Arousal responses and risk factors for sudden infant death syndrome

Abstract

Background: Failure to arouse from sleep has been postulated as a mechanism to explain the final pathway of sudden infant death syndrome (SIDS). Methods: We have reviewed the effects of the major risk factors for SIDS, prone sleep position, maternal smoking, prematurity and recent infection on arousability from sleep. In human infants it has been consistently demonstrated that arousal from sleep in response to a variety of stimuli is more difficult to induce from quiet sleep (QS) compared to active sleep (AS) over the first 6 months of life. Results: In the prone position both stimulus-induced and spontaneous arousability from both QS and AS were impaired at 2–3 weeks and 2–3 months, but not at 5–6 months of age in both term and preterm infants. In term infants exposed to maternal smoking during pregnancy both stimulus-induced and spontaneous arousability were impaired when infants slept supine in QS at 2–3 months of age. Healthy preterm infants showed no impairment in arousability compared with term infants at matched postconceptional ages. However, preterm infants with a history of apnoea and bradycardia of prematurity showed decreased arousal responses in both QS and AS and this impairment was positively correlated to their ‘perinatal risk score’. Infants who had recently suffered an infection requiring hospitalization showed decreased arousability in QS on the day of discharge when compared to 2 weeks later when they were completely well. Conclusions: In summary it has been found that the major risk factors for SIDS identified from epidemiological studies also decrease arousability from sleep in infants. We propose that this decreased arousability from sleep may be involved in the final pathway of SIDS.