Version May 2024
INTRODUCTION — Deficient or inadequate sleep may be caused by reduced total sleep time (decreased quantity), fragmentation of sleep by brief arousals (decreased quality), or mistimed sleep (circadian misalignment). Sleep deficiency arising from any cause results in reduced alertness, impaired performance, and compromised health.
Acute and chronic sleep deficiency result in measurable changes in cognitive performance, alertness, behavioral function, and emotional regulation, and these effects are particularly apparent in children. Susceptibility to such changes varies among individuals and is based on multiple factors including age, circadian preference, and genetic differences [1].
Importantly, racial, ethnic, and socioeconomic disparities exist in the prevalence of deficient sleep [2]. The associated adverse cognitive, behavioral, and emotional consequences of deficient sleep, particularly when there are cumulative risk factors, may disproportionately affect underrepresented and poor children, children exposed to trauma, and those living in alternative care settings [3-8].
This topic review will describe the clinical consequences of sleep deficiency and their manifestations in specific sleep disorders including obstructive sleep apnea (OSA) and insomnia. Other UpToDate topics with related content include:
●(See "Assessment of sleep disorders in children".)
●(See "Evaluation of suspected obstructive sleep apnea in children".)
●(See "Management of obstructive sleep apnea in children".)
●(See "Behavioral sleep problems in children".)
PATHOPHYSIOLOGY — Slow-wave sleep appears to be the most "restorative" form of sleep and thus is preferentially preserved in the face of insufficient total sleep. Rapid eye movement (REM) sleep also plays fundamental roles and is involved in cognitive functions such as the consolidation of memory and learning of new tasks. Both forms of sleep appear to play an integral role in the growth and development of the central nervous system.
Emerging literature suggests that developmental changes in sleep microstructure such as sleep spindle density are linked to fundamental cognitive parameters, including acquisition of executive functions in school-aged children and memory consolidation and general cognitive abilities in adolescence [9,10].
Sleep deficiency must be viewed in the context of normal sleep development, as sleep requirements vary across different ages (figure 1) [11]. Circadian misalignment also contributes to clinical consequences, especially in adolescents who often have a preference for later sleep onset and offset compared with environmental demands [12,13]. In toddlers, emerging evidence suggests that circadian misalignment in early development affects both napping patterns and nighttime sleep [14].
CLINICAL CONSEQUENCES OF SLEEP DEFICIENCY — Deficient sleep is associated with a variety of cognitive and behavioral consequences (table 1).
Attention, vigilance, and reaction time — Acute and chronic sleep loss or disruption consistently causes impairment in attention, vigilance, and reaction time. Many studies have demonstrated that sleep restriction impairs children's ability to respond quickly and accurately on neuropsychological measures of attention, including computerized performance tests, and leads to errors both of omission (failing to respond when a signal is present) and commission (responding when a signal is absent) [15]. The ability to work both accurately and efficiently is compromised, as individuals operating under conditions of sleep loss may arrive at the correct answer, but take a longer amount of time to do so, significantly impairing tasks that require speed and accuracy (eg, taking a standardized test, driving a car, or crossing a busy street).
The more complex the task, the greater the impact of sleep disruption. For example, children with fragmented sleep or with sleep loss experienced under experimental conditions show more performance deficits on more complex cognitive tasks [16]. Conversely, extending sleep above baseline by as little as 30 minutes in healthy children and adolescents has been found to result in significant improvement on cognitive tasks such as computerized tests [17] and visuospatial processing [18].
Executive functions — Sleep loss selectively impairs complex cognitive or "executive" functions (eg, time management, decision-making, organization, selective attention, judgment, motivation, self-monitoring and modifying behavior, predicting outcomes, problem-solving, planning, multitasking, impulse control, and emotional regulation). This is suggested by functional neuroimaging studies in adults and children, which indicate that sleep loss selectively impacts the prefrontal cortex (PFC) where these executive functions reside [19].
Short-term sleep restriction and deprivation in young children, school-aged children, and adolescents are associated with impairments in executive functions under conditions of experimental sleep manipulation. Related complex tasks such as classroom performance and simulated driving are also affected.
In addition to short-term impact of insufficient or poor quality sleep on attention and executive functions, there may be longer-term consequences as well [20]. For example, studies have shown that caregiver-reported sleep problems in school-aged children are associated with lower scores on neuropsychological tests and specifically on executive functions in adolescence [15]. Moreover, the role of circadian misalignment and evening chronotype on executive functions in adolescents is being increasingly recognized [21].
Memory — Sleep is now known to be an active process that is crucial for organizing and selectively retaining salient information; in particular, reactivation and reorganization of memory after learning occurs during sleep. Both slow-wave sleep and rapid eye movement (REM) sleep play active and important roles in regard to memory, particularly memory consolidation [22]. REM sleep may be particularly important for emotional memory processing and consolidating motor skills, while slow-wave sleep has an important role in consolidating learning about facts and knowledge.
Emerging evidence suggests that a period of sleep after learning a new task facilitates memory consolidation in children, and that caregiver-reported "poor" sleep and decreased sleep duration are associated with memory consolidation deficits, particularly poorer verbal working memory [20,23,24]. Similarly, day-to-day memory and other cognitive performance measure fluctuations in children may be linked to changes in sleep quality/quantity and daytime sleepiness. Similar finding are emerging in children with neurodevelopmental disorders such as autism [25]. Finally, several studies have documented the salutary effect of a daytime nap in young children on cognitive performance, including memory consolidation [26] and motor skill learning [27].
Academic performance — Disrupted sleep is associated with an overall decline in academic functioning. This relationship has been described in a number of studies assessing the impact of sleep disorders, such as obstructive sleep apnea (OSA) [28,29]. (See 'Sleep-related breathing disorders' below.)
Among otherwise healthy children, sleep restriction has been associated with worse academic performance [30]. Children who fail to obtain sufficient sleep are also more likely to exhibit other risky behaviors, including decreased physical activity and increased screen time, which may contribute to adverse effects on academic functioning [31].
Some evidence suggests that higher sleep efficiency (time asleep/time in bed), a measure of sleep consolidation, rather than sleep duration, is associated with better academic performance in typically developing school-aged children [32]. Good sleep quality also correlates with greater receptivity to the teacher, improved student self-image, and enhanced motivation to achieve.
Emotional regulation — The PFC and the amygdala (which is sometimes called the "emotional brain") participate in generating and regulating emotional responses. The neural connections between the PFC and amygdala are also vital. As an example, neuroimaging studies suggest that both anxiety disorders and depression in adolescents are characterized by dysfunctional and low levels of connectivity between these two brain regions.
Sleep loss appears both to impair emotional regulation in the amygdala and PFC and to disrupt the connections between these regions. This has been shown by functional neuroimaging studies in which sleep-restricted (adult) volunteers viewed emotional images and demonstrated an increased uptake (response) in the amygdala combined with a weaker connection between the amygdala and the PFC, implying a heightened emotional response with less emotional control [33]. REM sleep may play a particularly important role in emotional functioning and in the processing and retention of emotional memories.
Sleep loss impacts the level of emotional reactivity, the ability to regulate both positive and negative emotions, and the ability to accurately assess emotional reactions in others. These associations are present across the lifespan but appear to be most robust in children and adolescents [34]. Emotional reactivity and regulation are particularly important in children and adolescents as they learn to navigate complex emotional and social situations.
Sleep loss is associated with mood disturbances, including complaints of moodiness, irritability, emotional lability, increased negative emotions, depression, and anger. Even in young children, adequate sleep facilitates processes contributing to the development of social-emotional functioning [35,36]. Numerous studies in adolescents have reported a correlation between sleep loss and self-reported feelings of unhappiness, sadness or depression, hopelessness about the future, anxiety, a negative view of life, and self-harm [37-40]. This relationship is bidirectional, in that children and adolescents with anxiety and mood disorders are more likely to report poor sleep, while poor sleep also predicts later development of mood disorders [36,40]. An association has been reported in several studies of adolescents between suicidal thoughts and disrupted sleep. Conversely, sleep extension has been shown to improve mood and depressive symptoms in adolescents [41].
In addition to sleep loss, disruption of normal circadian rhythms (eg, by weekday-weekend changes in sleep schedule or early middle and high school start times), is also related to mood dysregulation. Interventions that result in increased sleep duration, such as delaying middle and high school start times, are also associated with improvements in mood as well as increased academic engagement [42-44]. Similarly, intrinsic circadian rhythm "preferences" or orientation, specifically a tendency towards "eveningness" (later bedtimes and wake times) versus "morningness" (earlier bedtimes and wake times), is associated with greater risk of depression and mood disorders [45].
Behavior — Motor hyperactivity is one of the most consistently reported symptoms in a number of sleep disorders, particularly in younger children, and may be construed as a behavioral compensation for an internal sense of sleepiness (in an attempt to remain awake), compounded by behavioral dysregulation. Accordingly, there is an overlap between sleep disorders including OSA and symptoms of attention deficit hyperactivity disorder (ADHD), as noted below. (See 'Sleep-related breathing disorders' below.)
Sleep loss promotes risk-taking and sensation-seeking behavior. A number of studies, including some in adolescents, have suggested that insufficient sleep is linked to changes in reward-related decision-making, so that sleep-deprived individuals tend to take greater risks and are less concerned about the potential negative consequences of their behavior [46,47]. These effects are mediated through the striatum (caudate, putamen, and nucleus accumbens), which is part of the basal ganglia and is particularly important for motivation and reward-related function. Risk behaviors during adolescence, such as substance use [48], driving while impaired [49], and self-harm behaviors [50], depend on a complex relationship between risk perception, assessment of the cost/benefit ratio of risky behaviors, and reward salience.
Disordered sleep in children has been associated with daytime behavioral disinhibition, including oppositional, defiant and aggressive behavior, and noncompliance as reported by teachers and parents/caregivers [46]. Disordered sleep includes not only decreased sleep duration but also factors such as prolonged sleep onset, increased wake after sleep onset, and the presence of sleep disorder symptoms [51]. The persistence of sleep problems in middle childhood has also been associated with worse emotional and behavioral functioning and quality of life [52].
Sleepy school children more often show bullying behavior and receive discipline referrals compared with their peers [53]. However, it is important to recognize that while children with poor quality and/or insufficient sleep demonstrate more problematic behavior, the converse may also be true. For example, an average of 30 minutes of sleep extension in school-aged children was reported to be associated with improvements in students' emotional lability and restless/impulsive behavior as rated by their teachers, and with decreased aggressive and oppositional behavior in school [54].
The behavioral and emotional effects of sleep loss may be further exacerbated by "weekend oversleep" [55]. This phenomenon is common among teens who are exposed to chronic sleep loss during the week and who attempt to compensate by shifting bed and wake times later and extending sleep on weekends, causing progressive disruption of circadian rhythms.
SPECIFIC SLEEP DISORDERS THAT MAY AFFECT COGNITIVE AND BEHAVIORAL OUTCOMES — The prevalence and types of sleep problems that occur throughout childhood must be understood in the context of normal development. As examples, separation anxiety in toddlers may be associated with increased bedtime problems; normal fears in preschoolers may result in nighttime fears and night wakings; and the relative prominence of adenotonsillar hypertrophy in early childhood is partly responsible for the relatively high prevalence of obstructive sleep apnea (OSA) in this age group. Parental/caregiver perception and reporting of sleep problems in children also varies across childhood, with caregivers of infants and toddlers more likely to be aware of sleep concerns than are caregivers of school-aged children and adolescents. Indeed, the very definition of a "sleep problem" by parents is often highly subjective and is commonly influenced by the amount of disruption caused to parents' sleep.
Data are still relatively sparse regarding the impact of interventions for pediatric sleep disorders on cognitive, mood, and behavioral outcomes, with the exception of studies focused on OSA and on behavioral insomnia in young children. Interventions for these disorders demonstrate a positive impact on sleep parameters. In addition, treatment for these disorders appears to have a positive impact on behavioral function and mood regulation, as well as academic performance, as discussed in the following sections.
Sleep-related breathing disorders — Sleep-related breathing disorders (SRBD) are common in children and encompass nocturnal breathing abnormalities ranging from habitual snoring to OSA. The term OSA refers to periodic episodes of nocturnal airflow restriction (hypopneas) or obstruction (apneas). A polysomnogram (PSG) is required for a definitive diagnosis of OSA. Behavioral comorbidity was included in some of the first descriptions of pediatric OSA [56,57], and is also emphasized in the consensus guidelines [58]. (See "Evaluation of suspected obstructive sleep apnea in children".)
Behavioral and cognitive manifestations — The behavioral and academic consequences of sleep loss described above, including problems with inattention, hyperactivity, impulsivity, irritability, or depressed mood may be the primary presenting complaints in children with SRBD, including primary snoring and OSA [59]. Because parents and caregivers may not associate these problems with sleep disorders, the clinician should have a high index of suspicion: children who present with behavioral, mood, attentional, or academic concerns should be systematically screened for nocturnal breathing symptoms suggestive of OSA and risk factors for OSA [60].
OSA in children has been associated with neurobehavioral symptoms, with fairly good consistency over many studies [61-67]. "Externalizing" behaviors are particularly frequent, including aggression, impulsivity, hyperactivity, oppositional behavior, and conduct problems [68-70]. As an example, among two cohorts of children scheduled to undergo adenotonsillectomy exclusively or almost exclusively for suspected OSA, inattentive and disruptive behaviors were common; approximately 30 percent met diagnostic criteria for attention deficit hyperactivity disorder (ADHD) [71,72]. A longitudinal Canadian study found that "early" (approximately nine months of age) and "late" (approximately 18 months of age) onset of caregiver-reported SRBD symptoms were both associated with increased behavioral problems at age two years [73].
Oppositional defiant disorder and conduct disorder or related disruptive behavior such as bullying are also common comorbidities in pediatric SRBD [53,74]. Other alterations include emotional dysregulation and "internalizing" behaviors such as irritability, mood instability, low frustration tolerance, depression/anxiety, social withdrawal, and increased somatic complaints. In one study, school-aged children with OSA, and particularly those with nocturnal oxygen desaturation, were more likely to have depressive symptoms than a normative sample [75]. A meta-analysis of studies in several different pediatric populations with OSA reached similar conclusions [76].
"Classic" symptoms of excessive daytime sleepiness (eg, difficulty waking in the morning, falling asleep at inappropriate times, or increased napping) are common in adults with OSA. These symptoms tend to be less obvious in children, except among those who are obese or have severe SRBD, but symptoms can often be identified when families are asked directly about sleepiness [61]. Sleepiness in children with OSA, as compared with controls, can also be documented objectively on Multiple Sleep Latency Tests (MSLT) [77,78].
The evidence regarding the effect of OSA on cognition is less robust than for behavioral manifestations [79-83]. A number of studies have suggested associations between OSA and impaired executive functions such as tasks involving reaction time, vigilance, and sustained and selective attention, including in otherwise healthy pediatric samples [84-86], obese children [87], and those with underlying neurocognitive deficits [88]. The relationship between OSA and neuropsychological functioning is also evident in studies assessing academic achievement in these children [60]. However, other areas of impairment are not necessarily consistent across studies. In particular, many studies have failed to find a dose-dependent relationship between pediatric sleep-disordered breathing severity and the degree of cognitive (or behavioral) impairment [89]. Some cognitive deficits, such as language delays and impairments in visual perception, motor functions, and memory, have been identified in very young children with only mild SRBD. For example, infants with persistent habitual snoring have been found to have lower scores on a standardized measure of infant/toddler development (Bayley scores) [90]. Similarly, impairments in behavior, attention and executive function have been identified across the spectrum of severity in pediatric sleep-disordered breathing [91]. Mechanisms linking OSA and impairments in cognitive function are under investigation [92,93].
It is likely that the association between OSA and behavioral or cognitive dysfunction in many studies may have been confounded by other factors that also increase the risk of cognitive impairment, including comorbid conditions (prematurity, asthma, obesity and co-occurrence with other sleep disorders); environmental and sociocultural influences (short sleep duration, exposure to secondhand smoke, and economic disadvantage); and genetic susceptibility (individual genetics and/or African American race). In cross-sectional studies, the observed association between low levels of academic achievement and OSA may represent the combined influence of a number of these risk factors for impaired learning and attention. This makes confirmation in longitudinal studies, and especially randomized controlled trials, all the more important.
Effects of treatment — Overall, there is robust evidence that treatment (adenotonsillectomy) for OSA has a positive impact on sleep parameters, as measured by PSG. There is also increasing evidence that treatment in otherwise healthy school-aged children diagnosed with mild to moderate OSA has a significant and sustained impact on measures of behavioral function, quality of life, and SRBD symptoms [94]. A benefit of treatment on cognitive outcomes is suspected, as noted above (see 'Behavioral and cognitive manifestations' above), but has not yet been proven by randomized controlled trials [95].
●Randomized trials – Some of the most compelling evidence about neurobehavioral effects of OSA in children comes from the Childhood Adenotonsillectomy Trial (CHAT), in which 464 children with OSA (mostly of mild to moderate severity) were randomized to receive early adenotonsillectomy versus watchful waiting for seven months [96]. Though it was not designed as a population-based epidemiologic study, CHAT did not show baseline differences in measures of attention and executive function between enrolled subjects and population means. These cognitive measures, which were the designated primary outcomes for the trial, also did not improve to different extents in the two study arms at follow-up. Reasons for this finding may be that there was relatively little behavioral pathology at baseline or that the seven-month follow-up was not long enough.
In contrast, CHAT did confirm robust and significant improvements in several other key secondary outcomes, including parent- and teacher-reported measures of behavior, quality of life, OSA symptoms, and PSG findings [97]. Normalization of PSG findings was observed in 79 percent of children in the adenotonsillectomy group, with lower rates of normalization in African American and obese children [96]. In the watchful waiting group, PSG normalization was also found in almost one-half (46 percent) of the subjects after seven months, but spontaneous resolution of symptoms such as inattention, hyperactive behavior, and sleepiness was much less common [97,98]. These findings indicate that adenotonsillectomy does have important benefits on behavioral symptoms associated with OSA. However, the improvement in controls also raises important questions about the indications for and efficacy of adenotonsillectomy for OSA. Careful observation without immediate surgical intervention may be warranted in some children. This study had the strengths of a randomized design and large, multicenter sample. It also had potential limitations due to limited duration of follow-up (seven months) and exclusion of children with severe OSA or with ADHD. (See "Management of obstructive sleep apnea in children", section on 'Choice of therapy'.)
A randomized trial in younger children with mild OSA (ages three to five years; n = 190) found no significant differences in cognitive function as assessed by global intelligence quotient (IQ; Woodcock-Johnson III Brief Intellectual Ability) for adenotonsillectomy compared with watchful waiting [99]. Improvements were documented in objective sleep quality, as measured by PSG, and in subjective OSA symptoms and daytime behavior, daytime napping, and overall health as reported by caregivers. The watchful waiting group then underwent adenotonsillectomy 12 months after the baseline assessment (late adenotonsillectomy group). A follow-up study in a subset of patients who attended 24-month follow-up (62 percent) reported improved sleep quality and reduced daytime napping in both groups that started shortly after the adenotonsillectomy, with no between-group differences in several measures of cognitive function [100].
●Other evidence – Observational studies of children undergoing adenotonsillectomy have generally reported postoperative improvements in subjective and objective measures of sleepiness, impulsivity, inattention, cognitive function [71,72,77,79,101], or behavior, as reported by parents [102]. As an example, in a comparison of 78 school-aged children scheduled for adenotonsillectomy with 27 children scheduled for unrelated surgical care, the former showed higher baseline scores on measures for hyperactivity, inattention, and objectively assessed daytime sleepiness [77]. One year after adenotonsillectomy, no significant differences persisted between groups in these neurobehavioral measures. Twenty-eight percent of the children scheduled for adenotonsillectomy met diagnostic criteria for ADHD at baseline, and one-half of these no longer met ADHD criteria at follow-up [71]. By contrast, a small observational study in preschool-aged children did not find effects on cognitive or behavioral outcomes [103]. A few studies suggest that alternative treatment modalities for OSA in children, such as positive airway pressure therapy, also may have positive impacts on sleep parameters, sleepiness, executive function, and quality of life [104-107].
An important unanswered question is whether children who snore, but do not qualify for a diagnosis of OSA based on PSG findings (ie, those with primary snoring), may still experience neurobehavioral consequences of their sleep-disordered breathing and potential benefits from adenotonsillectomy. Some children with primary snoring who do not meet PSG criteria for OSA undergo adenotonsillectomy because otolaryngologists often proceed to surgery for habitually snoring children without obtaining PSG first [108], and as many as one-half of such children would not have OSA if tested [77,96]. However, cross-sectional data suggest that children with PSGs negative for OSA often still have the neurobehavioral morbidity seen in OSA [77,109]. These children experience neurobehavioral improvement after surgery, similar to the improvement seen in children with OSA [71,110]. Analysis of the Pediatric Adenotonsillectomy Study (PATS) randomized trial may help to address these questions about children with frequent snoring who do not meet criteria for OSA on PSG [111].
Other key questions relate to the long-term effects of OSA on behavior and cognition, and the efficacy and ideal timing of intervention to prevent such long-term effects. Preliminary evidence suggests that snoring very early in life is associated with behavioral symptoms or cognitive impairment later in childhood. As an example, one prospective cohort study found that snoring at baseline predicted new development of hyperactive behavior four years later [112]. Similarly, a retrospective case-control study found that children in 7th and 8th grades who performed poorly, compared with those who performed well, more often had a parent-reported history of snoring in early childhood [113]. Finally, in a large cohort study, children who snored or had other parent-reported symptoms of OSA during infancy or early childhood, and then had no such symptoms thereafter, still showed increased probability of having hyperactive behavior at ages four and seven years [114]. These findings raise the possibility that the earliest possible detection and treatment of OSA might be beneficial, but questions of when and how to accomplish this remain largely unanswered [69]. Patient selection could require a better understanding of the variability in the natural history of OSA or SRBD in untreated or partially treated children, and of potential variation among children in genetic susceptibility to neurobehavioral effects of these sleep disturbances [1].
Restless legs syndrome/periodic limb movement disorder — Restless legs syndrome (RLS) is a common cause of sleep onset and sleep maintenance problems in children and frequently co-occurs with ADHD, mood disorders, and anxiety disorders. Two related disorders, periodic limb movement disorder (PLMD) and restless sleep disorder (RSD), appear to have similar neurobehavioral consequences and daytime impairments. (See "Restless legs syndrome and periodic limb movement disorder in children" and "Restless sleep disorder in children".)
Behavioral and cognitive manifestations — In children with RLS or PLMD, the most common daytime symptoms are neurobehavioral (eg, hyperactivity, inattentiveness, poor focusing). Explicit symptoms of excessive daytime sleepiness (eg, difficulty waking in the morning or drowsiness) are relatively uncommon. The difficulty falling asleep and frequent nighttime awakenings associated with these disorders may also promote mood dysregulation and behavior problems, including mood problems, anxiety, and disruptive behavior. (See "Restless legs syndrome and periodic limb movement disorder in children".)
There is a close association between ADHD or attentional difficulties and symptoms of RLS or PLMD. More than 40 percent of clinical samples of children with ADHD have been reported to have RLS symptoms, and approximately 25 percent of pediatric patients with RLS have been shown to have ADHD symptoms [115,116]. In children with both ADHD and RLS, the ADHD symptoms are typically more severe than in children with ADHD alone. Although the association between ADHD and sleep problems may reflect a reporting bias by caregivers, a meta-analysis of PSG studies in children with ADHD confirmed an increase in periodic limb movements of sleep in children with ADHD [117]. There is also an increased risk for depression and anxiety symptoms in children and adolescents with RLS. One study found that 64 percent of pediatric patients with RLS had one or more comorbid psychiatric disorders: mood disturbances in 29 percent of patients, anxiety disorders in 12 percent of patients, and behavioral disturbances in 11 percent of patients [118]. (See "Restless legs syndrome and periodic limb movement disorder in children", section on 'Comorbidity'.)
In view of these associations, clinicians should consider RLS and PLMD in the differential diagnosis for any sleep problem presenting with significant difficulties falling asleep, nighttime awakenings with restless sleep, or unexplained symptoms of daytime somnolence. In addition, RSD can also be associated with neurobehavioral symptoms (eg, inattentiveness, hyperactivity, and irritability). Moreover, for children with ADHD it is helpful to inquire about symptoms of RLS, even if the child has no overt sleep complaints.
Effects of treatment — Only a few studies in children and adolescents include any assessment of the impact of treatment of RLS on behavior, cognitive function, and mood. While some studies reported improvement in daytime function after treatment of RLS with iron [119], none of these were randomized clinical trials. Clinical case series and chart review studies have suggested that treatment with either supplemental iron, gabapentin, or dopaminergic agents may result in improved mood and may reduce or eliminate ADHD symptoms [120]. Preliminary results have suggested that there may be an important relationship between properties of psychotropic medication and pharmacogenomic factors in children and adolescents with symptoms of RLS, which may in turn impact treatment efficacy. For example, in children with RLS and comorbid depression and anxiety, bupropion is the preferred choice of antidepressant rather than selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs), which may exacerbate RLS. (See "Restless legs syndrome and periodic limb movement disorder in children", section on 'Children with anxiety and/or depression'.)
Insomnia — Insomnia or problem sleeplessness is characterized by difficulty initiating sleep, night wakings, or waking up too early, with accompanying impairment of daytime function. In children, the sleep disturbance may manifest as resistance to going to bed at the appropriate time or difficulty sleeping without caregiver intervention. (See "Risk factors, comorbidities, and consequences of insomnia in adults" and "Medical disorders resulting in problem sleeplessness in children".)
Behavioral and cognitive manifestations — Insomnia in young children and adolescents has well-established effects on function and quality of life, and also places a significant burden on caregivers and on the parent-child relationship. The clinical manifestations typically include observable alterations in behavior, mood, and cognitive functioning. A wealth of empirical evidence demonstrates that insufficient or interrupted sleep causes daytime sleepiness with significant impairment of performance and mood dysregulation (irritability, mood lability, more negative mood). As noted above, higher-level cognitive or "executive" functions such as decision-making and problem-solving appear to be particularly sensitive to the effects of disturbed, insufficient, and/or irregular sleep-wake patterns [121] (see 'Executive functions' above). In addition, these types of sleep problems appear to be an important precursor and potential early indicator of later mental health issues such as anxiety, depression, and substance use disorders (see 'Emotional regulation' above and 'Behavior' above). For example, insomnia seems to increase the risk of developing symptoms of conduct and oppositional defiant disorder, major depressive disorder, ADHD, and social phobia in young school-aged children [122].
The association between sleep and cognitive and behavioral outcomes is bidirectional, in that sleep problems appear to exacerbate cognitive or behavioral symptoms, and vice versa. This bidirectional causality is seen in several different groups of patients:
●Neurodevelopmental conditions – Children with underlying neurodevelopmental conditions, including intellectual disabilities, may be particularly vulnerable to developing sleep problems including insomnia, with accompanying impairments in mood, behavior, and cognition, compared with typically developing children [123-125]. For example, some of the core behaviors associated with autism spectrum disorder (ASD; eg, repetitive stereotypic behaviors, emotional dysregulation, self-stimulatory and self-injurious behaviors, poor communication skills, sensory integration deficits, unresponsiveness to social cues) may contribute to the genesis of sleep problems. Moreover, a number of psychosocial and environmental factors are likely to contribute to the high prevalence of severe sleep problems in these children, including learned maladaptive sleep patterns, inadequate parent limit setting, and increased parental awareness of sleep issues. Children and adolescents with ASD are also particularly prone to anxiety; thus, sleep problems related to separation anxiety, nighttime fears, and perseverative behaviors are commonly observed. Conversely, deficient sleep likely interferes with cognitive and behavioral function in these children, as it does in typically developing children.
Recommendations for clinical approaches to address sleep disturbance in individuals with ASD are available [126] and are discussed in more detail separately. (See "Autism spectrum disorder in children and adolescents: Pharmacologic interventions", section on 'Sleep disturbance'.)
●Mental health concerns – Virtually all psychiatric disorders in children and adolescents may cause sleep disruption, and sleep disruption can cause or exacerbate psychiatric symptoms. As a result of these bidirectional relationships, there is considerable overlap between symptoms of mental health disorders, such as mood dysregulation, inattentiveness, and disruptive behaviors, and features common to a wide range of sleep disorders, including sleep-disordered breathing (SDB) (see "Risk factors, comorbidities, and consequences of insomnia in adults", section on 'Psychiatric disorders'). As examples:
•ADHD appears to be associated an increased prevalence of insomnia, particularly difficulty initiating and maintaining sleep, as well as irregular sleep schedules and daytime sleepiness [127,128]. Conversely, many of the most common behavioral consequences of insufficient or disrupted sleep in children mimic or exacerbate symptoms of ADHD (ie, problems with attention and focusing, hyperactivity, poor impulse control, irritability and disturbed mood, and disruptive behaviors such as oppositionality and aggression) [129].
•Depression and anxiety disorders are commonly associated with insomnia [130]. Conversely, insomnia is also a risk factor for the later development of these conditions, and some studies have suggested that insomnia symptoms often precede the onset of major depressive disorder in adolescents [131]. The interaction between sleep disturbances and symptoms of mood dysregulation and anxiety may pose a diagnostic dilemma because of the similarities in presenting symptoms. Studies suggest that 40 to 50 percent of these children have night wakings, nightmares, and difficulty waking in the morning, as reported by their parents. At the very least, poor sleep can exacerbate mood disorders, which may lead to additional sleep disturbances in a negative downward spiral. Insomnia has been associated with suicidal ideation and attempts in adolescents.
●Other factors – While an evening chronotype is a well-known contributor to delayed sleep onset and "secondary" insomnia in adolescents, a similar relationship may also exist in younger children [132]. Genetic factors may play a role in risk for insomnia, although they have not been well-studied in children and may be confounded by parents with insomnia having biased perceptions of sleep disturbances in their children [133-136]. Rates of insomnia tend to be higher in females than males in adults as well as children, especially during adolescence [137]. Children from low socioeconomic households are also more likely to experience sleep concerns, including insomnia, further contributing to sleep disparities [138,139]. Childhood adversity, including abuse and neglect and witnessing violence, is a known risk factor for the development of insomnia in youth [140]. Global events such as the COVID-19 pandemic may influence insomnia risk for a variety of reasons [141].
Effects of treatment — For typically developing young children, the positive impact on sleep from behavioral interventions for bedtime resistance and problematic night awakenings is well-established [142]. In a number of these studies, improvements in mood and daytime behavior have been demonstrated as well. It is possible that some of these apparent improvements may reflect improvement in the caregivers' sleep and stress levels, which impact both caregivers' perceptions of their child's behavior and their parenting effectiveness. In addition, similar positive outcomes have been observed with behavioral interventions in special pediatric populations (eg, children with ADHD, anxiety and mood disorders, ASD, intellectual disabilities), demonstrating the robustness of behavioral interventions such as modified and unmodified extinction and positive routines [126,143]. (See "Behavioral sleep problems in children", section on 'Young children with behavioral insomnia'.)
There is also an emerging literature on pharmacologic treatment of insomnia in the pediatric population [144]. Most of these studies are in children with neurologic and developmental disorders and are focused on melatonin [145], usually in combination with behavioral interventions [146]. In general, melatonin seems effective in reducing sleep onset latency and appears to be well tolerated in children with ASD and ADHD, as well as typically-developing children; the vast majority of these studies have only assessed sleep parameters, although a handful have reported concomitant improvements in daytime variables such as behavior and parenting and family stress. (See "Medical disorders resulting in problem sleeplessness in children", section on 'Neurologic and neurodevelopmental disorders' and "Autism spectrum disorder in children and adolescents: Pharmacologic interventions", section on 'Sleep disturbance'.)
The efficacy of cognitive behavioral therapy for insomnia (CBT-I) in adults is well established, although there are fewer studies assessing the impact of this strategy in typically-developing children and adolescents [147]. Results thus far indicate that CBT-I can have positive effects on cognitive functions in adolescents, with notable improvements in visuospatial processing and phonologic working memory [148], as well as some components of executive function [149]. Other studies have reported anecdotal improvements in daytime functioning, coping, and sense of well-being. CBT-I may also result in a decrease in symptom severity in children with psychiatric disorders such as depression who also have insomnia. Finally, in adolescents with sleep onset insomnia in the context of delayed sleep-wake phase disorder, CBT-I plus bright light therapy has been shown to improve daytime functioning, including daytime sleepiness, fatigue, and depression symptoms [150].
Narcolepsy — Narcolepsy is a chronic neurologic disorder characterized by excessive and irresistible sleepiness often associated with cataplexy, hypnagogic hallucinations (vivid dream-like imagery at sleep onset), and sleep paralysis (a momentary inability to move the body as one is drifting off to sleep or waking up). Although relatively rare in comparison to chronic insomnia or OSA, narcolepsy is one of the more common causes of disabling daytime sleepiness beginning in adolescence or early adulthood. The clinical features, diagnosis, and management of this disorder are discussed in detail in separate topic reviews. (See "Clinical features and diagnosis of narcolepsy in children" and "Clinical features and diagnosis of narcolepsy in adults" and "Treatment of narcolepsy in adults".)
Behavioral and cognitive manifestations — Many children and adolescents with narcolepsy experience functional impairment, psychological distress, and decreased quality of life due to excessive daytime sleepiness and/or cataplexy, which may be exacerbated by a delay in diagnosis [151-154]. Patients with narcolepsy are more likely to have behavioral disturbances, depression, and problematic peer relationships [155]. In a study of Swedish children developing narcolepsy after an H1N1 vaccination, over 40 percent of patients had at least one psychiatric comorbid condition, including ADHD in 29 percent, major depression in 20 percent, generalized anxiety disorder in 10 percent, and oppositional defiant disorder in 7 percent [156]. Behavioral dysregulation (ie, temper tantrums) were reported in the overwhelming majority (94 percent). Increased levels of depressive symptoms, largely associated with fatigue, have been reported to affect some 25 percent of children with narcolepsy, with girls older than 10 years of age being especially vulnerable, and depression also seems to be a major contributor to the decrease in overall quality of life [157].
While most studies have found that children with narcolepsy do not have significant impairments in overall cognitive functioning (ie, IQ is within the normal range), specific learning and academic deficits have been described [158]. In the Swedish study cited above, children with narcolepsy were found to have decreased verbal comprehension and working memory on neuropsychological tests [156]. Due to the propensity for falling asleep in school and the attentional difficulties associated with narcolepsy, childhood narcolepsy with cataplexy represents a risk factor for subtle and heterogeneous cognitive impairments, which may result in academic failure. Patients with psychiatric comorbidity such as depression may be at increased risk for general cognitive dysfunction.
Effects of treatment — Nonpharmacologic treatments for narcolepsy in children and adolescents (eg, sleep schedules including napping, physical activity and diet, mindfulness and acupuncture) are endorsed by patients and families, but thus far there are few studies examining the efficacy of these interventions even in adults [159]. The cognitive and behavioral effects of pharmacologic therapies for narcolepsy are also understudied. A review of clinical experience in Europe focused largely on core symptom-related outcomes [160]. Several retrospective studies have reported improvements in academic and social functioning with various pharmacologic treatments for daytime sleepiness and/or cataplexy, although one retrospective chart review study suggested that treatment appeared to have no significant impact on health-related quality of life [161]. (See "Management and prognosis of narcolepsy in children".)
SUMMARY
●Acute and chronic sleep loss or disruption can impair the following functions (table 1) (see 'Clinical consequences of sleep deficiency' above):
•Attention, vigilance, and reaction time
•Complex cognitive or "executive" functions (including decision-making and impulse control)
•Memory functions (organizing and selectively retaining salient information)
•Academic performance
•Emotional regulation
•Behavioral regulation, resulting in motor hyperactivity (especially in young children) and increases in risk-taking behavior
●Sleep disorders such as obstructive sleep apnea (OSA) often result in daytime sleepiness, with cognitive and behavioral symptoms. These include "externalizing" behaviors (aggression, impulsivity, hyperactivity, oppositional behavior, and conduct problems), as well as "internalizing" behaviors (irritability, mood instability, low frustration tolerance, depression/anxiety, social withdrawal, and increased somatic complaints). Overt difficulty waking or drowsiness are relatively less common in children compared with adults. Treatment for OSA has a positive impact on sleep parameters as measured by polysomnography (PSG) and quality of life, and a number of studies have found that treatment has a significant and sustained positive impact on behavioral function and mood regulation, with potential, though less clearly demonstrated, benefit on cognitive functioning as well. (See 'Sleep-related breathing disorders' above.)
●Restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) in children can each be associated with behavioral manifestations, including hyperactivity, inattentiveness, and poor focusing. There is a close association between these sleep disorders and attention deficit hyperactivity disorder (ADHD) or other attentional difficulties. Affected children also have an increased risk for depression and anxiety symptoms. (See 'Restless legs syndrome/periodic limb movement disorder' above.)
●Insomnia in children and adolescents has well-established comorbidity including alterations in behavior, mood, and cognitive functioning. The relationship between sleep and cognitive and behavioral outcomes is inherently bidirectional. This is particularly apparent in children with neurodevelopmental conditions (eg, autism spectrum disorder [ASD] or intellectual disability) or mental health concerns (ADHD, depression, or anxiety). There is considerable empirical evidence that behavioral interventions for insomnia are effective for both typically developing children and those with comorbid psychiatric or neurodevelopmental disorders, although in the latter group, adjunctive pharmacotherapy may be warranted. (See 'Insomnia' above.)
●Many children and adolescents with narcolepsy experience functional impairment, mood disturbances, psychological distress, and decreased quality of life due to excessive daytime sleepiness and/or cataplexy. Patients with narcolepsy are also more likely to have behavioral disturbances such as temper tantrums, as well as problematic peer relationships. (See 'Narcolepsy' above.)
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