Clue to Sudden Infant Death Syndrome
Brain Stem Abnormality Seen in SIDS Babies, Study Shows
WebMD News Archive
Oct. 31, 2006 - Researchers have identified a brain defect they think is a major contributor to sudden infant death syndrome (SIDS).
The findings provide the strongest evidence yet of a specific neurological cause for SIDS, a little-understood condition that kills roughly 2,500 infants each year in the United States.
In the study, autopsy tissue taken from babies who had died of SIDS and other causes showed abnormalities in the lower brain stems of the SIDS babies. Among other things, this region of the brain is thought to help regulate breathing and arousal.
Environmental factors, such as stomach sleeping, overheating, and exposure to cigarette smoke are all believed to increase a baby's risk of death from SIDS.
But the search for a biological link has turned up little, until now.
"This is very good evidence that there definitely is a biological problem that contributes to SIDS," neuroscientist and study co-author David S. Paterson, PhD, tells WebMD.
"There very well may be other biological causes which have not been identified. This gives us a good starting point to keep looking," says Paterson, of Boston Children's Hospital.
The Serotonin System
Boston Children's Hospital neuropathologist Hannah Kinney, MD, has searched for a biological cause for SIDS for the past two decades.
She and Paterson had previously identified defects in the serotonin system of the lower brain stem in babies who had died of SIDS.
The brain stem serotonin system is believed to help coordinate breathing, blood pressure, sensitivity to carbon dioxide, arousal, and temperature. Serotonin works as a chemical messenger in this system.
Kinney and Paterson believe babies who die of SIDS actually suffocate from breathing the carbon dioxide they exhale during sleep.
Normal babies wake up when the air they breathe contains too much carbon dioxide and not enough oxygen, but the thinking is that babies susceptible to SIDS lack this arousal reflex.
In their latest study, which appears in the Nov. 1 issue of The Journal of the American Medical Association, the researchers confirmed their earlier findings and expanded on them.
They examined autopsied tissue from the lower brain stems of 31 infants who had died of SIDS and 10 infants who had died from other causes.
Multiple defects in the serotonin system of the SIDS babies were identified, including abnormally high numbers of neurons that make and release serotonin and deficiencies in certain serotonin receptor binding sites.
"Our hypothesis right now is that we're seeing a compensation mechanism," Paterson says. "If you have more serotonin neurons, it may be because you have less serotonin and more neurons are recruited to produce and use serotonin to correct this deficiency."
Male babies who died of SIDS had less serotonin receptor binding - necessary for serotonin to work -- than either female babies who died of SIDS or the babies who died of other causes. This may help explain why SIDS is twice as common in males as in females.