Articles: brain-injuries.
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Aggressive treatment of patients with severe head injury increases the chance for survival and good functional outcome in most cases. To prevent irreversible cerebral lesions, the key point of treatment is the management of intracranial hypertension caused by intracranial hematomas, brain edema and impaired circulation of cerebrospinal fluid (CSF). Therapeutic standards are surgery of traumatic hematoma, osmotherapy and mild hyperventilation for brain edema, and CSF drainage. In highly elevated intracranial pressure (ICP) administration of barbiturates and forced hyperventilation can be considered.
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Diffuse cerebral swelling after severe traumatic brain injury (TBI) develops more commonly in children than adults; however, models of diffuse brain injury in immature animals are lacking. The authors developed a new model of diffuse severe TBI in immature rats by modifying a recently described closed head injury model for adult rats. A total of 105 Sprague-Dawley immature rats (17 days old; average weight 38.5 +/- 5.46 g) were subjected to head impact using variable weights (0 g (sham), 75 g, 100 g, or 125 g) delivered from a height of 2 m onto a metal disk cemented to the intact cranium. ⋯ Weight loss, acute physiological instability, and acute neurological deficits were also indicative of an SI. Mortality was eliminated when ventilatory support was used during the peritrauma period. This model should be useful in studying the response of the immature rat to diffuse severe TBI.
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To estimate the potential benefit of increasing bicycle helmet use among children and adolescents in the United States. ⋯ There continues to be a need to advocate for greater use of bicycle helmets, particularly among young children. Helmet design changes should be considered to prevent mouth injuries.
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Although hypothermic circulatory arrest (HCA) has become routine practice in cardiac surgery, it is associated with substantial neurotoxicity. We tested the hypothesis that increased nitric oxide production during HCA participates in neuronal death. We previously described a canine survival model of HCA that produces a consistent neurologic deficit and histopathologic pattern of selective neuronal death. ⋯ We conclude that neurotoxicity after HCA involves a significant, early induction in neuronal nitric oxide synthase expression in neuronal processes leading to widespread augmented nitric oxide production in the brain.
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To identify early prognostic value of brain injury, a comparison was made between computerized tomography (CT) findings, coagulation abnormalities, and clinical features in 51 patients with closed head injury. The patients were divided into three groups according to their plasma level of fibrin-fibrinogen degradation product (FDP): normal group (FDP 10 micrograms/ml or less) in 20 patients; moderately abnormal group (FDP 10-40 micrograms/ml) in 15 patients; and highly abnormal group (FDP 40 micrograms/ ml or more) in 16 patients. Cases with a fatal clinical course were mostly associated with very high FDP level. ⋯ Although severe head injury (GCS 8 or less) was found in 44% of the highly abnormal group and 13% of the moderately abnormal group, normal group only had one case (5%). Very high FDP concentrations were found to be associated with combined hemorrhagic lesions and mass effect on CT scan, but not with a specific localization of brain damage. In summary, the evaluation of coagulation and fibrinolytic function in patients following closed head injury might have both diagnostic and prognostic value.