Articles: brain-injuries.
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The aim of this study was to analyze the effect of early surgical management protocol and other important clinical features on the prognosis of patients suffering from war missile skull base injuries. ⋯ Although the wounds were associated with a high mortality rate, this study showed that there are major differences in prognosis of patients with war missile skull base injuries with respect to certain presenting clinical features.
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Experimental neurology · Sep 1998
Interleukin-10 improves outcome and alters proinflammatory cytokine expression after experimental traumatic brain injury.
Traumatic injury to the central nervous system initiates inflammatory processes that are implicated in secondary tissue damage. These processes include the synthesis of proinflammatory cytokines, leukocyte extravasation, vasogenic edema, and blood-brain barrier breakdown. Interleukin-10 (IL-10), a cytokine with antiinflammatory properties, negatively modulates proinflammatory cascades at multiple levels. ⋯ Subcutaneous IL-10 administration (100 micrograms) at 10 min, 1, 3, 6, 9, and 12 h after TBI also enhanced neurological recovery. In contrast, intracerebroventricular administration of IL-10 (1 or 6 micrograms) at 15 min, 2, 4, 6, and 8 h after TBI was not beneficial. These results indicate that IL-10 treatment improves outcome after TBI and suggest that this improvement may relate, in part, to reductions in proinflammatory cytokine synthesis.
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Post-traumatic vasospasm after severe head injury is now a well known entity. However, all studies available in the literature have evaluated only the anterior cerebral circulation. We evaluated the incidence of basilar artery vasospasm in patients with severe head injury. ⋯ Basilar artery blood flow velocity is higher in patients with severe head injury. Patients with diffuse brain injury have a particularly high velocity. Thus, it may be an easy method to assess the severity of head injury. The temporal profile of basilar artery vasospasm needs to be established in severely head-injured patients to assess its clinical utility.
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Activity of calpains and caspase-3 inferred from proteolysis of the cytoskeletal protein alpha-spectrin into signature spectrin breakdown products (SBDPs) was used to provide the first systematic and simultaneous comparison of changes in activity of these two families of cysteine proteases after traumatic brain injury (TBI) in rats. Distinct regional and temporal patterns of calpain/caspase-3 processing of alpha-spectrin were observed in brain regions ipsilateral to the site of injury after TBI, including large increases of 145 kDa calpain-mediated SBDP in cortex (up to 30-fold), and enduring increases (up to 2 weeks) of 145 kDa SBDP in hippocampus and thalamus. By contrast, 120 kDa caspase-3-mediated SBDP was absent in cortex and showed up to a 2-fold increase in hippocampus and striatum at early (hours) after TBI. Future studies will clarify the pathological significance of large regional differences in activation of calpain and caspase-3 proteases after TBI.