Elsevier

Sleep Medicine

Volume 3, Supplement 2, December 2002, Pages S61-S65
Sleep Medicine

Arousal responses and risk factors for sudden infant death syndrome

https://doi.org/10.1016/S1389-9457(02)00168-5Get rights and content

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.

Introduction

Despite the dramatic decline in the incidence of sudden infant death syndrome (SIDS) following world-wide education programmes, SIDS still remains the major cause of death in infants between 1 month and 1 year of age [1], [2]. Arousal from sleep is believed to be an important survival mechanism that may be impaired in victims of SIDS [3]. A prospective study found that infants who subsequently died from SIDS had fewer body movements during sleep compared with controls [4]. Additionally, post-mortem examinations of infants dying of SIDS have identified abnormalities in brain regions associated with arousal [5].

Epidemiological studies in a number of western countries have identified various factors, which increase the risk of an infant dying from SIDS. The prone sleeping position has been identified as one of the major risk factors for SIDS in numerous studies [6], [7], [8], [9], [10], [11]. With the reduction in the incidence of infants being put to sleep prone, maternal smoking has become the major modifiable risk factor for SIDS [6]. Preterm and low birth-weight infants are also at increased risk for SIDS, and this increase is inversely related to gestational age [12], [13], [14], [15], [16], [17]. It has been estimated that approximately 20% of all SIDS cases occur in the preterm population [15], [16], [17]. Approximately half of the SIDS victims in some studies had slight respiratory infection prior to death [18]. Many of the developmental and environmental risk factors associated with SIDS, such as peak age of occurrence, seasonal distribution, prone sleeping and maternal smoking, are also associated with susceptibility of infants to infection, particularly that of upper respiratory tract infection [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29].

This paper will review the effects of these major risk factors for SIDS on infant arousability. The studies will focus on the work carried out by our laboratory over the past 5 years.

Section snippets

Methods

All subjects were recruited from the Monash Medical Centre, Melbourne, Australia. Written informed consent was obtained from parents prior to commencement of the study, and no monetary incentive was provided for participation. The Monash Medical Centre Human Ethics Committee granted approval for these projects.

Sleep state

Our studies have shown that arousal from sleep in response to air-jet stimulation is affected by sleep state in both term and preterm infants, with arousal thresholds being significantly elevated in QS compared to AS [31], [32], [33], [34], [35], [36], [37]. We have recently demonstrated that the same sleep-state difference in arousability occurs in response to 15% O2 over the first 6 months of life when arousability is measured as both probability of arousal and arousal latency [38].

Sleeping position

We have

Discussion

Arousal from sleep is an important response that may protect an infant from a life-threatening event and impairment in arousability has been postulated as a likely mechanism to explain SIDS [3]. Our studies have demonstrated that the major risk factors for SIDS identified from epidemiological studies, prone sleeping position, maternal smoking, prematurity and recent infection, also decrease arousability from sleep in infants. We propose that this decreased arousability from sleep may be

Acknowledgements

This project was supported by SIDSaustralia, Sudden Infant Death Research Foundation of South Australia and SIDassist.

References (58)

  • P. Franco et al.

    Prenatal exposure to cigarette smoking associated with a decrease in arousal in infants

    J Pediatr

    (1999)
  • K.L. Lewis et al.

    Deficient hypoxia awakening response in infants of smoking mothers: possible relationship to sudden infant death syndrome

    J Pediatr

    (1995)
  • F. Marchal et al.

    Ventilatory and waking response to laryngeal stimulation in sleeping mature lambs

    Respir Physiol

    (1986)
  • B.T. Thach

    Sleep, sleep position, and the sudden infant death syndrome: to sleep or not to sleep? That is the question

    J Pediatr

    (2001)
  • T. Dwyer et al.

    The decline in SIDS: a success story for epidemiology

    Epidemiology

    (1996)
  • B. Guyer et al.

    Annual summary of vital statistics 1997

    Pediatrics

    (1998)
  • Changing concepts of sudden infant death syndrome: implications for infant sleeping environment and sleep position

    Pediatrics

    (2000)
  • A. Kahn et al.

    Sleep and cardiovascular characteristics of infant victims of sudden death: a prospective case-control study

    Sleep

    (1992)
  • H.C. Kinney et al.

    Decreased muscarinic receptor binding in the arcurate nucleus in sudden infant death syndrome

    Science

    (1995)
  • E.A. Mitchell

    Sleeping position of infants and the sudden infant death syndrome

    Acta Paediatr

    (1993)
  • A.-L. Ponsonby et al.

    The Tasmanian SIDS case-control study: univariate and multivariate risk factor analysis

    Paediatr Perinatal Epidemiol

    (1995)
  • H. Brooke et al.

    Case control study of sudden infant death syndrome in Scotland, 1992–5

    Br Med J

    (1997)
  • E.A. Mitchell et al.

    Risk factors of sudden infant death syndrome following the prevention campaign in New Zealand: a prospective study

    Pediatrics

    (1997)
  • H. Oyen et al.

    Combined effects of sleeping position and the perinatal risk factors in sudden infant death syndrome: the Nordic epidemiological SIDS study

    Pediatrics

    (1997)
  • M.H. Malloy et al.

    Prematurity, sudden infant death syndrome and age of death

    Pediatrics

    (1995)
  • H.J. Hoffman et al.

    Risk factors for SIDS: results of the National Institute of Child Health and Human Development SIDS cooperative epidemiological study

    Ann N Y Acad Sci

    (1988)
  • D.R. Peterson

    Sudden unexpected deaths in infants. An epidemiologic study

    Am J Epidemiol

    (1966)
  • S.J. Standfast et al.

    The epidemiology of sudden infant death syndrome in upstate New York

    J Am Med Assoc

    (1979)
  • L. Stoltenberg et al.

    Does immunostimulation play a role in SIDS

  • Cited by (0)

    View full text