Effects of neonatal hyperbilirubinemia on the brainstem electric response

Abstract

TttE RESPONSES of the cochlear hair cells, the eighth nerve, and the auditory brainstem pathways to electrophysiologic tests t may produce a clearer picture of the auditory sequelae of hyperbilirubinemia than provided by .behavioral techniques. The si!e or sites of bilirubin involvement remain somewhat obscure, but the evidence suggests that the site is retrocochlear, because auditory nerve responses are usually delayed Or absent, whereas the cochlear microphonic responses of the inner ear are usually present) Chisin et al? observed that the cochlear responses were present in nine of 13 children who had hyperbilirubinemia as neonates; the neural response from the auditory nerve Was absent in 11 of these 13 children, whereas electrocochlear responses were absent in most patients with sensorineural loss without a history of hyperbilirubinemia. Other ~vork in infants with kernicterus supports the concept that in hearing loss secondary to hyperbilirubinemia, wave I, ihe auditory nerve responses in the brainstem electric response are either delayed or absent. It is hypothesized that when bilirubin concentration reaches a yet to determined critical value, hearing loss can 9 occur and wave I may not be well resolved in the evoked potential average. If this is correct, the later waves III and V might serve as early signals of bilirubin infiltration of the auditory system before hearing loss occurs. We explored the use of waves III and V as early indicators of neural involvement in hyperbilirubinemia.