Numerous studies in premature infants have shown that aspects of brain stem evoked responses (BAER) mature with increasing gestational age (ΓA) including the appearance of specific wave forms, decrease in latencies, and increase in relative amplitude. Studies in term infants have shown reversible acute BAER wave changes associated with hyperbilirubinemia, an increase in wave latencies and a decrease in amplitude followed by loss of wave form. However, no data is available for sequential changes in BAER over the first postnatal week in preterm infants in whom hyperbilirubinemia is common. Bilateral monaural BAER tests were performed on 5 of the first 7 days after birth in 54 infants £32 weeks gestation using 80 dB nHL unfiltered click stimuli presented at a repetition rate of 39.9/sec. BAER waveforms were categorized using a unique system based on response replicability and peak identification (1: replicable, wave I, V amplitude and latency measurable; 2: replicable, wave V measurable; 3: replicable, wave V not measurable; 4: no identifiable wave forms). Latencies for wave V were analyzed, when measurable, for the entire group and for individuals followed serially. Data were collected for risk factors associated with changes in BAER components or with hyperbilirubinemia-induced neurotoxicity: acidosis (pH<7.2), Apgar score<5 at 5 min, sepsis, hypoalbuminemia, and IVH. GA was assessed by obstetrical dating criteria or, when obstetrical data were inadequate, by Ballard exam. Of 8 infants 24-26 wk GA and 15 infants 26-28 wk GA, BAER responses were predominantly category 3,4. Of 6 infants 28-30 wk GA and 25 infants 30-32 wk GA, the majority of BAERs were category 1,2 and the progression of wave V latencies were analyzed over time and as a function of serum bilirubin. Max biliρυβιν levels in infants with BAER changes (3 each at 28-30 and 30-32 wk GA) ranged from 7.2 - 14.5 regardless of risk factors. Infants with normal progression of wave V had max biliρυβιν levels of 5.8 - 14.2. These results suggest that bilirubin levels as low as 7.2 in infants 28-32 wk GA may produce a bilirubin effect and, by extension, place these infants at risk for bilirubin toxicity.