the onset and/or progression of AD-like beta-amyloid peptide (Abeta) deposits, we studied the long-term effects of TBI in transgenic mice that overexpress human Abeta from a mutant Abeta precursor protein (APP) minigene driven by a platelet derived (PD) growth factor promoter (PDAPP mice). TBI was induced in 4-month-old PDAPP and wild type (WT) mice by controlled cortical impact (CCI). ⋯ Hippocampal atrophy and reduced Abeta deposits were not seen in hippocampus or cingulate cortex of sham-injured PDAPP mice or in any WT mice. These data suggest that the vulnerability of brain cells to Abeta toxicity increases and that the accumulation of Abeta deposits decrease in the penumbra of CCI months after TBI. Thus, in addition to providing unique opportunities for elucidating genetic mechanisms of AD, transgenic mice that recapitulate AD pathology also may be relevant animal models for investigating the poorly understood role that TBI and other epigenetic risk factors play in the onset and/or progression of AD.
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Previous studies of traumatic brain injury (TBI) and hemorrhagic shock (HS) models, have shown cardiorespiratory depression in ethanol-treated animals. This study investigated the effects of ethanol (ET) on brain lactate concentrations and acidosis in a TBI/HS model. ⋯ In this TBI/HS model, ethanol-induced increases in lactate concentrations in brain tissue and cerebral venous blood are associated with respiratory depression and reduced organ blood flow.
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Neurologic and neuropsychologic sequelae of crush head injury, which is produced by static forces occurring when the head is stationary and pinned against a rigid structure, were studied prospectively in a series of eight children ranging in age from 13 to 32 months. Hospital course, computed tomographic findings, and neurologic and developmental outcomes were examined. All children sustained pronounced cerebral trauma characterized by multiple fractures throughout the calvaria, extra-axial hemorrhages, and parenchymal contusions. ⋯ One year after the injury, five of the six children reevaluated had a good recovery. Motor scores were significantly lower than cognitive scores at baseline and showed the greatest degree of improvement over time. Neuropsychologic outcome after brain injury produced by static loading of the head is more favorable than from traumatic brain injury associated with dynamic loading.