deficit hyperactivity disorder (ADHD) is one of the most common childhood
behavioural disorders, with an estimated worldwide prevalence of approximately
5-15% in school-age children.1 Complaints of sleep problems in
children with ADHD are common in clinical practice and are reported in 45-55%
of cases.2 In the last decade, there has been a renewed interest in
the relationship between ADHD and sleep disorders.3 Several groups
have attempted to clarify the links between ADHD and sleep disorders. Research
in this topic is relevant from a theoretical standpoint, suggesting possible
novel etiopathophysiological models of ADHD as well as new insights into the
effects of sleep alterations on behavioural and cognitive functions.4-5
The proper detection and management of sleep problems in children with ADHD may
significantly reduce symptom severity and improve the quality of life of these
children as well as that of their families.6 Indeed, it has been
pointed out that any sleep disorder that results in inadequate sleep duration,
fragmented or disrupted sleep, or excessive daytime sleepiness can lead to or
contribute to problems with mood, attention, and behaviour.7
Critical Issue with Sleep Related
Studies in ADHD
studied sleep and alertness in children with ADHD using both subjective and
objective measures. There have been studies based on questionnaires filled out
by the children or their parents while others have used techniques such as
polysomnography, actigraphy and the Multiple Sleep Latency Test (MSLT).8
Results from both groups of studies are highly inconsistent. Some researchers
have reported significant differences between children with ADHD and controls,
while many studies have failed to replicate these findings.9 These
inconsistencies are often due different inclusion criteria used by these studies.10
There are also a few important reasons to account for the heterogeneity of
sleep studies in ADHD.
First, there are
marked differences in the evaluation methods for ADHD across studies, ranging
from simple evaluation of symptoms of hyperactivity, impulsivity and
inattention to a more rigorous application of different diagnostic criteria.
Standardized and stringent diagnostic criteria are appropriate for a proper
diagnosis of ADHD.11 The use of DSM-III criteria to assess the
relationship between sleep problems and ADHD also has some limitations. DSM-III
had included restless sleep as a defining characteristic of attention deficit
disorder, and hence studies conducted with DSM-III criteria may have been
confounded by the use of sleep disturbance as a diagnostic criterion12.
Therefore, the use of DSM-III-R and DSM-IV criteria minimizes subject-selection
bias.13 Second, only a few studies have excluded or controlled for
the effects of psychiatric comorbidity. Comorbid disorders frequently
associated with ADHD such as oppositional defiant disorder, depression and
anxiety disorders may account for some of the sleep disturbances found in ADHD.14
It has been reported that depression with a childhood or adolescent onset may
be associated with delayed sleep onset, problems with sleep maintenance, and
excessive daytime sleepiness.15 Children and adolescents with
anxiety disorders have also reported sleep-onset delay, problems with sleep
maintenance, and sleep-related involuntary movements.16 Children
with oppositional defiant disorder and conduct disorder too have clinically
presented with difficulty in sleep onset in subjective studies.17
Psychiatric comorbidity may thus influence the results of the studies comparing
sleep and alertness in children with ADHD versus control subjects.18
studies on sleep issues in ADHD did not exclude or control for medication
related factors and effects. Since pharmacological treatments for ADHD may
affect sleep and alertness, it is preferable that one assesses non-medicated
subjects to evaluate the relationship between sleep-alertness alterations and
ADHD.19 Systematic reviews and meta-analyses on the subject have not
been able to control for the above-mentioned potential confounding factors.20
It is possible
that the difficulties reported as significantly higher in children with ADHD
refer to inappropriate behavior in the context of problematic parent–child
interaction and parents of children with ADHD may more likely report high
levels of daytime and sleep-related problematic behaviours in a sort of a
‘negative halo effect’.21 Results from reviews on the subject do
suggest otherwise. Results suggest that some of the parentally reported
complaints about their children’s sleep may actually be due not only to
inappropriate parent–child interaction but also to objective sleep
disturbances.22 Another factors is the fact that that children with
ADHD present with a night-to-night variability in sleep patterns.23
Therefore, it is possible that parents are more likely to recall and thus
report as ‘typical’ those nights on which a child has significant bedtime
resistance or difficulty falling asleep. It has been pointed out that sleep
problems in ADHD are multifactorial i.e., they can be ascribed to many
underlying factors. Therefore, the correct identification of such factors
facilitates the appropriate management of sleep disturbances in this
population.24 There have been reviews of sleep related problems in
children and adults with ADHD but the present review restricts itself to ADHD
in children and adolescents alone.
ADHD, Restless Legs Syndrome
(RLS) & Periodic Limb Movements in Sleep (PLMS)
syndrome (RLS) is a common sensorimotor disorder characterized by an
irresistible urge to move the legs, which is often accompanied by uncomfortable
sensations in the legs or, less frequently, other body parts.25
These sensations are worse at rest, relieved by movement, and worse in the
evening or night and at rest. In RLS, patients frequently experience insomnia
from the leg discomfort and the need to move around.26 The diagnosis
of RLS is based on the revised RLS criteria developed by the International
Restless Legs Syndrome Study Group (IRLSSG).27 Children may report
RLS symptoms differently than adults, in part because of their limited ability
to describe RLS sensations and it has been noted that the clinical presentation
of RLS may differ in children.28
RLS also frequently have a related sleep disorder called periodic limb
movements in sleep (PLMS). PLMS are defined as movements that last 0.5–10
seconds and recur every 5 to 90 seconds in a series of ≥ 4.29
70-80% of adult patients with RLS have PLMS.30 PLMS have been
reported in children with RLS although their prevalence in children has not
been adequately studied.31 It has been correctly pointed out that
sleep disturbances may mimic ADHD symptoms in the evening or be associated with
ADHD symptoms.32 In these cases, the appropriate treatment of sleep
disturbances may significantly improve diurnal ADHD symptoms. In a review of
the literature, it was concluded that up to 44% of subjects with ADHD have been
found to have RLS or RLS symptoms, and up to 26% of subjects with RLS have been
found to have ADHD or ADHD symptoms.33 However, data should be
considered with caution given some methodological limitations of the reviewed
studies and it is probable that the real estimates of the prevalence of RLS in
ADHD and vice-versa are more conservative.34 Further large
epidemiological and clinical methodological studies are needed to assess the
real prevalence of RLS (diagnosed according to standardized criteria) in
children with ADHD (diagnosed according to DSM-IV criteria), as well as the
prevalence of ADHD in children with RLS.35
hypotheses have been proposed to explain the association between RLS and ADHD
(or ADHD-like symptoms). RLS associated sleep disturbance may cause
inattentiveness, moodiness and paradoxical overactivity, thus mimicking
symptoms of ADHD.36 Another hypothesis is that diurnal
manifestations of RLS (who have been reported in children) mimic ADHD symptoms.37
Some children who are seriously affected with RLS cannot sit in school during
the day for extended periods because they get up and walk around to relieve
their leg discomfort. Hyperactivity might thus lead to inattention through the
mechanism of leg discomfort in a subgroup of patients.38 In fact,
true ADHD and RLS can be comorbid conditions.39 ADHD and RLS might
share a common dopaminergic dysfunction.40 Since iron deficiency
(which is a co-factor in dopamine synthesis) has been implicated into the
pathophysiology of RLS41 and has also been reported in children with
ADHD42, it has been suggested that iron deficiency is a common
underlying pathophysiological factor to both RLS and ADHD. Genetic research in
both RLS and ADHD are currently under investigation but no concrete evidence
has been ascertained.43 Children with RLS can develop bedtime
opposition, probably because they associate bedtime with the occurrence of the
unpleasant RLS sensations. Parents may consider this refusal as the expression
of a general oppositional attitude, ignoring the real cause of the child’s
behaviour.44 It is also possible that ADHD worsens RLS symptoms.45
With regard to psychopharmacologic strategies for patients with both RLS and
ADHD, some case reports have demonstrated the efficacy of low doses of
dopaminergic agents (levodopa, pergolide, and ropinirole) in children diagnosed
with both conditions who were previously unsuccessfully treated with
psychostimulants.46 However, though dopaminergic agents are
considered the first-line treatment for adults with RLS, they are not approved
for use in children with RLS.47 No concrete evidence for iron
supplementation as therapy has been noted in this group though some anecdotal
A number of
studies have examined the relationship of ADHD to PLMS.49-51 A
recent meta-analysis summarizing several such studies showed an intimate link
between ADHD and PLMS.52 Since no randomized double-blind trials
have been conducted to assess the potential effectiveness of the dopaminergic
agents for ADHD and PLMS in children with both the conditions, this may
represent a research avenue for the future. Moreover, since PLMS may improve
after treatment with iron sulfate,53 in consideration of the
possible role of iron in ADHD, it would be worthwhile to conduct randomized,
placebo-controlled trials of iron supplementation for PLMS and ADHD.
ADHD, Narcolepsy and Daytime
characterized by excessive daytime drowsiness with or without sudden loss of
body tone under conditions of strong emotion (cataplexy). Hypnologic
hallucinations and sleep paralysis are frequently associated features.54
Arousals can be divided into phasic (tasks that require immediate attention)
and tonic (tasks that require sustained attention). One of the glaring deficits
in this area is that there has been no attempt to see if narcoleptic patients
are also hyperactive. It is theoretically possible that narcoleptics move more
in order to stay alert, but this has not been formally tested.55 More
than a third of adults with ADHD are drowsy, as determined by a score >12
on the Epworth Sleepiness Scale according to one study.56 In ADHD
patients, inattention scores correlated with the excessive daytime sleepiness
scores. Of course, daytime drowsiness may be caused by disorders (such as sleep
apnea) other than narcolepsy.57 To our knowledge, there is no study
that systematically evaluates individuals with ADHD for the presence of either
the MSLT findings of narcolepsy or secondary features of narcolepsy (sleep
paralysis, hypnagogic/hypnopompic hallucinations, or cataplexy).
symptoms of inattention are common in narcolepsy, but symptoms of
hyperactivity in narcolepsy need to be further explored. Drowsiness is common
in ADHD, but the prevalence of narcolepsy in ADHD remains to be determined. The
nature of excessive daytime sleepiness has yet to be determined: excessive
daytime sleepiness might be a primary disorder or the consequence of some other
sleep alteration.58 If excessive daytime sleepiness is actually a
primary disorder in ADHD, these findings suggest new potential therapeutic
strategies for a subgroup of children who present with ADHD associated with an
alteration in sleep or wakefulness, and who may not respond adequately to
first-line stimulant treatments, such as MPH and amphetamine salts.59
Wake promoting agents could be an important alternative to stimulants in these
children. The use of the wake-promoting, non-stimulant agent modafinil has been
proposed for this specific indication60, although the drug is not
approved for this use. Double-blind studies should be conducted to evaluate the
potential usefulness of this agent specifically in children with ADHD and
excessive daytime sleepiness.
Sleep Disordered Breathing,
Obstructive Sleep Apnea and ADHD
sleep apnea (OSA) is characterized by relaxation of throat muscles during sleep
and temporary obstruction of the airway for ≥ 10 sec. An apnea/hypopnea
index > 30/hour is considered severe and, over time, patients with OSA are
possibly more subject to hypertension, heart disease, and stroke.61-62
A number of studies have examined the relationship between sleep disordered
breathing and ADHD.63-64The possible mechanisms for the link between
OSA and ADHD are sleep fragmentation and episodic hypoxia. Sleep disruption
leads to non- restorative sleep that, together with intermittent hypoxia or
hypercarbia and the consequent disruption of cellular or chemical homeostasis,
may induce alterations in the neurochemical substrate of the prefrontal
cortex.65 This in turn may result in executive dysfunction with
adverse daytime effects such as poor planning, disorganization, rigid thinking,
difficulty in maintaining attention and motivation, emotional liability, and
over activity/ impulsivity.66 Another point in favour of this
hypothesis are the improvements in behaviour, neuropsychological functioning,
and sleepiness after treatment of sleep disordered breathing (SDB) .67
The results to date suggest that it is generally the milder forms of SDB that
tend to be more common in ADHD children than in controls. This may be due both
to the more frequent occurrence of milder as opposed to more severe OSA in the
pediatric community and to somnolence during the day in the severe cases,
There is a
‘primary’ ADHD with no OSA or other sleep disorders characterized by a reduced
sleep fragmentation at night (hypo arousal) and increased levels of daytime
sleepiness on MSLT, and a ‘secondary’ ADHD, i.e., due to sleep disorders (OSA,
PLMS), that, when treated result in improvement of the ADHD symptoms.69
To the best of our knowledge, no studies in obese children with ADHD have
considered the effect of weight reduction on the symptoms of ADHD in parallel
with the improvement of sleep disordered breathing.70 There is no
mention of a parallel treatment effect on OSA for the non-stimulants used to
treat ADHD, e.g. atomoxetine, bupropion, the α-2 adrenergic agents guanfacine
and clonidine, tricyclic antidepressants, or modafinil.71
It is possible
that OSA can cause mild inattention or hyperactivity, but it is still
questionable whether children with a diagnosis of moderate to severe ADHD
suffer from inattention or hyperactivity as a result of OSA. SDB may
contribute to some mild ADHD-like symptoms that can be readily misperceived and
may be the theoretical basis of overlap between the two diagnoses. Longitudinal
and prospective studies evaluating the treatment effect of both the disorders
may eventually clarify the relationship between OSA and ADHD.72
With regard to treatment strategies in this population, authors have reported
that children with ADHD and an apnea–hypopnea index >1 and <5 events/hour
improved significantly more after Aden tonsillectomy than after stimulant
treatment.73-74 This suggests that appropriate recognition and
surgical treatment of underlying SDB in children with ADHD might prevent the
need for long-term stimulant treatment. A recent longitudinal study has shown
that improvements are maintained 2.5 years after surgery.75
Circadian Rhythm Sleep Disorders
phase syndrome occurs primarily in adolescence and is characterized by sleep
onset insomnia if the individual tries to go to sleep early. In delayed sleep
phase syndrome, the individuals with a propensity to sleep at a later time than
normal is thought to be mediated through the biological clock located in the
suprachiasmatic nucleus of the hypothalamus.76 ADHD seems to be
characterized, in some cases, by a sleep onset insomnia characteristic of
delayed sleep phase syndrome.77 On the other hand, the reverse
relationship does not seem to hold, as a preliminary study suggests that ADHD
symptoms are not common in delayed sleep phase syndrome.78 It may be
that hyperactivity at night in ADHD causes a delayed sleep onset characteristic
of Delayed Sleep Phase Syndrome, but that the sleep disruption from a delayed
sleep onset is not enough to cause daytime inattention and hyperactivity characteristic
of ADHD.79 It has been reported that medication-free children with
ADHD and sleep-onset insomnia (SOI) exhibit a delayed evening increase in
endogenous melatonin levels.80 Therefore, it has been hypothesized
that SOI in ADHD is a circadian rhythm disorder due to a dim light melatonin
onset delay.81 This may underlie and contribute to symptoms of
bedtime discomfort with secondary resistance to go to bed, which may be
erroneously considered as the expression of a general ‘oppositional-defiant
a delayed evening increase in endogenous melatonin levels might contribute to
SOI in children with ADHD, some investigators have also assessed the effect of
light therapy (LT) in this population.83 To our knowledge, no
controlled study has been conducted to assess the efficacy of LT in children
with ADHD, with the exception of a case report.84 It is noteworthy
to report that, to date, pharmacological agents other than melatonin have not
been found effective for sleep-onset insomnia in randomized controlled trials.
In particular, a recent controlled trial85 reported that zolpidem at
a dose of 0.25 mg/ kg per day to a maximum of 10 mg failed to reduce the
latency to persistent sleep on polysomnographic recordings after 4 weeks of
treatment in children and adolescents with ADHD.
Increased Nocturnal Motor
Activity & Rhythmic Movement Disorder (RMD) in ADHD
Movement Disorder (RMD) primarily occurs in young children and is characterized
by head banging or body rocking prior to sleep onset and sometimes during sleep
itself. Most children outgrow the disorder. It is not truly considered a
disorder unless sleep-related injury is present (which is uncommon), or
daytime consequences related to reduced sleep quality are present. The disorder
often disappears as children age.86 ADHD seems to be more common in
RMD and, in turn, RMD seems to be more common in ADHD.87 The sample
sizes tested are small, and results need to be confirmed in larger series.
Whether sleep disruption from RMD leads to symptoms of ADHD, or whether a
program for increased motor activity has a common diathesis in both RMD and
ADHD bears further investigation.88 While some studies have showed
that MPH three-times daily does not impact upon sleep89 or causes
only a slight decrease in sleep duration90, others have reported
that a third daily dose of MPH does worsen sleep. Given these contrasting
findings, late-afternoon stimulant treatment cannot yet be recommended for ADHD
patients with high nocturnal motor activity, and further research to clarify
this controversial issue is welcome91.
Disorders of Partial Arousal and
Partial Arousal (DOA) consist of complex behaviours that are outside the
conscious awareness of the individual. Patients with DOA are difficult to
arouse and have little recollection of the events the next day. Subjects with
DOA may walk (sleep walking or somnambulism- SW), talk in a confused way
(Confusional arousals- CA) or run in a confused terror while screaming (Sleep
Terrors- ST or Night Terrors- NT). Children usually outgrow DOA but DOA may
recur in adulthood under conditions of emotional or physical stress.92-93
Despite scanty reports on Disorders of Partial Arousal in ADHD, this type of
parasomnia seems to be quite prevalent in ADHD, and probably depends on chronic
sleep deprivation via sleep fragmentation due to multiple arousals.94
Disorders of Partial Arousal frequently coexist with epilepsy but less so with
nocturnal seizures.95 Levetiracetam exerts a positive overall effect
not only upon epilepsy but also upon Disorders of Partial Arousal.96
The reverse prevalence, i.e., the prevalence of ADHD in Disorders of Partial
Arousal remains to be studied.97
Psychiatric Comorbidity in ADHD
comorbid disorders including oppositional disorder, conduct disorder, mood
disorders, anxiety disorders, learning disability, developmental coordination
disorder and tic disorder or Tourette’s syndrome are frequent in ADHD.98
Most of these psychiatric disorders might be associated with significant sleep
disturbances, from a subjective and, less consistently, objective standpoint.99
One must systematically evaluate associated psychopathologies in patients with
ADHD, especially when sleep problems are reported. The appropriate treatment of
comorbid disorders may improve sleep, but the clinician should keep in mind
that some medications used to treat these conditions may negatively impact
sleep (e.g., selective serotonin reuptake inhibitors).100
ADHD Medications and Sleep
stimulants (methylphenidate, amphetamine salts and lisdexamfetamine dimesylate)
are the first line, US Food and Drug Administration approved treatments for
ADHD, followed by the non-stimulant atomoxetine (ATX). However, non-approved
drugs, such as bupropion, tricyclic antidepressants, alpha-agonists and
modafinil are also used.101 It has been suggested that stimulants
used in the treatment of ADHD lead to sleep disturbances. In particular, it has
been reported in some studies that stimulants have effects on sleep-onset delay102,
night awakenings103, shorter sleep duration and dyssomnias.104
However; subjective and objective studies investigating the effects of
stimulants on sleep in ADHD have produced mixed results. While some
investigators have reported, among other outcomes, lengthened total sleep time,
increased sleep-stage shifts, increased number of rapid eye movement (REM)
sleep periods, elevated indices of REM activity, and REM-period fragmentation,
others did not confirm these findings.105 As stimulant use may be
associated with the so-called ‘‘rebound effect” (i.e., increase over base-line
values in ADHD symptoms when the medication wears off) it is also possible that
reported sleep problems may be linked with such restlessness rather than
occurring as a direct action of the agents themselves.106
effect of atomoxetine (ATX) on sleep in children with ADHD, in a recent
randomized, double-blind, crossover study comparing the effect of MPH given
three times daily and ATX given twice daily, it was found that MPH increased
sleep-onset latency significantly more than did ATX, considering both
actigraphic and PSG data. Moreover, both child diaries and parental reports
indicated a better quality of sleep with ATX compared with MPH.107
Both medications decreased night-time awakenings, but the decrease was greater
with MPH. Clearly, these results need to be replicated in additional studies.
Future Research Needs
increasing evidence of alterations of sleep in children with ADHD, albeit at
present there is still a lack of evidence on the most effective and safe
treatment strategies (both pharmacological and non-pharmacological). Looking
ahead, one of the most important issues in the research on the relationship
between ADHD and sleep disturbances is to conduct methodological sound studies
controlling for the possible confounding effects of psychiatric comorbidities
and ADHD on sleep variables. Once we gain further insight in the relationship
between ADHD and sleep, appropriate treatment strategies of sleep disturbances
in subjects with ADHD should be systematically addressed. One research area
which needs to be developed is represented by the effectiveness of behavioral
strategies for sleep problems in children with ADHD.108
evidence on the effectiveness of some medications (such as dopaminergic agents
for RLS) comes from single cases or case series, further large randomized
controlled studies on the effectiveness and tolerability of medication for
sleep disorders associated with ADHD are needed. Besides randomized controlled
trials on the effectiveness of pharmacological and non-pharmacological
treatments for sleep disturbances in ADHD, there are some under-explored areas
of research. The interesting issue of the relationship between ADHD and
narcolepsy or primary disorders of vigilance has yet to be fully explored.
Another area of research which is still under-developed is the relationship
between ADHD and parasomnias, which could provide important insights into the
pathophysiology of ADHD and could suggest useful treatment strategies to
improve sleep quality in ADHD.109 Finally, possible genetic
underpinnings and neuroimaging correlates of the association between sleep
disturbances and ADHD lay the ground work for fruitful and innovative avenues
occur frequently in the setting of several specific sleep disorders and vice
versa. We would recommend that clinicians be aware of the potential connection
between ADHD and the specific sleep disorders mentioned. We have two general
recommendations. First, because the various sleep disorders mentioned more
frequently have symptoms of ADHD than control populations, we recommend that
patients with these sleep disorders be queried about the symptoms of ADHD.
Second, since ADHD patients more frequently have symptoms of the various sleep
disorders in question, we also recommend that patients with ADHD be queried
about the sleep disorders in question. If these sleep disorders are present in
patients with ADHD, they should be addressed. In addition, there remains the
possibility that treatment of the associated sleep disorder may lead to
adjunctive improvement of the ADHD symptoms in conjunction with stimulant
therapy. In addition to strengthening already established connections, future investigations should explore
whether narcolepsy is characterized by paradoxical hyperactivity, whether ADHD
patients have a higher prevalence of narcolepsy, and whether patients with DOA
more frequently have ADHD symptoms.
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