Babies who die of sudden infant death syndrome usually appear to thrive right up to their last moments. It often seems as if the babies simply forgot to breathe.
Even autopsies have failed to reveal abnormalities associated with SIDS. However, a new study has found brain stem anomalies that may be at fault. They undermine the action of the chemical serotonin, which is critical to respiration, the researchers conclude.
Because the brain stem controls automatic functions such as breathing, problems within that structure have been considered culprits in SIDS. Previous studies found that babies who died of SIDS had fewer serotonin receptors in their brain stems than other babies did. The new study bolsters that finding and reports other abnormalities in the use of serotonin, notes David S. Paterson of Children’s Hospital Boston.
In the new study, Paterson, Hannah C. Kinney, also of Children’s Hospital, and their colleagues compared the brains of 31 infants who died of SIDS with those of 10 infants who had died suddenly of other causes. The scientists found that the babies who died of SIDS had as few as half as many serotonin receptors as the others did.
Surprisingly, the team also found that the neurons that produce serotonin were 30 percent to 50 percent more abundant in the babies that died of SIDS than in the other infants. Furthermore, in the babies that died of SIDS, each cell on average had fewer of the structures that recycle serotonin.
“There’s no doubt to us that there is a problem with the serotonin system,” Paterson says. He and his colleagues report the findings in the Nov. 1 Journal of the American Medical Association.
Today, researchers can detect such abnormalities only after an infant has died, but further work may lead to methods to determine which babies are at high risk of SIDS and, ultimately, to treatments for preventing it. Currently, doctors recommend preventive measures for all babies, including putting babies to sleep on their backs to ease breathing.
“This study makes it clear that infants who die with SIDS have many anomalies with serotonin function,” says Jack L. Feldman of the University of California, Los Angeles. He cautions, however, that other brain-chemical systems have not been thoroughly studied and may play equally strong roles.
Ralph E. Fregosi of the University of Arizona in Tucson admires the new work but says that the significance of the reported anomalies isn’t clear. The physical changes that the team found don’t necessarily imply that those parts of the brain were working badly. “There’s this hole in their beautiful anatomical data related to the function of the system,” he says.