The Aetiology of the Sudden Infant Death Syndrome: Current Ideas on Breathing and Sleep and Possible Links to Deranged Thiamine Neurochemistry

Wiley - Tập 8 Số 3 - Trang 322-336 - 1978
D. J. Read1,2
1*Associate Professor of Physiology and Consultant Physiologist at Royal Prince Alfred Hospital.
2Department of Physiology, University of Sydney and Department of Perinatal Medicine, King George V Memorial Hospital

Tóm tắt

Summary: The aetiology of the sudden infant death syndrome: Current ideas on breathing and sleep and possible links to deranged thiamine Neurochemistry.The sudden infant death syndrome (SIDS) is now the commonest cause of death between one week and one year of age in most western countries. An asphyxia/ death, with unrecognised hypoxic episodes during sleep in the preceding weeks, has been postulated from autopsy evidence for both acute and chronic hypoxia; the evidence includes Po2 values, intra‐thoracic distribution of petechiae, pulmonary arteriolar and right ventricular hypertrophy. Long‐term monitoring of infants resuscitated from a “near miss” SIDS demonstrates sleep apnoea, sometimes associated with episodic collapse and obstruction of the upper airway.Physiological studies in healthy babies and animals highlight factors leading to vulnerability to asphyxia in different phases of sleep. In REM‐sleep (rapid‐eye‐movement), inhibition of intercostal muscle activity leads to: inspiratory collapse of the rib‐cage, impaired reflex compensation for airway obstruction, overall lung‐deflation with reduction of O2‐stores and rapid hypoxaemia during apnoea. In REM‐sleep, breathing efforts are not augmented by hypercapnia and the defense against asphyxia depends on reflex responses to hypoxia.Sleep apnoea sometimes occurs in infants with a rare congenital defect of brain thiamine triphosphate. This draws attention to many similarities of modern SIDS and other infantile syndromes reported historically which involve deranged thiamine neurochemistry. Sudden unexpected deaths occur in apparently thriving infants of asymptomatic thiamine deficient mothers. Other similarities include: a peak incidence at 2–4 months of age; precipitation often by minor febrile episodes; seasonal and familial risk factors, with increased risk in twins; many common findings at autopsy.Although asymptomatic maternal thiamine deficiency is common in western communities ingesting high carbohydrate diets containing various thiamine antagonists, the effect on infant thiamine stores has received little attention.Future research is needed to evaluate SIDS incidence after identification and elimination of low thiamine states. Defective neural control of breathing during sleep should be evaluated in relation to thiamine‐neurochemistry, particularly to the leaky blood‐brain barrier, to glutamate and GAB A, to sympathetic denervation and to defective vagal reflexes of the lungs and larynx.

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Wiley

Tập 8 Số 3

322-336

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