Dr. Ivanenko is assistant professor of Clinical Psychaitry and Behavioral Sciences in the Division of Child and Adolescent Psychiatry at Northwestern University Feinberg School of Medicine at Children’s Memorial Hospital in Chicago, Illinois, and Pediatric Sleep Medicine Director at Children’s Memorial at Central DuPage Hospital in Winfield, Ilinois. Dr. Patwari is assistant professor of Clinical Pediatricsin the Department of Critical Care Medicine at Northwestern University Feinberg School of Medicine at Children’s Memorial Hospital.

Disclosure: Dr. Ivanenko is a consultant to Boehringer Ingelheim, NextWave Parmaceuticals, Inc., and Takeda Global Research & Development Center, Inc; and on the speaker’s bureau of sanofi-aventis. Dr. Patwari reports no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Anna Ivanenko, MD, PhD, 800 Biesterfield Rd, Suite 510, Elk Grove Village, IL 60007; Tel: 847-981-3660; Fax: 847-956-5108; E-mail: aivanenko@sbcglobal.net.


Focus Points

• Insomnia, parasomnias, and sleep-disordered breathing are common among children and adolescents.
• Behavioral insomnia includes limit-setting and association types.


Disturbances of sleep-wake function are common in children and adolescents, but still remain unrecognized and undertreated. Sleep disorders are even more prevalent in children with psychiatric disorders. Thus, it is important for healthcare providers to diagnose and manage sleep disorders in order to achieve most optimal patient outcomes. This article provides an overview of the most common pediatric sleep disorders, discusses the use of instrumental assessment of sleep and validated sleep questionnaires, and describes non-pharmacologicand pharmacologic treatments currently available for children and adolescents with sleep disorders.


Sleep disorders remain among the most prevalent clinical conditions in children and adolescents. In the past 2 decades, there has been an increased number of research studies emphasizing the importance of sleep for children’s growth, neurobehavioral development, and learning.

A multi-system heuristics model has been proposed to define the relationship between sleep and daytime functioning in children.1 The model implies bi-directional and mediational relationships between multiple intrinsic and extrinsic systems involved in the regulation of sleep-wake processes, and with behavioral and emotional control in children as they develop.

This article reviews the prevalence of sleep disorders in the pediatric population, describes subjective and instrumental methods of assessment currently used in sleep medicine, and defines available treatment options for children and adolescents with disorders of sleep and alertness.

Sleep Requirements Among Children and Adolescents

Sleep requirements and distribution of sleep stages vary across ages. Infants enter rapid eye movement (REM) sleep (also termed active sleep at this age) at the beginning of their sleep phase, and REM sleep constitutes ~50% of their total amount of sleep. The ratio between non-REM (NREM) sleep (also termed quiet sleep) and REM sleep increases dramatically during the first year of life, with REM sleep approaching ~20% to 25% of the total sleep duration by the end of the first year. According to a parental survey conducted by the National Sleep Foundation,2 total sleep amount decreases from an average 13.2 hours in newborns to 11.4 hours in 2-year-olds. 

Napping requirements vary among individuals and are influenced by cultural and social factors. Most children, however, stop napping by 5 years of age with few children requiring naps at 6–7 years of age.

Brief nocturnal awakenings are a normal part of the sleep process and occur in infants and toddlers on an average of 1.3 and 0.73 times, respectably.3 Infants that return to sleep without parental intervention are referred as “self-soothers,” as opposed to “signalers” that require parental interaction to fall back to sleep. Difficulty with falling asleep may progress into behavioral sleep disorders as they continue to be behaviorally reinforced by parents.

Numerous laboratory and field studies conducted in the past 25 years have indicated that the need for sleep does not decline with puberty, but remains an average of 9–10 hours/night. Adolescent growth and development is associated with physiologic changes in sleep homeostasis and a characteristic delay in the circadian sleep phase, leading to a later sleep onset time and often to subsequent sleep loss due to early school start times.

Epidemiology of Common Sleep Disorders in Children


The prevalence of sleep disorders in the general population of children is estimated to be between 25% and 40%, depending on the study sample.4 Difficulty falling and staying asleep with frequent nocturnal awakenings, fear of darkness, and bedtime refusal are among the most common types of sleep complaints reported by the parents. Because symptoms of insomnia in children are very distinct from those in adults and are highly influenced by behavioral and family factors, the diagnosis of “behavioral insomnia in childhood” was introduced into the International Classification of Sleep Disorders, Second Edition.5

Behavioral insomnia is defined as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep, and results in daytime functional impairment for the child or family.” Two types of behavioral insomnia in childhood have been defined as the limit-setting type and sleep-onset association type. In the limit-setting type, the child stalls or refuses to go to bed at an appropriate time, while the sleep-onset association type is characterized by the inappropriate or maladaptive associations, such as rocking, feeding, watching TV or listening to the radio, and parental presence in bed. The absence of certain conditions can cause significant delay in sleep onset and subsequent reduction in a total sleep time. Combined types present with both subtypes at the same time and are frequently seen in the families where parents have difficulties enforcing consistent behavioral limits.

Behavioral insomnia is commonly associated with prolonged nocturnal awakenings; once the child awakens in the middle of the night he is unable to return back to sleep without recreating the same sleep association.

The pathophysiology of insomnia in children is far less studied and understood compared to adults. However, there are reported cases of lifetime primary insomnia starting during childhood and continuing into adult age, as well as cases of psychophysiologic insomnia triggered by a stressful event and associated with increased somatized tension and arousal conditioned to the bedroom and bedtime activities.

Symptoms of insomnia have frequently been reported by parents of children and self-reported by many adolescents. According to the Sleep in America Poll,2 69% of parents reported their children having sleep problems, mainly with falling and staying asleep, occurring a few times a week, with up to 51% of adolescents reporting difficulties initiating sleep at least once a week.6 The prevalence of insomnia among adolescents varies depending on the sample and definition of insomnia used in the research study. Two of the most recent studies that used Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,7 classification criteria for insomnia found that 4% of teens reported symptoms of insomnia in the European countries sample.8 In the United States, 10.7% of adolescents had primary insomnia.9 Children with psychiatric, neurodevelopmental, and chronic medical conditions have a much higher prevalence of insomnia compared to healthy controls.10 For example, one of the studies indicated that ~50% of children and adolescents with insomnia who were referred to the pediatric sleep center had coexisting psychiatric diagnosis.11


Parasomnias are defined as behaviors associated with incomplete partial arousals during sleep or transitions into sleep, or following arousal from sleep. They occur both during NREM and REM sleep and can be very disruptive to the child and the family. Frequently seen parasomnias are rhythmic movements, sleepwalking, sleeptalking, nightmares, confusional arousals, sleep terrors, and nocturnal enuresis. Parasomnias are far more prevalent among children than adults, appear to be highly heritable, and tend to resolve spontaneously over the course of child development. Sleepwalking is reported occasionally in 20% to 40% of children 4–8 years of age. Frequent episodes of sleepwalking occur in ~3% to 4% of children. The prevalence of sleep terrors prevalence is ~3% in the general pediatric population. Confusional arousals are more frequently observed in infants and toddlers. They tend to be more disturbing to the family members and may last for up to 30–45 minutes with the child appearing confused, agitated, and incoherent. The exact pathophysiology of parasomnias is unknown, but they seem to represent maturation of systems within the central nervous system (CNS) involved in regulation of sleep and arousal. Psychological, environmental, and developmental factors influence parasomnias. Increased stress, emotional excitement, irregular bedtime, and sleep deprivation are known to increase the frequency of parasomnias and complicate their course.12 Parasomnias are more prevalent in children with psychiatric and neurologic disorders, and can be induced or exacerbated by certain psychological, medical conditions, and psychopharmacologic agents. Parental education and reassurance with regular and appropriate bedtime routines and stress management are effective interventions for parasomnias. While treating children with parasomnias, safety issues should be emphasized to prevent the child from possible accidental injury. Medication should be reserved only for severe or potentially dangerous cases.

Sleep Disordered Breathing

Primary snoring, upper airway resistance syndrome (UARS), and obstructive sleep apnea (OSA) are among the most common sleep-related breathing disorders in children. Habitual snoring has been estimated to have a prevalence of 10% to 27% among school-aged children with the peak at 2–8 years of age when adenotonsillar hypertrophy develops relative to the size of the upper airway. The prevalence of OSA among children is estimated to be 2% to 3%.13,14 Clinical symptoms of sleep disordered breathing (SDB) include continuous snoring, mouth breathing, witnessed breathing pauses, restlessness in sleep, and unusual sleeping positions. Nocturnal enuresis and parasomnias are overrepresented in children with SDB, and are frequently resolved after the treatment of SDB.

It is especially important for healthcare providers to be aware and to recognize symptoms of SDB in children and adolescents as it has a significant impact on their neurocognitive and behavioral development. Hyperactivity, inattention, aggressiveness, and impulsive behaviors have consistently been reported in children with SDB, along with some cognitive and performance deficits, academic failure, and excessive sleepiness.15-18 Sleep deficits, especially in younger children, often manifest with increased behavioral disinhibition, agitation, and mood lability. School problems and academic deficits have been reported in children with OSA, with subsequent improvement in academic grades following successful treatment of OSA.15-19 Quality of life is shown to be reduced in children with OSA and obesity, which can lead to depression, fatigue, and a decreased interest in daily life activities.20


The classical narcolepsy tetrad includes excessive daytime sleepiness, cataplexy, hypnogogic/hypnopompic hallucinations, and sleep paralysis. The pathophysiology of narcolepsy involves loss of orexin (ie, hypocretin) neurons in the hypothalamus that are involved in the control of sleep-wake cycle. The exact prevalence of narcolepsy is unknown. In Japan, the prevalence rate is as high as .16% versus only .02% among Israeli Jews. This discrepancy in the prevalence rate seems to be associated with certain human leukocyte antigen (HLA) haplotypes. HLA DQB1-0602 has been confirmed as one of the best markers of narcolepsy.21 The presence of cataplexy is specific for the diagnosis of narcolepsy. However, the vast majority of cases demonstrate excessive daytime sleepiness as a presenting symptom. The differential diagnosis of narcolepsy, especially in preadolescent children, frequently includes attention-deficit/hyperactivity disorder (ADHD), epileptic seizures, and depressive disorders. Since hypersomnia is frequently associated with major depressive disorder, it may be viewed as a part of the depressive symptomatology rather than intrinsic sleep disorder. There are cases of secondary narcolepsy caused by genetic disorders (eg, myotonic dystrophy type 1), Prader Willi syndrome, brain tumors, and head injuries.

Two or more sleep-onset REM periods on the Multiple Sleep Latency Test (MSLT; see below) are thought to be indicative of narcolepsy in adolescents and adults. Since the MSLT has not been validated in prepubertal children, it is more difficult to establish the diagnosis of narcolepsy in this age group. A thorough clinical history with daily sleep logs, actigraphy, polysomnography, and an MSLT should be used in the attempt to establish the diagnosis of narcolepsy in younger children.22

Restless Legs Syndrome and Periodic Limb Movement Disorder

RLS is a sensorimotor disorder manifest mostly at night and associated with an unpleasant sensation and urge to move one’s legs. The prevalence of RLS in the pediatric population is ~2%.23 Diagnostic criteria of RLS in children were published24 in 2003 with three different proposed categories, namely, definite RLS, probable RLS, and possible RLS. While RLS is a clinical diagnosis, periodic limb movement disorder (PLMD) requires nocturnal polysomnography or actigraphy to establish diagnosis. Periodic limb movements (PLMS) are brief muscle jerks lasting 0.5–5.0 seconds that usually occur at 20–90-second intervals during sleep. PLMS affect legs, toes, feet, and arms and may cause electroencephalogram (EEG) arousals from sleep. Most patients with RLS have PLMS, but there are cases of RLS that fail to demonstrate PLMS in sleep studies.25

Establishing the diagnosis of RLS in children is far more challenging than in adolescents or adults. Children typically describe their sensations as “bugs,” “ants crawling inside my legs,” “tickle,” “feeling uncomfortable,” or “hurts.” Parents usually report restless sleep in the children; they frequently observe their child rubbing or moving their legs excessively prior to falling asleep. Many children with RLS ask their parents to massage their feet or legs at bedtime to help with falling asleep. The differential diagnosis of RLS in children includes orthopedic problems, muscle soreness, skin problems, or neuropathies. It has been shown that ferritin serum levels <50 ng/ml are associated with RLS severity in children and adults.26,27 Supplementation with iron to achieve ferritin levels >50 ng/ml was shown to be effective in improving symptoms of RLS. Vitamin C usually enhances iron absorption, and children are usually recommended to take an iron supplement with orange juice or other fruit drinks that contain Vitamin C.

Numerous studies reported an association of RLS, PLMD, and ADHD in pediatric and adult patient populations. The prevalence of RLS/PLMD in children with ADHD varies between 25% and 44% depending on the study sample.28,29 The exact pathophysiology of these disorders and their complex relationship is poorly understood. However, the role of iron as part of the dopamine metabolic pathway has been proposed as one of the etiologic factors in both RLS and ADHD.30

Evaluation of Sleep Disorders in Children and Adolescents

The key difference between adults and children is that the developing child also has an evolving sleep pattern with continual changes in sleep requirements. As with most medical evaluations, the strongest clue to the underlying diagnosis lies with a thorough history. A focused history should be directed at determining abnormalities in sleep quantity or quality. Furthermore, a focused pediatric sleep history should include attention to the psychosocial history, daytime functioning, bedtime behaviors and routines, and nocturnal behavior. In addition to information gleaned from the history, objective information and quantitative evaluation can be obtained from questionnaires, sleep logs or diaries, polysomnography, actigraphy, and MSLT.

Psychosocial History

Psychosocial history speaks to the strong influence that environmental factors and consistencies with caretakers play in a child’s life. Questions should be directed at obtaining information regarding parental marital status, living arrangements, significant life events, and significant changes or stressors.

Daytime Functioning

In adults, a key question is whether the patient falls asleep at inappropriate times or has difficulty staying awake during certain daytime activities. However, rather then having a primary complaint of daytime sleepiness, young children often manifest daytime sleepiness with increased activity and teenagers may manifest sleepiness with emotional instability.4 Whether daytime sleepiness is a primary complaint or one that needs to be uncovered, it can result in poor daytime functioning such as problems with cognitive and school performance.31 Other important items to address are whether the patient takes naps and if he or she feels refreshed upon awakening in the morning or from the naps. It is important to keep in mind that depending on the age of the infant or child, daily naps may be normal. Further pathology can be uncovered when patients have complaints of unintentional sleep episodes, sleep paralysis, hypnagogic hallucinations, or cataplexy.32

Bedtime Routine

For parents of young children, dealing with bedtime behaviors can be both frustrating and exhausting. Parents should be asked about the patient’s evening routine, including the timing and consistency of bedtime activities. This includes any variances during weekends and holidays. Children with behavioral insomnia of childhood may interrupt this routine with behaviors such as stalling and resistance.4 Questions about the child’s sleeping environment should include co-sleeping, room sharing, light and noise level, room temperature, and presence of electronics (cell phone, computer, or television).

Nocturnal Behavior

The quality of sleep can be determined, in part, from asking about the timing and events related to night awakenings. This should include the frequency, duration, and parental response to awakenings. Respiratory symptoms, such as snoring, gasping, cessation of breathing, and mouth breathing also should be elucidated. Partial arousal parasomnias, such as sleep walking and talking, are common complaints and often are familial.33,34 A child with RLS may complain of leg pain, “creepy-crawly” feelings in the legs, or simply feeling the need to get out of bed several times to move around.35 Other questions regarding nighttime behaviors should include difficulties with seizures, enuresis, nightmares, night terrors, or rhythmic movements of extremities.

Questionnaires and Scales

Several questionnaires and scales exist for use by clinicians and researchers to evaluate sleep disorders. Useful questions that are designed for screening for sleep problems by the primary care physician are described in Table 1.31,36,37 Two common sleep scales that are used clinically for adults are the Stanford Sleepiness Scale and the Epworth Sleepiness Scale. The Pediatric Daytime Sleepiness Scale is an 8-item questionnaire used by clinicians for evaluating younger school age children.36 Other brief questionnaires designed for the screening of sleep problems include the BEARS and Ten-item Sleep Screener (TISS). The BEARS can be used for children 2–18 years of age and consists of five items, namely, “B”edtime problems, “E”xcessive daytime sleepiness, “A”wakenings during the night, “R”egularity of evening sleep time and morning awakenings, and “S”leep-related breathing problems or “S”noring.37 Another quick and simple questionnaire is the TISS. The TISS includes questions regarding the child’s snoring, excessive daytime sleepiness; difficulty with falling asleep at night; frequent moving at night; frequent waking at night; difficulty awakening in the morning; gasping, choking, and snorting in sleep; cessation of breathing during sleep; enough sleep compared to peers; and existence of a difficult temperament.31 If any of the answers suggest a sleep problem, then the clinician should seek further evaluation by a sleep specialist for the child.



More extensive questionnaires and scales include the Children’s Sleep Habits Questionnaire (CSHQ), Pediatric Sleep Questionnaire (PSQ), and Sleep Disorders Inventory for Students (SDIS). The CSHQ consists of 33 questions for children 4–10 years of age and is used primarily for pediatric sleep research.31

The PSQ is a 22-item instrument for children ages 2–18 years that yields a higher score based upon the presence of abnormal breathing during sleep, snoring, excessive sleepiness, abnormal behavior, and periodic limb movement disorder.38 Finally, the SDIS questionnaire, which is used to create the TISS, can be given to children 2–10 years of age (SDIS-C) or to adolescents 11–18 years of age (SDIS-A). The SDIS has 25 or 30 questions that can help diagnose OSA syndrome, PLMD, delayed sleep phase syndrome (DSPS), and excessive daytime sleepiness. The SDIS-A also covers RLS and narcolepsy.31

Sleep Diaries

The sleep diary provides a graphic method to track a 24-hour sleep-wake cycle. The patient or parent is instructed to record the times of daily sleep onset and awakenings over a period of 1–2 weeks. This can provide valuable information about consistencies and insufficiency in the patient’s sleep schedule, and can function as a reference to assess changes associated with different therapeutic interventions.


Polysomnography (PSG) is the primary method for determining sleep architecture and is the gold standard for evaluating sleep disorders (Table 2). This test is generally performed overnight in a sleep lab with supervising technicians. It records multiple channels of information including the EEG, electrooculogram (EOG), electromyogram (EMG), respiratory activity, electrocardiogram, and audi-visual monitoring.39 The different sleep stages are determined with the use of the EEG, EMG, and EOG signals. The EEG montage in adults requires placement of central and occipital leads. Additional leads can be used to evaluate for seizure activity and can be useful for pediatric sleep evaluations. The EMG and EOG are necessary to identify REM sleep. For respiratory activity, effort is determined by monitoring chest and abdominal wall movements, nasal and oral airflow is recorded with the use of thermistors or pressure transducers, and gas exchange is determined by the use of pulse oximetry and end-tidal carbon dioxide monitoring. The audiovisual components of a sleep study are important in providing information about seizures, sleep walking, snoring, and ensuring safety of the patient.





Actigraphy is used to provide an objective measure of the sleep-wake cycle based on the assumption that movement indicates wakefulness (Table 2). It is useful in assessing sleep quality and circadian rhythm patterns in a patient. The recording can be conducted over a series of days or weeks while the person follows a normal routine. Actigraphy can be conducted as outpatient with the patient wearing a small device similar in size to a large watch.

Multiple Sleep Latency Testing

The MSLT is used to determine daytime sleepiness and diagnose narcolepsy (Table 2). It is often performed the day after overnight PSG. The patient is instructed to take 4–5 naps at 2-hour intervals. REM latency is the time from the onset of sleep to first REM episode. A long latency to sleep onset indicates an alert patient. A short time to sleep onset indicates sleepiness. Normal sleep onset time in adults is 10–20 minutes and in children 10–12 minutes. An average sleep onset that is <5 minutes suggests the possibility of pathology. In children, this test is limited because it requires patient cooperation, daytime napping can be normal, and it has not been validated in children <6 years of age.35

Pharmacologic Treatments of Pediatric Sleep Disorders

Although pharmacologic agents are frequently prescribed to children with sleep disorders, none of them are approved by the US Food and Drug Administration for pediatric use, and there is significant lack of well-designed clinical research on the safety and tolerability of sedative hypnotics in pediatric populations.40
One recent study indicated that up to 81% of children with insomnia were prescribed medication to treat their clinical condition.41 Proper assessment and diagnosis of sleep disorders is the critical step in selecting a treatment approach that would address pathophysiology of sleep dysfunction rather than simply sedating the child. Non-pharmacologic treatments should always be considered prior to prescribing medications.


According to surveys, Clonidine is a central alpha-2-adrenergic receptor agonist with the onset of action within 1 hour. Clonidine is one of the most commonly prescribed medications by pediatricians to children and adolescents.41,42 It is being used off label in pediatrics for insomnia, especially among children with neurodevelopmental disorders and ADHD. The usual starting dose is 50 mcg with the gradual increase in 50 mcg increments.


Diphenhydramine is a histamine-1 receptor antagonist frequently used for sleep initiation and sleep maintenance problems in children of all ages. The minimal effective dose in children has been reported at 0.5 mg/kg. However, a recent randomized controlled clinical trial43 of diphenhydramine in infants showed it being no more effective than placebo for the treatment of nocturnal awakenings. Significant side effects can occur even at the therapeutic doses and may include impaired consciousness and anticholinergic side effects.


Melatonin, a product not regulated by the FDA, has been shown to be effective in the treatment of sleep-onset problems in children and adolescents. Double-blind, placebo-controlled trials of melatonin 5 mg were conducted in healthy normal elementary school-age children44 and in children with ADHD and comorbid insomnia45 showing significant improvement in sleep-onset latency.

Non-benzodiazepine Hypnotics

Non-benzodiazepine hypnotics are now available in the US and include zolpidem, zaleplon, and eszolpiclone. This group of pharmacologic agents is characterized by a rapid onset of action and relatively short half-lives. Only one study46 examined the pharmacokinetics of zolpiden in children and concluded that clearance of zolpidem is three times higher in children than in adults. Zolpidem appeared to be well tolerated by children and adolescents up to maximum dose of 20 mg. Episodes of hallucinations, sleep walking, and other complex behaviors in sleep has been reported from use of zolpidem and related hypnotics. Patients and their parents should be warned about potential risks associated with the use of non-benzodiazepines hypnotics.


Benzodiazepines are used infrequently in children with sleep disorders except in the treatment of parasomnias, such as sleep-walking and sleep terrors. Low doses of clonazepam from .25–.5 mg at bedtime is usually recommended for the treatment of parasomnias. Clonazepam has also been used to relieve symptoms of RLS and improve sleep continuity in children.


Modafinil is a non-stimulant-alerting agent that is well tolerated by children and adolescents. The pharmacologic treatment of excessive sleepiness associated with narcolepsy or idiopathic hypersomnia includes modafinil at 100–400 mg/day in divided doses.47


Stimulants, such as methylphenidate and dextroamphetamine products, have been widely used to treat excessive sleepiness but are far less studied in children with narcolepsy compared with those diagnosed with ADHD.48

Sodium Oxybate

Sodium oxybate was approved by the FDA in 2002 for the treatment of excessive daytime sleepiness and cataplexy in patients with narcolepsy. It is a powerful CNS depressant that increases slow-wave sleep, but has serious potential side effects in cases of overdose or abuse. One study49 demonstrated the effectiveness of sodium oxybate for the treatment of excessive daytime sleepiness associated with narcolepsy in a small sample of children.


Antidepressants with noradrenergic reuptake-inhibiting qualities have been used for the treatment of cataplexy in both adults and children. Tricyclic antidepressants, fluoxetine, venlafaxine, and more recently atomoxetine, have been shown to be effective in controlling cataplexy and other REM-related symptoms.

Dopaminergic Agents

Dopaminergic agents, such as carbidopa/levodopa, pramirexole, and ropinorole have been shown to be effective in the treatment of RLS in children in a few reports. In general, they appear to be well tolerated but may be associated with an augmentation phenomenon where symptoms of RLS worsen and appear earlier in the day with an increased dose of medication.


Gabapentin is a g-aminobutyric acid agonist approved for use in children with epilepsy and has shown to reduce RLS symptoms in children.

Nasal Steroids

Nasal steroids, like fluticasone alone50 or in combination with montelukast, have been shown to be effective in reducing the severity of OSA in children and helping to resolve residual symptoms of sleep-disordered breathing after adenotonsillectomy.51

Non-Pharmacologic Treatments of Pediatric Sleep Disorders

Parental Education

Parental education, especially during the prenatal period or shortly after the child’s birth, has shown to be very effective in preventing the development of behavioral sleep problems in the future. Parents are usually instructed on healthy bedtime routines, sleep and nap schedules, and how to entrain their infants into a normal circadian sleep cycle and how to develop appropriate sleep associations. Recent studies52 indicated that infants whose parents received sleep education achieved an average 1.3 hours more sleep per day than those whose parents did not have preventive education.

Disengagement of feeding from bedtime routine is shown to be helpful in reducing the need for further feedings during the night. Parents are usually instructed to place their infant in a crib while he or she is still awake to prevent sleep-onset association disorder requiring lengthy parental interventions like rocking, holding, and so forth.

Behavioral Interventions

Behavioral interventions represent the first-choice therapy for children with sleep disturbances associated with bedtime resistance, behavioral insomnia of childhood, circadian sleep disorders, and parasomnias.

Unmodified Extinction

Unmodified extinction, also known as the “crying out” approach, has been shown to be effective but particularly difficult for parents to implement.

Graduated Extinction

Graduated extinction involves putting the child to bed and checking periodically while progressively increasing the intervals between checks until the child learns to fall asleep without the need for parental presence.

Extinction with Parental Presence

Extinction with parental presence is another version of behavioral intervention where parents are instructed to sleep in a separate bed in the child’s room while ignoring the child’s crying. This type of sleeping arrangement is recommended to continue for ≥1 weeks until the child learns to fall and stay asleep consistently. Then, the parent returns to sleeping in a separate bedroom.

Positive Bedtime Routines

Positive bedtime routines along with sleep hygiene interventions have been shown to be effective in treating behavioral insomnias and bedtime resistance. Reinforcement can be used to improve the child’s sleep behavior and increase the compliance with a sleep schedule. Examples of tangible reinforcers include sticker charts, candy, toys, and desired play activities.

Scheduled Nocturnal Awakenings

Scheduled nocturnal awakenings are effective in reducing the frequency of spontaneous nocturnal awakenings, confusional arousals, night terrors, and other parasomnias. The protocol usually involves awakening the child for a brief period of time before his usual spontaneous awakening or partial arousal. In most cases, the combination of several interventions is used to achieve the optimal response and to minimize stress for the child and family.

Sleep Hygeine

Sleep hygeine, or improved sleep habits, is an essential intervention in the treatment of sleep disorders. Generally, sleep hygiene recommendations help promote a conducive environment for better nighttime sleep and daytime alertness.


Chronotherapy is an intervention directed toward improvement in the timing of the sleep-wake cycle. The approach is most commonly used to treat adolescents with delayed sleep-phase syndrome. Chronotherapy involves a gradual delay in the bedtime by ~2–3 hour increments every 2 days until a desired earlier bedtime is reached.

Light Therapy

Light therapy has been successfully employed to treat circadian rhythm sleep disorders by therapeutic bright light exposure (5,000–10,000 lux) in the morning for sleep phase advancement in cases of DSPS, and in the evening to delay sleep onset in patients suffering from advanced sleep phase syndrome.53

Imagery Rehearsal Therapy

Imagery rehearsal therapy was shown to be effective in one study54 of adolescents with chronic recurrent nightmares.

Surgical Treatment

Surgical treatment, including adenotonsillectomy, is usually the first-choice therapy for pediatric OSA.55 In up to 80% of children, OSA is resolved following adenotonsillectomy.56

Continuous Positive Airway Pressure

Continuous positive airway pressure is indicated for children and adolescents who either failed surgical intervention or are not surgical candidates.55


Sleep disorders are highly prevalent in children and adolescents, and often have a significant impact on their neurocognitive, emotional, and behavioral development. Consequences of sleep loss and sleep fragmentation in children include daytime sleepiness, inattentiveness, fatigue, impaired performance, increased irritability, aggression, and behavioral dyscontrol. It is important for practicing psychiatrists to differentiate psychiatric symptoms that might be attributable to sleep loss, and to intervene to prevent further deterioration in regulation of sleep and wakefulness.

There are few well-designed clinical studies addressing treatment algorithms for pediatric sleep disorders, especially using pharmacologic agents. Further studies on the effective practical approaches to treatment of insomnia, parasomnias, and disorders of excessive sleepiness in children are needed with the emphasis on psychiatric comorbidities and neurocognitive development. PP


1.    Beebe DW. Sleep and behavior in children and adolescents: a multi-system, developmental heuristic model. In: Ivanenko A, ed. Sleep and Psychiatric Disorders in Children and Adolescents. New York, NY: Informa Healthcare USA, Inc; 2008:1-10.
2.    Kintera.org. 2004 Sleep Poll Final Report. Available at: www.kintera.org/atf/cf/{F6BF2668-A1B4-4FE8-8D1A-A5D39340D9CB}/2004SleepPollFinalReport.pdf. Accessed January 5, 2009.
3.    Montgomery-Downs HE. Normal sleep development in infants and toddlers. In: Ivanenko A, ed. Sleep and Psychiatric Disorders in Children and Adolescents. New York, NY: Informa Healthcare USA, Inc; 2008:11-21.
4.    Meltzer LJ, Mindell JA. Sleep and sleep disorders in children and adolescents. Psychiatr Clin N Am. 2006;29(4):1059-1076.
5.    International Classification of Sleep Disorders. 2nd ed. Westchester, IL: American Society of Sleep Medicine; 2005.
6.    National Sleep Foundation. Children and Sleep. Sleep in America Poll, 2006. Available at: www.sleepfoundation.org/atf/cf/{F6BF2668-A1B4-4FE8-8D1A-A5D39340D9CB}/2006_summary_of_findings.pdf. Accessed January 5, 2009.
7.    Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association. 1994.
8.    Ohayon MM, Roberts RE, Zulley J, Smirme S, Priest RG. Prevalence and patterns of problematic sleep among older adolescents. J Am Acad Child Adolesc Psych. 2000;39(12):1549-1556.
9.    Johnson EO, Roth T, Schultz L, et al. Epidemiology of DSM-IV insomnia in adolescence: lifetime prevalence, chronicity, and an emergent gender difference. Pediatrics. 2006;117(2):e247-e256.
10.    Phillips C, Meltzer LJ, Mindell JA. Epidemiology of insomnia. In: Ivanenko A, ed. Sleep and Psychiatric Disorders in Children and Adolescents. New York, NY: Informa Healthcare USA, Inc; 2008:235-246.
11. 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):253-259.
12.    Stores G. Parasomnias of Childhood and Adolescence. Sleep Med Clin. 2007;2(3):405-417.
13.    Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med. 2001;164(1):16-30.
14.    Tang JP, Rosen CL, Larkin EK, et al. Identification of sleep-disordered breathing in children: variation with event definition. Sleep. 2002;25(1):72-79.
15.    Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics. 1998;102(3 pt 1):616-620.
16.    Chervin RD, Archbold KH, Dillon JE, et al. Inattention, hyperactivity, and symtoms of sleep-disordered breathing. Pediatrics. 2002;109(3):449-456.
17.    Urschitz MS, Eitner S, Guenther A, et al. Habitual snoring, intermittent hypoxia, and impaired behavior in primary school children. Pediatrics. 2004;114(4):1041-1048.
18.    O’Brien LM, Mervis CB, Holbrook CR, et al. Neurobehavioral correlates of sleep-disordered breathing in children. J Sleep Res. 2004;13(2):165-172.
19.    Gozal D. Obstructive sleep apnea in children: implications for the developing central nervous system. Semin Pediatr Neurol. 2008;15(2):100-106.
20.    Goldstein NA, Fatima M, Campbell TF, et al. Child behavior and quality of life before and after tonsillectomy and adenoidectomy. Arch Otolaryngol Head Neck Surg. 2002;128(7):770-775.
21.    Pelin Z, Guilleminault C, Risch N, et al. HLA-DQB1*0602 homozygosity increases relative risk for narcolepsy but not disease severity in two ethnic groups. US Modafinil in Narcolepsy Multicenter Study Group. Tissue Antigens. 1998;51(1):96-100.
22.    Guilleminault C, Zvonkinaa V, Tantrakul V, Kim JH. Advances in narcolepsy syndrome and challenges in the pediatric population. Sleep Med Clin. 2007;2(3):397-404.
23.    Picchietti D, Allen RP, Walters AS, et al. Restless legs syndrome: prevalence and impact in children and adolescents – The Peds REST study. Pediatrics. 2007;120(2):253-266.
24.    Allen RP, Picchietti D, Hening WA, et al. Restless legs syndrome: Diagnostic criteria, special considerations, and epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop at the National Institutes of Health. Sleep Med. 2003;4(2):101-119.
25.    Montplaisir J, Boucher S, Poirier G, et al. Clinical, polysomnographic, and genetic characteristics of restless legs syndrome. A study of 133 patients diagnosed with new standard criteria. Mov Disord. 1997;12(1):61-65.
26.    Sun ER, Chen CA, Ho G, et al. Iron and the restless legs syndrome. Sleep. 1998;21(4):371-377.
27.    Kotagal S, Silber MH. Childhood-onset restless legs syndrome. Ann Neurol. 2004;56(6):803-807.
28.    Cortese S, Konofal E, Lecendreux M, et al. Restless legs syndrome and attention-deficit/hyperactivity disorder. A review of the literature. Sleep. 2005;28(8):1007-1013.
29.    Picchietti MA, Picchietti DL. Restless legs syndrome and periodic limb movement disorder in children and adolescents. Semin Pediatr Neurol. 2008;15(2):91-99.
30.    Picchietti D. Is iron deficiency an underling cause of pediatric restless legs syndrome and of attention-deficit/hyperactivity disorder? Sleep Med. 2007;8(7-8):693-694.
31.    Luginbuehl M, Bradley-Klug KL. Assessment of sleep problems in a school setting or private practice. In: Ivanenko A, ed. Sleep and Psychiatric Disorders in Children and Adolescents. New York, NY: Informa Healthcare USA, Inc.; 2008:109-138.
32.    Sheldon SH. Diagnostic methods in pediatric sleep medicine. Sleep Med Clin. 2007;2(3):343-351.
33.    Guilleminault C, Palombini L, Pelayo R, Chervin RD. Sleepwalking and sleep terrors in prepubertal children: what triggers them? Pediatrics. 2003;111(1):e17-e25.
34.    Hublin C, Kaprio J. Genetic aspects and genetic epidemiology of parasomnias. Sleep Med Rev. 2003;7(5):413-421.
35.    D’Andrea LA. Evaluation of sleep disorders in children and adolescents. In: Ivanenko A, ed. Sleep and Psychiatric Disorders in Children and Adolescents. New York, NY: Informa Healthcare USA, Inc.; 2008:95-108.
36.    Drake C, Nickel C, Burduvali E, Roth T, Jeffereson C, Pietro B. The Pediatric Daytime Sleepiness Scale (PDSS): sleep habits and school outcomes in middle-school children. Sleep. 2003;26(4):455-458.
37.    Owens J, Dalzell V. Use of the ‘BEARS’ sleep screening tool in a pediatric residents’ continuity clinic: a pilot study. Sleep Med. 2005;6(1):63-69.
38.    Chervin RD, Hedger K, Dillon JE, Pituch KJ. Pediatric Sleep Questionnaire (PSQ): validity and reliability of scales for sleep-disorder breathing, snoring, sleepiness, and behavioral problems. Sleep Med. 2000;1(1):21-32.
39.    Kothare SV, Kaleyias J. The clinical and laboratory assessment of the sleepy child. Semin Pediatr Neurol. 2008;15(2):61-69.
40.    Mindell JA, Emslie G, Blumer J, et al. Pharmacological management if insomnia in children and adolescents: consensus statement. Pediatrics. 2006;117(6):e1223-e1232.
41.    Stojanovski SD, Rasu RS, Balkrishnan R, et al. Trends in medication prescribing for pediatric sleep difficulties in US outpatient settings. Sleep. 2007;30(8):1013-1017.
42.    Owens JA, Rosen Cl, Mindell JA. Medication use in the treatment of pediatric insomnia: Results of a survey of community-based pediatricians. Pediatrics. 2003;111(5 pt.1):e628-e635.
43.    Merenstein D, Diener-West M, Hallbower AC, et al. The trial of infant response to diphenhydramine: The TIRED study- a randomized, controlled, patient-oriented trial. Arch Pedaitr Adolesc Med. 2006;160(7):707-712.
44.    Smits MG, Nagtegaal EE, van der Heijden J, Coenen AM, Kerkhof GA. Melatonin for chronic sleep onset insomnia in children: a randomized placebo-controlled trial. J Child Neurol. 2001;16(2):86-92.
45.    Van der Heijen KB, Smits MG, Van Someren EJ, et al. Effect of melatonin on sleep, behavior and cognition in ADHD and chronic sleep-onset insomnia. J Am Acad Child Adolesc Psychiatry. 2007;46(2):233-241.
46.    Blumer JL, Red MD, Steinberg F, et al. Potential pharmacokinetic basis of zolpidem dosing in children with sleep difficulties. Clin Pharmacol Ther. 2008;83(4):551-558.
47.    Ivanenko A, Tauman R, Gozal D. Modafinil in the treatment of excessive daytime sleepiness in children. Sleep Med. 2003;4(6):579-582.
48.    Littner M, Johnson SF, McCall WV, et al. Practice parameters for the treatment of narcolepsy. An update for 2000. Sleep. 2001;24(4):451-466.
49.    Murali H, Kotagal S. Off-label treatment of severe childhood narcolepsy-cataplexy with sodium oxybate. Sleep. 2006;29(8):1025-1029.
50.    Brouillette RT, Manoukian JJ, Ducharme FM, et al. Efficacy of fluticasone nasal spray for pediatric obstructive sleep apnea. J Pediatr. 2001;138(6):838-844.
51.    Kheirandish L, Goldbart AD, Gozal D. Intranasal steroids and oral leukotriene modifier therapy in residual sleep-disordered breathing after tonsillectomy and adenoidectomy in children. Pediatrics. 2006;117(1):e61-e66.
52.    Symon BG, Marley JE, Martin AJ, Norman ER. Effect of consultation teaching behaviour modification on sleep performance in infants: a randomized controlled trial. Med J Aust. 2005;182(5):215-218.
53.    Chesson AL Jr, Littner M, Davila D, et al. Practice parameters for the use of light therapy in the treatment of sleep disorders. Standards of Practice Committee, American Academy of Sleep Medicine. Sleep. 1999;22(5):641-660.
54.    Krakow B, Sandoval D, Schrader R, et al Treatment of chronic nightmares in adjudicated adolescent girls in a residential facility. J Adolesc Health. 2001;29(2):94-100.
55.    American Academy of Pediatrics, Section of Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704-712.
56.    Lipton AJ, Gozal D. Treatment of obstructive sleep apnea in children: do we really know how? Sleep Med Rev. 2002;7(1):61-80.