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dc.contributorAas, Pålen_GB
dc.contributorMyhrer, Tronden_GB
dc.date.accessioned2018-10-11T12:25:54Z
dc.date.available2018-10-11T12:25:54Z
dc.date.issued2003
dc.identifier812
dc.identifier.isbn82-464-0803-8en_GB
dc.identifier.other2003/01278
dc.identifier.urihttp://hdl.handle.net/20.500.12242/1485
dc.description.abstractThe potential for exposure to chemical warfare nerve agents exists on the battlefield and as a terrorist threat to civilians. Nerve agents are irreversible inhibitors of the acetylcholinesterase enzyme and there-by induce hyperactivity of the cholinergic systems in the brain and in the periphery. Exposure causes a progression of toxic signs, including hypersecretions, fasciculations, tremor, convulsions, respiratory distress and death. A combined regimen consisting of prophylaxis and medical therapy is considered the most effective medical countermeasure for management of nerve agent poisoning of military personnel. In case of terrorist use of nerve agents against civilians, only post-exposure treatment is feasible. The use of prophylaxis and medical treatment or only medical treatment after exposure does not prevent the development of nerve agent-induced brain seizures. Prolonged epileptic seizures in a nerve agent casualty will produce profound, irreversible, brain damage that in turn will result in long-term deficits in cognitive function and behaviour. It is considered important to co-administer a GABAergic agonist, such as diazepam, with the currently used regime of carbamate prophylaxis and follow-up medical treatment with atropine and oxime. Experimental studies in NATO have shown that diazepam does not provide total protection against nerve agent induced brain injuries. An active research is, therefore, necessary to find better and more effective drugs. Several drugs have been studied and some drugs have shown to provide a better anticonvulsant effects than others. Future research will probably identify drugs that will be more efficient in protecting humans from injuries following exposure to nerve agents than the present ones in use.en_GB
dc.language.isonoben_GB
dc.titleAktuelle motmidler mot hjerneskader ved nervegasseksponeringen_GB
dc.subject.keywordNervegasseren_GB
dc.subject.keywordHjernesykdommeren_GB
dc.source.issue2003/01278en_GB
dc.source.pagenumber31en_GB


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