Abstract
Advances in the care of neonatal hyperbilirubinemia have led to a decreased incidence of kernicterus. However, neonatal exposure to high levels of bilirubin continues to cause severe motor symptoms and cerebral palsy (CP). Exposure to moderate levels of unconjugated bilirubin may also cause damage to the developing central nervous system, specifically the basal ganglia and cerebellum. Brain lesions identified using magnetic resonance imaging following extreme hyperbilirubinemia have been linked to dyskinetic CP. Newer imaging techniques, such as diffusion tensor imaging or single-photon emission computed tomography, allow quantification of more subtle white matter injury following presumed exposure to unbound bilirubin, and may explain more subtle movement disorders. New categories of bilirubin-induced neurologic dysfunction, characterized by subtle bilirubin encephalopathy following moderate hyperbilirubinemia, have been implicated in long-term motor function. Further research is needed to identify subtle impairments resulting from moderate-severe neonatal hyperbilirubinemia, to understand the influence of perinatal risk factors on bilirubin toxicity, and to develop neuroprotective treatment strategies to prevent movement disorders due to bilirubin toxicity.