Computed tomography was performed on 14 unconscious Kenyan children re
covering from cerebral malaria (seven of whom had another scan 12-120
days later) to elucidate the cause of intracranial hypertension and ne
urological sequelae. Brain swelling, defined as a loss of cerebrospina
l fluid spaces, was documented in six children, while a further two ha
d conspicuously small ventricles only. There was severe intracranial h
ypertension in the two children with definite brain swelling in whom i
ntracranial pressure was monitored. There was no evidence of acute hyd
rocephalus or vasogenic oedema. Four children with brain swelling also
had widespread low density areas suggestive of ischaemic damage. The
patterns of damage were not uniform but were consistent with a critica
l reduction in cerebral perfusion pressure (which was documented in th
e two in whom this was monitored), hypoglycaemia, or status epilepticu
s. All four had serious neurological sequelae. These data suggest that
brain injury in cerebral malaria may be due in part to secondary syst
emic and intracranial factors as well as to the direct effect of intra
vascular sequestration.