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Respiratory control during upper airway infection:Mechanism for prolonged reflex apnoea and sudden infant death with special reference to infant sleep position

FEMS Immunology & Medical Microbiology
Oxford University Press
Publication Date
DOI: 10.1016/s0928-8244(99)00076-0
  • Laryngeal Chemoreceptor
  • Prone Sleeping Position
  • Reflex Apnea
  • Seasonality
  • Respiratory Tract Infection
  • Sudden Infant Death Syndrome
  • Mathematics


Abstract The mortality rate of sudden infant death syndrome (SIDS) has been dramatically reduced after the supine sleeping position was recommended by health authorities. Concomitant with the decline in overall mortality rate, a marked attenuation of the seasonal distribution has been observed. So far, neither a satisfactory explanation of the previously noted seasonal variation, nor a generally accepted explanation for the preventive effect of supine sleeping position has been presented. Conceivably either the effect of some yet unidentified risk factor for sudden unexpected death in infancy was more prevalent during the dark and cold months of the year during the period when infants generally slept prone, or the effect of the risk factor(s) was more potent in the prone sleeping infant. Prolonged apnoea in infancy may lead to hypoxia, bradycardia and circulatory collapse. Reflex apnoea can be elicited by stimulation of chemoreceptors in the upper airway. The cardio-respiratory response to receptor stimulation is reinforced during a respiratory tract infection. Based on our own and others’ experimental data, it is suggested that the reduction in sudden infant mortality rate and in particular the attenuation of the seasonal variation is in part an effect of the reduced likelihood of laryngeal chemoreceptors being stimulated by stagnated airway secretions during upper airway tract infection in the supine sleeping infant.

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