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Published on: February 25, 2016
Arousal responses and risk factors for sudden infant death syndrome
Rosemary S C Horne1, Peter M Parslow, Dorota Ferens
1Department of Paediatrics and Ritchie Centre for Baby Health Research, Monash University, Melbourne, Victoria, Australia. rosemary.horne@med.monash.edu.au
Insights
Sudden infant death syndrome (SIDS) may be linked to infants’ difficulty waking from sleep. Major SIDS risk factors, including prone sleeping and maternal smoking, impair infant arousability, potentially explaining SIDS mechanisms.
Area of Science:
- Pediatrics
- Sleep Medicine
- Neonatology
Background:
- Sudden infant death syndrome (SIDS) remains a leading cause of postneonatal mortality.
- Arousal from sleep is a critical protective mechanism in infants.
- Failure to arouse has been proposed as a key mechanism in SIDS.
Purpose of the Study:
- To investigate the impact of major SIDS risk factors on infant arousability from sleep.
- To explore the relationship between specific risk factors and the ability of infants to respond to stimuli during sleep.
Main Methods:
- Systematic review of studies examining SIDS risk factors: prone sleep position, maternal smoking, prematurity, and recent infection.
- Analysis of infant arousal responses to stimuli during quiet sleep (QS) and active sleep (AS) in the first six months of life.
- Comparison of arousal thresholds in term and preterm infants, including those with apnea and bradycardia.
Main Results:
- Prone sleeping impaired arousal at 2-3 weeks and 2-3 months but not 5-6 months.
- Maternal smoking impaired arousal in term infants at 2-3 months.
- Preterm infants with apnea/bradycardia showed decreased arousal, correlated with perinatal risk score.
- Recent infection temporarily decreased arousal in quiet sleep.
Conclusions:
- Major epidemiological risk factors for SIDS are associated with decreased infant arousability.
- Impaired arousal from sleep may play a significant role in the final pathway of SIDS.
- Further research into arousal mechanisms is crucial for SIDS prevention strategies.
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.
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