Arguably, one of the largest gaps in epidemiological research is a lack of high quality prevalence data on insomnia disorders in ADHD (see Chapter 3). This is in large part because factors which may cause apparent “insomnia” such as restless legs syndrome or circadian rhythm disorder are frequently not measured in prevalence studies (Cortese, Faraone, Konofal, & Lecendreux, 2009). Thus, rates of insomnia may be overestimated in children and adolescents with ADHD whilst rates of conditions such as restless legs syndrome may be underestimated. Future research is required that involves large samples of children and adolescents with ADHD and comprehensively measures the range of sleep disorders that can present as behavioral insomnia. These studies should differentiate the burden of specific sleep disorders by ADHD presentation, to inform optimal management across the ADHD spectrum. If findings are to apply to the broader population of children and adolescents with ADHD, these studies should also include children and adolescents with common comorbid conditions such as autism spectrum disorder, given the significant rates of sleep problems in this disorder too (Veatch, Maxwell-Horn, & Malow, 2015).

Similar to our gap in knowledge about exact prevalence of insomnia disorders in ADHD, we also lack rigorous data on the prevalence of circadian rhythm disorders in ADHD, particularly Delayed Sleep-Wake Disorder. A delay of melatonin secretion in children with ADHD and insomnia compared to ADHD and no insomnia has been described (Van der Heijden, Smits, Van Someren, & Gunning, 2005) and some studies suggest an “eveningness” preference in children with ADHD compared with controls, which is associated with increased daytime sleepiness and resistance going to sleep (Durmuş, Arman, & Ayaz, 2017). However, it is not known whether other factors contribute to delayed sleep onset such as behavioral insomnias (e.g., limit setting disorder). Teasing out the relative contributions of delayed melatonin secretion, “eveningness” preference, and specific sleep disorders in the clinical presentation of delayed sleep onset would allow for more individualized treatments.

Chapter 11 raises some important considerations around gaps in epidemiological research in adolescents with ADHD. There are few studies employing subjective or objective measures of sleep and sleep problems in adolescents with ADHD. Some studies have used actigraphy but have small sample sizes (Mullin, Harvey, & Hinshaw, 2011) or have assessed ADHD based on parent report of physician diagnosis which may be inaccurate (Moore, Kirchner, Drotar et al., 2011). A series of studies using polysomnography to assess sleep in male adolescents has been conducted by Prehn-Kristensen et al. In their first study, they found differences in sleep onset latency, sleep efficiency and REM sleep duration compared with controls (aged 10–16 years) (Prehn-Kristensen, Göder, Fischer et al., 2011) but in a subsequent study (of younger adolescents aged 9–12 years), they found no differences (Prehn-Kristensen, Molzow, Munz et al., 2011). No girls were included in their samples. No studies have compared daytime alertness between adolescents with and without ADHD using objective measures such as the Maintenance of Wakefulness Test. Self-reported daytime sleepiness has been linked with poorer academic competence and subsequent poor and failing grades in college students with ADHD (Langberg, Dvorsky, Becker, & Molitor, 2014). There is a clear need for larger studies using objective sleep measures in adolescents with ADHD, that employ validated measures of ADHD and its subtypes, include girls, and examine actigraphy and PSG differences between adolescents with ADHD and controls, by age and pubertal maturation.

Similarly, there is dearth of longitudinal data on the natural history of sleep patterns and sleep disorders in children and adolescents with ADHD. The handful of studies that have examined sleep over time have been limited by relatively short durations (Lycett, Mensah, Hiscock, & Sciberras, 2014; Hansen, Skirbekk, Oerbeck, Wentzel-Larsen, & Kristensen, 2013a, 2013b), small sample sizes (Hansen, Skirbekk, Oerbeck et al., 2013a, 2013b), and insufficient girls to enable adequate power to detect possible sex differences over time. Sleep is measured by parent report and not objectively. Further, most studies lack sufficient numbers to enable examination of the associations between ADHD presentation and comorbidity status and the natural history of sleep disorders. Future research involving larger samples, longer follow-ups, with adequate ADHD measurement and purposeful oversampling for girls, is required. Studies using objective measures of sleep should also follow up children and adolescents to determine the persistence of sleep problems and how sleep impacts later academic, social–emotional, and cognitive functioning. Similar studies are required using self-reported sleep problems and patterns. Whether the persistence of ADHD versus the persistence of sleep problems leads to adverse functional outcomes is also another area ripe for further research.

The nature of the causes of sleep problems in adolescents (and indeed younger children and adults) with ADHD also require further research. In typically developing adolescents, maturational changes slow the homeostatic sleep drive leading to a shift in “eveningness” preference and delayed sleep onset (Jenni, Achermann, & Carskadon, 2005). This in turn leads to many adolescents trying to sleep in on weekends which in its own right is associated with poorer attentional functioning (O’Brien, & Mindell, 2005). Whether this occurs and to what extent in adolescents with ADHD is unknown. Comorbid conditions like depression and anxiety are common in adolescents with ADHD but their relative contributions to sleep problems over time (and vice versa) requires greater research, especially to tease out the contribution of other common risk factors in adolescents with ADHD such as comorbid autism, learning problems, substance abuse, screen time use, and cyber bullying. The role of stimulant medication in causing sleep problems in children and adolescents with ADHD remains controversial and evidence is mixed. In a rigorous, double blind cross-over trial in 65 children aged 10–17 years, higher doses of both extended-release dexmethylphenidate and extended release mixed amphetamine salts were associated with reduced sleep duration and later sleep start times, as measured by actigraphy (Santisteban, Stein, Bergmame, & Gruber, 2014). A recent meta-analysis of randomized controlled trials (RCTs) on the effects of stimulant medication on adolescent sleep, measured objectively, found that stimulant medications led to longer sleep latency, worse sleep efficiency, and shorter sleep duration (Kidwell, Van Dyk, Lundahl, & Nelson, 2015). However, the authors caution that publication bias, especially in the outcome of sleep efficiency, may mean that effects sizes may not be representative of all studies examining the effects of stimulants on the sleep of children with ADHD. In Chapter 11, Becker calls for “carefully controlled studies and longer-term studies that can tease apart relevant factors surrounding medication use (e.g., medication type and formulation, medication duration and adherence) … to better understand whether, how, and under what circumstances medication impacts sleep in adolescents with ADHD.”

In children and adolescents with ADHD, intraindividual or night-to-night variability of sleep/wake patterns appears more common than the variability in typically developing peers. A better understanding of the extent of this and whether intraindividual variability contributes to functioning may offer more targeted clinical sleep recommendations in ADHD. Finally, very little research has examined the role of sleep in an adolescent’s transition to adulthood and to university (college) and/or the workplace. Studies that measure sleep, ADHD symptom severity, comorbid mental health and adjustment before the transition are needed and should consider characteristics of the work environment (e.g., shift work) and educational setting (e.g., contact hours), and evaluate the extent to which sleep problems impact social, academic and workplace functioning and vice versa.

Several studies have described the prevalence of self-reported, common sleep disorders (i.e., insomnia, delayed sleep wake phase disorder, restless legs syndrome) in adults with ADHD (see Chapter 12) although the prevalence of periodic limb movements has received less attention. Further, data on the prevalence of sleep problems by ADHD presentation and comorbid mental health conditions in adults are limited. There is little research exploring the role of risk factors such as substance abuse in the exacerbation or development of sleep disorders in adults with ADHD, even though adults with ADHD are more likely to have tobacco and alcohol dependence than adults without ADHD (Kessler, Adler, Barkley et al., 2006; Park, Cho, Chang et al., 2011). Similarly, there is a lack of research exploring the link between obesity, sleep and ADHD, even though adults with ADHD are more likely to be obese than their peers.

One area that has yet to be explored is the relationship between sleep problems and brain development in children (and adolescents and adults) with ADHD. Patients with ADHD have deficits in executive functioning (working memory, inhibition) and motivation (altered processing of reinforcement and incentives), underpinned by disordered biochemical function involving multiple brain structures (De La Fuente, Xia, Branch, & Li, 2013). Research also shows that ADHD is a disorder characterized by delayed brain maturation (Shaw et al., 2007) but despite studies demonstrating the importance of sleep in promoting brain development in the general population, it is unknown how the presence of sleep problems influences brain development in young people with ADHD (Lunsford-Avery, Krystal, & Kollins, 2016).

A number of studies have shown that sleep problems and sleep restriction in children with ADHD are associated with even poorer executive functioning and neurobehavioral functioning (Hansen et al., 2013a, 2013b; Moreau, Rouleau, & Morin, 2013; Sciberras, DePetro, Mensah, & Hiscock, 2015), suggestive of underlying frontostriatal neural mechanisms. Similarly in the largest behavioral sleep RCT in children with ADHD conducted to date (N=244), receipt of the intervention was associated with better working memory function compared to children who received usual clinical care (Hiscock et al., 2015). Sciberras et al. (2015) found that self-reported sleep problems were associated with poorer directly assessed working memory in 5 to 13 year old children with ADHD (N=189). Hansen and colleagues (2013b) reported associations between attention, as measured by the Attention Network Test, and parent-reported sleep problems on the Children’s Sleep Habits Questionnaire in mixed sample of children with ADHD, anxiety and typically developing children aged 7 to 13 years. In this study, the aspect of attention that was most strongly associated with sleep problems related to the alert network involving the ability to maintain high sensitivity to incoming information. Moreau et al. (2013) also found that sleep duration, as assessed using actigraphy, was associated with poorer executive functioning in children with ADHD (N=43). Finally, an elegant study in which sleep was restricted in children with and without ADHD (N=43) by 1-hour over six nights demonstrated that sleep restriction was associated with poorer performance on the Conners Continuous Performance Test (Gruber, Wiebe, Montecalvo, Brunetti, Amsel, & Carrier, 2011).

It is highly likely that sleep problems contribute to additional neurodevelopmental maturation abnormalities in youth with ADHD (Lunsford-Avery et al., 2016). A number of studies have now explicitly examined the relationship between sleep parameters and brain development as assessed through brain imaging methods. For example, in the general population (N=720), parent-reported sleep problems from ages 2 to 6 years have been associated with smaller gray matter volume and thinner dorsolateral prefrontal cortex at age 7 years (Kocevska et al., 2017). This study demonstrated that more severe trajectories of sleep problems over childhood had more of an adverse impact on brain development. Another study of 177 14-years-old adolescents found that poorer sleep habits were associated with smaller gray matter volumes (Urrila et al., 2017). In particular, later weekend bedtimes were associated with smaller gray matter volumes across numerous regions (frontal, anterior cingulate, and precuneus cortex), while shorter weekday time in bed was associated with smaller gray matter volumes in frontal regions. This study was limited by adolescent report of habitual bedtimes and wake times on weekdays and weekends. Another study using a more rigorous measure of sleep found that increased variability in sleep duration (measured using sleep diaries) has been associated with altered white matter microstructure (lower fractional anisotropy) in a longitudinal study of 48 adolescents (Telzer, Goldenberg, Fuligni, Lieberman, & Galvan, 2015). In this study adolescents completed 14 day sleep diaries to assess sleep at time 1 (mean age 14.8 years) and at time 2 (mean age 15.9 years). White matter microstructure was assessed at time 1 using diffusion tensor imaging. This study demonstrated that variability in sleep at time 1 in particular, seemed important for brain development over and above the effects of overall sleep duration and variability in bedtimes. A fruitful area for future research is to examine whether there are indeed associations between sleep parameters and brain development in ADHD. It would be particularly interesting to examine these relationships over the transition to adolescence.

Adolescence is a crucial time point for young people with ADHD, a period during which developmental trajectories tend to diverge (Lunsford-Avery et al., 2016). This time is characterized by significant changes in sleep (as reviewed in other sections of this book), which could be underpinning these diverging trajectories. These alterations in sleep coincide with patterns in brain maturation characterized by peaking in the development of cortical brain volume and thickness before a decline in later adolescence (Giedd et al., 1999). Despite the availability of medication and psychological therapies to treat the condition, young people with ADHD are highly vulnerable and go on to have much worse outcomes than those without ADHD across the social, educational, and mental health sphere in adolescence. The factors contributing to poorer outcomes for young people with ADHD are poorly understood, particularly at the neurobiological level. The search for influential predictors of neurobiological outcomes is a priority, as this has the real potential to inform the development of new and effective treatments for the condition. Sleep problems may be one such predictor.

Whilst the recommendation of healthy sleep practices remains the mainstay of a clinician’s response to managing sleep problems, there is surprisingly little rigorous evidence for their effectiveness in ADHD (see Chapter 5). This is in part because healthy sleep practices are often offered in combination with specific behavioral strategies for the treatment of insomnias in trials. Thus, the relative contributions of individual healthy sleep practices to improving sleep is unclear. Further, in adolescents, many of the healthy sleep practices run counter to their preferences (e.g., later sleep onset, use of electronics in the bedroom) and research is needed on how best to engage adolescents in adopting healthier sleep patterns. Future research is also needed to develop and evaluate healthy sleep practice resources, like the ABCS of SLEEPING tool (see Chapter 5), in children with ADHD, given these resources are relatively low cost and could be easily implemented by frontline and specialist clinicians alike. Such research should determine the efficacy of healthy sleep practice resources on not only child sleep but ADHD symptom severity, daytime functioning and use of sleep medications as well.

There have been a handful of trials of behavioral strategies for behavioral insomnias in children with ADHD with most demonstrating benefits to sleep and in some cases, ADHD symptom severity (see Chapter 9). However, there have been no trials of strategies such as chronotherapy to address other common problems including delayed sleep wake phase disorder. Further, trials of interventions that aim to address sleep problems together with comorbid disorders (e.g., anxiety, oppositional defiance) are lacking and could offer benefits to those who do not respond to sleep interventions alone. Future trials of behavioral strategies must be “pragmatic,” that is representative of real-world samples of children with ADHD, to maximize generalizability of findings. Interventions that use technology (apps, wed-based platforms, biorhythm trackers) to deliver strategies and track responses to them could offer solutions to adolescents and hard to reach (e.g., rural) families of children with ADHD and sleep problems. However, no such interventions have been evaluated in ADHD.

Whilst placebo-controlled trials of the use of melatonin in children with ADHD have been conducted (finding improved sleep onset latency but not necessarily improved sleep duration and no effects on ADHD core symptoms, see Chapter 10), data on the long-term effectiveness and safety of melatonin are missing. There have been no RCTs of commonly used medications such as clonidine and antihistamines, despite their widespread use. Trials of the use of these medications, perhaps in the subset of children who do not respond to first line behavioral strategies, are needed.

Finally, the efficacy of newer therapies such as mindfulness for the treatment of behavioral insomnia in children and adolescents with ADHD remains to be explored.

As per the literature on treatments for behavioral sleep disorders, Chapter 10 highlights the lack of research on the treatment of medical disorders in ADHD, principally sleep disordered breathing, obstructive sleep apnea (OSA) and restless legs syndrome. Only one small, nonrandomized study (n=25 children received adenotonsillectomy, n=27 received methylphenidate, n=14 received no treatment, and n=20 healthy controls) has examined the natural history of mild OSA in ADHD (Huang, Guilleminault, Li et al., 2007). The study found that unlike healthy controls, mild OSA tends to persist in children with ADHD, albeit the children were only followed for 6 months. Children who received surgery had better behavioral and functional outcomes than children who did not. There have been no RCTs of adenotonsillectomy in children with ADHD and OSA and no RCTs of the medical treatments (i.e., intranasal steroids, oral montelukast) that have been found to improve mild OSA in trials with typically developing children (see Chapter 10). Clearly, randomized trials of medical and surgical treatment of mild OSA, with longer follow-up periods, are needed to determine the optimal treatment for children with ADHD and mild OSA.

Restless legs syndrome is another common medical sleep disorder in children with ADHD and is associated with low iron. In typically developing children, it is often treated with iron although evidence for its effectiveness is inconclusive (Allen, Picchietti, Auerbach et al., 2018). Few studies have evaluated the effect of iron treatment in children with ADHD. In one small RCT, a 12-week course of iron was associated with improved ADHD symptoms as rated by parents but not teachers (Konofal, Lecendreux, Deron et al., 2008). Larger, controlled trials evaluating the effects of iron supplementation in children with ADHD and low iron levels/restless legs syndrome, on ADHD symptoms and sleep, are required.

Few studies have focused on treatments in adolescents which is concerning given the large biological, socioemotional, and environmental changes that occur in adolescence. No studies of pharmacological interventions have been conducted in adolescent only samples with studies of melatonin spanning childhood and adolescence. Studies of behavioral interventions in adolescents are sparse with no studies to date examining whether treating sleep problems in adolescents with ADHD may lead to improvements in broader areas of functioning.

There are no guidelines specific to assessment and management of sleep problems in adults with ADHD. This is in large part because there are no trials of the efficacy of psychoeducation and cognitive behavioral therapy to treat sleep problems in adults with ADHD. Similarly, there have been no controlled trials of light therapy to treat delayed sleep wake phase disorders although one open trial found benefits to ADHD symptom severity and mood (Fargason, Fobian, Hablitz et al., 2017).