Proposal for mechanisms of protection of supine sleep against sudden infant death syndrome: An integrated mechanism review

Abstract

Supine sleep decreases sudden infant death syndrome (SIDS) incidence, however the mechanisms for this are unclear. The triple risk model for SIDS requires that one or more underlying abnormalities of breathing or autonomic control are present; these are rare, but brainstem defects are found in most SIDS cases. Supine sleep increases sympathetic nervous system tone, and level of state organization, and may therefore act as a stressor. This is evidenced by physiological arousal, and by delayed neurodevelopment in supine compared to prone sleepers. It is argued here that prone sleep position is the biological normative standard in healthy infants, supporting autonomic regulation. During rapid eye movement (REM) sleep (and other circumstances), a parasympathetic-mediated adverse autonomic event (AAE) may be spontaneously triggered. In healthy infants, gasping initiates autoresuscitation and recovery. Hypothesis: the underlying vulnerability to SIDS is specific to autoresuscitation from an AAE, the initial serotonin-dependent gasp is commonly compromised. Serotonin metabolism defects also influence sleep architecture, increasing the likelihood of AAE. The mechanism whereby supine sleep decreases SIDS may therefore be a stressor effect, disturbing sleep architecture to decrease REM and AAEs, and increasing sympathetic tone, which may prevent and counteract the purely parasympathetic-mediated AAE, thereby decreasing the risk of SIDS.