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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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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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 review our experience with craniocerebral injuries caused by plastic bullets, and to delineate prognostic factors for outcome. ⋯ Plastic bullet-induced craniocerebral injuries carry a lower morbidity and mortality rate compared with other gunshot wounds. However, plastic bullets do incur a significant risk of injury. Their use should be carefully regulated.
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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.