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Function of the Blood-Cerebrospinal Fluid Barrier in Human Cerebral Malaria: Rejection of the Permeability Hypothesis
David A. Warrell
David A. Warrell
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Sornchai Looareesuwan
Sornchai Looareesuwan
Faculty of Tropical Medicine, Mahidol University, Thailand
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Rodney E. Phillips
Rodney E. Phillips
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Nicholas J. White
Nicholas J. White
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Mary J. Warrell
Mary J. Warrell
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Helen M. Chapel
Helen M. Chapel
Department of Immunopathology, John Radcliffe Hospital, Oxford, England
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Suvit Areekul
Suvit Areekul
Faculty of Tropical Medicine, Mahidol University, Thailand
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Savanat Tharavanij
Savanat Tharavanij
Faculty of Tropical Medicine, Mahidol University, Thailand
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We tested the hypothesis that cerebral malaria is caused by blood-brain barrier inflammation and cerebral edema. In a group of 157 Thai patients with strictly defined cerebral malaria, cerebrospinal fluid (CSF) opening pressures were normal in 79% and were lower in fatal cases than in survivors (means ± 1 SD, 144 ± 58 and 167 ± 51 mm CSF, respectively, P = 0.051). CSF: serum albumin ratios (× 103) in 39 of them were significantly higher than in 61 British controls (medians 8.5 and 5.5, respectively, P = 0.04), but were no higher in 7 fatal cases. In a group of 12 patients this ratio was not significantly higher during coma than after full recovery (means ± 1 SD, 9.0 ± 6.2 and 6.7 ± 4.2, respectively, P > 0.1). CSF α2-macroglobulin concentrations were always normal. CSF: serum 77Br- ratios were elevated in 11/19 comatose cases but fell to normal 4 to 9 days later in 11/11 cases. Dexamethasone treatment had no significant effect on bromide partition. The percentage of an intravenously administered dose of 125I-human serum albumin detectable per ml of CSF 6 hr after intravenous injection was 2.4 ± 1.3 × 10-5 in 14 comatose patients and 4.4 ± 4.0 × 10-5 in 9 of them during convalescence (P > 0.1). These results demonstrate that the blood-CSF barrier is essentially intact in patients with cerebral malaria and give no support to the idea that cerebral edema is the cause of coma.
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