A new report suggests that SIDS is associated with a defect in 1 or more components of the medullary 5-hydroxytryptamine system.
A new report suggests that sudden infant death syndrome (SIDS) is associated with a defect in 1 or more components of the medullary 5-hydroxytryptamine (5-HT) system. Investigators compared autopsy findings in 41 infants who died from SIDS with findings in 7 infants with acute death from known causes (controls) and 5 infants who had been hospitalized with chronic hypoxia-ischemia before death. Investigators measured serotonin and metabolite tissue levels in 2 major components of the medullary 5-HT system, the raphé obscurus and paragigantocellularis lateralis (PGCL); levels of 5-HT's key biosynthetic enzyme, tryptophan hydroxylase (TPH2), and 5-HT1A receptor binding density.
Compared with controls, infants with SIDS had lower 5-HT and TPH2 levels, consistent with a disorder of medullary 5-HT deficiency. Serotonin levels in both the raphé obscurus and PGCL were 26% lower in the infants with SIDS than in age-adjusted controls. In the raphé obscurus, TPH2 levels were 22% lower in the SIDS infants than in controls, and 5-HT1A receptor binding was 29% to 55% lower in 3 medullary nuclei that receive 5-HT projections. The profile of 5-HT and TPH2 abnormalities in the SIDS and hospitalized groups differed significantly, suggesting that the primary mechanisms underlying 5-HT abnormalities in SIDS are not mediated by chronic hypoxia-ischemia (Duncan JR, et al. JAMA. 2010;303:430-437).