Fever: blessing or curse?
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Biomedical subjects
Publications and source records attributed to E Schwam.
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Flumazenil, a benzodiazepine antagonist, blocks the central effects of benzodiazepines by competitive interaction at the receptor site. Two double-blind, placebo-controlled, randomized studies in healthy volunteers (110/study) were performed to determine the minimal effective dose of flumazenil required to reverse the sedative, psychomotor and amnesic effects of benzodiazepines used to produce conscious sedation. Conscious sedation was produced by i.v. diazepam (12-30 mg) in one study and i.v. lorazepam (0.045 mg kg-1) in the other. Intravenous flumazenil (0.001, 0.003, 0.007 or 0.014 mg kg-1) or placebo was administered after diazepam or lorazepam. Assessment of sedation, psychomotor performance and recall/recognition were made both before and after the benzodiazepine as well as serially after flumazenil or placebo. Doses as low as 0.007 and 0.014 mg kg-1 flumazenil consistently reversed diazepam- and lorazepam-induced effects, respectively. The duration of reversal produced by varying doses of flumazenil (0.2, 0.6, 1.0 or 3 mg) was evaluated in 50 volunteers in a double-blind, placebo-controlled, parallel group study. A constant level of conscious sedation was produced by a continuous infusion of midazolam. Assessments of sedation and psychomotor performance were assessed both before and at varying times after the administration of flumazenil or placebo. Preliminary results indicate that the duration of reversal produced by 3.0 mg flumazenil was longer than that produced by any of the lower doses. While the mean duration of reversal produced by the lower doses was comparable, the 0.2 mg dose resulted in the greatest between subject variability and only partial rather than complete reversal. Two further double-blind, placebo-controlled studies were done in healthy volunteers (45/study) to evaluate the safety of flumazenil 1.0 mg or placebo given i.v. to reverse midazolam-induced sedation in subjects who had been treated for up to 14 days with either oral diazepam or triazolam. No clinically significant changes were noted in laboratory test values, electrocardiograms or vital signs monitored for up to 36 h after flumazenil or placebo in any pre-treatment group.
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Aged squirrel monkeys develop senile plaques in the brain that are similar to those occurring in aged rhesus monkeys and aged humans. These plaques consist of abnormal, swollen neurites around an amyloid core. In whole-hemisphere coronal sections through the level of the rostral temporal lobe, plaques are present in temporal cortex, amygdala, hippocampal formation and, occasionally, in other cortical regions. In more rostral sections through the frontal lobe, plaques are most common in orbitofrontal and frontal opercular cortical regions. In immunocytochemical preparations, some neurites show immunoreactivity with antibodies directed against phosphorylated neurofilaments and neuropeptide Y. Thus, plaques in these New World primates are similar in distribution and composition to those occurring in aged Old World primates.
We report a case of fulminant supraglottitis with dramatic external cervical swelling due to associated cellulitis. Blood cultures were positive for Neisseria meningitidis. The patient recovered completely after emergency fiberoptic intubation and appropriate antibiotic therapy. We summarize five other cases of meningococcal supraglottitis, all reported since 1995, and discuss possible pathophysiologic mechanisms.