Recent epidemiological studies have shown that cerebral palsy is only rarely associated with birth asphyxia and that there may be more important causative factors in the prenatal period. For this reason a series of 165 brains of infants who were stillborn or died in the early neonatal period was examined in order to identify the incidence and nature of prenatal brain damage. Seventeen (44%) of the stillborn infants showed evidence of brain damage thought to be related to circulatory disorders. The most frequent abnormality, widespread ischaemic damage to the white matter of the cerebral hemispheres, occurred in 10 (26%). Criteria for white matter ischaemia were reactive astrocytosis, macrophage infiltration, karyorrhexis and endothelial swelling or reduplication. This abnormality was only seen after 27 weeks gestation. In five (13%) of the stillborn infants, haemorrhage was seen in association with ischaemic damage and in only two (5%) did brain haemorrhage occur in utero without evidence of co-existing ischaemic damage. Of the 90 live-born infants, 12 (16%) of those surviving less than 3 days and three (20%) of 15 infants who lived between 3 and 7 days after birth showed ischaemic damage which was of prenatal origin. The most frequent pathological change in the infants studied was white matter gliosis occurring in infants who survived into or beyond the last trimester. This may interfere with normal myelination by diverting glial stem cells into reactive astrocytes and thus reduce the population of oligodendrocytes available to synthesize myelin and so cause permanent neurological damage.