There has been a resurgence in the incidence of marked hyperbilirubinemia resulting in the potential for bilirubin brain injury in infants previously considered low risk. This is due, in part, to the renewed interest in breast feeding, as well as early discharge of hospitalized term infants. From 1995-97 we have admitted 6 AGA term infants with marked hyperbilirubinemia in association with either clinical signs consistent with bilirubin injury or radiologic evidence of basal ganglia staining on MRI. All infants were breast fed and presented in the first week of life with nonhemolytic hyperbilirubinemia. Peak bilirubin values ranged from 26.4 mg/dL (451.4μmol/L) to 36.9 mg/dL (631 μmol/L). 5/6 infants had bilirubin values> 30 mg/dL (513 μmol/L). 5/6 infants presented with neurologic signs including muscle tone abnormalities (3/5), high pitched cry (2/5), lethargy(3/5), or seizures (1/5). 5/6 infants received exchange transfusions and all were treated with phototherapy and IV fluids. Four infants had initial MRIs; 3 demonstrated basal ganglia staining consistent with kernicterus. One of these three also had encephalomalacia with no history of perinatal asphyxia. 2/4 infants had abnormal BAERs; both also had abnormal MRIs. Follow-up examinations between ages 6 mos-2 yrs showed resolution of clinical signs in all but the infant with encephalomalacia who is left with mental retardation, cerebral palsy, and blindness. Two infants had second MRIs. In both, the basal ganglia staining disappeared. No infant demonstrated residual hearing impairment. In conclusion, we observed transient neurologic dysfunction in breast fed term infants with marked hyperbilirubinemia. Aggressive management of these infants is generally associated with a good outcome. We speculate that inadequate establishment of breast feeding coupled with early discharge and less opportunity for breast feeding counselling may play a role in this phenomenon.