American Academy of Sleep Medicine (2014) defines insomnia as a problem with sleep initiation, duration, consolidation, or quality that occurs despite adequate opportunity and circumstance for sleep; results in daytime impairments; and occurs three times or more per week. Problems that persist for at least 3 months may warrant a diagnosis of chronic insomnia. For information about how insomnia is classified according to the International Classification of Sleep Disorders (ICSD-3) and the DSM-5, see Chapter 3.

According to a recent review by Wynchank, Bijlenga, Beekman, Kooij, and Penninx (2017), the worldwide prevalence of insomnia symptoms in the general adolescent and adult population ranges from 31% to 56%. In the adult ADHD population, cross-sectional, clinical and population studies suggest that this figure may be as high as 43%–80%. Sleep-onset insomnia, defined as difficulty getting to sleep at the desired bedtime, and poor sleep quality, may be the most common sleep problems for both adolescents and adults with ADHD (Brevik et al., 2017; Fisher et al., 2014). For example, in a sample of 40 nonmedicated adults with ADHD, 78% reported having sleep-onset insomnia (Van Veen, Kooij, Boonstra, Gordijn, & Van Someren, 2010). Higher incidence of insomnia among adults with ADHD than the general population could be related to the presence of psychiatric comorbidity in this group (Schredl, Alm, & Sobanski, 2007) or could be symptoms of other underlying sleep problems such as a delayed sleep-phase disorder. In Fisher’s large study cited above, sleep-onset insomnia (difficulty falling asleep at the desired bedtime) and sleep maintenance problems were most the pronounced problems in adults with ADHD (Fisher et al., 2014).

Chapter 3 outlines the ICSD-3 and DSM-5 definitions of Circadian Rhythm Sleep–Wake Disorders. Circadian rhythm is the 24-hour cycle of physiological changes that results in sleep and alertness. A misalignment of sleep pattern timing in circadian rhythm sleep disorders can lead to disrupted sleep and impaired functioning. As per the ICSD-3, signs of a shift in the normal circadian rhythm indicating the presence of a delayed sleep–wake phase disorder include: evening diurnal preference, sleeping and rising later than normal, sleep-onset insomnia when trying to fall asleep earlier, and difficulty waking (Hvolby, 2015). This delay is common in adults with ADHD compared to those without, with one Dutch study of adults with ADHD aged 18–65 years showing a prevalence of 26% (n=202) compared with only 2% (n=189) in controls based on self-report (P<.001; Bijlenga, van der Heijden, et al., 2013). American (N=350) and Norwegian (N=10,000) studies using objective and subjective sleep measures suggest a prevalence rate of delayed sleep–wake phase disorder in the general adult population to be between 0.13% and 3.1% (Instanes et al., 2016). Another study (N=29) by Rybak, McNeely, Mackenzie, Jain, and Levitan (2007) found that 41% of adults with ADHD had a later circadian preference whereas only 18.5% reported a morning preference. There were medium to large associations between a greater degree of eveningness demonstrated and more self-reported ADHD symptoms (r=–.40, p=.039) and neuropsychological deficits such as impulsive, erroneous responding (r=–.54, p=.004) and poorer target discrimination when attempting to sustain attention (r=–.54, p=.004). Severity of ADHD symptoms, and comorbidity of ADHD and insomnia are associated with delayed sleep (Gamble, May, Besing, Tankersly, & Fargason, 2013; Van Veen et al., 2010). Sleep-onset delays for those with ADHD may be independent of age (Bijlenga, Van Someren, et al., 2013), as children and adolescents with ADHD are also more likely than healthy peers to experience delayed circadian rhythm functioning manifested as bedtime resistance or morning awakening difficulties (Imeraj et al., 2012).

Sleep-disordered breathing (SDB) refers to a range of sleep-related abnormalities characterized by periodic impairment of respiration during sleep (Lugaresi & Plazzi, 1997) (see also Chapter 10). When coupled with other symptoms such as snoring and excessive daytime sleepiness, a diagnosis of obstructive sleep apnea (OSA) syndrome should be considered. The literature on the prevalence of SDB and OSA in those with ADHD has been limited to the pediatric population (20%–30%; Youssef, Ege, Angly, Strauss, & Marx, 2011) with the exception of few small studies supporting this similar elevated frequency in adults. Surman et al. (2009) reported that of the six adults with clinically diagnosed ADHD in their study, all had polysomnographic evidence of SDB and impaired sleep quality. In another study by Levy, Fleming, and Klar (2009), 56% of the 78 severely obese adults with ADHD had OSA. Further large-scale studies with clinically diagnosed adults with ADHD without comorbidities are needed to understand the association of SDB, OSA, and ADHD. Nonetheless, these elevated rates are significantly higher than the estimated 3% occurring in the general population (Young et al., 1993).

Restless legs syndrome (RLS) is a neurological condition characterized by an unpleasant sensation in the feet or other limbs, a desire to move the limbs to relieve the discomfort and is often accompanied by motor restlessness (Walters et al., 1995) (see also Chapter 10). A propensity for symptoms to worsen at night or when the person is relaxed makes it difficult to fall asleep. The overall prevalence of RLS in the general population of adults is 2%–15% and increases with age, with higher rates found in women than men, and lower rates in Asian populations (American Psychiatric Association, 2013; Berger, Luedemann, Trenkwalder, John, & Kessler, 2004; Phillips et al., 2000; Rothdach, Trenkwalder, Haberstock, Keil, & Berger, 2000). Several studies have shown that compared with healthy controls, more adults with ADHD have RLS or symptoms with rates of around 20%–35% reported (Schredl et al., 2007; Snitselaar, Smits, & Spijker, 2016; Zak, Fisher, Couvadelli, Moss, & Walters, 2009). Conversely, ADHD is also more common among patients with RLS (26%) compared with patients with insomnia (6%) or controls (5%; Wagner, Walters, & Fisher, 2004).

Nocturnal motor activity, as measured by periodic limb movements in sleep (PLMS) using polysomnography (PSG), refers to periodic episodes of repetitive limb movements caused by contraction of muscles during sleep (Instanes et al., 2016). When these episodes occur at least three times night and are followed by a partial arousal or awakening (as measured by PSG), a formal diagnosis of PLMS can be made (ICSD-3). As compared to healthy controls, adults with ADHD in two small case–control studies (N=8–20) had increased PLMS and reported reduced sleep time and poor sleep quality despite significantly increased (Philipsen et al., 2005), or similar (Kooij, Middelkoop, van Gils, & Buitelaar, 2001) objective sleep duration. In the latter study, sleep problems were subsequently resolved with stimulant treatment (Kooij et al., 2001). Unlike the assessment of PLMS in adults with ADHD, PLMS in children with ADHD has been studied more extensively with strong evidence suggesting significantly higher prevalence than peers (Owens, 2005; Picchietti, England, Walters, Willis, & Verrico, 1998; Yoon et al., 2012).

Excessive daytime sleepiness affects around 37% of adults with ADHD (Oosterloo, Lammers, Overeem, de Noord, & Kooij, 2006) and like adolescents with ADHD (Cortese, Faraone, Konofal, & Lecendreux, 2009), these rates are higher than in healthy peers. Excessive daytime sleepiness is characterized by persistent tiredness and lack of energy with a tendency to fall asleep. It can be caused by chronic sleep deprivation and other underlying sleep disrupters such as OSA, RLS, and PLMS (Cortese et al., 2009), and is associated with increased ADHD severity (Gamble et al., 2013). Excessive daytime sleepiness may also indicate signs of narcolepsy when paired with an urge to fall asleep (Cortese et al., 2009), which often goes unrecognized and undiagnosed until adulthood despite frequently first presenting in late childhood and adolescence (Owens, 2005). A comparison study of daytime sleepiness and ADHD symptoms in adults with ADHD (n=61) and adults with hypersomnia (n=64) by Oosterloo et al. (2006) found a high percentage of symptom overlap between both groups using self-reported ESS and ADHD Rating Scale. Adults with ADHD (38%) fulfilled criteria for excessive daytime sleepiness, while adults with hypersomnia (19%) had scores that warranted a diagnosis of childhood onset adult ADHD. Given the overlap between symptoms of hypersomnia and ADHD, misdiagnosis of either disorders may occur. Studies of narcolepsy in adults with ADHD are lacking but one retrospective study found an 8–15 times greater likelihood of elevated childhood ADHD symptoms in adults with narcolepsy compared to adult controls (Modestino & Winchester, 2013).

A range of sleep problems are indicated in adults with ADHD as described above, however, research in this area is still early and the majority of studies have relied on self-report rather than objective measures of sleep. The first meta-analysis of sleep in adults with ADHD has recently been published with findings of impairment relative to controls in subjective measures of sleep problems but few differences in objectively measured sleep alterations (Díaz-Román, Mitchell, & Cortese, 2018). Only 13 studies met inclusion criteria for this review which necessitated adults (18 years and above), ICD or DSM diagnosis of ADHD and inclusion of a comparison group of adults without ADHD. Meta-analysis showed that adults with ADHD subjectively reported more problems in seven out of nine areas compared with controls: longer sleep latency [Standard Mean Difference (SMD)=0.67], more psychosomatic symptoms during sleep onset (SMD=0.64), night awakenings (SMD=0.56), general sleep problems (SMD=1.55), lower sleep quality (SMD=0.69), poorer sleep efficiency (SMD=–0.55), and higher daytime sleepiness (SMD=0.75). There were no differences in sleep duration and restorative value of sleep. In objective measures adults with ADHD differed in only two of five actigraphic parameters: having longer sleep-onset latency (SMD=0.80) and poorer sleep efficiency (SMD=-0.68) than controls. No differences were found in the nine polysomnographic parameters. Hence, additional research is required to understand if some of the subjectively reported difficulties are underpinned by objectively measured sleep alterations.

Psychiatric comorbidities are common in adults with ADHD with many independently associated with sleep problems. Mood and anxiety disorders are prevalent in ADHD and may be thought of as intrinsic to ADHD, similar to sleep problems (Kessler et al., 2006; Yoon et al., 2012). For example, an epidemiological cross-sectional study of N=6081 adults in Korea found a quadruple likelihood of these disorders occurring in adults with ADHD symptoms (Park et al., 2011). The link between mood disorders and sleep disturbances is well-recognized in adults in the general population (American Psychiatric Association, 2013) with some limited research showing this association in adults with ADHD (Hvolby, 2015; Hysing, Lundervold, Posserud, & Sivertsen, 2016). Insomnia and poor sleep quality, for instance, have been reported to increase the risk of depression, even after taking into account ADHD symptomology (Schredl et al., 2007).

Substance use is another common psychiatric comorbidity of ADHD, with up to 20% of adults with ADHD symptoms having nicotine dependence and 30% having alcohol dependence (Kessler et al., 2006; Park et al., 2011). Substance use may further exacerbate sleep problems in this group although there is limited research exploring these associations in adults with ADHD. There is also a lack of prospective studies to understand the direction of the relationship between psychiatric comorbidities and sleep problems in adults with ADHD.

In the general population of adults, numerous medical problems are linked with sleep disorders including diabetes, systemic hypertension, coronary heart disease, heart failure, stroke, chronic obstructive pulmonary disease, arthritis, fibromyalgia, Parkinson’s disease, cerebrovascular disease, obesity, and chronic pain (American Psychiatric Association, 2013; Avidan & Zee, 2011). Few of these associations have been investigated in adults with ADHD to date. In a recent systematic review, obesity was more prevalent among adults with ADHD (28%) than those without (16%) regardless of gender (Cortese et al., 2015), and is postulated to be a consequence of dysregulated eating behaviors and weight gain exacerbated by impulsivity and inattention (Cortese & Castellanos, 2014). Excess weight is a well-established predictor of SDB and other sleep difficulties such as decreased sleep duration and delayed sleep onset (Cortese, Konofal, Dalla Bernardina, Mouren, & Lecendreux, 2008; Young, Peppard, & Taheri, 2005). In adolescents with obesity, ADHD symptoms and daytime sleepiness have been correlated (Cortese et al., 2007), however, there is a lack of adult research directly exploring the link between obesity, sleep problems, and ADHD.

Sleep problems in the general adult population result from a myriad of biological, environmental, psychological, and behavioral factors (American Psychiatric Association, 2013). There are numerous studies showing that sleep disorders are heritable (Gehrman, Keenan, Byrne, & Pack, 2015). For example, many sleep disorders are familial and the prevalence of insomnia is higher among monozygotic relative to dizygotic twins (Watson, Goldberg, Arguelles, & Buchwald, 2006). Environmental triggers such as noise, light, temperature, and altitude can contribute to sleep problems such as insomnia (Obradovich, Migliorini, Mednick, & Fowler, 2017). Other causal factors can include major life events such as illness, chronic daily stress, alcohol and drug use, medical conditions, and the psychiatric conditions highlighted above (American Psychiatric Association, 2013). Numerous medications can contribute to sleep problems including central nervous system (CNS) stimulants, decongestants, antihypertensives, hormones, and psychotropics. Increasing age and gender are also risk factors for many sleep problems. The causes of sleep problems are complex and may share components with psychiatric disorders, as well as unique components related to sleep disturbances (Gehrman et al., 2015).

The etiology of sleep problems in ADHD is also likely to be multifactorial and vary across individuals (Owens, 2005). It can be difficult to distinguish between sleep disorders and ADHD as sleep problems may mimic ADHD symptoms, exacerbate ADHD symptoms, or ADHD may induce or impact the severity of sleep disturbances. For example, symptoms of inattentiveness and daytime cognitive and behavioral deficits can arise from prolonged sleep deficit. SDB can cause hyperactivity, inattention, and disrupted cognition and behavior (Hvolby, 2015). RLS similarly shares the symptoms of inattention and hyperactivity (Philipsen, Hornyak, & Riemann, 2006). OSA and insomnia symptoms mimic hyperactivity, impulsivity, and inattention (Gau et al., 2007; Philipsen et al., 2006). ADHD-related symptoms might therefore be caused by sleep problems rather than stemming from ADHD (Konofal, Lecendreux, & Cortese, 2010). Alternatively, sleep problems may worsen behavioral and cognitive ADHD symptoms (Park et al., 2011; Yoon et al., 2012). Three models outlining ADHD and sleep problems potential comorbidity are discussed below.

Dopamine and noradrenaline deficits are well documented as key neurochemical determinants of ADHD symptoms (Cortese, 2012; Cortese, Konofal, & Lecendreux, 2008; Volkow et al., 2009; Yoon et al., 2012). These neurotransmitters play roles in governing sleep disturbance and arousal (Salerno, Makris, & Pallanti, 2016), and perturbations of their transmission systems located in the midbrain and pons have been suggested to be at the basis of comorbid RLS and ADHD (Cortese et al., 2008), and RLS/periodic limb movements and ADHD (Ondo, Romanyshyn, Vuong, & Lai, 2004).

Structurally, abnormalities in brain areas regulating arousal, behavioral inhibition, self-regulation, and vigilance associated with ADHD have been postulated to result in sleep disturbances due to considerable overlaps in CNS centers controling sleep, arousal, and attention (Owens, 2005; Yoon et al., 2012). Dysfunctional sleep and attention are hypothesized to result from neural circuitry alterations in the cortical and brain stem regions that regulate arousal and attention, including neurotransmitter sites locus coeruleus (noradrenaline) and substantia nigra (dopamine) (Yoon et al., 2012). These areas encompass major sites implicated in the pathophysiology of ADHD, including the frontal, dorsolateral, prefrontal, ventrolateral, prefrontal, and dorsal anterior cingulate cortices, striatum (caudate and putamen), lateral temporal and parietal regions (Cortese, 2012; Owens et al., 2013) (see also Chapter 13). For example, numerous studies have demonstrated the significant impact of sleep deprivation on neuropsychological tests aiming to tap into frontal and prefrontal lobe functions, resulting in executive function impairments, emotional dysregulation, deficits in motor control, and major lapses in attention and vigilance (Dinn, Robbins, & Harris, 2001; Owens et al., 2013). Taken together, the interrelated but distinct brain areas implicated in both ADHD and sleep disorders may account for the disruption in one system adversely affecting the other.

There is growing evidence of a genetic basis for ADHD and sleep problems involving many genes of small individual effects. Twin studies show the association between ADHD in adulthood and poor sleep is higher in monozygotic than dizygotic twins suggesting genetic influences explain around 55% of the association (Gregory et al., 2017). A functional polymorphism of the catechol-O-methyltransferase (COMT) gene in those with ADHD is related to a persistence of poor sleep into adulthood (Gruber et al., 2006), and COMT haplotype (rs6269) has been associated with hyperactivity/impulsivity (Halleland, Lundervold, Halmøy, Haavik, & Johansson, 2008). Two studies in adults with ADHD indicate that a single nucleotide polymorphism in the CLOCK gene affects the molecular operation of the circadian clock (Kissling et al., 2008; Xu et al., 2010). A circadian rhythm phase delay was also attributed to an ablation of the rhythmic expression of two clock genes BMAL1 and PER2 over 24 hours (Baird, Coogan, Siddiqui, Donev, & Thome, 2011).

There are mixed findings for the first two models discussed above. Prospective longitudinal studies using objective measures of sleep problem in adults with ADHD are lacking. The complex interplay of the various factors cannot currently be deciphered and empirical support for these models remains limited until further research is done. Regardless, adults with ADHD report significantly more sleep problems than controls and objective measures suggest longer sleep-onset latency and poorer sleep efficiency (Díaz-Román et al., 2018), hence assessment and management of sleep problems in adults with ADHD is a clinical necessity in this group.