Mechanisms of pathogenesis in the Sudden Infant Death Syndrome

Abstract

The likely processes of the Sudden Infant Death Syndrome (SIDS) were identified many years ago (apnea, failed arousal, failed autoresuscitation, etc.). The neurophysiological basis of these processes and the neurophysiological reasons some infants die of SIDS and others do not are, however, only emerging now. We reviewed recent studies that have shed light on the way in which epidemiological risk factors, genetics, neurotransmitter receptor defects and neonatal cardiorespiratory reflex responses interact to lead to sudden death during sleep in a small number of normal appearing infants. As a result of this review and analysis, we hypothesize that the neurophysiological basis of SIDS resides in a persistence of fetal reflex responses into the neonatal period, amplification of inhibitory cardiorespiratory reflex responses and reduced excitatory cardiorespiratory reflex responses. The hypothesis we developed explores the ways in which multiple subtle abnormalities interact to lead to sudden death and emphasizes the difficulty of ante-mortem identification of infants at risk for SIDS, although identification of infants at risk remains an essential goal of SIDS research.