The beneficial effects of early dexamethasone administration in infants and children with bacterial meningitis.
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BACKGROUND: In experimental models of meningitis and in children with meningitis, dexamethasone has been shown to reduce meningeal inflammation and to improve the outcome of disease. METHODS: We conducted a placebo-controlled, double-blind trial of dexamethasone therapy in 101 infants and children admitted to the National Children's Hospital, San Jose, Costa Rica, who had culture-proved bacterial meningitis or clinical signs of meningitis and findings characteristic of bacterial infection on examination of the cerebrospinal fluid. The patients were randomly assigned to receive either dexamethasone and cefotaxime (n = 52) or cefotaxime plus placebo (n = 49). Dexamethasone (0.15 mg per kilogram of body weight) was given 15 to 20 minutes before the first dose of cefotaxime and was continued every 6 hours thereafter for four days. RESULTS: The demographic, clinical, and laboratory profiles were similar for the patients in the two treatment groups. By 12 hours after the beginning of therapy, the mean opening cerebrospinal pressure and the estimated cerebral perfusion pressure had improved significantly in the dexamethasone-treated children but worsened in the children treated only with cefotaxime (controls). At 12 hours meningeal inflammation and the concentrations of two cytokines (tumor necrosis factor alpha and platelet-activating factor) in the cerebrospinal fluid had decreased in the dexamethasone-treated children, whereas in the controls the inflammatory response in the cerebrospinal fluid had increased. At 24 hours the clinical condition and mean prognostic score were significantly better among those treated with dexamethasone than among the controls. At follow-up examination after a mean of 15 months, 7 of the surviving 51 dexamethasone-treated children (14 percent) and 18 of 48 surviving controls (38 percent) had one or more neurologic or audiologic sequelae (P = 0.007); the relative risk of sequelae for a child receiving placebo as compared with a child receiving dexamethasone was 3.8 (95 percent confidence interval, 1.3 to 11.5). CONCLUSIONS: The results of this study, in which dexamethasone administration began before the initiation of cefotaxime therapy, provide additional evidence of a beneficial effect of dexamethasone therapy in infants and children with bacterial meningitis. (+info)
Management of giant pseudomeningoceles after spinal surgery.
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Reduction of PrP(C) in human cerebrospinal fluid after spinal cord injury.
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It has been estimated that cerebrospinal fluid (CSF) contains approximately 80 proteins that significantly increase or decrease in response to various clinical conditions. Here we have evaluated the CSF protein PrP(C) (cellular prion protein) for possible increases or decreases following spinal cord injury. The physiological function of PrP(C) is not yet completely understood; however, recent findings suggest that PrP(C) may have neuroprotective properties. Our results show that CSF PrP(C) is decreased in spinal cord injured patients 12 h following injury and is absent at 7 days. Given that normal PrP(C) has been proposed to be neuroprotective we speculate that the decrease in CSF PrP(C) levels may influence neuronal cell survival following spinal cord injury. (+info)
Assessment of craniospinal pressure-volume indices.
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The rate of CSF formation, resistance to reabsorption of CSF, and aperiodic analysis of the EEG following administration of flumazenil to dogs.
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The effects of flumazenil, a benzodiazepine antagonist, on the rate of cerebrospinal fluid (CSF) formation (Vf), resistance to reabsorption of CSF (Ra) and the electroencephalogram (EEG) was determined in 12 dogs anesthetized with halothane (0.4%, end-expired) and nitrous oxide (66%, inspired) in oxygen. In six dogs the responses to flumazenil were measured during administration of midazolam (1.6 mg/kg followed by 1.25 mg.kg-1.h-1, intravenously) given along with inhalational anesthesia, whereas in the other six dogs the responses to flumazenil were measured during inhalational anesthesia without midazolam. Vf and Ra were determined using ventriculocisternal perfusion, and EEG activity was evaluated using aperiodic analysis. Flumazenil, 0.0025 and 0.16 mg/kg, was administered both when CSF pressure was normal and when CSF pressure was increased to 36-38 cmH2O by continuous infusion of mock CSF. Flumazenil produced no statistically significant change in Vf. Flumazenil did produce inconsistent and relatively small changes in Ra. Quantitative aperiodic analysis indicated changes in EEG activity only when the larger dose of flumazenil was given to dogs receiving midazolam. At normal CSF pressure the changes were consistent and were comprised of decreases in theta, alpha, and total hemispheric power. At elevated CSF pressure the changes were less consistent. It is concluded that smaller doses of flumazenil (which cause no EEG changes with the present method of analysis) and larger doses of flumazenil (which reverse midazolam-induced increase of theta and alpha activity) produce no change of Vf and no consistent change of Ra. Although flumazenil given in the presence of midazolam may increase Ra, thereby increasing CSF pressure and impairing contraction of CSF volume, this effect is not likely to be clinically important. (+info)
Pathophysiology of persistent syringomyelia after decompressive craniocervical surgery. Clinical article.
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