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Much that has been written on the pathophysiology of animal malarias is of doubtful relevance to the understanding of the mechanism of<jats:italic>Plasmodium falciparum<\/jats:italic>infection in man. The clinical picture of severe<jats:italic>P. falciparum<\/jats:italic>infection differs in several respects from severe animal malarias, even those of non-human primates. Cerebral dysfunction is the most common severe manifestation of falciparum malaria in man. Coma develops suddenly after a generalized convulsion or gradually towards the end of the first week of illness. There are signs of a symmetrical upper motor neurone lesion and brain-stem dysfunction, but only about 5% of survivors show persisting neurological deficit after 2 or 3 days of unconsciousness. The mortality of cerebral malaria depends on how it is defined and on the predominant age group and other factors. In patients with proved acute<jats:italic>P. falciparum<\/jats:italic>infection with unrousable coma, in whom other causes of encephalopathy have been excluded, the mortality is between 15 and 50% despite treatment with antimalarial drugs (Warrell, Looareesuwan, Warrell, Kasemsarn, Intaraprasert, Bunnag &amp; Harinasuta, 1982).<\/jats:p>","DOI":"10.1017\/s0031182000085826","type":"journal-article","created":{"date-parts":[[2011,8,23]],"date-time":"2011-08-23T11:24:30Z","timestamp":1314098670000},"page":"S53-S76","source":"Crossref","is-referenced-by-count":74,"title":["Pathophysiology of severe falciparum malaria in man"],"prefix":"10.1017","volume":"94","author":[{"given":"D. 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