Articles: brain-injuries.
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In the last two decades our understanding of the pathophysiology of severe head injury has significantly increased. It has become evident that secondary neuronal damage may occur and should be prevented. It is ischemia, similar to that seen with stroke and aneurysmal subarachnoid hemorrhage, that causes secondary brain damage. ⋯ Moreover, there are some new pharmacological concepts for changing the threshold for ischemia in brain tissue. At the present time, however, valid data concerning clinical use are still not available. Therefore, mild hyperventilation and sedation during the initial post-traumatic phase and lowering of intracranial pressure by osmotherapeutics remain the most important treatment modalities, as they were 20 years ago.
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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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Journal of neurotrauma · Nov 1996
Review Practice Guideline GuidelineThe use of mannitol in severe head injury. Brain Trauma Foundation.
Mannitol is effective in reducing ICP, and we recommend its use in the management of traumatic intracranial hypertension. Serum osmolalities greater than 320 mOSsm/L and hypovolemia should be avoided. Some data suggest that bolus administration is preferable to continuous infusion.
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J Int Neuropsychol Soc · Nov 1996
Randomized Controlled Trial Clinical TrialThe impact of posttraumatic seizures on 1-year neuropsychological and psychosocial outcome of head injury.
This study examined the relationship of posttraumatic seizures and head injury severity to neuropsychological performance and psychosocial functioning in 210 adults who were prospectively followed and assessed 1 year after moderate to severe traumatic head injury. Eighteen percent (n = 38) of the patients experienced 1 or more late seizures (i.e., seizures occurring 8 or more days posttrauma) by the time of the 1-year followup. ⋯ However, after the effects of head injury severity were controlled, there were no significant differences in neuropsychological and psychosocial outcome at 1 year as a function of having seizures. These findings suggest that worse outcomes in patients who develop posttraumatic seizures up to 1 year posttrauma largely reflect the effects of the brain injuries that cause seizures, rather than the effect of seizures.