Sleep in Children and Adolescents with Behavioral and Emotional Disorders

501

SLEEP MEDICINE CLINICS Sleep Med Clin 2 (2007) 501–511

Sleep in Children and Adolescents with Behavioral and Emotional Disorders Ronald E. Dahl, -

-

-

a,

MD

*, Allison G. Harvey,

Emotional disorders: bidirectional relationship between sleep and affective function Major depressive disorder Anxiety disorders Bipolar disorder Sleep and problems with behavioral and attentional control Attention-deficit–hyperactivity disorder Aggression–oppositional defiant disorder and conduct disorder Sleep in other psychiatric disorders Tourette’s

The interface between sleep problems and psychiatric disorders represents an extremely important dimension of child and adolescent mental health. This is most evident in the domain of emotional disorders (specifically depression, anxiety, and bipolar disorder), and there are equally compelling questions about the role of sleep in relation to attention deficit disorders and clinical problems with aggression. Emerging data also indicate that sleep is an important issue in autistic spectrum disorders (ASD) and other neurodevelopmental disorders. From a clinical perspective, there are at least three important reasons to address this interface between sleep problems and psychiatric disorders. First, sleep problems occur at high rates in several of

-

-

b

PhD

Eating disorders Autism A multicomponent behavioral sleep intervention for youth Providing the motivation Sleep and circadian education Stimulus control Bedtime worry, rumination, and vigilance Targeting media use and social activities Relapse prevention Summary References

these disorders. Sleep represents an important pragmatic domain for diagnosis and intervention. Second, not only are sleep symptoms seen at high rates in many child psychiatric disorders, but psychiatric symptoms occur at increased rates in several pediatric sleep disorders, such as narcolepsy, Kleine-Levin syndrome, restless legs syndrome and periodic limb movement disorder (PLMD), and obstructive sleep apnea syndrome (OSAS). Third, there is growing interest in identifying causal or etiologic links between sleep-arousal regulation and aspects of behavioral-emotional functioning; a deeper understanding of this interface may provide new insights and opportunities for early intervention.

a

University of Pittsburgh, 3811 O’Hara Street, Pittsburgh, PA 15213, USA Psychology Department, University of California, 3210 Tolman Hall, No. 1650, Berkeley, CA 94720–1650, USA * Corresponding author. E-mail address: [email protected] (R.E. Dahl). b

1556-407X/07/$ – see front matter ª 2007 Elsevier Inc. All rights reserved.

sleep.theclinics.com

doi:10.1016/j.jsmc.2007.05.002

502

Dahl & Harvey

Addressing the full range of issues and questions at this interface of sleep and mental health, and considering these issues across the full developmental range from infancy through adolescence, exceeds the space limitations for this article. Accordingly, two primary areas are explored: sleep and emotional disorders (where the largest number of studies have been conducted), and sleep in behavioral disorders (focusing on attention disorders and clinical problems with aggression). This is followed by a brief consideration of sleep in several other psychiatric disorders. Finally, a multicomponent behavioral treatment aimed at improving sleep and sleep-wake schedules in children and adolescents, and the rationale and relevance of this intervention to a wide range of youth with sleep problems and affective or behavioral symptoms that might be attributable to (or exacerbated by) insufficient sleep is described.

Emotional disorders: bidirectional relationship between sleep and affective function Over the past decade, there has been increasing interest in understanding the bidirectional relationship between sleep disturbances and problems with emotion regulation in children and adolescents. There is growing evidence that problems with sleep can create or exacerbate emotional problems, and that emotional difficulties can interfere with sleep. Evidence from the sleep deprivation literature suggests that one of the strongest adverse effects of sleep deprivation is increased negative mood [1–3]. This is consistent with evidence suggesting that rapid eye movement (REM) sleep may be particularly important in emotional processing and mood regulation [4]. Another set of adverse consequences of sleep deprivation includes fatigue, tiredness, and diminished motivation, which can have a negative impact on affective functioning. Other observations have indicated that insufficient sleep can result in greater variability or lability of mood, leading to speculations about impaired emotion regulation. Theories include impaired frontal cortical modulation of affect [5], and sleep-deprivation causing lapses in self-monitoring of affective state. Lapses in self-monitoring of affective state also may have relevance to understanding why sleep deprivation can exacerbate difficulties with aggression and other domains of self-regulation of attention and behavior. There also are interesting questions about the causal links in the other direction (ie, why emotional difficulties lead to high rates of sleep disruption). These include questions about the role of

emotional arousal interfering with sleep, questions about anxiety and vigilance interfering with sleep, and the role of bedtime ruminations and worries [5–7]. Broadly speaking, these ideas reflect the concept that sleep and vigilance represent opponent processes, a theme developed further in the anxiety disorder section later. Independent of these intriguing theoretical questions, these bidirectional interactions (and the potential for a vicious cycle of negative effects) have important clinical implications, particularly among children and adolescents because they are still developing their abilities to control emotions. These issues become even more important when considered in relation to youth who struggle with specific emotional disorders, as reviewed next.

Major depressive disorder Major depressive disorder (MDD) is prevalent in young people [8] and has been linked strongly to sleep problems across the lifespan. In particular, several studies have reported a relationship between MDD and disturbance in subjective sleep in children and adolescents [9,10]. Findings on objective sleep problems in children with depression have yielded mixed results, with some studies finding poor sleep quality in depressed children [11], whereas several have not [12–14]. A recent large controlled study by the authors’ research group reported that children with depression reported many subjective sleep complaints but did not reveal objective polysomnography (PSG) evidence of disturbed sleep [9]. After puberty, however, studies of adolescent depression have found stronger evidence of objective sleep disturbances, especially prolonged sleep latency and increased cortisol in the period near sleep onset [15,16]. One meta-analysis revealed that the sleep of depressed individuals with a mean age of less than 20 years was largely indistinguishable from controls [17]. Furthermore, in contrast to the robust finding in adults that reduced REM latency predicts the recurrence of depression in depressed adults [18], findings about predictive value of REM latency in children and adolescents have not been as strong [19]. This could have something to do with the maturity of the central nervous system. Other investigators have examined the microarchitecture of sleep (focusing on measures of intrahemispheric and interhemispheric coherence) and have reported some changes in sleep measures associated with depression [20]. These investigators have argued that these findings may indicate alterations in neurodevelopment in some individuals with depression.

Sleep Problems and Psychiatric Disorders

Anxiety disorders Youth anxiety is common, impairing, and strongly associated with later anxiety and mood disorders [21]. Insomnia, nightmares, or nocturnal panic attacks are prominent features of sleep disturbance that spans across many anxiety disorders [22]. In studies from the Pittsburgh group [16,23], young people with anxiety disorders showed increased levels of cortisol in the period near sleep onset, and more evidence of objective sleep problems when compared with healthy controls or those with MDD. These sleep findings held even when those with comorbid MDD were excluded from the anxiety group. In comparison, the objective sleep measures in the children and adolescents with MDD were similar to those of the control group. Moreover, in contrast to the findings in the MDD group (where subjective sleep complaints were the primary findings), the sleep problems in the anxiety group were more evident in PSG-based sleep measures than in subjective sleep measures. The only variable for which both objective and subjective differences for anxiety disorders emerged was sleep latency. The correlations between anxiety symptoms and sleep latency were consistent with this pattern. Most strikingly in the objective measures of sleep latency, youth with anxiety disorders showed sleep latencies that were greater than the control or MDD groups on night 2 in the laboratory but not on night 1. Sleep latency typically decreases with adjustment to the sleep laboratory environment, with youth typically falling asleep more quickly on the second night; however, this decrease was not evident in the anxiety group [23]. It is possible that anxiety interferes with the processes of adjusting to sleeping in the laboratory. There is also prospective evidence showing that persistent insomnia is associated with an increased risk of developing an anxiety disorder [24–26]. More recently, a large study looking at the association of insomnia with anxiety disorders and depression in youth [27] explored the direction of the association between insomnia and anxiety disorders and major depression among a community-based sample of adolescents. Data from a community-based sample of 1014 youth aged 13 to 16 found that the lifetime associations of Diagnostic and Statistical Manual-IV (DSM-IV) insomnia with anxiety disorder and with depression were moderate (odds ratio 5 3.2–6.8). Among those with comorbid disorders, anxiety disorders preceded insomnia 73% of the time, whereas insomnia occurred first in 69% of comorbid insomnia and depression cases. Any prior anxiety disorder was associated with an increased risk of insomnia, adjusting for gender, race and ethnicity, and

depression before insomnia (odds ratio 5 3.5). Prior insomnia, however, was not significantly associated with onset of anxiety disorders. Prior depression was not associated with onset of insomnia, but prior insomnia was associated with onset of depression adjusting for gender, race and ethnicity, and any prior anxiety disorder (odds ratio 5 3.8). These results suggest distinct natural courses of development between DSM-IV insomnia, anxiety, and depression during adolescence. Additionally, insomnia may have independent, and potentially etiologically distinct, directional associations with anxiety disorders versus depression. The occurrence of sleep problems in young people with anxiety disorders could reflect vigilance processes and the biased information processing that are postulated to characterize early onset anxiety [28]. For instance, children and adolescents with anxiety disorders tend to shift their attention toward potential threats [29]. Because vigilance interferes with the feelings of safety that are critical to the onset and maintenance of sleep [30], it may contribute to the longer sleep latency and less frequent deep sleep in the young people with anxiety in the authors’ study. Specifically, stage 4 sleep is postulated to be particularly important to vigilance and safety [30] because deep sleep requires a sense of security about one’s surroundings, a core feature in the development of a vigilance-avoidance model has implications for understanding sleep problems in childhood and adolescence [5]. At the most fundamental level, sleep and vigilance represent opponent processes. Physiologically, going to sleep requires turning-off awareness and responsiveness to threats in the external environment. Because of this loss of vigilance and responsiveness, sleep is naturally restricted to safe times and places (eg, animals and birds tend to sleep in safe burrows, nests, or temporal niches that minimize dangers). In the anxiety disorders, one important domain for assessing the safe conditions that permit or promote sleep focuses on social and emotional appraisals of threat [5,31]. Although these tendencies have adaptive advantages (inhibiting sleep in truly dangerous environments), they also have costs: high levels of anxiety and vigilance based in perceived threats can lead to chronic sleep difficulties. A major source of difficulty for children and adolescents is rooted in presleep onset worries and ruminative thinking at bedtime, which naturally increase vigilance and interfere with going to sleep. Yet, it can be equally problematic if anxious youth avoid these distressing bedtime worries by staying up (or getting back out of bed) to engage in very late hours of school work, watching television, or socializing (by Internet or cell phones). These patterns of behavior often lead to difficulty getting to sleep until very late on

503

504

Dahl & Harvey

school nights resulting in insufficient sleep because of the need to get up early for school. Without effective intervention, this pattern of vigilance and avoidance can lead to extremely problematic sleep habits and patterns in adolescents with anxiety disorders (a treatment approach to address this is described in the final section of this article).

Bipolar disorder The emergence of bipolar disorder during childhood and adolescence is of particular concern because it may have a more severe presentation and course [32–37]. In adults with bipolar disorder, the case for sleep contributing to mood disturbance is fairly compelling: sleep loss is highly correlated with daily manic symptoms [38]; among patients with bipolar disorder, sleep disturbance is the most common prodrome of mania and the sixth most common prodrome of depression [39]; and induced sleep deprivation triggers hypomania or mania in a proportion of patients [40–45]. In youth with bipolar disorders, rates of significant sleep disturbance range from 35% to 45% [46]. In these younger samples, however, research and clinical questions relating to the possible link between sleep disturbance and mood are yet to be addressed.

Sleep and problems with behavioral and attentional control Another major domain of the interface between sleep and psychiatric disorders is the link between sleep and regulation of behavior and attention, especially its relevance to attention-deficit–hyperactivity disorder (ADHD) and aggression. There has been a long interest in the role of sleep deprivation (or sleep fragmentations such as occurs in OSAS, PLMD, and narcolepsy) as causing difficulties with focused attention that mimic or exacerbate symptoms of ADHD, including evidence that improvements in sleep can have a positive impact on attentional functioning [47,48]. Theses issues are considered in relation to ADHD and problems related to aggression in the following sections.

Attention-deficit–hyperactivity disorder There has been considerable interest (and controversy) in the relationship between sleep and attention disorders. For decades, clinical investigators have described high rates of sleep problems in youth with attentional problems. This has included several lines of evidence: (1) that behavioral sleep problems (or simply insufficient sleep) may exacerbate or mimic ADHD; (2) evidence that children with OSAS have high rates of ADHD and improvement in behavioral symptoms in response to

treatment of OSAS; (3) evidence that restless legs syndrome and PLMD are associated with ADHD; (4) that narcolepsy in children is associated with ADHD; and (5) that response to stimulants in some ADHD youth could reflect treatment for sleep deprivation. One of the first important issues to be considered is the distinction between subjective and objective measures of sleep. More specifically, as one moves from studies using highly subjective measures (eg, parental questionnaires) to more objective measures (sleep logs, actigraphy, and PSG studies) the rates of sleep problems (and effect sizes in controlled studies) steadily diminish. Although subjective reports of sleep complaints are highly prevalent in ADHD samples, objective evidence of sleep abnormalities is much weaker. There is an extensive literature (and several conceptual and methodologic issues pertinent to these issues) making a comprehensive discussion beyond the scope of this article. These issues have been addressed in two recent systematic reviews. One by Cortese and colleagues [49] reviewed evidence on sleep and alertness in children with ADHD controlling for potential confounding factors. They excluded studies not using DSM-III-R or DSM-IV criteria for diagnosis and studies not excluding or controlling for psychiatric comorbidity or medication. They performed a meta-analyses based on the remaining studies. The primary objective measures that emerged as significant were as follows: the proportion of subjects who fell asleep during the Multiple Sleep Latency Test, the number of movements in sleep, and the apnea-hypopnea index (each of these was significantly higher in children with ADHD than in controls). They found no significant differences in other objective parameters (sleep-onset latency; number of stage changes; percentages of stage 1 sleep, stage 2 sleep, slow wave sleep, or REM sleep; REM sleep latency; and sleep efficiency). Limited evidence from subjective studies suggested no significant differences in sleeponset difficulties and bedtime resistance between children with ADHD and controls, after controlling for comorbidity and medication status. They noted, however, that data on sleep duration, night and morning awakenings, and parasomnias are still very limited. A second meta-analysis by Sadeh and colleagues [50] took a rigorous approach to systematic review of this area, focusing only on studies with objective measures, and considering a range of factors including age, gender, inclusion of adaptation night, and comorbidity. They found only one PSG variable to reveal a small but significant effect size: PLMD (d 5 0.26; P < .05; 95% confidence interval 0.04–0.49).

Sleep Problems and Psychiatric Disorders

Taken together, these studies raise several important issues. There is some evidence that PLMD and OSAS may contribute to ADHD. It seems that youth with ADHD may show more daytime sleepiness when this is assessed with objective measures, such as Multiple Sleep Latency Test (most studies, however, did not perform this test). More broadly, the data suggest the important possibility that many youth with ADHD may show behavioral sleep problems at home (eg, resisting going to bed, or difficulty settling amidst multiple distractions), which may not show up on laboratory studies where staff are controlling many behavioral aspects of sleep. Clearly, additional large controlled studies are needed to further disentangle these complex but important questions.

Aggression–oppositional defiant disorder and conduct disorder It seems that sleep deprivation increases irritability and some tendencies toward aggression in both human and animal studies, showing increased aggression and impulsivity following experimental sleep loss. Rats, for example, show increases in aggression and defensive fighting after sleep deprivation. One recent study found that animals that were easy to handle at baseline became irritable and aggressive following modest amounts of sleep deprivation, with evidence of related changes in synaptic plasticity associated with these behavioral changes [51]. Clinical studies of children and adolescents also have revealed associations between sleep deprivation and irritability or aggression and difficulties with self-regulation in youth [5,52,53]. Most relevant is a recent study by Haynes and colleagues [54] that examined behavioral and emotional changes in adolescents with substance-related difficulties undergoing a behavioral sleep treatment. This study reported that improvements in sleep time were associated with significant decreases in the reporting of aggressive thoughts and actions. Taken together, these data suggest that inadequate sleep in adolescence may contribute to aggressive thoughts and actions, and that increased or improved sleep may reduce problematic aggression at least in some cases. This represents an important area for future research with very significant clinical and social policy implications.

Sleep in other psychiatric disorders Tourette’s Another example of a child psychiatric disorder where sleep seems to be important is Tourette’s syndrome. Numerous studies have documented sleep disruptions, including evidence of tics disrupting all stages of sleep [55]. These findings raise clinically

significant questions not only because sleep deprivation seems to make the tic symptoms worse, but also because of the frequent comorbidity with ADHD and other behavioral problems, because the sleep fragmentation may contribute to or exacerbate daytime symptoms. Treatment studies are needed to improve sleep and then examine both tics and other behavioral symptoms in response to improved sleep.

Eating disorders Disorders relating to eating typically have an onset during adolescence. Minimal research has been conducted to investigate whether there is an association with sleep disturbance and eating disorders, and most research conducted to date is correlational. The results published to date indicate that adolescent girls with anorexia nervosa exhibit more awakenings and lower sleep efficiency and slow wave sleep, relative to age- and gendermatched controls [56,57]. Bulimia nervosa seems to be characterized by sleep onset and sleep offset that is delayed by 1 hour [58]. The authors interpreted this finding as connected with time-consuming daytime binge-purge cycles. At the other end of the spectrum, there is growing evidence that sleep problems influence the risk for obesity. Sleep deprivation increases appetite, weight gain, and insulin intolerance through metabolic and neuroendocrine responses to sleep loss [59]. Although most of this work has been done in adults, there are emerging data showing the same pattern of findings in children [60–62]. Given the enormous epidemic of obesity and type-2 diabetes in children and adolescents, this raises a compelling set of questions about the role of sleep loss and erratic sleepwake schedules contributing to obesity, probably the single largest public health concern relevant to physical health and well-being in the United States.

Autism There has been emerging interest (and several recent studies) focusing on sleep problems in autism spectrum disorders (ASD)—neurodevelopmental disorders characterized by social deficits (impaired social motivation and social skills) in children who also typically show restricted range of interests and some repetitive behaviors. Numerous studies have reported that parents of children with ASD endorse high rates of sleep problems, with estimates ranging from 40% to 85% of youth experiencing significant problems with sleep. Moreover, given the heavy demands of caring for these children, the sleep problems seem to be particularly problematic, probably because they lead to sleep deprivation among parents who are often fatigued by the other demands of caretaking for special needs youth.

505

506

Dahl & Harvey

Understanding the causes of sleep problems in ASD children is at an early stage of progress. Clearly, behavioral problems and difficulties settling are part of the problem, and in one study, 65% of the families of ASD youth reported co-sleeping (compared with less than 10% of controls) [63]. In addition, there has been evidence that many ASD youth have increased anxiety, even though the anxiety may not be manifest in traditional symptoms (perhaps because of the social deficits). More recently, investigators have used objective measures (actigraphy and PSG) with strong evidence of sleep disturbances in ASD children. One particularly intriguing study in this area, by Malow and colleagues [64], reported EEG evidence of prolonged sleep latency and decreased sleep efficiency among ASD children reported by their parents as poor sleepers. Most interestingly, the ASD children with objective sleep problems showed significantly higher rates of anxiety, depression, and aggressive behavior compared with ASD children without sleep problems. Significant correlations were observed between PSG measures of sleep latency and these affective and behavioral symptoms, raising compelling questions about the direction of effects (ie, Are the emotional and behavioral problems leading to difficulties falling asleep? Or is sleep deprivation exacerbating emotional and behavioral difficulties in the daytime?). There are several treatment studies showing promising preliminary results in ASD children, including behavioral interventions [65,66] and an open (uncontrolled) study of sustained-release melatonin [63]. There is a need for more treatment studies, including an investigation as to whether improving sleep may have a positive effect on cognitive, affective, and social functioning.

A multicomponent behavioral sleep intervention for youth One of the most common clinical issues at the interface between sleep and psychiatric symptoms is when youth present with some combination of sleep problems and daytime symptoms that could be attributed to (or exacerbated by) insufficient sleep. The most pragmatic issue often is to what degree the mood or attention symptoms might be improved by better sleep (or a more regular sleepwake schedule compatible with daytime school schedules). The simplest way to address this, given the complexities and uncertainties of medication effects, is to use a behavioral intervention to improve sleep and to see the degree of improvement in daytime function. This is a particularly important issue in relation to affective disorders. Mood disorders are common

in adolescents, and 75% of depressed adolescents report difficulty falling asleep and most have late night and erratic sleep-wake schedules and difficulty falling asleep. This occurs in a context where many normal high school students have late or erratic bedtimes and insufficient sleep on school nights, with at least some daytime symptoms impacting mood and motivation, such as difficulty waking up on time for school, and daytime symptoms of tiredness, low motivation, and irritability. It can be very difficult to disentangle symptoms caused by the mood disorder and symptoms caused by problems with sleep and sleep-wake schedules. Because both domains (erratic and late-night bedtimes among high school students and affective disorders in adolescence) are quite common problems with overlapping features, the authors advocate the pragmatic approach of a behavioral intervention to improve sleep and regularize sleep-wake schedules, and then see how the mood, motivation, and attention symptoms change as a function of better sleep. Essential to this approach is the availability of effective treatments for this set of problems, particularly psychological and behavioral treatments that help youth develop better sleep habits, skills, and attitudes to maintain healthy sleep-wake schedules across adolescence. Intervention in childhood and adolescence seems especially important because there is a growing literature indicating that sleep problems predict the development of depressive disorders across the lifespan [67]. Accordingly, a multicomponent sleep treatment that was specifically designed to improve sleep in youth age 9 to 18 who have comorbid symptoms of anxiety or depression (or who are at risk for developing affective disorders) is described. This treatment has been developed and refined in conjunction with an early intervention research study, and data collection is currently underway to formally evaluate the effectiveness. Four sources of information have been drawn from in designing this treatment. First, interventions that are known to be effective for treating sleep disturbance in adults have been adapted [68], where there is preliminary evidence for the effectiveness of these approaches for sleep disturbance that is comorbid with psychiatric disorder in adults [69], and modified from a developmental perspective to target youth across a range of ages spanning early to late adolescence. Second, the experience of Bootzin and Stevens [70], who have published the only empirically supported behavioral sleep treatment study of adolescents, in work on sleep disturbance in adolescents with substance use disorders, has been drawn on. Third, the authors have been engaged in a collaboration with

Sleep Problems and Psychiatric Disorders

Dr. Greg Clarke to develop a manualized sleep intervention specifically for youth with unipolar depression as part of a randomized controlled trial. Fourth, the authors have collaborated with experts in motivational interviewing techniques (Dr. Melanie Gold and Dr. Daniel Shaw) to incorporate a Motivational Interviewing (MI) approach, which seems to be an essential element, particularly in adolescence where motivation to change bedtime patterns and habits is crucial to treatment effectiveness. Before describing the intervention, the importance of starting with a thorough assessment, including 1 to 2 weeks of sleep diary, should be emphasized. The initial assessment of youth with symptoms of insomnia should start with a thorough clinical interview with the patient and their family members to obtain information about the duration, frequency, and severity of nighttime sleep disturbance, including estimates of the key sleep parameters: sleep onset latency, number of awakenings after sleep onset, total amount of time awake after sleep onset, total sleep time, and an estimate of sleep quality. This information should encompass both weekday and weekend schedules and should assess the regularity of the schedule and the average schedule. The onset and duration of the insomnia and type of symptoms (ie, sleep onset, sleep maintenance, early morning or late morning awaking problems or combinations of these) should be assessed. A description of the daytime correlates and consequences of insomnia is a key domain of importance, as is gauging parental responses to the insomnia. In addition, it is crucial to obtain information about medications (prescription and over-the-counter) and conduct a screen for the presence of psychiatric disorders and medical problems (including other sleep disorders). Asking the patient to complete a sleep diary each morning, as soon as possible after waking, for 1 or 2 weeks provides a wealth of information including an insight into the night-to-night variability in sleeping difficulty and sleep-wake patterns and the presence of circadian rhythm disorders, such as delayed sleep phase disorder. An assessment should also include an exploration of the youth’s fears, because fear, distress, or any cognitive or emotional cue that prevents an overall sense of safety is likely to be antithetical to sleep (because sleep onset requires turning off awareness, responsiveness, and vigilance). Adolescents can often get into the habit of mentally reviewing or replaying worrisome thoughts or memories of stressful events. Some youth with stressful memories or specific fears manage to avoid these during the day through distracting activities, but at night (especially when trying to fall asleep) rumination on these distressing thoughts becomes

problematic. Assessment should also focus on sleep-wake schedules on weekends and holidays and on school nights because many youth develop a partial delayed sleep phase syndrome by following very late bedtimes on weekends despite the need to wake up early on school days. This treatment is typically delivered in six weekly sessions lasting 50 minutes. Between sessions, home projects are aimed to encourage practice opportunities to ensure generalizability of session content. Progress is monitored with daily sleep diaries. At the outset, research is urgently needed to empirically evaluate treatment, especially the efficacy and effectiveness, and to adapt the intervention to reflect the unique features of the different disorders (eg, the motivational component may need to be enhanced for depression, and the stimulus control intervention may need to be altered for youth with bipolar disorder).

Providing the motivation Many sleep-incompatible or sleep-interfering behaviors used by youth are rewarding (eg, text messaging with friends into the night, and freely surfing the Internet once parents have gone to bed). Moreover, as children move into adolescence, parental influence over bedtime and bedroom activities wanes. Hence, treatment is begun with a motivational component designed to assist the young person to find their internal motivation for enhancing sleep. This component involves exploring the pros and cons of change, supporting self-efficacy, eliciting self-motivational statements, generating solutions to potential barriers to change, and identifying social supports for change.

Sleep and circadian education By increasing knowledge, this component helps target specific factors and behaviors that interfere with good sleep. This is particularly important as children move into adolescence, a period where multiple sleep-interfering factors converge, including the pubertal phase delay in the circadian system causing a tendency to shift toward later bedtimes and increased autonomy to decide on bedtimes. Education about circadian influences on sleep is critical. As discussed elsewhere in this issue, adolescence is characterized by a biologically based tendency toward a more delayed sleep phase, a key developmental feature of the sleep-wake cycle of adolescents, and, thus, helping adolescents understand these circadian influences (and the importance of sleep patterns on weekends and holidays) is essential to establishing good sleep on school nights. This intervention component has two aims: to correct unhelpful sleep habits while developing new healthy sleep habits, and to maintain these new

507

508

Dahl & Harvey

healthier habits. The following target behaviors are typically addressed: (1) use of electronic devices in the bedroom during the presleep period; (2) the vastly different sleep-wake schedules that are adopted on weekdays relative to weekends and holidays; (3) because bright light exposure in the morning helps to counter phase delay in circadian rhythm, youth are encouraged to obtain morning exposure to bright light (eg, outdoor sunshine or bright artificial light); and (4) daytime naps and caffeine use are discouraged. After the initial session, the following steps are followed to correct habits: behavioral contracts and monitoring healthy sleep behaviors and sleep-unfriendly behaviors on a daily basis. The maintenance of healthy habits is achieved by regular check-ins on progress throughout the remaining sessions and by including targets of change from this component in relapse prevention.

consequences of thought suppression while in bed; and scheduling a presleep wind down period before bedtime. The authors’ approach to reducing vigilance is to provide education and increased awareness of vigilance, and to provide training on actively directing attention to deactivating stimuli in the bedroom environment. An additional element is to teach youth how to replace bedtime worry and rumination with a focus on how to remember and savor positive experiences [73].

Targeting media use and social activities A central issue influencing bedtime is the use of electronic media (Internet, cell phones, MP3 players) for entertainment and social interaction at night. A crucial aspect of achieving earlier sleep onset requires a behavioral contract by each individual wherein they voluntarily choose a time for turning off all access to these devices.

Stimulus control

Relapse prevention

The aims of stimulus control are to regularize the sleep-wake cycle and reverse maladaptive conditioning between the bed and not sleeping by limiting sleep-incompatible behaviors within the bedroom environment, while increasing cues for sleep-compatible behaviors. The stimulus control component involves providing a detailed rationale for and assisting the patient to achieve the following: (1) use the bed and bedroom only for sleep (ie, no television watching or text messaging); (2) get out of bed and go to another room whenever one is unable to fall asleep or return to sleep within approximately 15 to 20 minutes and return to bed only when sleepy again; and (3) arise in the morning at the same time (no later than plus 2 hours on weekends) and gradually move closer to a regular schedule 7 days a week [70]. Based on clinical experience treating anxious youth with stimulus control, when they are out of bed because they are unable to fall asleep, engaging in a diary writing task is encouraged. The goal of this is to reduce the attraction of sleep-interfering activities, such as the Internet and television.

The goal is to consolidate and maximize maintenance of gains and to set the child and parent on a trajectory for continued improvement. It is guided by an individualized summary of learning and achievements. Areas needing further intervention are addressed by setting specific goals and creating a specific plan for achieving each goal.

Bedtime worry, rumination, and vigilance There is a clear need to address bedtime worry, rumination, and vigilance. Vigilance and worry interfere with sleep because they activate distress and physiologic arousal [71,72]. This treatment component includes diary writing or scheduling a ‘‘worry period’’ to encourage the processing of worries several hours before bedtime; creating a ‘‘to do’’ list before getting into bed to reduce worrying about future plans or events; training to disengage from presleep worry and redirect attention to pleasant (distracting) imagery; demonstrating the adverse

Summary This article focuses on the interface between sleep problems and psychiatric disorders, with an emphasis on the bidirectional effects of sleep and affective function. It addresses sleep in emotional disorders (depression, anxiety, and bipolar disorder) and considers a set of compelling questions about the role of sleep in relation to attention deficit disorders and clinical problems with aggression. It describes emerging data indicating that sleep is an important issue in ASD and several other child psychiatric disorders. It also describes a multicomponent behavioral treatment aimed at improving sleep and sleep-wake schedules in children and adolescents, including the rationale and relevance of this intervention to a wide range of youth with sleep problems and affective or behavioral symptoms.

References [1] Dinges DF, Pack F, Williams K, et al. Cumulative sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per night. Sleep 1997;20:267–267. [2] Pilcher JJ, Huffcutt AI. Effects of sleep deprivation on performance: a meta-analysis. Sleep 1996;19:318–26.

Sleep Problems and Psychiatric Disorders

[3] Van Dongen HPA, Maislin G, Mullington JM, et al. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation. Sleep 2003;26:117–26. [4] Stickgold R, Hobson JA, Fosse R, et al. Sleep, learning, and dreams: off-line memory reprocessing. Science 2001;294(5544):1052–7. [5] Dahl RE. The regulation of sleep and arousal: development and psychopathology. Dev Psychopathol 1996;8:3–27. [6] Dahl RE. The regulation of sleep-arousal, affect, and attention in adolescence: some questions and speculations. In: Carskadon MA, editor. Adolescent sleep patterns: biological, social and psychological influences. Cambridge (UK): Cambridge University Press; 2002. p. 269–84. [7] Harvey AG, Tang NK, Browning L. Cognitive approaches to insomnia. Clin Psychol Rev 2005; 25(5):593–611. [8] Birmaher B, Williamson DE, Brent DA, et al. Childhood and adolescent depression: a review of the past 10 years. Part I. J Am Acad Child Adolesc Psychiatry 1996;35(11):1427–39. [9] Bertocci MA, Dahl RE, Williamson DE, et al. Subjective sleep complaints in pediatric depression: a controlled study and comparison with EEG measures of sleep and waking. J Am Acad Child Adolesc Psychiatry 2005;44(11):1158–66. [10] Ivanenko A, Barnes ME, Crabtree VM, et al. Psychiatric symptoms in children with insomnia referred to a pediatric sleep medicine center. Sleep Med 2004;5(3):253–9. [11] Emslie GJ, Rush A, Weinberg W, et al. Children with major depression show reduced rapid eye movement latencies. Arch Gen Psychiatry 1990; 47(2):119–24. [12] Dahl RE, Puig-Antich J, Ryan ND, et al. EEG sleep in adolescents with major depression: the role of suicidality and inpatient status. J Affect Disord 1990;19(1):63–75. [13] Puig-Antich J, Goetz R, Hanlon C, et al. Sleep architecture and REM sleep measures in prepubertal children with major depression: a controlled study. Arch Gen Psychiatry 1982;39(8): 932–9. [14] Young W, Knowles JB, MacLean AW, et al. The sleep of childhood depressives: comparison with agematched controls. Biol Psychiatry 1982;17(10): 1163–8. [15] Dahl RE, Ryan ND, Matty MK, et al. Sleep onset abnormalities in depressed adolescents. Biol Psychiatry 1996;39(6):400–10. [16] Forbes EE, Williamson DE, Ryan ND, et al. Perisleep-onset cortisol levels in children and adolescents with affective disorders. Biol Psychiatry 2006;59:24–30. [17] Benca RM, Obermeyer WH, Thisted RA, et al. Sleep and psychiatric disorders: a meta-analysis. Arch General Psychiatry 1992;49(8):651–68 [discussion: 669–70].

[18] Reynolds CF III, Perel JM, Frank E, et al. Opentrial maintenance nortriptyline in geriatric depression: survival analysis and preliminary data on the use of REM latency as a predictor of recurrence. Psychopharmacol Bull 1989;25(1): 129–32. [19] Rao U, Dahl RE, Ryan ND, et al. The relationship between longitudinal clinical course and sleep and cortisol changes in adolescent depression. Biol Psychiatry 1996;40(6):474–84. [20] Armitage R, Hoffmann R, Emslie G, et al. Sleep microarchitecture in childhood and adolescent depression: temporal coherence. Clin EEG Neurosci 2006;37(1):1–9. [21] Pine DS, Cohen P, Gurley D, et al. The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Arch Gen Psychiatry 1998;55(1): 56–64. [22] Harvey AG, Hairston IS, Gruber JL, et al. (in press - a). Sleep and anxiety. In: Antony MM, Stein MB, editors. Handbook of anxiety and the anxiety disorders. Oxford (UK): Oxford University Press. [23] Forbes EE, Bertocci MA, Gregory AM, et al. (in review). Objective sleep in pediatric anxiety disorders and major depressive disorder. Sleep, in press. [24] Patten CA, Choi WS, Gillin JC, et al. Depressive symptoms and cigarette smoking predict development and persistence of sleep problems in us adolescents. Pediatrics 2000;106(2):E23. [25] Breslau N, Roth T, Rosenthal L, et al. Sleep disturbance and psychiatric disorders: a longitudinal epidemiological study of young adults. Biol Psychiatry 1996;39:411–8. [26] Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders: an opportunity for prevention? J Am Med Assoc 1989;262:1479–84, 29. [27] Johnson EO, Roth T, Breslau N. The association of insomnia with anxiety disorders and depression: exploration of the direction of risk. J Psychiatr Res 2006;40(8):700–8. [28] Mogg K, Millar N, Bradley BP. Biases in eye movements to threatening facial expressions in generalized anxiety disorder and depressive disorder. J Abnorm Psychol 2000;109(4):695–704. [29] Taghavi MR, Neshat-Doost HT, Moradi AR, et al. Biases in visual attention in children and adolescents with clinical anxiety and mixed anxietydepression. J Abnorm Child Psychol 1999;27(3): 215–23. [30] Tikotzky L, Sadeh A. Sleep patterns and sleep disruptions in kindergarten children. J Clin Child Psychol 2001;30(4):581–91. [31] Worthman C, Melby MK. Toward a comparative developmental ecology of human sleep. In: Carskadon MA, editor. Adolescent sleep patterns biological, social, and psychological influences. Cambridge (UK): Cambridge University Press; 2002. p. 69–117.

509

510

Dahl & Harvey

[32] Birmaher B, Axelson D, Strober M, et al. Clinical course of children and adolescents with bipolar spectrum disorders. Arch Gen Psychiatry 2006; 63:175–83. [33] Cate Carter TD, Mundo E, Parikh SV, et al. Early age at onset as a risk factor for poor outcome of bipolar disorder. J Psychiatr Res 2003;37: 297–303. [34] Geller B, Craney JL, Bolhofner K, et al. Two-year prospective follow-up of children with a prepubertal and early adolescent bipolar disorder phenotype. Am J Psychiatry 2002;159:927–33. [35] Geller B, DelBello MP. Bipolar disorder in childhood and early adolescence. New York: Guilford; 2003. [36] Perlis R, Miyahara S, Marangell L, et al. Longterm implications of early onset in bipolar disorder: data from the first 1000 participants in the systematic treatment enhancement program for bipolar disorder (STEP-BD). Biol Psychiatry 2004;55:875–81. [37] Tohen M, Angst J. Epidemiology of bipolar disorder. In: Tsuang MT, Tohen M, editors. Textbook in psychiatric epidemiology. 2nd edition. New York: Wiley-Liss; 2002. p. 427–44. [38] Barbini B, Bertelli S, Colombo C, et al. Sleep loss, a possible factor in augmenting manic episode. Psychiatry Res 1996;65:121–5. [39] Jackson A, Cavanagh J, Scott J. A systematic review of manic and depressive prodromes. J Affect Disord 2003;74:209–17. [40] Colombo C, Benedetti F, Barbini B, et al. Rate of switch from depression into mania after therapeutic sleep deprivation in bipolar depression. Psychiatry Res 1999;86:267–70. [41] Kasper S, Wehr TA. The role of sleep and wakefulness in the genesis of depression and mania. Encephale 1992;18:45–50. [42] Leibenluft E, Albert PS, Rosenthal NE, et al. Relationship between sleep and mood in patients with rapid-cycling bipolar disorder. Psychiatry Res 1996;63:161–8. [43] Wehr TA, Sack DA, Rosenthal NE. Sleep reduction as a final common pathway in the genesis of mania. Am J Psychiatry 1987;144:201–4. [44] Wu JC, Bunney WE. The biological basis of an antidepressant response to sleep deprivation and relapse: review and hypothesis. Am J Psychiatry 1990;147:14–21. [45] Zwi R, Shawe-Taylor M, Murray J. Cognitive processes in the maintenance of insomnia and co-morbid anxiety. Behavioural and Cognitive Psychotherapy 2005;33:333–42. [46] Harvey AG, Mullin BC, Hinshaw SP. Sleep and circadian rhythms in children and adolescents with bipolar disorder. Dev Psychopathol 2006; 18:1147–58. [47] Chervin RD, Dillon JE, Archbold KH, et al. Conduct problems and symptoms of sleep disorders in children. J Am Acad Child Adolesc Psychiatry 2003;42(2):201–8.

[48] Dahl RE, Pelham WE, Wierson M. The role of sleep disturbances in attention deficit disorder symptoms: a case study. J Pediatr Psychol 1991; 16(2):229–39. [49] Cortese S, Konofal E, Yateman N, et al. Sleep and alertness in children with attention-deficit/hyperactivity disorder: a systematic review of the literature. Sleep 2006;29(4):504–11. [50] Sadeh A, Pergamin L, Bar-Haim Y. Sleep in children with attention-deficit hyperactivity disorder: a meta-analysis of polysomnographic studies. Sleep Med Rev 2006;10(6):381–98. [51] Marks CA, Wayner MJ. Effects of sleep disruption on rat dentate granule cell LTP in vivo. Brain Res Bull 2005;66(2):114–9. [52] Chervin RD, Archbold KH, Dillon JE, et al. Inattention, hyperactivity, and symptoms of sleepdisordered breathing. Pediatrics 2002;109(3): 449–56. [53] Ireland JL, Culpin V. The relationship between sleeping problems and aggression, anger, and impulsivity in a population of juvenile and young offenders. Journal of Adolescent Health 2006;38:649–55. [54] Haynes PL, Bootzin RR, Smith L, et al. Sleep and aggression in substance-abusing adolescents: results from an integrative behavioral sleep-treatment pilot program. Sleep 2006;29:512–20. [55] Cohrs S, Rasch T, Altmeyer S, et al. Decreased sleep quality and increased sleep related movements in patients with Tourette’s syndrome. J Neurol Neurosurg Psychiatry 2001;70(2):192–7. [56] Nobili L, Baglietto MG, De Carli F, et al. A quantified analysis of sleep electroencephalography in anorectic adolescents. Biol Psychiatry 1999; 45(6):771–5. [57] Nobili L, Baglietto MG, Beelke M, et al. Impairment of the production of delta sleep in anorectic adolescents. Sleep 2004;27(8):1553–9. [58] Latzer Y, Tzischinsky O, Epstein R, et al. Naturalistic sleep monitoring in women suffering from bulimia nervosa. Int J Eat Disord 1999;26(3): 315–21. [59] Spiegel K, Tasali E, Penev P, et al. Brief communication: sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 2004;141(11):846–50. [60] Bass J, Turek FW. Sleepless in America: a pathway to obesity and the metabolic syndrome? Arch Intern Med 2005;165(1):15–6. [61] Beebe DW, Lewin D, Zeller M, et al. Sleep in overweight adolescents: shorter sleep, poorer sleep quality, sleepiness, and sleep-disordered breathing. J Pediatr Psychol 2007;32(1):69–79. [62] Snell EK, Adam EK, Duncan GJ. Sleep and the body mass index and overweight status of children and adolescents. Child Dev 2007;78(1): 309–23. [63] Giannotti F, Cortesi F, Cerquiglini A, et al. An open-label study of controlled-release melatonin

Sleep Problems and Psychiatric Disorders

[64]

[65]

[66]

[67]

[68]

in treatment of sleep disorders in children with autism. J Autism Dev Disord 2006;36(6):741–52. Malow BA, Marzec ML, McGrew SG, et al. Characterizing sleep in children with autism spectrum disorders: a multidimensional approach. Sleep 2006;29(12):1563–71. Weiskop S, Richdale A, Matthews J. Behavioural treatment to reduce sleep problems in children with autism or fragile x syndrome. Dev Med Child Neurol 2005;47(2):94–104. Wiggs L, Stores G. Sleep patterns and sleep disorders in children with autistic spectrum disorders: insights using parent report and actigraphy. Dev Med Child Neurol 2004;46(6):372–80. Perlis ML, Smith LJ, Lyness JM, et al. Insomnia as a risk factor for onset of depression in the elderly. Behav Sleep Med 2006;4:104–13. Morin CM, Bootzin RR, Buysse DJ, et al. Psychological and behavioral treatment of insomnia:

[69]

[70]

[71]

[72] [73]

an update of recent evidence (1998–2004). Sleep 2006;29:1396–406. Smith MT, Huang MI, Manber R. Cognitive behavior therapy for chronic insomnia occurring within the context of medical and psychiatric disorders. Clin Psychol Rev 2005;25:559–92. Bootzin RR, Stevens SJ. Adolescents, substance abuse, and the treatment of insomnia and daytime sleepiness. Clin Psychol Rev 2005;25: 629–44. Espie CA. Insomnia: conceptual issues in the development, persistence, and treatment of sleep disorder in adults. Annu Rev Psychol 2002;53: 215–43. Harvey AG. A cognitive model of insomnia. Behav Res Ther 2002;40:869–94. Bryant FB, Veroff J. Savoring: a new model of positive experience. Mahwah (NJ): Lawrence Erlbaum Associates, Publishers; 2006.

511