Does sleep correlate with neurodevelopmental outcomes in preterm and term infants in early-preschool children?

Sleep has been long considered an important contributor to optimal neurodevelopmental outcomes. Increasingly, sleep is being studied and validated for its role as an early biomarker of overall brain health, including developmental and neurodegenerative risk, and as an opportunity to serve as a tool for intervention to improve physical, cognitive, social, and psychological trajectories. With this stated, there is ongoing need to better understand sleep in individuals from birth longitudinally, with specific attention to gestational age at time of delivery. In this issue of Journal of Clinical Sleep Medicine Bijlsma et al¹ have performed a nested study evaluating objective and subjective measures of sleep in children at the (corrected) age of 3 years with participants from 2 ongoing large, prospective, observational cohort studies of children born full-term (gestational age [GA] > 37 weeks) and very-preterm (GA < 30 weeks) with no perinatal complications. Parent-reported questionnaires, including the Brief Infant Sleep Questionnaire (BISQ) and the Munich Chronotype Questionnaire (MCQ), as well as objective sleep measures including at least 3 days of actigraphy and sleep diary data, were collected from 97 very-preterm and 92 full-term children.¹ No significant differences for sleep problems and other parent-reported sleep parameters were identified between groups. Actigraphy data suggest an increased sleep duration in children born very preterm; these children woke up 21 minutes later than full-term children (adjusted P = .001).¹ Overall, circadian rhythm and consolidation of sleep and daytime napping were similar between groups. The implications of a later waking in preschool-aged children born preterm based on actigraphy are unclear.

Prior research has identified prematurity as a risk factor for problematic sleep, including impaired sleep quality, excessive daytime sleepiness, and differences in total sleep duration during infancy, childhood, and adolescence.² The underlying mechanism for sleep dysfunction is unknown but has been postulated to be a consequence of central nervous system immaturity, medical comorbidity, or insufficient exposure to maternal circadian signaling that may be further compounded by environmental factors that can also affect circadian entrainment and sleep quality (ie, lights, sound, or medical management).² Sleep has also been shown to provide value as an accurate predictor of neurodevelopmental progression, as illustrated by a study that evaluated 29 newborns in a neonatal intensive care unit at risk for seizures with polysomnography and near-infrared spectroscopy; abnormalities of the neonatal sleep patterns predicted worse neurodevelopmental outcomes at 18 months of age.³ Similar findings that suggest the relevance of ultradian rhythm to neurodevelopmental outcomes have been seen across various ages.⁴

The current study is limited by a relative lack of diversity and noninclusion of children with a history of comorbidity related to prematurity. This may reduce generalizability of the findings. There are no objective evaluations of detailed sleep characteristics by either electroencephalogram or polysomnography, such as rapid eye movement/non-rapid eye movement cycling, to further characterize comparison between cohorts that may have led to improved understanding of relevance to current neurodevelopmental status. Characterization of current sleep status compared to prior time points for participants would be valuable for understanding the trajectory of premature vs term infants, as would including neurodevelopmental assessments for additional comparison. If prior time points were included, stratification of breast vs bottle feeding would have been important. Parental morningness or eveningness, parents’ socioeconomic status, and cosleeping also were not described. Fewer participants from the full-term population were recruited. Studies using questionnaires are always subject to recruitment bias, because parents whose children have sleep issues often tend to volunteer in order to gain more information on their children’s conditions.

Despite these limitations, the novel findings of similar objective and subjective measures of sleep in preterm and term infants at age 3 years may provide additional support for the concept of developmental “catch up.” Traditionally, neurodevelopmental assessments in early childhood are performed and adjusted for GA until 3 years of age,⁵ with the expectation that irrespective of GA similar milestones will be achieved by age 3 years, unless there is other medical or neurologic pathology. Therefore, the results of this study may further reinforce the concept that similar brain maturation may be expected by 3 years of age irrespective of GA. Future studies should include additional circadian characterization with evaluation of urinary melatonin and genetic evaluations (CLOCK genes) along with parent-reported questionnaires and actigraphy to provide a comprehensive assessment of factors influencing the timing of sleep. The assessment of parental habits as they relate to sleep routines, response to bedtime resistance, and nocturnal awakenings may provide insight into other external factors that may influence term and preterm infants’ sleep habits. Finally, as described above, additional characterization of detailed sleep features with polysomnography or electroencephalography in a larger cohort, in combination with neurodevelopmental assessments, may provide meaningful insight into either biomarker or interventional factors that will inform medical decision-making and recommendations.

DISCLOSURE STATEMENT

The authors report no conflicts of interest.