Development of infant sleep processes

The development of infant sleep processes occurs parallel to and in conjunction with physical and cognitive development. Sleep evolves rapidly in the first year of life and outcomes depend on both developmental and ecological factors. Nighttime sleep duration increases with age (generally nighttime sleep becomes consolidated and daytime sleep decreases in the first year of life) and becomes stable at 6 to 17 months. Most variability occurs in the first 5 months, though sleep in the first year is highly variable overall. This large variability may reflect differences in environmental factors ; however, the impact of intrinsic factors should also be highlighted.

The development of infant sleep processes occurs as biological rhythms including body temperature changes and hormones such as melatonin and cortisol reach mature levels. The coordination of these biological rhythms and their synchronization with the times of day develop rapidly over the first 6 months of life to develop the circadian system. Infants are born with low levels of melatonin (transferred from the mother), which dissipate by 1 week, and infant melatonin secretion does not rise to detectable levels until approximately 6 weeks. Melatonin levels are still very low at 12 to 16 weeks, but by 6 months, they are a stable part of the sleep-wake cycle. Exposure to morning light decreases daytime melatonin production and is an important part of developing a consolidated sleep schedule. Temperature rhythms generally mature earlier at about 1 week. Early morning waking coordinates with increased body temperature by about 6 weeks, at approximately the time when melatonin first becomes detectable. Weeks later, nighttime sleep, sundown, and the decrease in body temperature become coordinated and the duration of nighttime sleep begins to increase. Cortisol secretion is also related to the sleep-wake cycle. Secretion peaks in the early morning and triggers an increase in glucose and metabolism during the day when energy demand is highest. Cortisol is at its lowest at about 12 to 4 a.m. when melatonin production is higher. Overall, the circadian pattern of sleeping at night and being awake during the day develops in the first 4 to 6 months of life.

In addition to the biological development of sleep processes, the rapid acquisition of new skills and abilities during the first year of life can affect infant sleep. Infants develop an understanding of object permanence and can experience separation anxiety, which generally peaks between 6 and 18 months. Separation anxiety can lead to increased sleep disruptions—both difficulty separating at bedtime and difficulty self-soothing and returning to sleep independently during nighttime arousals. Additionally, the development of new gross motor skills can negatively influence sleep, particularly sitting up, pulling to stand, and walking, as infants will often experiment with new skills during brief nighttime arousals leading to longer, more sustained arousals. As new motor skills begin to emerge, infants can get “stuck” until they have mastered a particular skill. For example, around 9 months of age, babies can often pull to stand but may have difficulty getting back to sitting or lying down without help.

Infant insomnia

Insomnia in infants is generally characterized by difficulty falling asleep independently as well as night wakings and is influenced by both developmental and behavioral/ecological factors. Because infants’ feeding and sleep schedules are emerging, difficulty falling asleep and night wakings are generally not characterized as insomnia before age 6 months. As many as 20% to 30% of parents complain about night wakings. ^, A higher number of night wakings has been associated with ecological factors such as breastfeeding back to sleep, not sleeping in a separate room, giving a bottle during the night, bringing the child into the parents’ bed, and an irregular bedtime routine. ^, In addition to the environmental factors that are typically modifiable, there are also intrinsic factors associated with infant insomnia including temperament, prematurity, and neurodevelopmental conditions. While other factors impact infant insomnia, including maternal factors, substance exposure, and sleep disorders such as obstructive sleep apnea, those are outside the scope of this chapter.

Temperament and insomnia

Temperament is generalized as the individual differences in emotional reactivity and mood that are biologically determined and stable across the lifespan. Infant temperament can be categorized as easy, slow-to-warm-up, and difficult, though these can also be understood as the level of inborn reactivity to stimuli. Certain inborn temperament traits may, to some extent, mediate infant sleep quality, for example, through the ability to “self-soothe.” Infant sleep and temperament variables have notable effects on each other and on familial variables in an interactive way. As an infant’s temperament becomes more reactive or “difficult,” more disruptions in sleep can be observed.

Studies on infant sleep and temperament have found a correlation between infant sleep and reactivity. For example, infants with a negative reactivity type (also described as a negative mood) were found to have more symptoms of insomnia. Mindell and Lee assessed infant sleep and mood in a large sample ( n = 1351) of mothers and infants (ages 3–13 months) in Brazil. Significant relationships were identified between sleep and mood, as measured by the Brief Infant Sleep Questionnaire (BISQ). Parental perception of infant mood was correlated with sleep outcomes, including night wakings, nighttime sleep duration, and parent reports of sleep problems. In addition, negative mood was related to increased sleep fragmentation and decreased sleep duration, including later bedtime, earlier wake times, and increased sleep problems. Another study by De Marcas et al. utilized objective measures of sleep (actigraphy) and infant reactivity (laboratory measures) at 3, 6, and 12 months of age. An inverse effect was found, particularly in girls, wherein higher reactivity was associated with lower sleep quality. Both hyper- and hyporeactivity predicted poor quality sleep among infants at all time points. The authors suggested that these results may account for some inconsistencies in the relationship between infant temperament and sleep. An additional longitudinal study utilized maternal reports of infant sleep duration, night wakings, and temperament. Infants with more reactive temperaments, particularly boys, had shorter sleep duration and a greater number of night awakenings.

Infant sleep has also been demonstrated to relate to the temperamental characteristics of approachability, adaptability, and emotion regulation. A longitudinal study that sought to assess the relationship between infant sleep/wake patterns, temperament, and development over the first year of life assessed infants at 3, 6, and 11 months via parental sleep diaries, actigraphy, the Early Infant Temperament Questionnaire (EITQ), and the Revised Infant Temperament Questionnaire (RITQ). All three time points studied showed that nocturnal sleep was positively correlated with the temperamental trait of increased approachability. At 11 months, increased diurnal sleep was correlated with increased adaptability, and at 12 months, decreased daytime sleep was correlated with better levels of emotion regulation.

A more recent longitudinal study on infant temperament and sleep revealed some aspects of temperament measured at 6 months of age were related to greater sleep problems at 12 months. In this study, mothers of over 1000 infants rated infant temperament using The Infant Behavior Questionnaire-Revised Short Form (IBQ-R-SF) and infant sleep using the BISQ at both 6 and 12 months of age. The authors found higher Negative Affectivity at 6 months of age was significantly related to greater sleep problems (increased night wakings, long sleep-onset latency, and ability to fall asleep independently) at 12 months after controlling for sleep quality at 6 months. Additionally, Regulation and Surgency traits at 6 months were associated with ability to fall asleep independently at 12 months. These findings suggest temperament is related to later sleep problems in infants within the first year of life.

While temperament is understood to be set at birth, maternal and familial factors have been shown to affect temperament and infant sleep. One study examined the moderating link of infant temperament on mothers’ emotional availability (EA) at bedtime and objectively assessed infant sleep development from 1 to 6 months via actigraphy. In a sample of 72 mother-infant dyads, infant sleep was assessed via actigraphy, and maternal EA and maternal reports of infant temperament were coded from bedtime videos at 3 and 6 months. While little evidence was found to support the main effects of either infant temperament or maternal EA, the results indicate a strong effect of infant temperament, particularly surgency (the tendency to experience and maintain positive affect), moderating the link between maternal EA at bedtime and infant sleep duration.

Furthermore, infant sleep and temperament have been shown to be associated with both maternal depression and family functioning. In one longitudinal study, 131 families were assessed with temperament and sleep data collected at the 8-month time point and maternal depression data collected at 15 months. Variability in infant sleep efficiency moderated the relationship between infant temperament and maternal depressive symptoms. Difficult temperament in the infant was associated with maternal depressive symptoms when infant sleep efficiency was variable, but not when infant sleep efficiency was consistent. These results highlight the complex links between infant sleep, temperament and maternal mental health.

Current research demonstrates that infants with more difficult temperament experience increased insomnia symptoms. While typical developmental processes and temperament relate to insomnia symptoms, other intrinsic factors such as prematurity and neurodevelopmental conditions also play a role.

Prematurity and insomnia

Many infants born preterm have sleep problems, altered sleep patterns, and increased insomnia symptoms as compared to term counterparts. For example, preterm newborns have been shown to spend 90% of each day sleeping as compared to term newborns, who spend about 70% of their day asleep. Sleep disruptions often occur in preterm infants due to features of neonatal intensive care including continuous light and sound which disrupt circadian rhythms, respiratory support, and a variety of comorbidities.

Recent studies suggest that preterm birth impacts sleep duration and night wakings, possibly in contradictory ways. One cross-sectional study looked at the sleep characteristics of very low-birth-weight (birth weight <1500 g) infants compared to full-term infants at the age of 12 months to examine whether the sleep behaviors of preterm infants differed from those of full-term infants. The authors found that at 1 year after preterm birth, preterm infants had a greater number of night wakings and slept less during the night than term counterparts. A successive study by the same authors found an overall reduction in overall sleep duration in preterm infants compared to term infants, when measured at 1 and 2 years of age. Conversely, other studies have found that preterm infants had increased sleep duration as compared to term infants. Even with increased sleep duration, more night wakings were noted. One study found that compared to term controls, 6-month-old infants born preterm had longer nocturnal sleep duration, more night awakenings, and longer daytime sleep.

Several studies have found no significant difference in the sleep of preterm and term infants. One study found no differences in parental reports of sleep duration, number of night wakings, or sleep-onset difficulties in preterm infants (median 34.1 weeks gestational age) and term controls. Similarly, a study by Hoppenbrouwers and colleagues found that beyond the neonatal period, preterm birth does not impact the development of sleep states, with a similar percentage of time spent in active sleep, quiet sleep, and wake time.

While there is variability among study results, many preterm infants have altered sleep patterns characterized by insomnia symptoms such as increased night wakings. It is clear that further studies are needed, given the lack of research on the impact of preterm sleep on sleep outcomes. This is especially true as several mediators may impact the relationship between gestational age at birth and sleep development, such as the degree of prematurity, growth restriction in the fetus, sleep-disordered breathing, occurrence of neurodevelopmental disorders, and chronic inflammation. ^,

Neurodevelopmental conditions and insomnia

Neurodevelopmental disorders manifest in early development and cause specific or global deficits in learning and cognition which are evidenced across areas of functioning including sleep. Infants with certain neurodevelopmental conditions do not display the same trajectory of sleep as typically developing infants and are at a greater risk of having insomnia symptoms. While there are neurodevelopmental conditions that are associated with poor sleep (e.g., motor disorders), we limit our discussion to those conditions which can be diagnosed in infancy and which have evidence of sleep disruption. Namely, autism spectrum disorder, trisomy 21, intellectual disability, and other neurogenetic syndromes characterized by disrupted sleep (e.g., Smith-Magenis syndrome). Congenital blindness and visual impairment, which can cooccur with neurodevelopmental conditions, are also associated with insomnia symptoms due to the impact on the circadian system.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with a high rate of comorbid sleep problems. The prevalence rate of sleep problems is between 50% and 80% in children with ASD. Insomnia symptoms in ASD typically include prolonged sleep onset, prolonged night wakings, early wakings, difficulty maintaining sleep, and daytime fatigue. While symptoms of ASD may be present during infancy, ASD is most commonly diagnosed after 3 years of age (e.g., van’t Hof et al.). As such, very little research has been conducted on infant sleep disturbance in ASD. A recent study of parent-reported sleep characteristics using the BISQ for over 1000 infants revealed the frequency of night wakings at 12 months old is associated with ASD screening scores at 24 months old. In contrast, ratings of nighttime and anytime sleep and sleep onset latency at 12 months were not found to relate to ASD screening scores at 24 months. MacDuffie and colleagues examined differences in parent-reported sleep onset difficulties using the Infant Behavior Questionnaire-Revised (IBQ-R) in infants at low and high risk of developing ASD, as well as infants at high risk who did and did not develop ASD. Sleep onset difficulty ratings and structural neuroimaging data were collected at 6, 12, and 24 months to examine the relation between sleep problems and subcortical brain volumes. Results of this study revealed sleep onset difficulties were more common in 6- and 12-month-old infants who were later diagnosed with ASD. This study also found a relationship between sleep onset problems in high-risk infants who developed ASD and hippocampal volume trajectories between 6 and 24 months. Though more research is needed, these preliminary findings suggest night wakings and sleep onset problems may precede ASD diagnosis.

Trisomy 21, also known as Down syndrome, is the most common genetic cause of intellectual disability (ID) and is associated with sleep disorders. While obstructive sleep apnea (OSA) is known to be prevalent in infants with trisomy 21 (e.g., Goffinski et al.), less is known about behavioral sleep disturbances in trisomy 21 within the first year of life. Studies that have examined behavioral sleep disturbances in children with trisomy 21 have included a large age range (e.g., birth to 18 years in Rosen et al.), have not included a control group, or have used measures not validated for infants. Very few studies have examined sleep in trisomy 21 with infant-only samples. McKay and Angulo-Barroso (2006) investigated sleeping patterns and leg activity overnight in infants 3 to 6 months with trisomy 21 using ankle activity monitors over 48 hours. Infants with trisomy 21 had more sleep disturbances compared to TD infants, including less sleep, more night activity, and greater sleep fragmentation. In a recent study by Yau et al. infant and toddler sleep habits in 104 individuals aged 6 to 36 months with trisomy 21 and 489 TD individuals of the same age range were measured with the BISQ. Parent-report of sleep habits revealed parents of infants and toddlers with trisomy 21 had more sleep problems, room sharing, and reduced night-time and total sleep over 24 hours. Parents in the trisomy 21 group were also more likely to be present when their child fell asleep. While snoring accounted for increased night waking, it did not account for reduced sleep time, whereas parental presence did. When controlling for snoring and parental presence during sleep onset, children with trisomy 21 had no significant difference in duration of sleep over a 24-hour period, as they slept less at night but more during the day. These findings suggest signs of insomnia such as parental presence at bedtime, more night activity, and greater sleep fragmentation may also contribute to sleep loss in infants with trisomy 21 in addition to sleep-disordered breathing.

Insomnia symptoms such as long sleep onset latency, night and early morning wakings, and bedtime struggles are more common in children with intellectual disability (ID) than in typically developing children, with prevalence rates varying between 23% and 86%. ^, Insomnia symptoms vary by neurodevelopmental condition, and many studies on children with ID include mixed groups with some having a specific genetic diagnosis and others not. As with research on other neurodevelopmental populations, very little sleep research has been conducted on infants with various forms of ID. Thus, while insomnia has been frequently documented in children with ID, more research is needed to determine whether insomnia symptoms emerge within the first year of life.

Smith-Magenis syndrome (SMS) is a genetic disorder characterized by neuropsychological and behavioral difficulties, as well as sleep disruptions typically related to inverted circadian rhythm of melatonin. ^, While sleep disruption related to inverted circadian rhythms has been documented in children and young adults with SMS, ^, very little is known about sleep in infants with this condition. Most research on the development of infants with SMS to date has been conducted using very small sample sizes using subjective descriptions, chart reviews, and retrospective observations. Observations of infants with SMS have revealed reduced overall sleep, lethargy, and placid behavior, ^, which could be related to insomnia and/or circadian rhythm problems. However, more research is needed to determine whether infants with SMS display symptoms of insomnia or whether inverted circadian rhythms are the primary sleep problem in this population.

Infants with congenital blindness and visual impairment (VI) are at greater risk of having sleep difficulties due to reduced light input which impacts melatonin production and sleep-wake patterns. Parents of young children who are blind or VI have reported settling difficulties as well as prolonged and more frequent night wakings relative to TD children. Fazzi and colleagues’ (2008) study included infants as young as 10 months and slightly over half the sample was under 20 months, suggesting insomnia symptoms of settling difficulties and night wakings may present before the toddler years in children with VI. Additionally, sleep behavior was not found to be related to the presence of associated disabilities (e.g., cortical visual impairment, epilepsy) within the VI group, suggesting sleep disturbance may be most related to circadian rhythm differences related to VI as opposed to other neurological pathologies.

In sum, neurodevelopmental conditions such as ASD and trisomy 21 as well as VI are associated with greater sleep difficulties in infancy and childhood. While more research is needed on insomnia symptoms in infants with developmental conditions, the current literature suggests insomnia symptoms may present within the first year of life in these populations. Insomnia symptoms documented in infants with neurodevelopmental and acquired conditions are variable, with sleep onset/settling difficulties and night wakings noted in ASD and VI as well as increased parental presence at bedtime, greater night activity, and greater sleep fragmentation noted in trisomy 21. While infants with SMS display sleep disturbances that could be related to insomnia such as reduced overall sleep and lethargy, more research is needed to parse insomnia symptoms from circadian rhythm differences in this population. Overall, greater attention to investigating insomnia symptoms in infants with developmental disorders and other disabilities is needed to inform targeted sleep interventions for these populations.