Sleep influences on homeostatic functions: implications for sudden infant death syndrome

The mechanisms underlying the sudden infant death syndrome (SIDS) appear to have origins in the fetal environment resulting in neural damage which lat er compromises responses to breathing or blood pressure challenges during s leep. The deficits appear to involve alterations in neurotransmitter recept ors within regions involved in chemoreception and cardiovascular control. S IDS risk is enhanced by pre- and postnatal nicotine exposure, and possibly by hypoxic experiences. The prone sleeping position plays a significant rol e in risk, as do head positions that minimize facial escape from enclosed s paces; elevated body temperature may also be a factor. Compensatory mechani sms, including diminished gasping ability, relative failure to arouse to a safer state, or a failure to recruit respiratory efforts to overcome a bloo d pressure loss have been the object of recent research efforts. The findin gs suggest that the fatal event involves a neurally-compromised infant, cir cumstances that challenge vital physiology, most likely during sleep, at a particular developmental period. (C) 2000 Elsevier Science B.V. All rights reserved.