Medullary serotonin defects and respiratory dysfunction in sudden infant death syndrome

David S. Paterson*, Gerard Hilaire, Debra E. Weese-Mayer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


Sudden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an infant less than 12 months of age that occurs during sleep and remains unexplained after a complete autopsy, death scene investigation, and review of the clinical history. It is the leading cause of postneonatal mortality in the developed world. The cause of SIDS is unknown, but is postulated to involve impairment of brainstem-mediated homeostatic control. Extensive evidence from animal studies indicates that serotonin (5-HT) neurons in the medulla oblongata play a role in the regulation of multiple aspects of respiratory and autonomic function. A subset of SIDS infants have several abnormalities in medullary markers of 5-HT function and genetic polymorphisms impacting the 5-HT system, informing the hypothesis that SIDS results from a defect in 5-HT brainstem-mediated control of respiratory (and autonomic) regulation. Here we review the evidence from postmortem human studies and animal studies to support this hypothesis and discuss how the pathogenesis of SIDS is likely to originate in utero during fetal development.

Original languageEnglish (US)
Pages (from-to)133-143
Number of pages11
JournalRespiratory Physiology and Neurobiology
Issue number1-2
StatePublished - Aug 31 2009


  • Infant
  • Pregnancy
  • SIDS

ASJC Scopus subject areas

  • Physiology
  • General Neuroscience
  • Pulmonary and Respiratory Medicine


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