Shapiro S M
Waisman Center on Mental Retardation and Human Development, Departments of Neurology and Pediatrics, University of Wisconsin-Madison.
Hear Res. 1991 May;53(1):41-8. doi: 10.1016/0378-5955(91)90212-r.
Bilirubin toxicity causes encephalopathy associated with lesions of the central auditory nervous system. Abnormal brainstem auditory evoked potentials (BAEPs) in jaundiced Gunn rats made acutely bilirubin toxic suggest abnormal input into the superior olivary complex, which might result in abnormal binaural interaction. Binaural difference waves (BDWs), obtained by subtracting the sum of two monaural BAEPs from a binaural BAEP, were obtained in 16- to 20-day-old jaundiced Gunn rats before and after injection of sulfadimethoxine, which produces bilirubin neurotoxicity by promoting net transfer of bilirubin out of the circulation into brain tissue. Reliable BDWs were recorded with onset 4.5 ms after the stimulus, followed by a large, often bimodal, positive peak occurring at about 6 ms. Following injection of sulfadimethoxine to produce bilirubin neurotoxicity, there was loss of BDW amplitude (21% +/- 14% of baseline, P less than 0.0001) and increase in latency (0.62 +/- 0.42 ms, P = 0.03) in bilirubin-toxic jaundiced rats compared to baseline, but no significant changes in nonjaundiced controls treated similarly. This documents abnormal BDWs in acute bilirubin encephalopathy suggesting that abnormalities of functions dependent on binaural processing of auditory information may be found as neurologic sequelae to bilirubin toxicity. BAEP BDWs may be a sensitive method for detecting neurophysiological abnormalities due to bilirubin toxicity.
