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Published on: May 10, 2019
Brainstem auditory evoked responses in very low birthweight infants with chronic lung disease
Ze D Jiang1, Rong Yin, Andrew R Wilkinson
1Children's Hospital, Shanghai Medical University, Shanghai, China. zedong.jiang@paediatrics.ox.ac.uk
Insights
Chronic lung disease (CLD) in very low birthweight (VLBW) infants significantly impairs neonatal auditory function, affecting both peripheral and central pathways. This auditory dysfunction is evident at term age, highlighting a critical developmental concern for these vulnerable infants.
Area of Science:
- Neonatology
- Neuroscience
- Audiology
Background:
- Very low birthweight (VLBW) infants with chronic lung disease (CLD) face high risks of neurodevelopmental impairment.
- Prolonged oxygen dependence is a common complication in VLBW infants with CLD.
Purpose of the Study:
- To investigate the impact of neonatal CLD on auditory function in VLBW infants.
- To assess peripheral and central auditory pathways using brainstem auditory evoked response (BAER).
Main Methods:
- Brainstem auditory evoked response (BAER) was performed on VLBW infants with CLD and compared to healthy VLBW infants and normal term infants.
- Auditory function was evaluated at 37-42 weeks postconceptional age.
Main Results:
- CLD infants exhibited significantly longer latencies for waves I, III, and V compared to term controls (p<0.001).
- Abnormal wave latencies were observed in 21.2% (wave I), 24.2% (wave III), and 42.4% (wave V) of CLD infants.
- Prolonged I-V intervals, indicative of central auditory impairment, were found in 21.2% of CLD infants.
Conclusions:
- Neonatal CLD significantly impairs auditory function in VLBW infants, affecting both peripheral and central auditory pathways.
- Auditory abnormalities are present at term age in VLBW infants with a history of CLD.
Unlabelled:
Very low birthweight (VLBW) infants who had prolonged oxygen dependence due to chronic respiratory problems, typically neonatal chronic lung disease (CLD), are at high risk of neurodevelopmental impairment. To assess the effect of CLD on neonatal auditory function we studied brainstem auditory evoked response (BAER) in VLBW infants who suffered CLD but no other major perinatal complications or problems. At 37-42 week postconceptional age, the latencies of waves I, III and V in CLD infants were all significantly longer than in normal term infants (all p<0.001). The differences between CLD infants and the term controls were greater for the later waves than for the earlier waves. Abnormally prolonged wave latency (>2.5 SD of the mean measurement) was seen in 7 (21.2%) CLD infants for wave I, suggesting peripheral auditory impairment, 8 (24.2%) for wave III and 14 (42.4%) for wave V. I-V interval in CLD infants was significantly longer than in the term controls (p<0.001). Seven (21.2%) infants had abnormally prolonged I-V interval, suggesting brainstem or central auditory impairment. Of these infants, 2 had both prolonged wave latencies and prolonged I-V interval, suggesting both peripheral and central auditory impairment. Similar abnormalities were found in CLD infants when compared with the BAER in birthweight- and age-matched healthy VLBW infants without CLD.
Conclusion:
Neonatal auditory function is impaired, both peripherally and centrally, at term age in VLBW infants who suffer neonatal CLD.
