The role of sleep disturbances in the onset and maintenance of psychiatric disorders in childhood and adolescence: A review of subjective and polysomnographic findings

Abstract

Purpose of Review:

To summarize subjective and polysomnographically-measured sleep disturbances in children and adolescents with psychiatric conditions, including anxiety, mood, and neurodevelopmental disorders and high-risk syndromes for psychosis. Evidence for the role of disrupted sleep in the onset and maintenance of each diagnostic category is considered.

Recent Findings:

Although subjective sleep complaints are common and transdiagnostic among youth with psychiatric disorders, evidence for disruptions in traditional polysomnographic measures (e.g., total sleep time) is inconsistent. However, physiological sleep abnormalities (e.g., delta or sigma power, rapid eye-movement density) may characterize specific mental health conditions. Overall, sleep disturbances appear to be precursors to, and sustainers of, psychiatric symptoms in youth.

Summary:

Future studies may elucidate physiological sleep processes underlying subjective sleep complaints in youth with psychiatric disorders and would benefit from polysomnographic methodology standardization, diverse/representative samples, incorporation of circadian measures, and inclusion of polysomnography as an outcome in behavioral sleep intervention clinical trials.

Introduction

The importance of sleep in supporting mental health has been observed by medical professionals for over a century (1). Moreover, the close ties between sleep health and psychiatric well-being emerge early in life (2). Childhood and adolescence are critical developmental periods for onset of psychiatric disorders, from the first identification of neurodevelopmental disorders in early childhood (i.e., Autism Spectrum Disorder, ASD; Attention Deficit/Hyperactivity Disorder, ADHD), to the proliferation of anxiety disorders in middle childhood, to the emergence of mood disorders, suicidal ideation, and psychosis, frequently occurring during adolescence (3). Importantly, behavioral and/or physiological sleep disturbances are implicated in each of these diagnostic categories, highlighting sleep as a transdiagnostic biological process underlying general mental health (4).

Sleep health is complex and multi-faceted, however, defined not just by the amount of sleep, but also by the length of time it takes to fall asleep, nocturnal awakenings, sleep efficiency (degree to which time spent in bed is time spent asleep), and perceived sleep quality (5). Additionally, sleep is a brain-based phenomenon, and important sleep aspects are only observable through objective measurements, including time spent in sleep stages (i.e., light, deep, or rapid-eye movement (REM) sleep) and brain-wave patterns across the night (6, 7). Evidence for disruptions to different facets of sleep—as reported by children and their caregivers, or objectively-measured using gold-standard assessment (polysomnography, PSG)—suggests both commonalities and differences in the sleep disturbances observed across childhood psychiatric disorders (2). In this review, we summarize the pediatric literature examining subjective and PSG-measured sleep in five diagnostic categories, including: Anxiety Disorders, ADHD, ASD, Mood Disorders (including Suicidality), and Psychosis. Additionally, we consider evidence for a role of sleep in the onset and maintenance of each diagnostic category. Rather than providing an exhaustive overview of all studies on these topics, this review seeks to paint a broad picture of the best evidence for sleep as a potentially modifiable factor for the onset and maintenance of psychiatric disorders among children and adolescents, and to allow for a high-level comparison of commonalities and differences regarding sleep disturbances across diagnostic categories during this critical period of development.

Brief Primer on Sleep Terms

Sleep is determined by the interaction of two independent biological processes. The homeostatic sleep drive is a pressure to sleep that accumulates across a period of wakefulness and dissipates during sleep. Circadian rhythms are 24 hour fluctuations in alertness and propensity for sleep (8). Disruptions to either process, as well as environmental factors (e.g., light exposure, caffeine use), result in sleep disturbances and disorders, such as insomnia. Sleep is composed of ~90-minute cycles of sleep stages, defined in part by corresponding EEG-measured brain-wave patterns. NREM sleep includes stages 1 (N1; theta waves), 2 (N2; sigma waves/sleep spindles, K-complexes), and 3 (N3/slow-wave sleep; delta waves). REM sleep, when vivid and emotionally salient dreams occur, is characterized by beta waves, and awakenings are associated with alpha waves (6, 7). Sleep spindles, characteristic of N2, are short waxing and waning bursts of EEG activity (10–15 Hz oscillations) lasting 0.5 to 3 seconds, and the density of sleep spindles (number of sleep spindles per 30 or 60 second epoch) (9) is believed to promote cognition, memory, and learning in children and adolescents (10, 11). NREM slow wave activity (SWA), characteristic of N3, is defined as density of high amplitude oscillations (<5 Hz, delta waves) (12) and is believed to reflect the restorative functions of sleep, including the role of sleep in promoting neural plasticity, brain functions, and cognition in pediatric populations (13, 14). See Table 1 for a sleep term overview.

Table 1.

Sleep Terms

Component	Definition	Subjective	PSG
Duration	Length of sleep period	Sleep Duration	Total Sleep Time (TST)
Latency	Length of time from lights out to sleep onset	Sleep Latency	Sleep-Onset Latency (SOL)
Continuity	Number and/or length of nocturnal awakenings	Nocturnal Awakenings	Wake After Sleep Onset (WASO)
Efficiency	Proportion of time spent in bed in which person is asleep	Sleep Efficiency	Sleep Efficiency (SE)
Quality	Perception of how restorative sleep is	Sleep Quality	N/A
Sleep Architecture	Stages of sleep cycle	N/A	N1 (Stage 1, “Light” sleep) N2 (Stage 2, “Light” sleep) N3 (Slow Wave Sleep, “Deep” sleep) REM (Rapid Eye Movement sleep)
Sleep Physiology	Power and amplitude of brain waves during sleep	N/A	Delta (.5–4 Hz, Slow Wave Activity) Theta (4–7 Hz) Alpha (8–12 Hz) Sigma (12–16 Hz, Sleep Spindles) Beta (13–30 Hz) Gamma (30–40 Hz)

Sleep Across Child Development

Sleep patterns and physiology normatively shift across child development. Sleep shortens from 10–13 hours in preschool to 8–10 years in adolescence, and sleep timing shifts later with the onset of puberty. The length of sleep cycles increases from infancy (50 minutes) to 90–110 minutes by school-age. Infants spend about 50% of sleep in NREM and 50% in REM, and REM percentage declines across childhood and adolescence to 25% by adulthood. Regarding NREM, N3 is greatest in early childhood, and declines steeply in adolescence, while N1 and N2 increase as youth approach adulthood. Adolescent sleep changes include shifts in both biological sleep processes: sleep drive accumulates more slowly and circadian phase shifts later. Importantly, developmental sleep changes are integrally tied to brain maturational processes (15–17).

Pediatric Sleep and Psychiatric Disorders

In this section, we summarize the pediatric literature examining subjective and PSG-measured sleep in each diagnostic category and consider evidence for a role of sleep in the onset and maintenance of each disorder. Table 2 summarizes findings from PSG studies across diagnostic categories.

Table 2.

Polysomnography-measured sleep disturbances in psychiatric disorders of childhood and adolescence

Strong Support (Meta-analysis or Systematic Review)
Diagnostic Category	Results
ADHD	Slow wave activity (SWA, delta EEG power) is higher in children but lower in adolescents; Abnormalities in cyclic alternating pattern subtype 1 (EEG-synchronized slow-waves)
ASD	Shorter total sleep time (TST), longer sleep onset latency (SOL), and greater wake after sleep onset (WASO)
Depression	Longer sleep onset latency (SOL), lower sleep efficiency (SE), increased light sleep, and increased REM density; Some support for abnormalities in SWA patterns overnight and reduced sleep spindles
Some Support (Individual Studies)
Diagnostic Category	Results
Anxiety Disorders	Mixed findings regarding increased sleep onset latency (SOL) and wake after sleep onset (WASO) and reduced Stage 3 (N3), REM periods, REM latency and NREM spindle activity
Psychosis (CHR)	Increased sleep onset latency (SOL) and wake after sleep onset (WASO), reduced sleep spindle duration, or higher NREM sleep gamma EEG power
Psychosis (EOS)	Greater REM and NREM beta EEG power. deficits in spindle activity (amplitude, duration, density, and/or frequency)
Suicidality	Longer sleep onset latency and REM latency, greater Stage 1 (N1) and REM density, less Stage 3 (N3)

Abbreviations: ADHD, Attention Deficit Hyperactivity Disorder; ASD, Autism Spectrum Disorder; CHR, Clinical High Risk; EOS, Early Onset Schizophrenia, NREM, Non-Rapid Eye Movement sleep; REM, Rapid-Eye Movement sleep

Anxiety Disorders

Anxiety disorders are the most prevalent psychiatric conditions of childhood, impacting ~20% of youth (18), and include separation anxiety, specific phobia, social anxiety disorder, generalized anxiety disorder (GAD), and panic disorder (19). Childhood anxiety disorders elevate risk of a range of psychiatric conditions in adulthood, including substance use, depression, and suicidality (18). Although sleep disturbance is included in the diagnostic criteria of one anxiety disorder (GAD), it represents an overlapping feature underlying the range of pediatric anxiety disorders (20).

Subjective.

Up to 85% of clinically anxious children and their caregivers report sleep problems, including bedtime resistance, delayed sleep onset, shorter sleep duration, greater night time anxiety, nightmares, and daytime sleepiness (2, 20). Subjectively-measured sleep disturbances are present across diagnostic classifications of pediatric anxiety disorders (20). Regarding GAD specifically, endorsement of subjectively-reported sleep problems during clinical evaluation may predict subsequent receipt of a GAD diagnosis for children and adolescents presenting to a behavioral health clinic (21).

PSG.

Results from PSG studies with children with anxiety are few and inconsistent (2). Individual studies have suggested increased SOL (22, 23) and awakenings (22), and reduced N3 (22), REM periods (24), REM latency (23), and NREM spindle activity (25), compared to healthy controls or other clinical groups (e.g., depression), but there are few commonalities in findings across studies. Methodological differences, including lab- versus home-based recordings and the number of recorded nights (single versus multiple nights), likely contributes to mixed findings (2).

Prior to onset.

Sleep disturbances prospectively predict anxiety symptoms in childhood (26), beginning early in life. Specifically, more caregiver-reported sleep problems in preschoolers are cross-sectionally related to greater anxiety symptoms and higher separation anxiety among children aged 2–6 (27), and a recent longitudinal study of preschoolers (mean age=3.6 at baseline) found that sleep disturbances at earlier time points predicted increased anxiety at later time points over two years, but not the reverse (anxiety did not predict later sleep problems) (28). A recent review suggests that early childhood sleep problems predict the presence of anxiety disorders in adolescence (29).

Role in maintenance.

Subjectively-reported sleep disturbances and anxiety disorders are bi-directionally related in youth, each increasing the severity of the other (30). A handful of PSG studies have linked sleep physiology with clinical outcomes in pediatric anxiety disorders. NREM spindle activity has been positively associated with worry symptoms, and spindle density in frontal regions has been negatively associated with global functioning (31). Increased N3 has been related to lower negative affect while increased REM is associated with more somatic complaints among youth with GAD (32). These preliminary results require replication. Notably, evidence suggests that behavioral sleep interventions may not only improve sleep, but also reduce anxiety, in pediatric samples (33, 34).

Attention Deficit-Hyperactivity Disorder (ADHD)

ADHD affects up to 1 in 10 youth (35) and is characterized by developmentally-inappropriate levels of inattention, hyperactivity, and/or impulsivity accompanied by pervasive social, familial, and academic impairments (19). DSM-5 criteria mandate onset prior to age 12; however, a growing literature supports a “late-onset” ADHD phenotype, with symptoms emerging in adolescence (36). Empirical and clinical interest in links between ADHD and sleep are of long-standing; as a historical note, the DSM-III included “moves about excessively during sleep” as a symptom of the disorder (37).

Subjective.

Elevated sleep complaints, as reported by youth with ADHD and their caregivers, are well-established (38, 39). As a potent illustration, a recent review identified 119 manuscripts querying subjective sleep complaints in pediatric ADHD (40). Common sleep complaints among youth with ADHD include general “sleep problems” as well as specific difficulties with bedtime resistance, longer SOL, shorter sleep duration, reduced SE, poorer sleep quality, and greater daytime sleepiness (38–40).

PSG.

Results from PSG studies suggest few consistently-observed differences in traditional measures such as TST, SOL, WASO, SE, or sleep architecture (stages) between youth with ADHD and their typically developing peers (41). An accumulating literature, however, highlights spectral sleep-EEG abnormalities which may characterize pediatric ADHD. A recent meta-analysis indicated that compared to their peers, slow wave activity (SWA; delta EEG power) is higher in children but lower in adolescents with ADHD compared to healthy controls as well as abnormalities in cyclic alternating pattern subtype 1 (EEG-synchronized slow-waves) (42). As SWA is closely tied to brain maturation and reflective of homeostatic sleep processes (43), this may suggest atypical patterns in neurodevelopment and sleep pressure accumulation in youth with ADHD (42).

Prior to onset.

For many youth with ADHD, sleep disturbances are present prior to the age of typical diagnosis (age 5–12). Cross-sectional studies with preschoolers have shown relationships between elevated ADHD symptoms and greater parent-reported sleep problems, longer sleep latencies, shorter sleep durations, and greater daytime sleepiness (44–48). Further, longitudinal studies have suggested that shorter sleep duration, greater sleep problems, bedtime struggles, and longer sleep latencies in infancy/toddlerhood are related to increased ADHD symptoms at age 5 (49–52), as well as bidirectional links between ADHD symptoms and shortened sleep duration and increased awakenings across the toddlerhood and preschool (53, 54).

Role in maintenance.

Sleep problems increase symptom burden in pediatric ADHD. Specifically, sleep disturbances are associated with greater core ADHD symptom severity (inattention, hyperactivity/impulsivity), increased externalizing (e.g., oppositional defiant behaviors) and internalizing (i.e., anxiety, depression) behaviors, and deficits in executive functioning and cognition (40). Further evidence suggesting that sleep plays a role in the maintenance of ADHD symptoms and related morbidity is provided by clinical trials evaluating behavioral sleep interventions, which have shown that treating sleep in children and adolescents with ADHD not only improves sleep, but also core ADHD symptoms and executive functioning (55, 56).

Autism Spectrum Disorder (ASD)

The last decade has seen a sharp rise in ASD prevalence, owing to increased community awareness and medical and public health efforts to better understand characteristic features of ASD (57). In the U.S.A., ASD occurs in 1 in 36 children, and is 4 times more common among boys than girls (58). ASD is characterized by persistent deficits in communication (e.g., socioemotional reciprocity; nonverbal communicative behaviors; building relationships) and restrictive or repetitive behaviors and activities (e.g., hand gestures, lining up objects, insistence on a certain route to home) (19).

Subjective.

Caregiver-reported sleep problems among autistic youth are well-documented in research, including challenges in establishing a bedtime routine, higher bedtime resistance and/or anxiety, difficulty initiating and maintaining sleep, repetitive behaviors when falling asleep, and daytime sleepiness (59, 60). Likewise, autistic youth endorse prolonged SOL, more awakenings, decreased SE, and higher daytime sleepiness (60, 61).

PSG.

PSG findings vary across studies, and include shorter time in bed, reduced TST (by ~50 minutes), prolonged SOL, and lower SE (59–61) among autistic children compared to neurotypical peers. A minority of studies suggest greater WASO, decreased REM latency, and lower REM density (60, 61), as well as increased proportion of N1, lower spindle density, shorter spindle duration, lower cyclic alternating pattern during N3, and decreased A1 and increased A2/A3 during light sleep in autistic youth as compared to neurotypical children (59–61).

Prior to Onset.

Sleep disturbances for autistic children have been documented in the first two years of life, attributed to neurobiological alterations in the developing brain. Emerging evidence suggests sleep onset problems in the first year of life precede ASD diagnosis and are associated with altered neurodevelopmental trajectories (hippocampal volume) among infants at high familial risk for ASD (62).

Role in Maintenance.

Sleep disturbances may exacerbate ASD features such as greater social withdrawal and repetitive and restrictive behaviors. Among autistic youth, sleep disturbances are also associated with impaired cognitive development and emotional and behavioral problems, including anxiety and aggression (63). Evidence from a large, prospective birth cohort in the Netherlands suggests sleep problems may be a part of the ASD construct (64).

Mood Disorders

Mood disorders are significant causes of functional impairment among youth. Depression is characterized by low mood and/or anhedonia for ≥2 weeks, accompanied by somatic, psychomotor, and cognitive changes (19). The U.S. prevalence of major depression among adolescents has doubled in the last decade (8.1% to 15.8%) (65). Bipolar Spectrum Disorders (BSD) are defined by periods of mania/hypomania (i.e., elated and/or irritable mood accompanied by increased energy, agitation, and/or grandiosity), which may alternate with depressive episodes (19). Although rare in childhood, BSDs may be preceded by non-specific anxiety symptoms, depressive episodes, and disordered sleep (66). Notably, both depression and mania/hypomania diagnostic criteria include sleep disturbance (19).

Subjective.

Subjectively-measured sleep disturbances, including poor sleep quality, disrupted sleep-wake cycles, nightmares, and sleep disorder symptoms (i.e., insomnia, hypersomnia) are reported in 75–90% of youth with depression (67, 68). Noted impairments among caregivers and youth with BSD include erratic sleep patterns, restless sleep, intense nightmares, prolonged SOL, frequent nighttime awakenings, and increased total time awake (67, 69). A longitudinal study found that self-reported sleep disturbances were associated with elevated clinician-rated mania and depression symptoms in adolescents with BSD over a 2-year period (69).

PSG.

Per meta-analysis, adolescents with depression exhibit longer SOL, lower SE, and increased light sleep and REM density compared to healthy controls (68). Additional studies have suggested abnormalities in SWA (NREM delta EEG power) and/or sleep spindles in adolescents with depression (for a review, see: 70); including higher frontal SWA (71), lower initial SWA in females (72), and lower initial SWA and/or flatter pattern of SWA decline overnight in males (73, 74), as well as reduced sleep spindle activity among adolescents with depression, particularly for females, (75) and associations between lower sleep spindle activity and greater depression symptom severity (76). In a recent large study of 102 adolescents with major depression, increased REM latency and N2 duration and less N3 and REM durations were observed compared to peers without depression (77).

Less is known about PSG-measured sleep in pediatric BSD. One older study found decreased SE, increased nighttime awakenings, increased N3, and decreased REM compared to controls (78). A more recent study found reduced N2, higher REM density, and longer first REM duration in a pediatric sample with BSD compared to healthy controls and/or those with ADHD (79). Small sample sizes of these studies (both n=13 with BSD) limit conclusions regarding generalizability of findings.

Prior to Onset.

Evidence suggests sleep disturbances (as early as age 5) are precursors to depression among youth (80). A recent meta-analysis found that a history of sleep disturbance was associated with a 1.5 to 2-fold increase in the odds for depression or BSD in adolescence and young adulthood (81). In a prospective epidemiological study, difficulties initiating and maintaining sleep were predictive of later BSD in a sample of adolescents and young adults (82). Among youth at familial risk for BSD, childhood sleep disorder confers increased risk of mood disorders, and is implicated in the developmental trajectory of BSD (83). Although evidence for a prospective role for insomnia in the occurrence of psychiatric illness is strongest for depression, there is suggestion of insomnia’s role in the development of other psychiatric disorders, including BSD, via alterations in emotional regulation and circadian cycles (81, 84).

Role in Maintenance.

There is considerable overlap in the cognitive and behavioral consequences of disrupted sleep, depression, and BSD, including low mood, irritability, and diminished decision-making. Poor sleep exacerbates mood symptoms and negatively impacts quality of life and treatment outcomes. Sleep disturbances may persist despite successful treatment for depression, which in turn may be a hallmark for depression recurrence. Reduced SE and prolonged SOL have been identified as distinct markers for short-term relapse (within one year) of depression in adolescents. Insomnia may also be a trigger for BSD relapse, including manic episodes (67, 80).

Suicidality

Suicidality is defined by persistent thoughts of death, making plans for one’s own death, acts of self-harm with life-ending intent, and completed suicide. Worldwide, suicide is a leading cause of death among young people with far-reaching social and economic consequences (85, 86). In the last decade, suicidal contemplation, planning, and attempts has increased among U.S. youth (87). Suicide is the second leading cause of death among 10–24 year olds (88).

Subjective.

Insomnia, nightmares, short (<7 hr) or long (>9–10 hr) duration, and weekend oversleep (≥2 hour increase) are associated with youth suicidality (89, 90). Cross-sectional and prospective studies link sleep-related complaints with increased risk of suicidal ideation (79%–135%), plans (58%), and attempts (92%) (91). A recent review of longitudinal studies found that sleep problems with greater specificity (e.g., initial insomnia) were more predictive of suicidality among adolescents than less specific complaints (e.g., feeling tired), and that sleep problems have greater utility as a proximal short-term risk factor than a long-term predictor (92). Data supports a curvilinear dose-response relationship between self-reported sleep duration and adolescent suicidal ideation and attempts (89, 90, 93).

PSG.

A recent PSG study suggested longer SOL and REM latency, higher N1 and REM density, and less N3 among youth hospitalized during a suicidal crisis compared to non-suicidal adolescents (94). Further, shorter REM latency, greater REM, and awakenings were related to poorer inhibition accuracy in response to emotional stimuli, and greater N2 and less N3 were associated with fewer neural resources activated by inhibitory processing, especially in the context of negative emotional valence. This suggests REM sleep and nocturnal awakenings may be associated with failures in inhibition during emotional processing, and the depth of NREM sleep may be associated with fewer neural resources available for inhibition (95).

Prior to Onset.

Impaired sleep is postulated to increase risk of suicidality via its effect on cognitions and perceptions, yielding: deficits in executive functioning (i.e., problem solving, impulse control); impaired emotional regulation and reactivity; a hyperarousal state (lower fear of death, increased pain tolerance); perceptions of isolation, loneliness, and burdensomeness; and rumination on negative self-appraisal and feelings of hopelessness (89). Further, without the ability to engage sleep as a mechanism to break cycles of compromised thought, risk for suicidality is intensified.

Role in Maintenance.

Affective reactivity is a proximal mechanism through which sleep disturbances are proposed to influence and maintain risk for suicidal thinking. Among youth at high-risk for suicidal behavior, worse sleep quality than usual (relative to an individual’s mean) predicts next-day suicidal ideation via reduced affective reactivity to positive interpersonal events and heightened affective reactivity to negative interpersonal events (96).

Psychosis

Psychotic disorders affect 1% of the population, and are characterized by aberrant thinking and perceptions (delusions, hallucinations); negative symptoms (e.g., amotivation, flattened affect); and cognitive deficits (e.g., impaired attention, memory) (19). Although typically diagnosed in early adulthood, an emerging body of research has investigated sleep disturbances in adolescents at clinical high-risk (CHR) of psychosis, who display attenuated psychosis symptoms (97). As these youth are at elevated risk of developing psychosis, research in adolescents at CHR may inform understanding of the role of sleep in the etiology and prevention of psychotic disorders (98).

Subjective.

Adolescents at CHR report greater frequency and severity of sleep disturbances, including greater overall sleep problems and specific concerns regarding poor sleep quality, more awakenings, fragmented sleep, and increased nightmares. Per recent meta-analysis, there is no consistent indication of shorter sleep duration in this population via self-report, suggesting concerns reported by CHR adolescents center more specifically on disruptions to sleep continuity and quality (97).

PSG.

Only a handful of PSG studies have examined sleep disturbances in adolescents at CHR. Increased SOL (99) and WASO (100) have been observed. Regarding spectral EEG findings, research from one group has shown reduced spindle duration, particularly in the centro-parietal and prefrontal regions (101), and higher NREM sleep gamma EEG power in the fronto-parieto-occipital area (100). Replication of PSG findings among adolescents at CHR is critically needed.

Prior to Onset.

Sleep disturbances predict worsening of attenuated psychosis symptoms over time, and thus may play a role in conversion to a psychotic disorder (102). Longitudinal studies show that subjectively-measured shorter sleep duration (103) and disrupted sleep continuity (104) are associated with greater positive symptoms 1 to 2 years later among youth at CHR, although only sleep continuity remained a predictor of later positive symptoms after controlling for baseline psychosis symptom severity (104). In a study developing a predictive model for transition from CHR to first-episode psychosis, subjective sleep disturbances were an identified component, doubling conversion risk (105). Finally, a recent study suggests that subjectively-measured sleep disturbances predict increased psychosis symptoms over time, but not vice versa, among adolescents at CHR (106).Role in Maintenance. Sleep disturbances may play a role in the maintenance and exacerbation of attenuated psychosis in adolescents at CHR (97, 102). Greater subjective sleep disturbances are related to increased positive and negative symptoms and worsened psychosocial functioning (107–109), and increased NREM gamma power in medial fronto/parietal areas is positively related to increased negative symptoms (100). Sleep disturbances are also associated with cognitive impairment among youth at CHR; for example, poorer subjective sleep quality is related to worsened procedural learning (110), and spindle frequency is correlated with working memory deficits (101). A recent randomized, controlled pilot trial of a cognitive-behavioral sleep intervention, adapted for adolescents at CHR, provided promising preliminary evidence for sustained improvements in sleep, as well as reduced depression, anxiety, and paranoia (111), suggesting a possible role of sleep disturbance in psychosis etiology (112).

Early Onset Schizophrenia.

Additional evidence for a role of sleep disturbances in schizophrenia onset and maintenance comes from the literature investigating early onset schizophrenia (EOS), in which schizophrenia onsets during childhood and/or adolescence. EOS is conceptualized as phenomenologically and neurobiologically similar to adult-onset schizophrenia, but may represent a more severe form of the disorder associated with more pronounced developmental, neural, and genetic risk factors (113). Studies with EOS populations have suggested greater beta power during REM and NREM sleep (114) and deficits in sleep spindle activity (amplitude, duration, density, and/or frequency) and coherence compared to healthy and clinical (i.e., depressed) controls. Further, diminished spindle activity has been associated with severity of positive and negative symptoms as well as cognitive impairment (memory consolidation, processing speed) among youth with EOS (115, 116). Notably, a recent study demonstrated overlap in the genetic variants for schizophrenia and sleep spindle activity among healthy adolescents, highlighting sleep spindle deficits as a possible endophenotype for psychosis (117).

Conclusions

Subjectively-measured sleep disturbances such as bedtime resistance, prolonged SOL, shorter sleep duration, nighttime awakenings, poor sleep quality, nighttime anxiety, nightmares, and daytime sleepiness are prominent features across psychiatric disorders of childhood, highlighting the transdiagnostic nature of problematic sleep underlying behavioral health concerns. In contrast, PSG findings are inconsistent regarding observed sleep problems within psychiatric diagnostic categories, likely due to inconsistency in or limitations of methods (e.g., home versus lab PSG, number of nights of recording, small or unrepresentative samples). Specifically, procedures that rely on only 1 night of in-lab PSG recording may result in elevated estimates of sleep disturbances due to the first night effect, in which discomfort with sleeping in an unfamiliar location interferes with typical sleep patterns (118). In-home recordings may reduce the impact of the first night effect for children and adolescents (119); however, research suggests that multiple nights of recording (≥3) remain necessary to obtain a stable measure of an individual’s habitual sleep, as sleep patterns vary from night to night (120).

Other methodological limitations in the PSG studies reviewed include small samples (often N<30), variability in the presence or absence of comorbid diagnoses, mixed samples of youth receiving inpatient or outpatient care, and potential medication confounds, all of which increase the challenge of comparing results across studies. For example, psychotropic medications such as stimulants or selective serotonin reuptake inhibitors (SSRIs) may alter a range of physiological sleep metrics as measured by EEG, including SWA (NREM delta EEG power) among youth with ADHD (42) and measures of REM latency and percentage among adolescents with depression (121). In addition, many studies including wide age ranges (e.g., collapsing across childhood and adolescence, or extending into young adulthood), which is problematic given the significant shifts in sleep behavior and physiology occurring across development (15–17).

In addition, PSG results differ across psychiatric disorders. Notably, although differences in traditional PSG indices such as TST, SOL, WASO, and SE are observed in some disorders (i.e., mood disorders, ASD), there is little consistent evidence of such impairments in others (i.e., ADHD, anxiety disorders), despite the high degree of subjective sleep complaints associated with these conditions. This apparent discrepancy, between the high frequency of reported sleep disturbances among youth with psychiatric disorders compared to healthy controls paired with a lack of reliable group differences in PSG measures, begs a critical question: what is different about the sleep of children and adolescents with psychiatric disorders that underlies subjectively-reported sleep complaints?

The answer may lie in the physiology of their sleep, in which commonalities across disorders may emerge. For example, findings to date suggest abnormalities in the amount and pattern of SWA (NREM delta power) overnight in ADHD and depression, REM density in pediatric mood disorders, and sleep spindles (NREM sigma power) in youth with anxiety disorders, ASD, CHR for psychosis, and EOS. It is possible that these physiological differences may contribute to the perceived sleep complaints of youth with psychiatric disorders. For example, in adults, greater REM and less N3 are indicators of poor sleep quality (122), and NREM sleep EEG spectral indices (e.g., lower delta power; greater alpha, sigma, beta power) are related to poorer perceived sleep quality even when traditional indices (i.e., TST, SE, WASO) are similar to that of healthy controls (123). Whether physiological processes similarly underlie subjectively-reported sleep disturbances in pediatric psychiatric populations is yet unknown.

Beyond possible sleep differences among psychiatric versus non-psychiatric youth populations, accumulating evidence across the disorders reviewed suggests that sleep disturbances are frequently present prior to onset, often as early as the preschool years, and following onset, likely play a role in maintaining psychiatric and related concerns in youth, including inattention, mood and anxiety symptoms, cognition deficits, and social impairments. Perhaps the strongest support for the role of sleep in the development and exacerbation of childhood psychiatric conditions comes from behavioral sleep treatment research. Across conditions, when sleep is enhanced through behavioral sleep interventions, downstream positive effects on mental health symptoms are observed (124), leading researchers to suggest that sleep plays a causal role in driving psychiatric symptoms (125). Although replication of such findings is clearly warranted, evidence in this review suggests that early detection and treatment of sleep problems may represent a critical opportunity for prevention and amelioration of psychiatric conditions in youth.

Where does the field go from here? In order to better understand and treat the biological sleep processes underlying subjective sleep complaints among youth with psychiatric disorders, scientific consensus on best methods for PSG data collection in children (e.g., multiple nights of PSG may improve reliability (120)) and standardization in future research would allow for better comparison of results across studies. Studies should further ensure adequate representation of the diverse population of youth with sleep and mental health concerns (126). Given significant psychiatric comorbidity in childhood, future research may investigate links between sleep physiology and cross-cutting biobehavioral dimensions (e.g., negative valence, positive valence, cognitive systems) rather than focusing on specific diagnostic classifications (127). Although not covered in the current review, circadian rhythm disruptions are implicated in pediatric mental health (128), and future studies combining objective circadian measures (e.g., dim light melatonin onset) with PSG may allow for disentangling of circadian versus homeostatic drivers of physiological sleep disruptions in youth. Finally, incorporation of PSG measures as outcomes (e.g., NREM delta, sigma power) in clinical trials of behavioral sleep interventions for youth with mental health conditions may clarify the specific physiological sleep processes underlying psychiatric symptoms and elucidate brain-based sleep processes (e.g., improved homeostatic sleep pressure) underlying treatment gains (112).

Despite the transdiagnostic nature of sleep complaints in youth with psychiatric conditions and a possible role for sleep in prevention of mental health conditions, sleep disturbances remain under-assessed and under-treated in pediatric populations (129). Advancing knowledge of the biological sleep processes underlying onset and maintenance of mental health conditions in children and adolescents may facilitate targeted assessment, prevention, and intervention strategies to improve psychiatric health across the lifespan.