New autopsy data provide the strongest evidence yet that
sudden infant death syndrome (SIDS) has a concrete biological basis. In the November 1 issue of the Journal of the American
Medical Association, Children's Hospital Boston researchers show that babies who die from SIDS have significant
abnormalities in the
brainstem's serotonin
system, which is thought to help coordinate breathing, blood pressure,
sensitivity to carbon dioxide and temperature.
Neuropathologist
Hannah Kinney, MD,
neuroscientist David
Paterson, PhD, and
colleagues examined
brainstem tissue from 31
infants who died from SIDS and 10 who had died from other causes. They documented the most comprehensive set of defects known to date: deficiencies in the serotonin receptor 5HT1A, an abnormally high number of
neurons that make and release serotonin; a preponderance of
immature serotonergic neurons; and insufficient amounts of the
serotonin transporter protein, which "recycles" serotonin so neurons can reuse it. Male SIDS infants had significantly fewer 5-HT1A
receptors than females, offering a possible explanation why boys
succumb to SIDS twice as often as girls.
A current theory on the cause of SIDS is that when babies sleep face-down or when their faces are covered by bedding, they re-breathe exhaled
carbon dioxide. Normally, the rise in CO2 activates neurons in the brainstem that stimulate respiratory and arousal centers in the brain, causing the baby to wake up, turn his head and breathe faster. Kinney believes that defects in the serotonin system can cause SIDS by impairing these
protective reflexes.
Although more research is needed, Kinney, Paterson and colleagues believe that factors such as maternal smoking and alcohol use during early fetal development may derail development of the brainstem serotonin system. Based on their findings, they hope to develop a diagnostic test to identify
infants at risk for SIDS. They also envision a drug to protect infants.
