Visual Evoked Potentials in Infants With Diffuse Periventricular Leukomalacia

Abstract

Periventricular leukomalacia (PVL) is characterized by necrosis of the cerebral white matter in the dorsolateral portions of the lateral ventricles. PVL causes motor, sensory, and cognitive deficits. The aim of this study was to analyze the conduction characteristics of the visual pathway in infants with diffuse PVL using visual evoked potentials (VEPs). We studied 11 healthy infants (mean age 3.3 ± 1.3 months) and 17 with diffuse PVL (mean age 2.9 ± 0.8 months and mean gestational age 31.9 ± 3.1 weeks). The N75, P100, and N135 wave latencies; the interwave N75-P100 and P100-N135 latencies; and the N75-P100 and P100-N135 amplitudes were measured in the occipital leads. VEPs were recorded during binocular stimulation at an angle of 120′ from the Fz-Oz lead. Healthy children had mean N75, P100, and N135 wave latencies of 84.4 ± 5.8, 143.4 ± 30.6 and 222.9 ± 40.4 ms, respectively. The mean interwave N75-P100 and P100-N135 latencies were 59.0 ± 28.6 and 79.5 ± 13.6 ms, respectively. Compared with the healthy group, infants with PVL had longer N75 and N135 latencies at 92.3 ± 15.3 ( P = .05) and 265.0 ms ± 60.3 ( P = .05), respectively. The interwave latency P100-N135 (105.5 ± 29.1 ms; P = .017) was longer in children with PVL than in healthy infants. Infants with diffuse PVL had mild alterations in their N75, P100 and, particularly, their N135 latencies. These increases in P100-N135 interwave latencies could be because of damage to the geniculocortical pathways and V2-V3 networks.