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[From the murine model to human cerebral malaria].

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.