Sudden infant death syndrome: an update and new perspectives of etiology

Abstract

Sudden infant death syndrome (SIDS) is a condition in which an infant, usually in the early postnatal period and nearly always before 6 months of age, dies during sleep for unexplained reasons and the standard autopsy fails to disclose an etiology. Various physiological explanations of risk factors include the prone sleeping position, overheating by excessive bundling, viral upper respiratory tract infections, parental smoking at home, and birthing injury resulting in an insult to the inner ear and central chemoreceptor zone, an immaturity that involves CO2 chemoreceptors that regulate respiratory control. Neuropathological studies and theories implicate: (1) hypoplasia or defective transmitter function in the medullary arcuate nucleus, a derivative of the rhombencephalic lip of His; (2) synaptic or receptor immaturity of the nucleus of the fasciculus solitarius, the "pneumotaxic center"; and (3) functional impairment of the serotonergic raphé nuclei of the pontine and medullary ventral median septum and other serotonergic neurons of the brainstem. Additional neurological risk factors for SIDS include perinatal neuromuscular diseases, infantile epilepsies or status epilepticus, and genetic metabolic encephalopathies.