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Autonomic function and SIDS

There is an extensive literature suggesting that disordered autonomic function, including cardiorespiratory control, may be involved in sudden infant death syndrome (SIDS), by rendering an infant liable to sudden death in a variety of ways, from loss of cardiorespiratory, upper airway or temperature control, singly or in combination (1-4) Adults with autonomic neuropathy are known to die suddenly and unexpectedly ( 5 ) . Infants with SIDS and/ or an apparent life-threatening event (ALTE) have been shown to have decreased beat-to-beat variability, a higher resting heart rate (6) and excessive sweating (7) compared with controls, all of which can indicate autonomic dysfunction in adults. In 1959, Gastaut & Gastaut demonstrated increased potency of the oculocardiac reflex in children under five years of age and that the younger the subject the more easily is cardiac arrest caused through vagal sensitivity (8). Further interest in autonomic dysfunction and SIDS was demonstrated by Salk et al. in 1974 (9) and by Schwartz et al. 1976 (10). The recent report of recurring hypothermia in ALTE infants may be additional evidence of poor autonomic control of heat production in brown fat (sympathetic cholinergic activity) ( 1 I ) . In addition, maintenance of upper airway expiratory resistance, which is important in maintaining a functional residual capacity, and thereby protecting against end-expiratory apnoea, is under autonomic control.