The significance and the role of cerebral edema in the pathogenesis of hypotoxic-ischemic encephalopaty (HIE) is controversial. It is not clear if cerebral edema is in itself a major determinant of brain damage or if it is merely a secondary terminal event. We tried to answer to this question by recording simultaneously the intracranial pressure (ICP) and the cerebral electrical activity in 17 term infants with grade 2-3 HIE. The recordings were made with a non invasive pneumatic applanation transducer (ICP) and a continuous 8 channel EEG monitoring for a period of at least 72 hours during the first week of life. Repented standardized neurological examinations were also performed and the severity of neurological impairment was graded using a clinical score. The aim of the study was to identify a possible correlation between an increase in ICP (as an expression of brain edema) on the one hand and a worsening of the EEG and clinical abnormalities (as an expression of brain damage) on the other hand. There were no significant or consistent variations of the EEG and clinical findings with increasing peak ICP in the infants studied. Our results do not support the hypothesis that cerebral edema, with a concomitant increase in ICP, plays a pathogenic role in the development of neuronal necrosis and brain damage in HIE.