Is human malarial coma caused, or merely deepened, by sequestration?

• Published in: Trends in parasitology Vol. 25; no. 7; pp. 314 - 318
• Main Authors: Clark, Ian A, Alleva, Lisa M
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ltd 01.07.2009; Elsevier
• Subjects: Biological and medical sciences; Brain - blood supply; Cell Adhesion; Coma - complications; Coma - epidemiology; Coma - parasitology; Cytokines - metabolism; Gastroenterology and Hepatology; Human parasitic diseases due to arthropods; Humans; India - epidemiology; Infectious Disease; Infectious diseases; Malaria, Cerebral - complications; Malaria, Vivax - complications; Malaria, Vivax - epidemiology; Malawi - epidemiology; Medical sciences; New Guinea - epidemiology; Parasitic diseases; Malawi; New Guinea; India; Human; Parasite
• ISSN: 1471-4922; 1471-5007
• DOI: 10.1016/j.pt.2009.04.003

Much research into falciparum malaria coma assumes the primary event to be vascular obstruction by parasitized red blood cells. Recent evidence that vivax malaria, caused by a parasite traditionally thought not to block blood flow, seems to alter brain function to the same degree as falciparum malaria has seriously questioned this. These data are a timely call to reassess whether vascular obstruction should still be considered the primary cause of the coma of falciparum disease. They add to a growing literature that suggests that enhancement of brain-origin cytokines, such as tumour necrosis factor, by non-brain systemic inflammation and an appreciation of the degree to which neuronal homeostasis depends on them provide a more fruitful research direction.