Studying children and adolescents poses methodological challenges. The primary research design for adult sleep deprivation studies, in which participants stay “in lab” to allow for greater control of sleep and activity schedules, is less of an option for child researchers because parents are often reluctant to leave their children in the care of unfamiliar adults, participants may be resistant to a prolonged stay away from home, and children's sleep may be particularly subject to disruption in an unfamiliar environment ^6-7. Further, children are a vulnerable population, for whom additional protections against risk may be required. Although it appears that any health effects of short-term sleep restriction are reversible with 1-2 nights of recovery sleep, researchers must consider the risk of events that could occur during sleep restriction (e.g., a poor school grade, auto accident for young drivers) and attempt to mitigate that risk. As a result, there have been few experimental studies.

High-quality studies using multiple research designs are needed, because each has strengths and weaknesses. Correlational, case-control and quasi-experimental studies lend themselves well to assessing the real-world associations between sleep and daytime function, often in impressively large samples that promote subgroup analyses and generalization of findings. However, the potential for uncontrolled confounding factors (e.g., parent work schedules, parenting styles, family structure, child daytime activities/habits, teen employment) limits causal inferences, and measurements of both sleep and outcome variables are often imprecise. In contrast, experimental studies allow for more confident attribution of causality and more measurement precision, but in much smaller samples and employing methods and measures that do not map cleanly onto real-world circumstances.

Like research designs, different cognitive and behavioral assessment techniques have complementary strengths and weaknesses ⁸. Questionnaires have the advantages of easy administration, low cost, and ready assessment of real-world functioning, but are prone to reporter biases. Office-based standardized neuropsychological tests avoid such bias and can parse out specific cognitive skills. However, some domains of functioning, particularly attention and executive functioning (e.g., planning, organization, mood and behavior regulation) are difficult to assess in an office-based testing environment ^9-10. Direct, systematic ratings of child behaviors by trained observers can provide an objective perspective in applied settings, but are logistically very difficult; the two studies that have used such techniques in the sleep-behavior literature used “simulated” classrooms, rather than embedding raters in subjects’ schools ^11-12.

Even so, findings have not been universal. At least one large study has suggested that sleep is minimally associated with academic knowledge ¹⁹. Of note, that study relied heavily on office-based tests of academic knowledge, which are only partial predictors of classroom performance. Classroom performance is also dependent upon skills that are difficult to test in the office, including sustained attention, behavior regulation, planning, and organization ²⁰. Indeed, school-identified learning problems did significantly correlate with poor parent-reported sleep quality in that study. However, this effect disappeared after statistically covarying for symptoms of attention-deficit/hyperactivity disorder (ADHD), which led the authors to speculate that any apparent link between sleep and learning problems could be due to the confounding effects of ADHD. Alternatively, however, symptoms of ADHD may not represent confounding factors, but rather the mechanism by which poor sleep quality was linked to learning problems.

Indeed, inadequate sleep has been linked to difficulties with attention, impulse control, and behavior regulation ^21-24, with potential consequences that extend beyond the classroom. Poor sleep quality is associated with crash risk in teen drivers ²⁵, and short sleep has been linked to accidental injuries in young children ^26-28 and adolescents ²⁷, as well as risk-taking behaviors in adolescents ²⁹. Because poor regulation of attention and behavior are key features of ADHD, some have concluded that a subgroup of children with primary sleep problems may be misdiagnosed with ADHD. The relationship between ADHD and sleep is complex, however, and the reader is referred to the relevant chapter in this volume and several other recent reviews for detailed coverage ^30-32.

The links between sleep and other psychiatric diagnoses, including depression and anxiety disorders, are similarly complex and extend beyond the current discussion. Briefly, sleep problems are disproportionately present in many psychiatric conditions, and the direction of causation appears to be reciprocal, rather than unidirectional (see ref ³³ for reviews). There is also evidence that the presence or severity of sleep disturbance predicts psychiatric symptom severity and functional impairment ^{e.g. 34-35}. However, it is difficult to know how to apply this information to the general population; whereas sleep disruption appears to be linked to mood, studies have yielded mixed associations between sleep duration and emotional functioning ^36-38. Indeed, within one study, parent-reported mood problems and behavior problems had variable associations with sleep duration depending on the source of information on behavior/ mood (parent vs self-report) and sleep duration (parent versus actigraphy)³⁹.

Of perhaps greater interest are studies of the daytime functioning of children and adolescents with obstructive sleep apnea (OSA), a largely treatable disorder in which the upper airway is chronically and/or repeatedly obstructed during sleep. As reviewed by Beebe ⁴⁰, OSA has been linked to poor classroom grades, sleepiness, inattention, hyperactivity, oppositional behaviors, and mood dysregulation (but not ongoing mood disturbance) in the vast majority of relevant studies, most of which have targeted children aged 5-12 years of age. We recently extended those findings through the adolescent years ²⁰. Office-based tests of intelligence have yielded inconsistent results in children with OSA, with the most consistent evidence of IQ deficits during the preschool and early grade-school years ⁴⁰. Other tests of cognition have yielded mixed results, but there is some evidence of poor scores on tests of attention, executive functioning, and learning/memory in children with OSA ^40-42. OSA is of particular interest here not only because a large number of studies have examined behavioral outcomes of children with this condition, but also because treatments focus on the airway and would not be expected to impact behavior in a manner independent of sleep. Non-randomized studies have shown improved daytime functioning following surgical intervention for uncomplicated OSA ^{40, 43}, bolstering the suggestion that OSA is causally related to daytime dysfunction. However, the field awaits the results of the CHildhood AdenoTonsillectomy (CHAT) study, an ongoing large randomized adenotonsillectomy trial for OSA with blinded outcome measures.

There have been studies that have linked other treatable sleep conditions, most notably Restless Legs Syndrome (RLS) and Periodic Limb Movement Disorder (PLMD), to daytime dysfunction, particularly to hyperactivity/impulsivity and inattention ^44-45. However, compared to OSA, studies have been few, causal implications are unclear, and intervention data are difficult to interpret because the relevant sleep treatments can also directly impact daytime functioning. For more information on RLS, see Durmer and colleagues’ paper in this volume.

Outside of OSA, only a handful of correlational and case-controlled studies of pediatric sleep have employed objective measures of cognitive functioning. In two, poor quality sleep was significantly associated with poor attention, working memory, and/or impulse control ^22-23. A recent study linked objectively-defined short sleep with lower IQ test scores ⁴⁶. However, others have reported either no relationship between sleep duration and IQ ⁴⁷ or an association only for males and on selected aspects of intelligence ⁴⁸. Two large-sample studies on young children have arrived at conflicting results with respect to overall cognitive functioning and sleep ^49-50.

First, compared to when they are well-rested, sleep-deprived children fall asleep more easily during the day, self-report sleepiness, and look sleepier ^{7, 11, 59-62}. Second, children are less attentive when sleep-deprived. It has proven difficult to demonstrate this on formal attention tests, but shortened sleep results in visibly more inattentive behaviors, whether reported by individuals who are not blind to sleep condition ^{7, 11}, teachers who were likely blind to sleep condition ⁶², or observers whose condition-blind state was rigorously maintained ¹⁷. Third, no experimental study has yet shown that sleep restriction induces hyperactivity, impulsivity, or other externalizing behaviors in children, despite correlational and case-control evidence that this “should” occur. Fourth, there is some evidence that depriving children of sleep affects their higher-level cognitive skills. One study documented diminished creativity and reasoning skills following a single night of shortened sleep, but overall study results were mixed⁶³. Another reported that sleep-deprived adolescents showed diminished higher-level executive functioning skills according to parent- and self-report forms ⁷. Fifth, there is evidence that that the impact of sleep deprivation is substantial enough to result in real-world impairment. Sleepiness and inattention in real-world settings have been reported by teachers, parents, and subjects ^{7, 61-62}. One study also found deficits in executive functioning as applied to daily life ⁷, and two studies reported learning difficulties in a simulated or real classroom ^{12, 62}.

Developmental changes are evident in the brain throughout the lifespan, but the most dramatic neurodevelopment occurs during childhood, guided by an interaction between genetic programming and environmental factors ^65-66. Chronic or extreme exposure to stress or toxins during development can lead to aberrant neural connections, resulting in disruption of cognitive, behavioral, or emotional functioning ⁶⁶. Inadequate sleep may be one such exposure; animal models have demonstrated that even short-term sleep deprivation can alter neural plasticity ^67-73. Further, a rodent model of OSA suggests a developmental gradient, with particularly marked effects on the brain and on learning during the time period equivalent to early childhood ^74-75. These findings are notable in light of human data which suggest that OSA has the greatest effect on behavioral functioning in boys under age 8 ⁷⁶, and on intelligence in preschool children ⁴⁰. Human exposures to inadequate sleep can be prolonged, so even “low level” exposure might result in changed neurodevelopmental patterns and trajectories over time. Notably, the anterior brain regions that show the most protracted development across childhood are also those that are believed to experience the greatest functional impact of sleep deprivation ^77-79.

There have been few publications on the neural response to sleep deprivation in children, but non-invasive technologies hold promise for shedding additional light. Four relevant studies have been published. Magnetic resonance spectroscopy conducted on school-aged children with severe OSA found region-specific chemical abnormalities suggestive of neuronal injury ⁸⁰. Also, in young children with “subclinical” sleep-disordered breathing, altered neuronal processing of speech sounds has been detected via evoked response potentials, leading study authors to speculate that the brain may be attempting to compensate for sleep disturbance ⁸¹. A similar explanation was evoked to explain altered activation-deactivation patterns in attention-related brain regions of adolescents during sleep restriction ⁶⁴. These adolescents also showed electroencephalographic slowing in a simulated classroom while sleep-deprived ¹². All of these findings are preliminary, and at present it is impossible to draw coherent conclusions due to differences in samples, research designs, and measures. However, these studies support the suggestion that inadequate sleep can substantively alter neural processing.

Paralleling neurodevelopment, key functional skills develop across childhood. While academic skills are most easily appreciated as requiring learning, it is no exaggeration to state that every foundation skill necessary for adult functioning matures substantially during childhood and adolescence. To the degree that sleep deprivation impacts a young child's ability to engage with and learn from his or her environment—and the evidence reviewed above suggests that it does—maturation may be delayed or disrupted. Older children and adolescents may be vulnerable in other ways, as their behaviors can have costly, irreversible consequences ⁷⁸. For example, there is a spike in accidental injuries during adolescence ⁷⁸, and adolescent school underperformance increases the odds of school drop-out, failure to enroll in or complete college, adult mental illness or substance abuse, and low occupational attainment ^82-86. If sleep quality or quantity affect injury risk or school success—and the above evidence suggests this to be the case—then the long-term legacy of pediatric sleep problems may be considerable.

In humans, it is neither feasible nor ethical to experimentally expose children to prolonged sleep restriction. However, longitudinal studies can examine the natural associations between inadequate sleep and later functioning. Over a dozen relevant studies have been published, and a well-replicated finding is that childhood sleep problems (variously defined) predict the development of anxiety and depressive symptoms over time, even after controlling for baseline mood difficulties and other potential confounds. This has been reported across timeframes spanning preschool to mid-childhood ^87-88, preschool to mid-adolescence ^89-90, mid-childhood to late childhood ^{39, 91}, mid-childhood to young adulthood ⁹², and adolescence to young adulthood ⁹³. Longitudinal associations between sleep problems and externalizing behaviors such as hyperactivity, aggression or conduct have tended to be weaker or less consistent, but also have been reported ^{39, 87-88, 92}. Consistent with such associations, the presence of loud snoring, a hallmark symptom of OSA, in young children has been shown to predict later hyperactivity and poor school performance ^94-95. Finally, sleep problems at ages 3-8 years have also been found to predict the early onset of substance use in adolescents ⁹⁰.

Such longitudinal relationships have not always been straightforward, however. One group has suggested that inadequate sleep has the greatest effects in children from homes in lower socioeconomic strata ^{39, 47}. In several other studies, the initial presence of sleep problems was less important in predicting later functioning than whether these problems persisted or worsened over time ^{38, 96-97}. Such complexity has also been evident in studies of cognitive and learning outcomes. Especially among children from low income homes, the presence of sleep problems in 3^rd grade predicts intellectual stagnation, and longer sleep predicts better reading development, over the following two years ⁴⁷. Persistent or worsening sleep problems during childhood also predict poorer scores later on tests of executive functioning, but not memory, nonverbal reasoning, vocabulary, or fine motor skills ^97-99.