Article révisé par les pairs
Résumé : Prevention campaigns to avoid risk factors for the occurrence of sudden infant death syndrome (SIDS) during sieep have ied to a significant decrease in the number of infants dying suddeniy and unexpectedly during sieep. Despite a growing amount of evidence, the understanding of the mechanisms responsible for SIDS is stilt iargeiy incomplete. We will review the most recent epidemiotogicai, electrophysiologicai, genetic and pathological research on this topic. From these data, a comprehensive model for SIDS has been proposed: the death wouid resuit from the combination of three factors (a prenatal vulnerability, a critical developmental period and an exogenous postnatal stress) and three potential mecbanisms (deficiencies in breathing, autonomie and sleep-wake controis). 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 controis during sleep. Genetic, metaboiic, nutritbnal or toxic prenatal brainstem injury could be responsible for these deficits. The infant's vulnerability lies latent until he/she enfers the critical developmental period from 2 to 6 months when significant changes in sleep-wake, breathing and autonomie 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. © 2005 Elsevier Masson SAS. All rights reserved.

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