Sudden infant death syndrome from epidemiology to pathophysiology

Pevention campaigns to avoid risk for the occurrence of sudden infant death syndrome (SIDS) during sleep have led to a significant decrease in the number of infants dying suddenly and unexpectedly during sleep. Despite a growing amount of evidence, the understanding of the mechanisms responsible for SIDS is still largely incomplete. We will review the most recent epidermiological, electrophysiological, genetic and pathological research on this topic. From these data, a comprehensive model for SIDS has been proposed: the death would result from the combination of three factors (a prenatal vulnerability, a critical developmental period and an exogenous postnatal stress) and three potential mechanisms (deficiencies in breathing, autonomic and sleep-wake controls). As arousal represents the last chance of survival when an infant is exposed to a life-threatening challenge during sleep, failure to arouse could be involved in the final pathway of SIDS. An infant could be vulnerable to SIDS because of a deficiency in cardio-respiratory or in sleep/wake behaviour controls during sleep. Genetic, metabolic, nutritional or toxic prenatal brainstem injury could be responsible for these deficits. The infant's vulnerability lies latent until he/she enters the critical developmental period from 2 to 6 months when significant changes in sleep-wake, breathing and autonomic controls occur. The accident has a greater probability of occurring when the infant is exposed to an infection, or an unfavourable environmental factor which enhances the immature cardio respiratory and sleep/wake behaviours of the infant.