 Acute morbidities can contribute to adverse neurodevelopment outcomes in preterm infants born at 30 wks gestation, but neural damage occurring after resolution of acute morbidities may be more subtle and related to cycles of inflammation and repair in the developing brain. One possible contributor to these more subtle injuries is intermittent hypoxia IH, defined as repetitive cycles of hypoxia and re-oxygenation, which occur commonly in convalescent premature infants. Caffeine treatment can improve both motor and cognitive neurodevelopmental outcome in premature infants, especially at higher doses, but mechanisms are unclear.The Caffeine for Apnea of Prematurity CAP Trial in infants born preterm at 1250 g reported 1 shorter duration of positive pressure ventilation and reduced rate of bronchopulmonary dysplasia BPD in infants treated with caffeine during the early postnatal wks prior to 34-35 wks postmenstrual age PMA, 2 improved motor function and reduced rates of developmental coordination disorder at 5 years, and 3 diffusion changes by MRI consistent with improved white matter microstructural development. Although potential mechanisms for this caffeine effect were not studied in these reports, a recent study of very preterm infants in postnatal weeks 1-10 showed for the first time a direct link between IH and motor, cognitive and language impairment at 18 months corrected age adjusted risk gradient p0.005.Notably, the greatest risk gradient was at postnatal ages 9-10 wk, consistent with a contributory role of later IH present after stopping routine caffeine treatment. These data emphasize the potential importance of recurrent episodes of IH, as convalescing infants approach term-equivalent age, on later cognitive, language and motor impairments. 