WORCESTER, Mass. A potentially life-threatening challenge characterized by pauses in breathing that can last for more than 20 seconds, apnea of prematurity (AOP) affects more than 50 percent of premature infants and is almost universal in the smallest of preemies. Caused in part by an underdeveloped central nervous system that can't adequately regulate breathing outside of the womb, especially during sleep, AOP is not yet fully understood by scientists and remains a grave concern among neonatologists and parents alike. New research published in the October issue of Pediatrics by clinical scientists at the University of Massachusetts Medical School suggests that heredity may play a strong role in determining an infant's susceptibility to AOP and could lead to the development of more effective treatments and screening methods.
Because it causes gaps in breathing, AOP can lead to reduced oxygen levels and a slowed heart rate in premature infants, as well as permanent disabilities and long-term damage to internal organs. Requiring around-the-clock monitoring, infants with AOP often must be gently jostled or rubbed to encourage inhalation and continued breathing, but such activities wake the baby, depriving it of much needed sleep. In severe cases, pharmaceutical interventions, such as caffeine, may be required. While the permanent consequences of AOP and its treatments have yet to be fully studied, infants with AOP are more likely to have cognitive and behavior problems, and other long-term disabilities.
"AOP is a medical puzzle," said David Paydarfar, MD, professor of neurology and physiology at the University of Massachusetts Medical School. "Our research seeks to explain why there is so much variability in the incidence and severity of apnea in premature infants and why some infants outgrow the problem much sooner than others."
Elisabeth B. Salisbury, PhD, assistant professor of neurology, Paydarfar, and colleagues compared the rates of AOP in 2
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University of Massachusetts Medical School