The relationship between sleep and sudden infant death.

Infants epidemiologically at high risk for SIDS demonstrate a variety of abnormalities in sleep-state organization, maturation, and sleep-state modulation of cardio-respiratory control mechanisms. These involve both the REM and quiet-sleep states and are seen in twins who have had no evidence of clinical cardio-respiratory compromise during infancy as well as in near-miss infants who have suffered serious cardio-respiratory failure. Although these infants have higher levels of REM sleep around 40 weeks, of special concern is the decrease in the maturation of the quiet system, which becomes evident after 44 weeks, and the reported quiet-sleep abnormalities in reflex control of respiration and arousal. The source of these abnormalities is environmental rather than genetic and most likely occurs prenatally. During the critical period for SIDS, infant sleep begins to coalesce from a series of naps to more prolonged night time sleep periods that last up to 8 hours. We believe that the ability to maintain physiologic homeostasis during prolonged sleep is a challenge facing infants who are epidemiologically at risk for sudden infant death. The challenge facing sleep research is the more complete understanding of the relationship between prolonged inhibition, homeostasis, arousal, and development.