News

Study Finds Abnormalities in Brain Region That Regulates Breathing, Sleep

The brains of infants who die of sudden infant death syndrome (SIDS) produce low levels of serotonin, a brain chemical that conveys messages between cells and plays a vital role in regulating breathing, heart rate, and sleep, reported researchers.

The researchers theorize that this newly discovered serotonin abnormality may reduce infants' capacity to respond to breathing challenges, such as low oxygen levels or high levels of carbon dioxide. These high levels may result from re-breathing exhaled carbon dioxide that accumulates in bedding while sleeping face down. The findings appear in The Journal of the American Medical Association.

"We have known for many years that placing infants to sleep on their backs is the single most effective way to reduce the risk of SIDS," says Alan E. Guttmacher, MD, acting director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. "The current findings provide important clues to the biological basis of SIDS and may ultimately lead to ways to identify infants most at risk as well as additional strategies for reducing the risk of SIDS for all infants."

For this study, senior author Hannah C. Kinney, MD, of Harvard Medical School and Children's Hospital Boston, and her colleagues examined small samples of tissue from the medulla, a region at the base of the brain that regulates basic functions such as body temperature, breathing, blood pressure, and heart rate. The researchers analyzed brain tissue from infants who died from SIDS and controls who died of other causes. Included in the analysis were 35 infants who died of SIDS, 5 infants who died unexpectedly of other causes, and 5 infants who were hospitalized and died for reasons associated with a lack of oxygen.

The researchers found that serotonin levels were 26% lower in tissue from infants who died of SIDS than in tissue from the group of infants who had otherwise died unexpectedly. Measurements of tryptophan hydroxylase, an enzyme needed to make serotonin, also were 22% lower.

In earlier work comparing SIDS cases with other infant deaths, researchers showed that the brains of infants who died of SIDS had higher concentrations of cells that use serotonin in the medulla oblongata, a region of the brain stem. For the current study, the researchers set out to see if this meant the SIDS infants' brains in fact had altered levels of the brain chemical.

This abnormality appears to fit into the triple-risk model of SIDS, which holds that SIDS occurs only when three elements come together: an infant with an underlying vulnerability, a critical period of development, and an external stressor. The researchers speculate in this case that the low serotonin level would cause the underlying vulnerability. The first year of life is the critical period of development for stabilizing vital functions such as breathing. The final element of the model, sleeping face down, might provide the external stressor.

"It's no one single factor but a culmination of abnormalities that result in the death," Kinney says. In fact, in 88% of the SIDS cases they examined, the researchers found two or more risk factors, such as the infant's sleep position, an illness, or exposure to cigarette smoke.

— Source: National Institutes of Health