Elsevier

Early Human Development

Volume 66, Issue 2, February 2002, Pages 89-100
Early Human Development

Arousal from sleep in infants is impaired following an infection

https://doi.org/10.1016/S0378-3782(01)00237-7Get rights and content

Abstract

Numerous studies have postulated a link between recent infection and Sudden Infant Death Syndrome (SIDS). In this study we contrasted arousal responses from sleep in infants on the day of discharge from hospital following an infection with those when fully recovered and also with well age-matched control infants.

Thirteen term infants comprised the infection group and nine well infants acted as age-matched controls. All infants were studied using daytime polysomnography and multiple measurements of arousal threshold (cm H2O) in response to air-jet stimulation applied alternately to the nares were made in both active sleep (AS) and quiet sleep (QS).

All infants were studied on two occasions: firstly, immediately before discharge from the Paediatric ward, and secondly, 10–15 days later when they were completely well in the case of the infection group.

Arousal thresholds in QS in the infection group were significantly elevated on the day of discharge (262±48 cm H2O) compared with 10–15 days later (205±31 cm H2O, p<0.05). Thresholds in the control group were not different between studies.

This study provides evidence that arousability from QS is impaired following an infection and we postulate that this may explain the increased risk for SIDS following infection observed in previous studies.

Introduction

Although the underlying pathophysiological processes involved in Sudden Infant Death Syndrome (SIDS) are still unexplained, significant progress in the understanding of a number of risk factors associated with SIDS has been made through extensive epidemiological studies. Many of the developmental and environmental risk factors associated with SIDS are also associated with susceptibility of infants to infection, particularly that of upper respiratory tract infection. The number of SIDS cases is greater during winter [1], coinciding with the seasonal increase in respiratory viral infections [2]. The peak period for vulnerability to SIDS, between 2 and 4 months of age, is also the period when infants are particularly vulnerable to infection as stores of maternal antibodies are decreased before the infant's immune system has fully matured [3], [4]. In addition, infants have been demonstrated to be particularly vulnerable to heat stress during this period [5]. SIDS occurs more frequently in the lower socio-economic classes in developed countries in which infectious diseases are also more common [6].

Infection can also been linked with the major risk factors for SIDS. The prone sleeping position, identified as the major risk factor for SIDS in numerous studies, [1], [7], [8], [9], [10], [11], [12] has been found to be an even greater risk when associated with a recent illness [9]. In addition, bacterial counts from nasal swabs were elevated when infants slept prone [13]. Many studies have found that maternal smoking is associated with an increased incidence of SIDS [10], [11], [14] and infants and children with parents who smoke have increased levels of respiratory tract infections [15]. Cigarette smoke may also alter the pathophysiology following viral infections [16]. Approximately half of the SIDS victims in some studies had slight respiratory infection prior to death [4].

Infection also changes both the amount and nature of sleep in both humans and animals, quiet sleep (QS) being increased in both depth and duration [17], [18]. The close temporal association between SIDS and sleep has led to the hypothesis that SIDS may result from a failure to arouse from sleep [19]. In previous studies our group have demonstrated that arousal thresholds in QS are elevated compared to active sleep (AS), and that QS thresholds increase with the length of time the infant has been asleep in both term and preterm infants [20], [21]. In addition. infection is often associated with sleep fragmentation, which is known to impair arousal responses in both animals and humans [22], [23]. In the current study we investigated the effects of a recent infection on arousability from sleep.

Section snippets

Subjects

Approval for this project was granted by the Monash Medical Centre Human Ethics Committee and infants were studied after informed parental consent was obtained. Subjects were recruited from the Paediatric ward at Monash Medical Centre, Melbourne. The patient admissions book was examined daily for infants born at term (38–42 weeks of gestation), aged between 1 and 4 months with a diagnosis of either a respiratory infection or nonrespiratory infection. A paediatrician (TMA) confirmed the

Demographics of the study groups

There was no difference between the mean gestational age at birth or birth weight of the infection and control groups of infants, nor was there a difference between the mean ages at which the two groups were studied.

Arousal threshold

In the infection group of infants (N=13) arousal thresholds in QS were significantly elevated on the day of discharge at Study 1 (262±48 cm H2O) compared with Study 2 (205±31 cm H2O) when infants were fully recovered (p<0.05). There was no significant difference between the mean

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 [19]. Moreover, it has been postulated that the increased risk for SIDS associated with infection may result from elevated body temperatures during infection [26]. This study has provided evidence that arousal from QS is impaired in infants following a recent infection.

Arousal thresholds determined for the

Acknowledgements

This project was supported by the Sudden Infant Death Research Foundation of South Australia. The authors thank the staff of the Paediatrics Ward at the Monash Medical Centre, and the parents and infants who participated in this study. We also wish to thank Professor Adrian Walker for his comments on drafts of this manuscript.

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