title: [From the murine model to human cerebral malaria].
abstract: The pathophysiology of cerebral malaria remains incompletely understood. Several mechanisms have been proposed to explain the aetiology of the neurological signs including reduction of cerebral blood flow, parasite toxin, hyperproduction of nitric oxide, immune response. Different models of murine and primate have been developed to investigate the different hypothesis. The role of nitric oxide was analysed in the murine and human malaria. Cerebral blood flow reduction is not compatible with the absence of sequelae observed in the majority of recovering cerebral malaria patients. Experimental data from primates and mice show that cerebral sequestration picture of circulating cells did not implicate the development of neurological signs. Brain haemodynamic data from human also argue for a "luxury perfusion" rather than a diminution of blood flow during cerebral malaria. The role of coinfection in the occurrence of cerebral malaria is discussed.
authors.affiliation: Laboratoire de Biologie Parasitaire et Chimiothérapie, URA CNRS 114, Muséum National d'Histoire Naturelle, Paris, France.
authors.forename: D
authors.initials: D
authors.lastname: Diakite
authors.forename: M C
authors.initials: MC
authors.lastname: Rahimy
authors.forename: P B
authors.initials: PB
authors.lastname: Falanga
mesh_terms: D000818:Animals; D002560:Cerebrovascular Circulation / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D007239:Infections / Q000150:complications; D016779:Malaria, Cerebral / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D010961:Plasmodium / Q000472:pathogenicity
chemical_list: D009569:Nitric Oxide
vernacular_title: Du modèle murin au neuropaludisme humain.