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Potential Neuroregulatory Basis for SIDS

Friday, 25 July 2008 22:50 F. Bruder Stapleton, MD
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SIDS cases had significantly more serotonergic system abnormalities than did controls.

Summary

Although sudden infant death syndrome (SIDS) is the leading cause of mortality during the first year of life, no unifying neurophysiologic basis has been identified. The serotonergic (5-hydroxytryptamine [5-HT]) system of the medulla oblongata helps regulate autonomic and respiratory function and has been implicated as a cause of SIDS. Investigators in California compared markers of 5-HT function in frozen medullae obtained at autopsy in 31 infants (15 males) who died from SIDS and 10 infants (8 males) who died suddenly from other causes (controls).

The number of medullary 5-HT neurons was significantly higher in SIDS cases than in controls. In most nuclei analyzed, 5-HT1A receptor binding density was significantly reduced in SIDS cases. Although 5-HT transporter (5-HTT) binding did not significantly differ between cases and controls, the ratio of 5-HTT binding density to 5-HT neuron count was significantly lower in SIDS cases. The mean 5-HT1A receptor binding density was significantly lower in male SIDS cases than in female SIDS cases; the mean binding density for both male and female cases was significantly lower than the binding density for controls. In an analysis that compared markers among subsets of SIDS cases with different risk factors, the authors found no association between 5-HT neuron count or 5-HTT binding density and other SIDS risk factors.

Comment

These data demonstrate extensive abnormalities in the serotonergic system of the medulla oblongata in a small group of predominantly white SIDS victims. Further studies to determine how the 5-HT neuroregulatory system might lead to sudden death are imperative. The fact that more than half of SIDS cases in this study were sleeping prone or on their sides at the time of death reminds us of the need for continued support of the Back to Sleep campaign.

Reviewed by Ramaz Mitaishvili, MD

 
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