Sudden infant death syndrome: The role of central chemosensitivity

Clinical and basic research on Sudden Infant Death Syndrome (SIDS) has focused on sleep-disordered cardiorespiratory control during a critical period of brainstem maturation. Recently, some SIDS cases have been reported to have abnormalities of the arcuate nucleus of the medulla. The human arcuate nucleus is thought to be homologous to the medullary raphe in rats and cats, a widely projecting serotonergic system that is functionally linked to both respiration and sleep. Neurons of the medullary raphe are now known to be highly sensitive to respiratory acidosis in vitro and are candidates for central chemoreceptors. The relevance of changes in the arcuate nucleus to the mechanisms of death in SIDS remains controversial. However, based on this new data, a specific hypothesis is proposed here. in combination with immaturity of respiratory control mechanisms, dysfunction of arcuate neurons may lead to a fatal exaggeration of a normal physiologic inhibition of central chemoreception during sleep. The major elements of this working hypothesis are testable in animal experiments and clinical studies.