SIDS is almost invariably sleep-related. Viable syndrome aetiology must be
compatible with its many epidemiologically diverse risk factors, each of wh
ich directly or indirectly associates with the creation of psychological an
d/or physiological infant stress, and the subsequent disruption of normal,
contented sleep. During essential deep 'rebound' recovery sleep, arousal ab
ility and upper airway muscle tone decrease further to that in normal sleep
, with subsequent upper airway obstruction. When stress impact causes suffi
cient sleep disruption and physiological fatigue, a failure to arouse and s
o restore sufficient tone to overcome such obstruction results: in sudden,
unexpected death. SIDS has therefore many causes which share a final lethal
mechanical pathway. Evidence is presented Fur obstructive apnoea during sl
eep as being the primary syndrome death mode, for sleep disruption, reduced
arousal ability, and infant stress in SIDS, and for risk factor associatio
n with the creation of this stress. Specific infant vulnerability in the fi
rst 6 months of life to stress predominantly I-elated to total dependency o
n a carer for gratification of need, and to obstructive sleep apnoea due to
normal anatomical, physical, and respiratory immaturity , including rapid
physiologic al fatigue, and peaks in sleep and thermal stress vulnerability
, are discussed. Further reasons fur the limited age period of SIDS, and fo
r reduced neonatal risk, are given. Prone sleeping risk can relate to posit
ional airway obstruction during normal sleep without prior infant stress. M
uch of SIDS aetiology appears to concern factors related to socio-economic
deprivation and subsequent sub-optimal infant care. (C) 2001 Elsevier Scien
ce Ireland Ltd. All rights reserved.