Postnatal abnormality in brainstem neural conduction in neonatal bronchopulmonary dysplasia survivors

To investigate postnatal neural conduction in the auditory brainstem in neonatal bronchopulmonary dysplasia (BPD) survivors.

Thirty-two very preterm BPD survivors were studied at 57-58 weeks of postconceptional age. Brainstem auditory-evoked response was studied using maximum length sequence. Wave latencies and intervals were analyzed in detail. The controls were 37 normal term infants and 35 very preterm non-BPD infants.

Compared with normal term controls, BPD survivors showed significantly shortened I-III interval but significantly prolonged III-V interval and greater III-V/I-III interval ratio. Compared with very preterm non-BPD controls, BPD survivors showed a significant shortening in waves III latency and I-III interval, moderate prolonged III-V interval, and significantly greater III-V/I-III interval ratio. These differences were generally similar at all click rates used. The slopes of latency- and interval-click rate functions in BPD survivors did not differ significantly from the two control groups.

Brainstem neural conduction in BPD survivors differed from normal term and age-matched non-BPD infants; neural maturation is accelerated in caudal brainstem regions but delayed in rostral regions. Neonatal BPD survivors are associated with differential maturation in neural conduction at caudal and rostral brainstem regions, which may constitute an important risk for postnatal neurodevelopment in BPD survivors.

We found that brainstem neural conduction at PCA 57-58 weeks in neonatal BPD survivors differs from normal term and age-matched non-BPD infants. No major differences were found between normal term and very preterm non-BPD infants in brainstem auditory conduction. Neural conduction in BPD survivors is accelerated in caudal brainstem regions but delayed in rostral regions. Neonatal BPD survivors are associated with differential maturation in neural conduction at caudal and rostral brainstem regions. The abnormality may constitute an important risk for postnatal neurodevelopment in BPD survivors.