Abstract

The hypoxia induced by decreased cerebrocortical blood flow contributes to the neurologic deficits found in many survivors of Hib meningitis. Because reduced blood flow is measurable within 48 hours of acquisition of bacteria, the inability of antibiotic therapy to prevent sequelae is more easily understood insofar as damage has already occurred by the time treatment is initiated. Hydrocephalus is probably due to severe choroid plexus necrosis with aqueductal occlusion. These deficiencies, along with the neuronopathy, contribute to permanent cerebrocortical deficits, including impaired learning ability.

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