Dr. Gerald Popelka's overall research effort centers on increasing our understanding of auditory function in the developing human neonate. This effort is driven by the critical role audition plays in the normal development of language and speech and the need to optimize all interventions for pre-lingual hearing loss including hearing aids and cochlear implants. Human auditory development differs significantly from that of most other organisms necessitating innovative experiments be carried out directly on newborns in well baby, special care and intensive care nurseries. Measurement systems must be non-invasive, integrated, very small and insensitive to the many forms of ambient acoustic and electrical noise found in these environments, yet remain precise and repeatable.
Under a series of carefully controlled experiments we recently showed that the auditory system undergoes systematic and repeatable neural maturation during the first two days after birth, both across subjects and in individual neonates. This effect clearly is associated with neural development at the level of the brainstem because the experimental approach allowed control of maturational effects associated with other auditory structures such as the external ear, the middle ear and the cochlea, non-auditory developmental factors such as birth weight, gestational age, and general health of the neonate, and a variety of exogenous variables such as exposure to maternal anesthetic at delivery. This early auditory neural maturation may be associated with apoptosis (programmed cell death) or dendritic pruning. Current research involves understanding the relationship between auditory function and exposure to bilirubin, a molecule that results from the normal catabolism of maternal senescent red blood cells and a potential detriment to normal auditory development. Significant bilirubin exposure is experienced by 60% of well babies and much higher percentages in the remaining neonates.

This molecule is known to permanently affect auditory function at extremely high exposures. However, its chronic or acute effects at lower exposures are largely unknown. Our experimental approach is to measure auditory function simultaneously with precise measures of bilirubin exposure at several points in time during the first few days after birth. A correlation of these two measures, after compensating for normal neural development, will establish the relation between auditory neural function and bilirubin exposure. Several related projects support these experiments. We are developing a life-sized neonatal hearing simulator that contains computers, electronics and transducers that can be programmed to simulate normal and impaired neonatal cochlear and auditory neural responses. This device will help us to understand the measurement process by determining the effects of known sources of acoustic and electrical noise and by investigating interactions among the various measures.
We also are developing and incorporating measures of bilirubin production derived from measures of carbon monoxide concentration in the breath and measures of bilirubin accumulation derived from transcutaneous optical techniques. Future efforts will involve the development of improved non-invasive measures of bilirubin production and accumulation and improved auditory neural measures. Potentially useful clinical procedures resulting from this research include improvements in neonatal hearing screening achieved from simulator-based training of nursery personnel, expansion of neonatal breath analysis to include other hemolytic conditions, improvements in non-invasive measures of bilirubin concentration, and the use of non-invasive auditory neural measures for early detection of impending toxic bilirubin exposure to improve intervention for hyperbilirubinemia.


