Identifying infants at risk for sudden infant death syndrome.
OBJECTIVE
This review examines recent research relevant to the underlying pathophysiology and risk factors for sudden infant death syndrome.


RESULTS
Current research focuses on the linkage between known risk factors and vulnerability, genetic contributions, and the role of dysfunctional brainstem neurotransmission in the pathogenesis of this syndrome. While social inequalities, prematurity, maternal smoking, infant sleeping practices and sleep environment, arousal failures and environmental pollutants remain important risk factors, new evidence is emerging that certain genetic polymorphisms may contribute to vulnerability. New neuropathological studies have provided strong support for abnormal brainstem serotonergic function. Since serotonin influences a wide range of physiological systems including breathing, the cardiovascular system, temperature, and sleep-wake cycles, this finding strongly supports the hypothesis that sudden infant death syndrome is the result of dysregulation of the autonomic nervous system and provides biological plausibility for certain risk reduction strategies.


CONCLUSIONS
Despite a putative diagnostic shift, sudden infant death syndrome remains the most common cause of death from 1 month to 1 year of age. Recent studies confirmed established risk factors and have suggested new genetic vulnerabilities. Finally, new evidence supports a key role for abnormalities in brainstem serotonin systems in the pathophysiology of this syndrome.
Sahni
Rakesh
R
Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. rs62@columbia.edu
Fifer
William P
WP
Myers
Michael M
MM
D000818:Animals; D020022:Genetic Predisposition to Disease; D006801:Humans; D007223:Infant; D012307:Risk Factors; D013398:Sudden Infant Death / Q000209:etiology* / Q000235:genetics