D. A. WarrellN. VeallP. ChanthavanichJuntra KarbwangN. J. WhiteS. LooareesuwanR. E. PhillipsPraneet PongpaewMahidol UniversityNuffield Department of Clinical MedicineMRC Clinical Research Centre2018-06-142018-06-141988-09-03The Lancet. Vol.332, No.8610 (1988), 534-538014067362-s2.0-0023719252https://repository.li.mahidol.ac.th/handle/123456789/15608In 12 patients comatose with cerebral malaria, cerebral blood flow was 52·2 (SE 4·0) ml/100 g per min, within the reported range for healthy controls, but cerebral vascular resistance was raised at 1·66 (0·19) mm Hg/ml per 100 g per min. Cerebral oxygen consumption (1·90 [0·23] ml/100 g per min), and cerebral arteriovenous oxygen content difference (3·5 [0·43] ml/dl) were subnormal, while cerebral venous pO 2 (5·7 [0·2] kpA) was raised. After recovery of consciousness there were significant decreases in arterial lactate concentration (2·44 [0·45] to 1·19 [0·45] μmol/l) and cerebral lactate production (17·4 [7·9] to 5·6 [1·1] mmol/100 g per minute). These results provide evidence of cerebral anaerobic gly colysis associated with inadequate oxygen delivery to the brain consistent with either inhibition of cerebral oxidative metabolism or the microcirculatory obstruction envisaged in the "mechanical" hypothesis for cerebral malaria. © 1988.Mahidol UniversityMedicineArticleSCOPUS10.1016/S0140-6736(88)92658-X