The study included for biochemical analysis 35 infants dying from SIDS, 5 infants with acute death from known causes (controls), and 5 hospitalized infants with chronic hypoxia-ischemia (a reduction in oxygen supply combined with reduced blood flow to the brain). Tissue samples were obtained via autopsy and levels of serotonin and several enzymes, including serotonin (5-HT) and tryptophan hydroxylase (TPH2), were measured and analyzed.
The researchers found that serotonin levels were 26 percent lower in SIDS cases compared with age-adjusted controls in the raphé obscurus and the paragigantocellularis lateralis (PGCL), regions of the brain. In the raphé obscurus, TPH2 levels were 22 percent lower in the SIDS cases compared with controls. Also, 5-HT levels were 55 percent higher in the raphé obscurus and 126 percent higher in the PGCL in the hospitalized group compared with the SIDS group.
"In this article we report the presence of lower levels of medullary 5-HT and TPH2 in infants dying from SIDS, pointing to a deficiency, as opposed to an excess, of 5-HT in the pathogenesis of the disorder," the authors write. "We now postulate that SIDS can be viewed as a disorder caused by a defect in 1 or more components of the medullary 5-HT system …"
SIDS remains the leading cause of postneonatal (from one month to one year after birth) infant death in the United States. It is believed to result from abnormalities in brainstem control of autonomic function and breathing during a critical developmental period. "Abnormalities of serotonin (5-HT) receptor binding in regions of the medulla oblongata [a region in the brainstem] involved in this control have been reported in infants dying from SIDS," the authors write. They suggest these abnormalities may play a role in the inability of an infant to respond to a life-threatening challenge, such as asphyxia, during sleep.
Citation: Duncan et al., 'Brainstem Serotonergic Deficiency in Sudden Infant Death Syndrome', JAMA, February 2010, 303(5):430-437
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