Abstract
In preterm infants the visual evoked potential (VEP) is attenuated at P.O, levels below 2.5 to 3.0 kPa. However, progressive VEP attenuation in terms of delayed latency and decreased amplitude is also observed at higher stimulation frequency (P<0.005). The degree of VEP attenuation may indicate low substrate delivery to the visual tracts. 26 preterm infants (GA 25-34 weeks) were investigated daily during the first three days of life. Single flash VEPs were recorded at different stimulation intervals (2, 4 and 30 sec) and oxygen delivery to the brain (OD) was calculated from the product of cerebral blood flow and the arterial oxygen content. In all infants a VEP was present. The VEP parameters and the degree of attenuation was neither related to OD (1.2 to 6.2 ml/100g/min) nor to perinatal data and postnatal age. Furthermore, there was no difference between infants who survived and those who developed cerebral lesions or died. The results indicate that the neurons generating the VEP are supported sufficiently at very low levels of OD. VEP attenuation in preterm infants cannot be interpreted as imminent ischemia.
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