Central auditory processing disturbances have been described in kernicterus, but electrophysiologic studies to date have only assessed brainstem function. We assessed brainstem and cortical auditory function in the Gunn rat model of acute bilirubin neurotoxicity using brainstem auditory evoked potentials (BAEPs) and CAEPs recorded simultaneously from a scalp electrode over the contralateral temporal lobe in 10 pairs of 17-day-old jj rats given fentanyl ip., 100 μg/kg initially and 50 μg/kg q1/2h. Reproducible baseline latencies were obtained for BAEP waves I, I-II and I-III at 1.04±0.14 (mean±SD), 1.16±0.24 and 2.18±0.18 msec, and CAEP waves P1, N1, P2 and N2 at 15.7±4.8; 26.7±2.0; 45.4±3.8; 83.7±11.0 msec, respectively. After baseline recordings, one jj (experimental) was given sulfadimethoxine 100 mg/kg ip. to produce acute bilirubin toxicity; a littermate control jj received saline; recordings continued for ≥6h. In the experimental group, BAEP wave I-III and I-II latencies increased vs. baseline and vs. controls at 4h and 6h(p<0.01 each), while the amplitude of III decreased at 2, 4 and 6h (p<0.05,.01 and.01, respectively). The latency of cortical N1 and P2 increased at 6h (p<0.05 and 0.01, respectively). In 4/10 experimental rats but only 1/10 controls (p=0.12, chi-square), the large positive CAEP P2 wave split into two component peaks(Figure, arrows). These findings demonstrate cortical auditory dysfunction with acute bilirubin toxicity. Dysfunction in these areas in humans may relate to central auditory processing and language disorders. CAEPs may provide useful diagnostic and prognostic information in humans with neonatal hyper-bilirubinemia.

figure 1

Supported by NIH NIH R01 DC00369