Like most threads on SDN, this one has gotten off topic. I'll try to get it back.
Kernicterus is due to deposition of unconjugated bilirubin in the basal ganglia that can lead to severe neurologic defects and even death in the newborn human. It can be due to decreased levels of albumin (freeing up UCB to cross the BBB), congenital deficiencies of liver enzymes (i.e. Crigler-Najarr), and megaloblastic anemia from use of drugs like sulfonamides during periods of physiologic jaundice in the newborn among other things.
It seems that a lot of people here are confused about why this only occurs in neonates and not in adults that suffer from hyperbilirubinemia. There may be many factors at play, but it seems that the number one factor (especially for board questions) is that the BBB in the infant is not fully developed, allowing for increased passage of substances into the brain parenchyma. I've bolded that last part for the ones here who seem to not understand this concept.
Edit: BBB = Blood-Brain Barrier