Medullary serotonin defects and respiratory dysfunction in sudden infant death syndrome

David S. Paterson; Gerard Hilaire; Debra E. Weese-Mayer

doi:10.1016/j.resp.2009.05.010

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

Pediatrics

Research output: Contribution to journal › Article › peer-review

52 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	133-143
Number of pages	11
Journal	Respiratory Physiology and Neurobiology
Volume	168
Issue number	1-2
DOIs	https://doi.org/10.1016/j.resp.2009.05.010
State	Published - Aug 31 2009

Funding

The authors would like to thank the “Naitre et Vivre” Association for their financial support to the organization of the International Symposium on Respiratory Control (Saint Maximin, France) and the Scottish Cot Death Trust, Evelyn Deborah Barrett Fellowship, CJ Foundation for SIDS, First Candle/SIDS Alliance, CJ Murphy Foundation, National Institute of Child Health and Human Development, and Children's Hospital Mental Retardation Core Grant for their support.

Keywords

Infant
Pregnancy
SIDS

ASJC Scopus subject areas

Physiology
General Neuroscience
Pulmonary and Respiratory Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.resp.2009.05.010

Cite this

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abstract = "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.",

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N2 - 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.

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Medullary serotonin defects and respiratory dysfunction in sudden infant death syndrome

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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