Articles: brain-injuries.
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Posttraumatic headache is a general term for pain localized in the head or neck, occurring after head trauma and of varied aetiology and pathogenesis. In many cases one only finds a time-dependent relation to trauma, but no causal one. There is no uniform, typical "posttraumatic headache". ⋯ A reciprocal influence exists between these functionally disturbed structures and a relation to psychogenic factors, which are essential co-factors. Usually it is difficult to decide whether posttraumatic headaches are exclusively caused by organic or psychogenic factors. Probably both factors are involved to an individually different degree.
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Sixteen patients each received infusions of 1 g of mannitol per kg over 5 to 10 minutes, and serial determinations of intracranial pressure (ICP), systemic arterial blood pressure (SABP), central venous pressure, cerebral perfusion pressure (CPP), hematocrit, hemoglobin, serum Na+, K+, osmolarity, and fluid balance were carried out for 4 hours. Urine output was replaced volume for volume with 5% dextrose in 0.45% NaCl solution. We tested the hypothesis that patients with high (greater than or equal to 70 torr) CPP would respond less well to mannitol by either ICP or CPP criteria than patients with low (less than 70 torr) CPP. ⋯ These data suggest that mannitol infusion is at least partly dependent upon hemodynamic mechanisms that allow vasoconstriction to occur with reduction in cerebral blood volume and that little may be gained by using mannitol when CPP greater than or equal to 70 either by SABP, ICP, or CPP criteria because vasoconstriction is already nearly maximal. This mechanism is not exclusive of other potential mechanisms of action. Mannitol "rebound" may be a function of net dehydration, hemoconcentration, and SABP decline.
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We analyzed the charts and CT scans of 49 cases of civilian .22 caliber gunshot wounds of the brain admitted to the University of Alberta and Royal Alexandra Hospitals between 1975 and 1985. The average age of the patients was 30 years, 88% were males, 88% were suicide attempts. There were no deaths among patients with an initial coma score above 12 whereas the mortality rate was 85% for those admitted with a score of 7 or less. ⋯ We recommend that no treatment be given those cases with an admission coma score of 3 and/or fixed pupils and that simple scalp wound debridement be employed with those having a coma score of 7 or less. Tract exploration and retrieval of bullet fragments is not indicated, as retained fragments carry a very low incidence of complications (e.g. abscess formation). In patients in good condition (GCS greater than or equal to 12) the management of intracranial hematomas should be independent of their etiology and approached aggressively.
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In 60%-90% of cases head injury is a part of multisystem trauma and of very decisive importance for the post-traumatic prognosis. Hypoxia, hypercarbia, and hypotension increase the primary lesion and cause secondary brain damage. Therefore, emergency measures must be directed to the essentials of sustaining vital functions, i.e. intubation/ventilation/oxygenation and stabilization of the circulatory system. ⋯ Anesthesia in patients with severe head injury must involve only those techniques that do not further increase an already elevated intracranial pressure. As inhalational anesthetics, including nitrous oxide, elevate the intracranial pressure to varying extents due to cerebral vasodilation with a concomitant rise in intracranial blood volume, these substances have to be avoided whenever raised intracranial pressure cannot be excluded. Narcotics, benzodiazepines, small dosages of barbiturates, and long-lasting muscle relaxants can be regarded as useful.