Sudden Infant Death Syndrome
Is Serotonin the Key Factor?
- Author Affiliation: Department of Pediatrics, Pediatric Respiratory Medicine, Rush University Medical Center, Chicago, Ill.
- Corresponding Author: Debra Ellyn Weese-Mayer, MD, Department of Pediatrics, Pediatric Respiratory Medicine, Rush University Medical Center, 1653 W Congress Pkwy, Chicago, IL 60612 (debra_e_weese-mayer{at}rsh.net).
Since this article does not have an abstract, we have provided the first 150 words of the full text.
- KEYWORDS:
- AUTONOMIC NERVOUS SYSTEM
- BLACKS
- ETHNIC GROUPS
- INFANT MORTALITY
- SEROTONIN AGONISTS
- SUDDEN INFANT DEATH
Neuropathological studies have identified a key role for the serotonin (5-hydroxytryptamine [5-HT]) pathways in sudden infant death syndrome (SIDS). Panigrahy et al1 reported a decrease in 5-HT receptor binding in the arcuate nucleus, raphé obscurus, and other medullary regions that contain 5-HT cell bodies in SIDS cases in the United States. Similarly, Ozawa and Okado2 reported a decrease in 5-HT receptor binding in the dorsal nucleus of the vagus, solitary nucleus, and ventrolateral medulla in SIDS cases in Japan. Subsequently, Kinney et al3 confirmed their prior observations of altered 5-HT receptor binding in medullary regions in Native American Indians, a group at high risk for SIDS.
In this issue of JAMA, Paterson and colleagues4 report that “SIDS cases had a significantly higher number and density of 5-HT neurons . . . and a significantly lower density of 5-HT1A receptor binding sites . . . in regions of the medulla involved in homeostatic …
