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Central serotonin pathways implicated in sudden infant deaths

BMJ 2006; 333 doi: https://doi.org/10.1136/bmj.333.7576.1013-c (Published 09 November 2006) Cite this as: BMJ 2006;333:1013

The exact cause of sudden infant death syndrome (SIDS) is unknown. But evidence is mounting that the defect lies somewhere within the serotonergic pathways of the medulla oblongata. The latest neurological study found clear and significant differences in serotonin neuropathology between 31 SIDS cases and 10 control infants who had died from accidents, infections, or congenital disease. Medullary samples from the cases had more serotonergic neurones, a lower density of one type of serotonin receptor, and a relative lack of the serotonin transporter compared with similar samples from controls, suggesting fairly extensive defects in synthesis, release, and clearance of serotonin, and therefore neurone firing, associated with SIDS.

The authors suspect that these defects are developmental and could interfere with the usual autonomic mechanisms regulating breathing and other functions during sleep. A child with defective central serotonin pathways may not respond properly to transient hypoxia or hypercarbia when face down for example, or when sharing a bed with an adult.

The study was small, and the controls were less than ideal—pre-existing disease might have unknown effects on markers of serotonin function—but a linked editorial says the weight of evidence now favours a role for serotonin in the pathogenesis of at least some cases of SIDS (pp 2143-4).

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