In a longitudinal study of 217 infants delivering at < 37 completed weeks gestation, Doppler flow velocity waveforms were obtained, and resistance index (RI) values calculated from the middle (MCA) and anterior (ACA) cerebral arteries during the first 10 days of life. Sixty infants demonstrated ultrasound evidence of cerebral pathology, of which five cases were congenital, and an additional 13 cases were complicated by patent ductus arteriosus during the study period. The Doppler data obtained during the first week of life from the remaining 42 infants who developed cerebral pathology, and 15 infants who had evidence of metabolic acidosis at delivery without ultrasound evidence of cerebral pathology were compared with local reference data obtained from non-acidotic infants with normal cranial ultrasound from 24 h of age. In those infants who had evidence of minor periventricular haemorrhage alone (Grade I/II PVH), there was no significant difference between the ACA or MCA RI during the study period compared with the reference data. In those groups of infants who demonstrated major PVH (Grade III/IV) or persistent periventricular flares, the ACA and MCA RI was found to be consistently significantly higher than the reference group throughout the study period. In those infants who developed ultrasound evidence of periventricular cystic leukomalacia (PVCL), the MCA RI was significantly lower than the reference data between 48 and 72 h of age, there being no significant difference in the ACA RI. The Doppler findings in those infants with evidence of metabolic acidosis at delivery (umbilical arterial pH < 7.20; BD > 8 mmol/l) but with normal ultrasound findings were similar to those infants who developed PVCL, namely a significant fall in MCA RI between 48 and 72 h of life, with no significant difference in the ACA RI during the study period. These findings suggest that variable changes in cerebral vascular resistance occur with the evolution of, or as a consequence of the development of cerebral pathology in the pre-term infant, and these changes of increased and decreased vascular resistance are discussed. Further investigation of the changes occurring in the cerebral circulation in the early neonatal period of infants who develop PVCL is required to clarify the vascular changes taking place, but if the findings of this study are confirmed, this technique may provide a means of identifying infants at risk of developing ischaemic cerebral pathology at an early stage when it may be possible to initiate therapeutic intervention to limit the cerebral damage.