Although the cause of SIDS deaths remains unknown, a new study sheds light on what researchers suspect will be an important clue that could lead to new treatments.

The scientists describe a group of brain cells that are responsible for gasping. When infants don’t get enough oxygen they become hypoxic, and gasping is the way normal breathing is restored.

But if these so-called respiratory pacemaker cells malfunction, a baby doesn’t gasp, breathing doesn’t restart, and SIDS is the result, they speculate.

“We think that in children who die of SIDS, gasping is disturbed and sighing is disturbed,” explained lead researcher Jan-Marino Ramirez, an associate professor of organismal biology and anatomy from the University of Chicago. “The sigh and the gasp are very important resuscitation mechanisms.”

When babies are placed on their tummy, their airways can become blocked. Normally, infants will start to sigh and gasp, which wakes them up and restores breathing.

“What we suspect in SIDS babies is that they don’t have this defense response,” Ramirez said. “They don’t generate a sigh, and they don’t generate the gasp, which is why they slowly become more and more hypoxic.”

Other studies have shown that SIDS infants have reduced sighs and disturbed gasping, Ramirez noted.

In experiments with brain cells, or neurons, Ramirez’s team looked at nerve cells responsible for sighs and gasps. They found that when hypoxia occurs, most neurons shut down, according to their report in the July 8 issue of Neuron.

“The only neurons that are active during hypoxia are those that depend on sodium channel mechanisms,” Ramirez said. A sodium channel is a protein channel that allows only sodium ions to pass through it.

“When you have to gasp, you need these sodium mechanisms,” he said. “If you block them, as we did, then you eliminate the gasp.”

Other studies have found that SIDS babies have decreased levels of serotonin, an important neurotransmitter involved in many body functions, including breathing. “When there is a decrease in serotonin, there is decreased activation of these gasping neurons,” Ramirez said.

“This finding is the missing link,” Ramirez said. “People knew that gasping and sighing was disturbed, and we knew that serotonin was disturbed, but we were not able to connect the two. Now we can.”

Ramirez believes that if this finding proves to be true, one could look for sodium channel mutations that may affect breathing. “We might be able to identify infants prone to SIDS,” he said.

Ramirez cautions that SIDS results from a combination of factors, including serotonin and sodium channel problems as well as sleep position. “If they all come together, then you have SIDS,” he said.

Disruptions in sodium channels are also related to heart rhythm problems and epilepsy, both of which are common in SIDS-prone children, Ramirez said.

Ramirez is continuing to look into the SIDS problem by experimenting with serotonin and sodium channels in mice.

SIDS expert Dr. Warren G. Guntheroth, a professor of pediatrics at the University of Washington, thinks the findings of this study are interesting but have no clinical value.

Guntheroth agrees there are two separate neurological functions, one that controls normal breathing and another that controls gasping, and that gasping is triggered by hypoxia.

“However, if you have trouble with your sodium channel, you probably have an inherited disorder. And SIDS is not inherited,” he said. “All of the things that would make SIDS an inherited disorder are not there, based on the recurrence rates of SIDS in families.”

Disorders in the sodium channel and decreased serotonin levels raise serious questions about cause and effect, Guntheroth said. “There is no way on earth that you can tell after death whether that was a result or the cause of death,” he added.

Asked whether the work by Ramirez and other researchers is identifying causes of SIDS, Guntheroth said, “No. They still remain a mystery.”