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Function of the Blood-Cerebrospinal Fluid Barrier in Human Cerebral Malaria: Rejection of the Permeability Hypothesis

David A. Warrell^*,,, Sornchai Looareesuwan^*, Rodney E. Phillips^*,,, Nicholas J. White^*,,, Mary J. Warrell^*,,, Helen M. Chapel, Suvit Areekul^* AND Savanat Tharavanij^*

^* Faculty of Tropical Medicine, Mahidol University, Thailand
Nuffield Department of Clinical Medicine and Sir William Dunn School of Pathology, University of Oxford and The Liverpool School of Tropical Medicine, Liverpool
Department of Immunopathology, John Radcliffe Hospital, Oxford, England

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 (x 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 ₂-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 x 10^-5 in 14 comatose patients and 4.4 ± 4.0 x 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.

Accepted for publication April 6, 1986.