Bilirubin toxicity remains a significant problem despite recent advances in the 
care of jaundiced (hyperbilirubinemic) neonates. A recent surge in reported 
cases of classical kernicterus, due in part to earlier hospital discharge and 
relaxation of treatment criteria for hyperbilirubinemia, and new reports of 
hyperbilirubinemia-induced auditory dysfunction using evoked potential based 
infant testing and hearing screening, underscore the need to better understand 
how hyperbilirubinemia causes brain damage in some infants, especially because 
the damage is preventable. Recent progress in understanding bilirubin binding 
and neurotoxicity resulting from unbound or "free" unconjugated bilirubin, how 
bilirubin affects the central nervous system in vivo and in vitro, and the use 
of new clinical tools in neonates, for example magnetic resonance imaging 
revealing bilateral lesions in globus pallidus and subthalamus, and abnormal 
brainstem auditory evoked potentials with normal inner ear function, may lead to 
improved detection and prevention of neurologic dysfunction and damage from 
bilirubin. Finally, the concern is raised that partial or isolated neurologic 
sequelae, for example auditory neuropathy and other central auditory processing 
disorders, may result from excessive amount and duration of exposure to free, 
unconjugated bilirubin at different stages of neurodevelopment.