NICHD-Funded Researchers Uncover Abnormal Brain Pathways in SIDS Victims

A team of researchers funded by the National Institute of Child Health and Human Development (NICHD) has found that infants who died of Sudden Infant Death Syndrome (SIDS) have abnormalities in several parts of the brainstem. The researchers presented their work at the joint meeting of the Pediatric Academic Societies and American Academy of Pediatrics societies today in Boston.

The finding builds upon the results of an earlier study that found abnormalities in the brain region known as the arcuate nucleus in children who died of SIDS.

"These findings show that SIDS infants have a more global biological deficit than we previously believed--one that may originate early in fetal life," said Dr. Marian Willinger, of NICHD's Pregnancy and Perinatology Branch.

The findings were presented by the senior author of the study, Dr. Hannah Kinney and a researcher at Children's Hospital and Harvard Medical School in Boston.

The researchers found that structures in the brainstem of SIDS infants were less likely to bind to the neurotransmitter serotonin than were the brains of infants who had died of other causes. Neurotransmitters are molecules that brain and nerve cells use to communicate. These molecules are produced in brain and nerve cells and bind to special receptor molecules on neighboring cells, in much the same way a key fits into a lock.

Serotonin is found throughout the brain. Specifically, the SIDS victims in the study were found to have decreased binding of serotonin in the nucleus raphé obscurus, a brain structure that is linked to the arcuate nucleus, as well as in four other brain regions. These brain regions are thought to play a crucial role in regulating breathing, heart beat, and body temperature, and arousal. The brain structures have their origin in a part of the rhombic lip, a region of the developing embryo that later gives rise to key structures in the brain stem.

The researchers have also published their findings in the Journal of Neuropathology and Experimental Neurology: Volume 59, Number 5, 2000, pp. 377-384.

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