Sudden infant death syndrome: a theory

Neurosci Biobehav Rev. 1993 Fall;17(3):305-12. doi: 10.1016/s0149-7634(05)80014-4.

Abstract

A hypothesis, and supporting evidence, is presented for the sudden infant death syndrome (SIDS). Our model is as follows. Fetal hemoglobin levels are abnormally elevated in SIDS infants, which contributes to a state of chronic hypoxia. Chronic hypoxia produces pronounced depressive effects on the respiratory system during slow wave sleep (a state of normal respiratory depression). These depressive effects are particularly manifest during that period of development in which slow wave sleep begins to occupy a very large percentage of total sleep time in infants -2-4 mo of age. A downward spiral is initiated in slow wave sleep such that hypoxia-induced decreases in ventilation produce more extreme hypoxia leading to further respiratory depression and ultimately death due to a cessation of respiration.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Female
  • Fetal Hemoglobin / metabolism*
  • Fetal Hypoxia / blood*
  • Humans
  • Infant
  • Infant, Newborn
  • Pregnancy
  • Sudden Infant Death / blood*
  • Sudden Infant Death / etiology

Substances

  • Fetal Hemoglobin