Yale research team offers SIDS explanation

A Yale School of Medicine research team may have found an answer to why one out of every 1,000 babies in the industrial world dies from sudden infant death syndrome.

The team, which included senior investigator Dr. George Richerson, associate professor of neurology and physiology, clarified how specific neurons in the brain might play a key role in preventing asphyxiation.

Richerson said certain neurons in the brain that produce serotonin are very responsive to an increase in carbon dioxide in the blood but may be defective in infants who die of SIDS.

“One of the biggest problems is that SIDS occurs in normal infants, and there’s no warning,” Richerson said.

In healthy babies and adults, these neurons react to aberrant levels of carbon dioxide during sleep by alerting the body to wake and breathe deeply, as abnormal carbon dioxide levels in the blood can have fatal effects.

The paper published by Richerson and his colleagues shows that these particular serotonin-containing neurons wrap around large blood vessels in the brainstem as if their specific function is to monitor the blood carbon dioxide levels.

“[The paper] clearly shows that these neurons are specialized to sense carbon dioxide,” Richerson said.

Improper regulation of carbon dioxide levels, a probable result of abnormalities in these neurons, could be a link to the cause of SIDS. A study done last year at Harvard revealed these abnormalities in the neurons of infants who died from SIDS.

“One goal [of this research] is to develop a test that you could easily administer to infants to determine if their serotonin neurons are functioning normally,” Richerson said, indicating that at-risk babies could then be monitored and potentially saved.

The cause of SIDS — the leading killer of children in their first year of life — is still not entirely known, but the prevalent theory is that there is a problem with infants’ breathing during sleep.

Risk factors include a face-down sleeping position, low birth weight, and premature birth. Richerson added that there is always an “exogenous stressor” present. The current culprit is believed to be babies sleeping face down on their stomachs.

“The normal response would be that the infant would wake up a little bit, move its head to relieve the obstruction, and breathe faster,” Richerson said. But if these regulatory neurons are not functioning properly, carbon dioxide, a waste product of respiration, can reach high levels in the bloodstream without eliciting action.

Richerson added that these neurons are naturally inhibited during sleep in all normal people, a fact that may explain why SIDS occurs only during sleep.

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