eMedicine Specialties > Pediatrics: Developmental and Behavioral > Medical Topics

Sleep Disorder: Problems Associated With Other Disorders

Dennis A Nutter, Jr, MD, Consulting Staff, Department of Psychiatry, Northeast Georgia Medical Center
Guy K Palmes, MD, Program Director, Assistant Professor, Department of Psychiatry, Section of Child and Adolescent Psychiatry, Wake Forest University; Benyam Tegene, MD, Fellow, Department of Psychiatry, Wake Forest University Baptist Medical Center

Updated: Apr 4, 2007

Introduction

Background

Sleep disturbances in youth represent highly common phenomena that, in severe forms, can interfere with daily patient and family functioning. Interest in pediatric sleep problems continues to increase, yet further investigation is needed to develop empirically based detection and treatment of pediatric sleep disorders.

The consequences of untreated sleep problems may include significant emotional, behavioral, and cognitive dysfunction. The magnitude of these sequelae is inversely proportional to the child's overall ability to adapt and develop in spite of the sleep disturbance. Nevertheless, sleep regulation remains a critical part of health for youths. Elevated rates of sleep problems exist among children and adolescents with neurodevelopmental, nonpsychiatric medical conditions and psychiatric disorders.

Reciprocal relationships occur between sleep disorders and comorbid psychiatric disorders. For example, when a given child with recurrent depression has an exacerbation, sleep problems often increase simultaneously. On the other hand, disrupted and inadequate sleep alone can produce behavioral, affective, and cognitive dysfunction.

Neurobiologically, closely linked modulatory systems appear to regulate sleep, alertness, and attention span. This article focuses on the most prevalent sleep problems among youths that are typical and distinctly unique from adult sleep disorders. Night terrors, nightmares, and sleep apnea are covered only briefly because they are discussed in other articles.

This article uses classifications and definitions from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text Revision (DSM-IV-TR) along with more operationally defined problems when appropriate.

Childhood sleep disorders are classified in the following three categories: dyssomnias, parasomnias, and medical-psychiatric disorders. Adolescents with substance use disorders represent a significant proportion of sleep-disordered youths.

Patients with dyssomnias present with difficulty initiating or maintaining sleep or with excessive daytime somnolence. The DSM-IV-TR defines dyssomnias as primary disturbances in the quantity, quality, or timing of sleep. These disorders are believed to be a consequence of central nervous system abnormalities that alter the sleep process.

Parasomnias result in disruption of an existing state of sleep. Arousals, partial arousals, and sleep-stage transition impositions define this category. An alternative definition of these phenomena describes deviated behavioral or physiological events that transpire during sleep, specific sleep stages, or sleep-wake transitions. Insomnia or excessive sleepiness is uncommon in parasomnias despite intrusion upon sleep. These are dyssomnia symptoms as noted above. Most parasomnias affect otherwise healthy youths and commonly subside over the course of adolescence. These disorders are typically viewed as transient developmental phenomena, although children with parasomnias were recently found to display higher rates of sleep-onset delay, night awakenings, bedtime resistance, and reduced sleep duration compared to a community control group.

Medical-psychiatric–associated sleep disorders comprise the neuropsychiatric conditions that typically include sleep disturbances. Attention deficit hyperactivity disorder (ADHD), gastroesophageal reflux disease (GERD), pervasive developmental disorders (PDD), mental retardation (MR), Down syndrome, Prader-Willi syndrome, Tourette disorder, nocturnal asthma, depressive disorders, anxiety disorders, mania, neuromuscular disorders, nocturnal seizures, Kleine-Levin syndrome, chronic fatigue syndrome, headaches, and blindness with associated sleep disorder are representative of this category of medical-psychiatric–associated sleep disorders.

Pathophysiology

Dyssomnias

Primary hypersomnia: Youths with primary hypersomnia have normal sleep efficiency, sleep/wake cycles, and sleep architecture. Patients with primary hypersomnia present with a normal variant sleep pattern except for longer sleep needs. It may be a lifelong pattern. No other identifiable cause exists for the excessive somnolence that continues for at least 4 weeks.

Primary or idiopathic insomnia: The pathogenesis of primary hypersomnia is poorly defined. Patients with primary or idiopathic insomnia may have a lifelong inability to initiate and maintain sleep with associated sequelae.

Sleep-state misperception: Youths with sleep-state misperception may have normal polysomnography. The pathology of sleep-state misperception is associated with an underestimate or misperception of the child's sleep duration, which results in the patient's mistaken belief of having experienced inadequate sleep.

Psycho-physiological insomnia: This disorder is related to psychological stressors that interfere with sleep onset or maintenance.

Narcolepsy: Rapid eye movement (REM) sleep mechanisms are dysregulated in youths with narcolepsy, but evidence also exists of nonrapid eye movement (NREM) and circadian sleep-wake cycle abnormalities. REM-associated sleep phenomena intrude into the awakened state. Sleep attacks (sleep), cataplexy (abrupt atonia precipitated by strong emotions), hypnagogic and hypnopompic hallucinations (experienced as dreamlike events immediately before sleep onset or upon awakening) are characteristic of narcolepsy. Excessive daytime somnolence leading to irresistible/involuntary sleep (sleep attacks) may occur. The role of the neuropeptide hypocretin (Orexin) and human leukocyte antigen (HLA)–DR2/DBQ1 as a genetic-neuroimmune interaction is being considered in current research on this issue. Narcolepsy is consistent with the polygenic model of development in most human cases.

Obstructive sleep apnea syndrome (OSAS): The pathophysiology of OSAS is poorly understood. Alterations exist in alveolar ventilation and oxygenation. OSAS is associated with adenotonsillar hypertrophy; however, most youths with adenotonsillar hypertrophy do not experience OSAS. Upper airway neuromotor dysfunction is possible in the initiation of OSAS.

Periodic limb movements in sleep (PLMS): PLMS is more prominent in NREM stage 1 and 2 sleep. PLMS is strongly associated with ADHD and restless legs syndrome (RLS) in the pediatric population. The response to dopaminergic agents and the association with ADHD suggest that PLSM may be a dopaminergic dysfunction. Characteristic movements may aid in further understanding of the pathology of PLMS. Repetitive flexion of lower extremities (more common) or upper extremities occurs in youths with PLMS with a 0.5- to 5-second duration occurring 5-90 seconds apart. Repetitive jerks are associated with frequent awakenings and daytime somnolence or insomnia. The pediatric population with PLMS often experiences inattention, overactivity, and mood lability due to associated sleep disruption/fragmentation. PLMS can occur without RLS.

RLS: The response to dopaminergic agents and the association to ADHD implicate that RLS is a dopaminergic dysfunction. Leg discomfort in patients with RLS is associated with a strong urge to move legs, and the relief with movement may ultimately reveal a pathophysiology similar to that of akathisia. Most patients with RLS have PLMS. The pediatric population with RLS often experiences inattention, overactivity, and mood lability due to associated sleep disruption/fragmentation.

Limit-setting sleep disorder: This is a parent-child transactional model with potentially numerous biopsychosocial variables that influence interactions. It is not simply a failure to set limits but has a more complex pathogenesis and ultimately pathophysiology. Children with limit-setting sleep disorder resist or refuse to go to bed at an appropriate time. Limit-setting sleep disorder may be related to underlying pathophysiology as observed in ADHD and other neurodevelopmental disorders or may be a combined medical-behavioral issue.

Insufficient sleep syndrome: This is a condition of chronic sleep deprivation without an underlying disease process. Youths with insufficient sleep syndrome may experience an increased need for sleep during puberty and adolescence. Insufficient sleep syndrome may represent a poor compensatory ability for sleep loss and includes failure to adequately synchronize sleep-wake behaviors and adapt to environmental demands, such as school. The patient with insufficient sleep syndrome attempts to decrease sleep debt incurred during the week by sleeping later on the weekends. They are unable to obtain sufficient sleep because of school, extracurricular, occupational, and other societal demands.

Circadian sleep disorders: A circadian clock/oscillator located in the suprachiasmatic nuclei of the anterior hypothalamus influences the wakefulness or alertness phase. A circadian clock potentiates alternate or diurnal phases of the sleep-wake cycle. A free-running human sleep-wake cycle is 25 hours; however, the cycle entrained by the environment results in a 24-hour cycle. Sleep and associated processes are at opposite phases or periods in patients with circadian sleep disorders. Circadian sleep disorders may represent a poor compensatory ability for sleep loss and includes failure to adequately synchronize sleep-wake behaviors and adapt to environmental demands, such as school. This disorder is frequently observed in adolescents with delayed sleep phase.

Parasomnias

Parasomnias are sleep-related phenomena disrupting normal sleep. Events can take place during sleep-wake transitions, arousal, or REM sleep. Sleep stages and other variables are related to pathogenesis.

Sleepwalking: Sleepwalking is described as partial arousal from sleep during slow-wave stages 3 and 4. It is most common during the initial third stage of the sleep period.

Bruxism (persistent grinding of the teeth): Bruxism is considered as a stereotyped movement disorder or rhythmic disorder. It is more frequent during the early part of sleep and may be related to stress and/or anxiety or dentition abnormalities. Bruxism is not limited to sleep but may also occur while the child is awake. Basal ganglia dysfunction has been hypothesized.

Nightmares: Nightmares appear to be related to the same etiology as other anxiety-related experiences. They occur during REM sleep.

Sleep terrors: Sleep terrors are associated with autonomic arousal and screaming. They transpire during the first third of sleep in the slow-wave sleep cycle.

Primary nocturnal enuresis: Bladder instability, which is an uninhibited or reduced threshold for detrusor contraction during bladder filling, and urethral instability, which is a failure of urethral sphincter to adequately relax with bladder filling, are characteristic of youths with primary nocturnal enuresis. Youths with primary nocturnal enuresis may have a relative resistance to an antidiuretic hormone at night. Genetic factors contribute significantly in primary nocturnal enuresis with linkage studies positive on chromosome 8. No correlation exists with sleep stage.

Rhythmic movement disorders: These disorders are related to the developmental age of the child. Head banging and body rocking are the most common presentations of this disorder. Rhythmic movement disorder occurs during sleep onset and stages 1 and 2 sleep (light sleep).

Confusional arousals: In a confusional arousal, the child may awaken from stage 1 and 2 sleep frightened and crying. Only minimal autonomic arousal occurs opposed to the high degree observed in sleep terrors. The patient usually fully awakens before returning to sleep. Confusional arousals are associated with higher rates of delayed sleep onset, night awakening, decreased sleep duration, and bedtime resistance.

Frequency

United States

Surveys report a 20-25% prevalence of youths with some type of sleep problem. The following problems are commonly reported in children aged 2-15 years:

• Nightmares (30%) are more common in younger youths.
• Sleepwalking with at least more than 1 episode occurs in 25-30% of youths and is most common in children aged 3-10 years.
• Insomnia occurs in 23% of youths.
• Enuresis occurs from 8% in children aged 4 years to 4% in children aged 10 years.
• Bruxism is reported in 10% of youths and may occur in people of any age.
• Grinding and clenching teeth at night is reported in 5-8% of adults.
• Sleep rocking or head banging is reported in 5% of youths, with head banging being common in infants and in children aged 9 months to 12 years.
• OSAS is the most common reason for sleep laboratory referral and affects an estimated 2% of children.
• Narcolepsy (0.01-0.20%) may be underestimated in children because a classic tetrad of symptoms is uncommon in this age group.
• Bedtime resistance in school-aged children has been reported at 15% and is often associated with limit-setting disorder.

International

See US frequency.

Mortality/Morbidity

• Learning difficulties, emotional lability, attentional deficits, disruptive behaviors, social and school impairments, family dysfunction, low self-esteem, depression, anxiety, cognitive dysfunction hyperactivity, irritability, and memory impairment represent common comorbidities and often exert bidirectional or reciprocal influences.
• OSAS may lead to cor pulmonale, pulmonary hypertension, right-sided heart failure, growth retardation, and failure to thrive.

Clinical

History

Sleep disorders are classified into 4 broad categories according to the DSM-IV-TR. These are primary sleep disorders, sleep disorders related to another mental disorder, sleep disorders due to a general medical condition, and substance-induced sleep disorders. Primary sleep disorders are subdivided into dyssomnias, which are characterized by abnormalities in the amount, quality, or timing of sleep, and parasomnias, which are characterized by abnormal behavioral or physiological events that occur in association with sleep stages or sleep-wake transitions. Key history areas are as follows:

• When evaluating a child or adolescent for a sleep disorder, obtaining a thorough sleep history cannot be overemphasized. A sleep diary usually kept for about 2 weeks provides information regarding night-to-night variability over time. Sleep diaries also are helpful in tracking patient compliance with behavioral interventions and response to treatment. Rating scales have been developed to quantify subjective sleepiness of patients. The Epstein Sleepiness Scale and Stanford Sleepiness Scale are examples.
  
  
  • Temporal history
  • When the problem began
  • Predisposing, precipitating, and perpetuating factors
  • Review of evening activities and bedtime rituals
  • Sleep environment
  • Latency to sleep onset
  • Arousals - When, duration, frequency, behavior during awakening, and ease with which child returns to sleep
  • History of snoring, breathing pauses, sleepwalking, talking, enuresis, and nocturia
  • Sleep position
  • Nightmares and sleep terrors
  • Seizure symptoms - Tongue biting, chewing, blood on bed clothes, and encopresis
  • Time of morning awakening, sleep paralysis, and early-morning headache
  • Total sleep time
  • Restorative sleep
  • Daytime sleepiness, fatigue, and school performance
  • Questions about depression, anxiety, worries or concerns, hyperactivity, and irritability
  • Frequency and duration of naps
  • Existing comorbid disorders
  • Substance use
  • Use of caffeine, alcohol, drugs, medications (prescription or over-the-counter [OTC]), and herbal preparations
  • Family history of sleep disorder or metabolic disorder
  • Parents' sleep habits
  • Efforts made to control symptoms
  • Overall impact of sleep disturbance on family
     
• Dyssomnias
  
  
  • Primary insomnia: Insomnia is defined as the subjective symptom of inadequate sleep quantity and quality. Patients with primary insomnia report difficulty falling asleep or maintaining sleep. Chronic insomnia may produce poor concentration and a low level of energy. Other symptoms include a decreased sensation of well-being and poor productivity. Some patients with primary insomnia feel that the sleep was not restorative. Distress due to inability to sleep may lead to a vicious cycle of frustration and insomnia.
  • Primary hypersomnia: Patients with primary hypersomnia require more sleep despite long and good sleep (about 12 h), usually require naps in the daytime, and are not refreshed by short naps.
  • Narcolepsy: Patients with narcolepsy may experience (1) excessive daytime sleepiness with irresistible daytime sleep attacks; (2) sleep paralysis, in which the individual awakens unable to move; (3) cataplexy, which may be subtle initially (eg, wobbly knees, dizziness) but may progress to sudden falls following a strongly experienced emotion; (4) hypnagogic hallucinations; and (5) feeling of refreshment after a sleep attack.
  • OSAS: Children with OSAS have a history significant for loud snoring, breathing pauses, mouth breathing, restless sleep, and increased perspiration at night. Snoring is the most common presenting symptom. Hyperactivity and failure to thrive are more common symptoms of childhood obstructive apnea. Other symptoms in children with OSAS include excessive daytime sleepiness, morning headaches, and behavioral changes (paradoxical hyperactivity as children try to stay awake). These children also experience emotional lability, changes in school performance, and cardiac failure.
  • Delayed sleep phase syndrome (DSPS): Of the circadian rhythm sleep disorders, DSPS is the most common, with a prevalence of about 7% for adolescents. It is characterized by early insomnia, little or no difficulty maintaining sleep, and difficulty waking in the morning.
     
• Parasomnias
  
  
  • Nightmare disorder: Nightmares affect 10-50% of children aged 3-6 years. Nightmares occur during REM sleep usually in the second half of the night. After a nightmare, the child is alert and can clearly describe in detail scenes and frightening images. Nightmares are common during stressful times or after frightening events, such as frightening movies. Nightmares are well remembered in the morning. If nightmares are severe and frequent, they may affect daytime functioning. In posttraumatic stress disorder (PTSD), nightmares may be associated with flashbacks, numbing, reenacting the events, and avoidance.
  • Night terrors (pavor nocturnus): This form of sleep disturbance occurs in the first 3 hours of sleep. The child is not awake but appears agitated. Abrupt, usually agitated, arousal from slow-wave sleep takes place. Night terrors are associated with autonomic arousal (eg, tachypnea, tachycardia, diaphoresis) and screaming. The child is often inconsolable during the episode. The episode terminates spontaneously after about 3-5 minutes and the child quickly returns to sleep. Recall of the event in the morning is poor. This type of disturbance may be associated with an ongoing illness or fever.
  • Sleepwalking disorder (somnambulism): The sleepwalker is difficult to arouse and usually has no recollection of the event in the morning. Actions taking place during sleepwalking frequently vary.
  • Bed-wetting (enuresis): In primary enuresis, no period of nighttime dryness occurs for more than 6 months. In secondary enuresis, a relapse of bed-wetting occurs after a period of at least 6 months of dryness. This sleep disturbance may be associated with shame and low self-esteem.
     
• Sleep disorders related to medical and psychiatric conditions: A wide variety of medical and psychiatric disorders may result in sleep disruption. The clinician must first establish the presence of a general medical condition. Furthermore, the clinician must determine whether the sleep disturbance is causally related to the medical illness through a physiological mechanism. Cluster headaches occur more frequently during the night than in the daytime. Sleep-related headaches usually awaken the patient and fragment sleep.
  
  
  • Insomnia related to another mental disorder is characterized by reports of difficulty falling asleep, frequent awakenings during the night, or a marked feeling of nonrestorative sleep that has lasted for at least 1 month and is associated with daytime fatigue or impaired daytime functioning.
  • Hypersomnia related to another mental disorder is characterized by reports of either prolonged nighttime sleep or repeated daytime sleep episodes for at least 1 month. In both insomnia and hypersomnia related to another mental disorder, the sleep symptoms cause significant distress or impairment in social, occupational, or other important areas of functioning.
     
• Diagnostic criteria for sleep disorders caused by a general medical condition include the following:
  
  
  • A prominent disturbance in sleep that is sufficiently severe to warrant independent clinical attention
  • Evidence from the history, physical examination, or laboratory findings that the sleep disturbance is the direct physiological consequence of a general medical condition
  • Disturbance that is not better accounted for by another mental disorder (eg, an adjustment disorder in which the stressor is a serious medical illness)
  • Disturbance that does not occur exclusively during the course of a delirium
  • Disturbance that does not meet the criteria for breathing-related sleep disorder or narcolepsy
  • Sleep disturbance that causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
     
• The following medical conditions fragment sleep, lead to excessive sleepiness during the day, and affect the individual's concentration and performance in the day to various degrees. In pediatric populations, epilepsies occurring during sleep account for 30% of seizure disorders. Epilepsy appears to fragment sleep and causes impairment in daytime functioning. The sleep disturbances associated with developmental CNS disorders generally reflect fragmentation with frequent awakenings, difficulty in initiating sleep, and early morning awakenings. The physical abnormalities associated with Down syndrome and Prader-Willi syndrome that occlude the upper airway often lead to OSAS. Blind individuals experience cyclic disorders because of the lack of cues that continually reset the internal clock to fit the 24-hour day/night cycle.
• Klein-Levin syndrome: Klein-Levin syndrome refers to a constellation of symptoms that include episodes of excessive somnolence, overeating, and sexual disinhibition. Behavioral disturbances, such as irritability and confusion, are associated with Klein-Levin syndrome. Occasional hallucinations have been reported. Klein-Levin syndrome is 3 times more frequent in boys than in girls. Symptoms typically begin during adolescence, either gradually or abruptly. Onset follows a flu-like illness or injury with loss of consciousness in half the cases. Klein-Levin syndrome has a course that remits and relapses, with relapses occurring at intervals of weeks to months. Symptoms may last from 12 hours to 3 weeks. Klein-Levin syndrome usually resolves spontaneously during late adolescence or early adulthood.
• Down syndrome: Airway hypotonia leads to obstructive apnea that is not associated with obesity, age, or congenital heart disease. Central apnea also is common and is associated with significant desaturation.
• ADHD: Paradoxical hyperactivity in children with ADHD encourages them to stay awake. Emotional lability may be observed. Children with ADHD tend to have fewer arousals and shorter arousals than adults. These children also tend to have obstructive hypopnea with relatively few complete apneic events. Children with ADHD have a strong tendency to fall asleep during the day. Children with ADHD have high rates of RLS and PLMS, and they have a higher prevalence rate for OSAS comorbidity.
• Tourette syndrome: Approximately 50% of children with Tourette syndrome have sleep disturbances. Nocturnal awakenings and movements increase when tics persist into sleep. Comorbidity exists with obsessive-compulsive signs, traits associated with increased sleep latency, decreased REM sleep, and deceased REM sleep latency. Children and adolescents with this movement disorder are at risk for parasomnias. Patients with Tourette syndrome have a higher incidence of enuresis.
• Rett syndrome: This is associated with prolonged sleep latency. Short and fragmented sleep results in low sleep efficiency.
• Prader-Willi syndrome: Obesity, hyperphagia, and developmental delay are the most common features. Obesity can cause obstructive sleep apnea. An increased frequency of apneas, decreased nadir of oxygen saturation, increased maximum heart rate, and blunted respiratory response to hypercapnia during NREM sleep all may occur in patients with Prader-Willi syndrome. Sleep time and slow-wave sleep increase during the day and at night.
• Upper airway resistance syndrome: This results in REM fragmentation and extra daytime sleep (EDS).
• Menstrual-associated periodic hypersomnia: This is another cyclic sleep disorder, noted during the first few years after menarche. Attacks generally last 1-2 weeks after ovulation, with sudden resolution occurring at the time of menses.
• Sleep-related GERD: This is characterized by regurgitation of stomach contents into the esophagus during sleep. It is very common in patients using theophylline as a respiratory stimulant for apnea of prematurity or asthma.
• Nighttime exacerbations of childhood asthma: These are common and may lead to significant sleep disruption.
• Atopic dermatitis: Children with atopic dermatitis tend to have increased sleep-onset difficulty, night awakenings, and decreased sleep duration due to pruritus and medications, such as antihistamines and corticosteroids.
• Chronic illness: Children with chronic illnesses, such as juvenile rheumatoid arthritis (JRA) or sickle cell disease, can experience sleep difficulties.

• Insomnia related to another mental disorder is the most frequent diagnosis (35-50%) among individuals who present to sleep disorder facilities for evaluation of chronic insomnia. In young children, separation anxiety, stress, and trauma may result in nighttime awakening, nightmares, or resistance to going to bed.
• Patients who have major depressive disorder or dysthymic disorder often report difficulty falling asleep or staying asleep or early morning awakening with inability to return to sleep. Hypersomnia can be a feature of depression, especially major depression with atypical features. Children and adolescents with major depressive disorder generally present with less subjective sleep disturbance and fewer polysomnographic changes than do older adults with a similar degree of depression.

• Prepubertal children with depression are more likely to experience insomnia (75%) than hypersomnia (25%); after puberty, hypersomnias predominate. Hypersomnia is a common feature of depressive disorders in adolescents and young adults, and insomnia is more common in older adults.

• Individuals with generalized anxiety disorder often report difficulty falling asleep and may awaken with anxious thoughts in the middle of the night. Panic attacks can arouse patients and cause insomnia. Significant insomnia is often observed during exacerbations of schizophrenia and other psychotic disorders but rarely is a predominant symptom. Other mental disorders that may be related to insomnia include adjustment disorders, somatoform disorders, and personality disorders.
• Substance-induced sleep disorder most commonly occurs during intoxication with substances, such as alcohol, amphetamine and related substances, caffeine, cocaine, opioids and sedatives, hypnotics, or anxiolytics. Substance-induced sleep disorder can also occur in association with withdrawal from these same classes of substances.

• Diagnostic criteria for substance-induced sleep disorder includes the following:
  
  
  • Prominent disturbance in sleep that is sufficiently severe to warrant independent clinical attention
  • Evidence from the history, physical examination, or laboratory findings of either (1) symptoms developed during or within a month of substance intoxication or withdrawal or (2) medication use related etiologically to the sleep disturbance
  • Disturbance that is not better accounted for by a sleep disorder that is not substance induced
     
• Evidence that the symptoms are better accounted for by a sleep disorder that is not substance induced might include the following:
  
  
  • Symptoms precede the onset of the substance use (or medication use).
  • Symptoms persist for a substantial period (eg, about 1 mo) after the cessation of acute withdrawal or severe intoxication.
  • Symptoms are substantially in excess of what would be expected given the type or amount of the substance used or the duration of use, or other evidence exists that suggests an independent non–substance-induced sleep disorder.
  • Disturbance does not occur exclusively during the course of an episode definable as delirium.
  • Sleep disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
     
• Alcohol-induced sleep disorder
  
  
  • Alcohol-induced sleep disorder typically occurs as the insomnia type. Alcohol, which often facilitates sleep onset, can lead to decreased REM sleep and sleep disruption. Acute intoxication initially results in increased sleepiness and reduced wakefulness for 3-4 hours.
  • An increase in stages 3 and 4 of NREM sleep is a typical feature of this initial stage. Following these initial effects, increased wakefulness, restless sleep, and, often, vivid and anxiety-laden dreams during the second half of the night are experienced by the individual. In addition, alcohol can increase the number of obstructive sleep apnea events and result in fragmented sleep. With continued habitual use, alcohol continues to show a short-lived sedative effect for several hours, followed by sleep continuity disruption for several hours.
  • During alcohol withdrawal, sleep architecture is grossly disturbed. Sleep tends to be fragmented and accompanied by an increase in the amount and intensity of REM sleep. Vivid dreams often accompany this stage of sleep.
     
• Amphetamines and other stimulants: During the period of acute intoxication, amphetamines produce sleep disruption associated with increased sleep latency, reduced total sleep time, fragmented sleep, an increase in body movements, and a decrease in REM sleep. Slow-wave sleep tends to be reduced. During withdrawal from long-term amphetamine use, hypersomnia with prolonged nocturnal sleep duration and excessive daytime sleepiness tends to be the rule.
• Caffeine-induced sleep disorder: This is characterized by insomnia during intoxication and by hypersomnia and excessive daytime sleepiness during withdrawal. Caffeine is known to result in increased wakefulness and sleep fragmentation, which may be documented on a polysomnographic test as prolonged sleep latency, multiple arousals, and a decrease in slow-wave sleep.
• Cocaine: Use of cocaine results in increased sleep latency, reduced total sleep time, and fragmentation of sleep architecture during intoxication. Cocaine withdrawal is associated with hypersomnia.
• Opioids: Short-term use of opioids produces increased sleepiness and reduced REM sleep. Insomnia and frequent arousals become common with prolonged use. Opioid withdrawal generally produces symptoms and signs of CNS hyperactivity, although some patients may report hypersomnia.
• Sedative-hypnotic medications: Use of sedative-hypnotic medications produces an increase in sleepiness and polysomnographic findings of decreased REM sleep and an increase in sleep-spindle activity. On the other hand, long-term use of sedatives may be accompanied by symptoms of insomnia and tolerance to these medications. Withdrawal from sedative-hypnotics and anxiolytics is associated with anxiety and insomnia. The manifestation of withdrawal symptoms depends on the half-lives of these drugs. Withdrawal from drugs with short half-lives typically produces insomnia. Medications with long half-lives are associated with symptoms of excessive sedation during their use.

Physical

Full physical examination is warranted and should focus on the causes and consequences of sleep-related disorders. Significant things to look for in a physical examination are as follows:

• Level of consciousness
• Physical features
• • Head circumference
  • Weight and indicators of failure to thrive
  • Features suggestive of congenital anomalies
  • Size of the posterior pharynx
• Physical causes of airway blockage such as enlarged tonsils or adenoids
• Obesity, neck circumference
• Systemic signs of heart failure such as clubbing or cyanosis
• Signs indicative of seizure activity
• Tooth injuries on tongue
• Incontinence
• Postictal changes in sensorium

Differential Diagnoses

Workup

Other Tests

• Sleep laboratory studies are very helpful when indicated, but most common pediatric sleep problems do not require formal sleep laboratory testing. Most sleep problems resolve with behavioral treatments. A detailed sleep history, thorough physical examination, and sleep logs provide the foundation for accurate diagnosis, treatment, and possible referral for polysomnography. Atypical presentations, snoring associated with daytime somnolence, behavioral-emotional problems, apneic or hypopneic episodes, suspicion of narcolepsy, abnormal and disruptive movements in sleep, unexplained or recalcitrant sleep difficulties, or daytime sleepiness indicate a need for sleep studies.
• Overnight polysomnography and next-day multiple sleep latency testings represent the most commonly used sleep studies. Clinical suspicion of any of the following disorders should prompt referral for sleep studies:
• • Sleep-related seizurelike activity
  • Sleep-related gastroesophageal reflux
  • Nighttime asthma or persistent cough
  • ADHD or Tourette syndrome associated with restless sleep and disrupted daytime functioning
  • RLS and PLMS - Relatively common in these patients
  • Recurrent REM sleep behaviors
  • Severe bruxism
  • Snoring and hypopnea or apnea
  • Recalcitrant or unexplained and daytime somnolence
  • Suspected narcolepsy
• Multiple sleep latency tests aid in clarifying unexplained excessive daytime sleepiness and narcolepsy symptoms.

Treatment

Medical Care

This section primarily reviews cognitive-behavioral treatments (CBT) effective in treating a broad range of childhood behavioral sleep problems. Treatment modalities can be adapted easily to the youth's developmental level. Furthermore, consider the role of sleep hygiene in all sleep problems. The effectiveness of CBT for childhood sleep disorders has been well demonstrated in controlled studies and clinical case reports. Specific interventions for sleep problems have gained the status of established evidence-based interventions. The issues that received the most attention pertain to settling problems and night awakenings in infants and toddlers. These topics have been extensively studied, with an impressive volume of well-controlled and informative clinical studies. Clinical research of all other sleep problems and in other age ranges is still very limited.

Pharmacologic treatments of sleep disorders lack adequate and significant empirical data. Given the lack of data supporting pharmacological treatment, initially use behavioral and cognitive strategies in most cases. Because of the paucity of adequate empirical studies, pharmacotherapy data are limited to treatment in select sleep disorders.

• Limit-setting problems, bedtime resistance, and frequent nightly awakenings represent common problems encountered in pediatric practice. Cognitive-behavioral techniques use relatively straightforward and safe strategies for enhancing overall parenting effectiveness as well as ameliorating the aforementioned problems.
  
  
  • Extinction technique: This technique involves the parents putting their child to bed at a designated time and ignoring the child's or infant's protests until an established time the next morning.
  • Graduated extinction: Many parents may experience or perceive pure extinction as overly taxing or cruel; therefore, a graduated extinction technique may be used. This may include progressive time delays in responding to bedtime protests or refusals (ie, a checking technique), or it may include comforting the child for increasingly shorter intervals when checking on the child.
  • Positive routine-stimulus control techniques: This technique involves developing a consistent, pleasurable, and calming nighttime routine, with pleasurable activities being halted if the child protests or throws a tantrum. The child is then put to bed.
  • Scheduled awakenings: Parents awaken the child approximately 15 minutes prior to the child's typical nightly awakening times. The scheduled awakenings gradually are stopped or weaned.
     
• Nocturnal enuresis: History and physical examination usually are sufficient to rule out urological abnormality. Routine dipstick urinalysis, growth/height trajectory, and blood pressure are used to exclude other medical causes of enuresis. Children younger than 6 years should be managed with child and family reassurance that the enuresis is developmentally normal.
  
  
  • Alarm clock method: An alarm is set before the most probable time of the event based on the trend of enuretic episodes. The alarm may be set for a predetermined time, such as 2-3 hours after usual onset of enuresis. Children eventually avoid wetting themselves before the alarm is triggered, unlike the bell and pad method. Longer treatment duration results in a higher success rate.
  • Parent education: Parents need to know that sleep hygiene practices serve as prevention of enuresis. Fluid restriction, bedtime voiding, and parent awakening later are components of sleep hygiene (see Patient Education). The earlier the child begins practicing sleep hygiene, the better. Individual families may require creative combinations of the aforementioned interventions.
  • Desmopressin and nocturnal enuresis: Desmopressin reduces nocturnal urine production, has better short-term results than the alarm method, is effective in 50-85% of individuals, and generally is well tolerated. Recidivism after discontinuation can present a problem.
  • Imipramine and nocturnal enuresis: Imipramine is effective, but concern exists for potentially serious adverse effects. Imipramine dosing is 25-100 mg depending on the age and size of the patient. Risks involved in imipramine use often outweigh the benefits for the relatively benign problem. The use of imipramine requires ECG at baseline, with titration and dose increases and periodic monitoring. The clinician should monitor blood pressure and pulse rate and review cardiovascular system issues at each visit.
     
• Sleep-related fears and anxiety: Treatment for sleep-related fears and anxiety include relaxation training, guided imagery, positive self-talk, positive reinforcement for increasingly successful efforts, systematic desensitization, and gradual exposure to child-determined hierarchy of sleep-related fears or anxiety. The child progresses from envisioning less threatening fears to conquering in vivo actual feared objects or situations. Exposure-response prevention is combined with relaxation techniques and positive reinforcement for treatment gains.
• OSAS: Adenotonsillectomy is the primary treatment modality in children with OSAS. Positive airway pressure is needed in cases of continued postsurgical symptomatology. Continuous positive airway pressure (CPAP), variable pressure devices (eg, bilevel positive airway pressure [BiPAP]), and on-demand pressure when airflow is impeded (D-PAP) may be needed. Weight loss can be helpful for obese patients.
• PLMS: Focus cognitive and behavioral therapy on alleviating stress and promoting relaxation. Dopaminergic therapy may be necessary; however, only limited data on dopaminergic therapy in youths are available. Pergolide (withdrawn from US market March 29, 2007) is effective in treating ADHD or Tourette syndrome and comorbid sleep disorder. Caffeine restriction can be helpful. Low-dose Depakote has been shown to be effective in a small case series of adults.
• RLS: Focus cognitive and behavioral therapy on alleviating stress and promoting relaxation. Dopaminergic therapy may be necessary; however, limited data exist for treatment in youths. Pergolide (withdrawn from US market March 29, 2007) has been found to be effective in treating ADHD or Tourette syndrome and comorbid sleep disorder. Caffeine restriction may be helpful. Low-dose Depakote has been shown to be effective in small case series of adults.
• Circadian rhythm disorders
  
  
  • Light therapy resets suprachiasmatic nuclei.
  • Melatonin acts directly upon suprachiasmatic nuclei. The effect of light on phase shifts is opposite. Phase delay requires morning dosing of melatonin. Advanced sleep phase syndrome requires evening dosing.
  • In manipulating the internal sleep-wake clock, gradually delaying sleep onset resynchronizes the internal clock. Delay sleep onset by 15-minute increments each night until desired sleep time is established.

Surgical Care

Adenotonsillectomy may be indicated for OSAS.

Consultations

Depending upon patient presentation, the following consultations may be necessary:

• Pulmonologist
• Developmental medicine specialist
• Neurologist
• Child psychologist, child psychiatrist, or developmental-behavioral pediatrician
• Sleep specialists (Multiple disciplines may have expertise, and the child may benefit from interdisciplinary evaluation and treatment planning.)
• Otolaryngologist
• Substance abuse evaluation

Diet

Weight loss is recommended for patients with obesity and OSAS.

Medication

Many of the medications described below are not approved by the Food and Drug Administration (FDA) for adolescents and children.

Vasopressin analogs

Desmopressin is a synthetic antidiuretic hormone with actions mimicking vasopressin. It is used for treating enuresis.

Desmopressin (DDAVP)

For use in primary nocturnal enuresis in children > 6 y. Increases cellular permeability of collecting ducts, resulting in reabsorption of water by kidneys.

Dosing

Adult

0.2-0.6 mg PO qhs

Pediatric

Nasal spray: 20 mcg (0.2 mL) intranasally qhs
Tablets: 0.1-0.4 mg PO qhs

Interactions

Coadministration with demeclocycline and lithium decrease effects; fludrocortisone and chlorpropamide increase effects of desmopressin

Contraindications

Documented hypersensitivity; platelet-type von Willebrand disease; any potential for water intoxication

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Renal abnormalities; history of electrolyte imbalance

Dopamine agonists

Preliminary efficacious results for treatment using these agents have been noted in youths with RLS and PLMS. Findings are based on nonrandomized non – placebo-controlled study. Pergolide was withdrawn from the US market March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. Do not abruptly stop pergolide. Health care professionals should assess patients' need for dopamine agonist (DA) therapy and consider alternative treatment. If continued treatment with a DA is needed, another DA should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.

Pergolide (Permax)

Pergolide withdrawn from US market. Not FDA-approved for RLS or PLMS. Potent and long-acting dopamine agonist. Reduces tonic stimulation of dopaminergic D-2 receptors located on intrastriatal cholinergic neurons.

Dosing

Adult

0.05 mg PO hs for first 2 d initially; gradually increase by 0.05 mg/d q3d over next 12 d, followed by increments of 0.25 mg/d q3d until optimal therapeutic dosage is achieved, generally 0.25-0.5 mg is effective

Pediatric

Not established, limited data exist: 0.4-1 mg/d PO divided qid

Interactions

Dopamine antagonists (eg, phenothiazines, butyrophenones, thioxanthenes, metoclopramide) may diminish effect; because pergolide mesylate is more than 90% bound to plasma proteins, exercise caution if pergolide is coadministered with other drugs known to affect protein binding

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May cause valvular heart disease (yearly echocardiograms recommended for patients on chronic therapy); inhibits secretion of prolactin; causes transient rise in serum concentrations of growth hormone and decrease in serum concentrations of luteinizing hormone; adverse effects include nausea, hypotension, hallucinations, and somnolence; use caution in patients who have been treated for cardiac dysrhythmias; may cause or exacerbate preexisting states of confusion and hallucinations or dyskinesia

Tricyclic antidepressants

These agents are used for treating narcolepsy and enuresis. Please note that scant data exist for use in childhood narcolepsy. Sudden death has been reported in 8 children, possibly related to use of imipramine and desipramine; findings have been inconclusive about the causes of these deaths. No FDA indication exists for use in children with narcolepsy and enuresis.

Imipramine (Tofranil)

Inhibits the reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) at presynaptic neuron. May be useful in pediatric ADHD as well as enuresis and possibly pediatric-onset narcolepsy.

Dosing

Adult

Not established

Pediatric

10 mg PO qd initially and, if tolerated but not effective, increase dose to 25 mg PO qd; titrate upward slowly by 25 mg/wk to effectiveness or intolerable adverse effects

Interactions

Increases toxicity of sympathomimetic agents (eg, isoproterenol, epinephrine) by potentiating effects; inhibits antihypertensive effects of clonidine

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; acute recovery phase following myocardial infarction; concurrent use of MAOIs or fluoxetine or coadministration in the previous 2 wk (avoid)

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Overdose may be lethal; may impair mental or physical abilities required for performance of potentially hazardous tasks; cardiovascular disease; conduction disturbances; seizure disorders; urinary retention; hyperthyroidism; patients receiving thyroid replacement; frequent ECG monitoring advised

Anticonvulsants

Valproic acid was efficacious in small case series for adults with RLS and PLMS.

Valproic acid (Depakene, Depakote)

It is likely that all forms of valproic acid have similar efficacy. The following preparations can be used: 250-mg tab, 125-mg sprinkle caps, or 250 mg/5-mL liquid (US preparations).

Dosing

Adult

125-600 mg PO qhs when used in investigational studies for RLS and PLMS

Pediatric

Not established

Interactions

Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce valproate levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely); valproate may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; valproate may displace warfarin from protein-binding sites (monitor coagulation test results); may increase zidovudine levels in HIV seropositive patients

Contraindications

Documented hypersensitivity; hepatic disease/dysfunction; history of thrombocytopenia due to valproic acid

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Thrombocytopenia and abnormal coagulation parameters have occurred; the risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations >110 mcg/mL in females and 135 mcg/mL in males; carefully monitor patients early in treatment; monitor periodically while the patient is stable; adolescent women may experience substantial weight gain and irregular menses and can develop polycystic ovaries; thrombocytopenic effect, particularly at higher doses and during intercurrent illnesses, may cause bruising/bleeding; mitochondrial syndromes may be worsened by valproic acid, thus use with extreme caution; do not use in pregnant adolescents or sexually active adolescents not taking adequate birth control

Hormones

These agents are used for treating circadian rhythm disturbances.

Melatonin

Used to treat circadian rhythm disturbances in blind patients without light perception.

Dosing

Adult

1-10 mg PO qhs

Pediatric

Administer as in adults

Interactions

Coadministration with other CNS depressants may result in excessive somnolence; fluvoxamine increases melatonin levels; may increase blood pressure and heart rate of patients on nifedipine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May cause dysphoria, headache, nausea, pruritus, and elevated alkaline phosphatase; caution with liver impairment, cardiovascular disease, neurologic disorders, or depression

Sedative/hypnotic agents

Studies for these drugs are limited to adults, and no FDA indications are approved for children younger than 18 years.

Eszopiclone (Lunesta)

Nonbenzodiazepine hypnotic pyrrolopyrazine derivative of the cyclopyrrolone class. The precise mechanism of action is unknown, but believed to interact with GABA-receptor at binding domains close to, or allosterically coupled to, benzodiazepine receptors. Indicated for insomnia in adults to decrease sleep latency and improve sleep maintenance. Short half-life of 6 h. Higher doses (ie, 2 mg for elderly and 3 mg for nonelderly adults) are more effective for sleep maintenance, whereas lower doses are (ie, 1 mg for elderly and 2 mg for nonelderly adults) are suitable for difficulty in falling asleep.

Dosing

Adult

Nonelderly adults: 2 mg PO hs; may increase to 3 mg PO hs prn
Elderly persons: 1 mg PO hs initially; not to exceed 2 mg PO hs
Severe hepatic impairment: Do not exceed 2 mg PO hs

Pediatric

<18 years: Not established

Interactions

Contraindications

CYP3A4 and CYP2E1 substrate; potent CYP3A4 inhibitors (eg, ketoconazole, itraconazole, clarithromycin, nefazodone, ritonavir, nelfinavir) increases AUC, Cmax, and t1/2 and therefore potential toxicity (decrease dose); potent CYP3A4 inducers (eg, rifampicin) increases clearance; coadministration with alcohol or other CNS depressants may increase effect and toxicity (decrease dose); coadministration with olanzapine may decrease DSST scores; sleep onset may be delayed if taken with or immediately after a high-fat or heavy meal

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May cause dysgeusia, headache, or cold-like symptoms; rare adverse effects associated with hypnotics include short-term amnesia, confusion, agitation, hallucinations, worsened depression, or suicidal thoughts; high doses (ie, 6-12 mg) produce euphoric effects similar to those of diazepam 20 mg; anxiety, abnormal dreams, nausea, and upset stomach may occur within 48 h after discontinuing; alertness may be affected the following day, use caution operating machinery or driving a car; caution with severe COPD or hepatic disease

Ramelteon (Rozerem)

Melatonin receptor agonist with high selectivity for human melatonin MT₁ and MT₂ receptors. MT₁ and MT₂ are thought to promote sleep and be involved in maintaining circadian rhythm and normal sleep-wake cycle. Indicated for insomnia in adults characterized by difficulty with sleep onset.

Dosing

Adult

8 mg PO qhs 30 min before bedtime on empty stomach

Pediatric

Not established

Interactions

Major substrate of cytochrome P450 CYP1A2 and minor substrate of CYP2C and CYP3A4; strong CYP1A2 inhibitors (eg, fluvoxamine) increase AUC up to 190-fold and C_max 70-fold; strong CYP inducers (eg, rifampin) decrease total exposure by mean of 80%; strong CYP3A4 inhibitors (eg, ketoconazole) and strong CYP2C9 inhibitors (eg, fluconazole) may increase serum levels

Contraindications

Documented hypersensitivity; strong cytochrome P450 CYP1A2 inhibitors (eg, fluvoxamine); severe hepatic impairment

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May affect reproductive hormones in
adults (eg, decreased testosterone levels, increased prolactin levels), further study required to determine safety in prepubescent and pubescent children; caution with mild hepatic impairment; adverse effects leading to discontinuation in clinical trials included: dizziness, nausea, fatigue, headache, and worsening insomnia

Follow-up

Prognosis

• Dyssomnias
• • The treatment of primary insomnia often is difficult.
  • Associated anxiety is often responsive to psychotherapy.
  • Narcolepsy is a lifelong illness.
  • Cataplexy, hypnagogic hallucinations, and sleep paralysis may diminish in frequency over time.
  • Tonsillectomy and adenoidectomy relieve symptoms in about 70% of patients with OSAS. CPAP is indicated for patients who partially respond to surgery or in whom surgery is contraindicated.
  • The success of DSPS treatment depends to a large extent on how much the adolescent is motivated. The new schedule needs to be maintained rigidly in order to avoid relapse of DSPS.
• Parasomnias
• • Most children with parasomnias outgrow this condition when younger than 10 years or demonstrate a progressive decrease to comparable prevalence to that of the adult population.
  • Approximately 88% of all enuretic children outgrow this condition by the time they are aged 13 years. The prevalence of enuresis in patients aged 13 years is 2%, which is similar to the prevalence rate in the adult population.
• Sleep disorder related to a general medical condition: Prognosis depends on treatment of underlying medical condition.
• Sleep disorder related to a substance use: Prognosis depends on treatment of the addiction.

Patient Education

• Because human beings spend a third of their time sleeping, emphasize the need for good sleep hygiene to children, adolescents, and their families. Sleep hygiene includes the following:
• • Keeping the room quiet, dark, and comfortable
  • Practicing a simple bedtime ritual that includes voiding
  • Limiting time spent in bed
  • Not eating or drinking heavily for about 3 hours before bedtime
  • Maintaining the bedroom for sleeping only
  • Removing distractions, such as TV
  • Avoiding medications
  • Considering the effect of sleep partners (including pets)
  • Maintaining a consistent sleep schedule
  • Avoiding naps
  • Exercising regularly
  • Taking a hot bath or drinking something warm before bedtime
• For excellent patient education resources, visit eMedicine's Sleep Disorders Center. Also, see eMedicine's patient education articles Disorders That Disrupt Sleep (Parasomnias), Night Terrors, Narcolepsy, REM Sleep Behavior Disorder, Periodic Limb Movement Disorder, and Sleeplessness and Circadian Rhythm Disorder.

References

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2. Bazil CW. Sleep, Sleep Apnea, and Epilepsy. Curr Treat Options Neurol. Jul 2004;6(4):339-345. [Medline].

3. Billiard M. The Klein-Levin syndrome. In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. Vol 1. Philadelphia, Pa:. WB Saunders Co;1989.

4. Challamel M, Cochat P. Enuresis: Pathophysiology and Treatment. Sleep Medicine Reviews. 1999;(3):313-324.

5. Drake ME, Hietter SA, Bogner JE, Andrews JM. Cassette EEG sleep recordings in Gilles de la Tourette syndrome. Clin Electroencephalogr. Jul 1992;23(3):142-6. [Medline].

6. Ferri R, Curzi-Dascalova L, Del Gracco S, Elia M, et al. Respiratory patterns during sleep in Down syndrome: Importance of central apneas. J Sleep Res. Jun 1997;6(2):134-41. [Medline].

7. Gangwisch JS, Heymsfield SE, Boden-Albal B. Short Sleep Duration as a Risk Factor for Hypertension. Analyses of the First National Health and Nutrition Examination Survey. Hypertension. 2006;Online First:Online First. [Full Text].

8. Hertz G, Cataletto M, Feinsilver SH, Angulo M. Sleep and breathing patterns in patients with Prader Willi syndrome (PWS): Effects of age and gender. Sleep. Jun 1993;16(4):366-71. [Medline].

9. Jankovic J, Rohaidy H. Motor, behavioral and pharmacologic findings in Tourette's syndrome. Can J Neurol Sci. Aug 1987;14(3 Suppl):541-6. [Medline].

10. Kuhn BR, Elliott AJ. Treatment efficacy in behavioral pediatric sleep medicine. J Psychosom Res. Jun 2003;54(6):587-97. [Medline].

11. Marcus CL, Keens TG, Bautista DB, von Pechmann, et al. Obstructive sleep apnea in children with Down syndrome. Pediatrics. Jul 1991;88(1):132-9. [Medline].

12. Marcus CL. Pathophysiology of childhood obstructive sleep apnea: current concepts. Respir Physiol. Feb 2000;119(2-3):143-54. [Medline].

13. Moline M, Broch L, Zak R. Sleep Problems Across the Life Cycle in Women. Curr Treat Options Neurol. Jul 2004;6(4):319-330. [Medline].

14. Nee LE, Caine ED, Polinsky RJ, Eldridge R, et al. Gilles de la Tourette syndrome: clinical and family study of 50 cases. Ann Neurol. Jan 1980;7(1):41-9. [Medline].

15. Owens JL, France KG, Wiggs L. Behavioral and cognitive-behavioral interventions for sleep disorders in infants and children: A Review. Sleep Medicine Reviews. 1999;3:281-302.

16. Picchietti DL, Walters AS. Moderate to severe periodic limb movement disorder in childhood and adolescence. Sleep. May 1 1999;22(3):297-300. [Medline].

17. Picchietti DL, Walters AS. Restless legs syndrome and periodic limb movement disorder. Child Adolesc Psychiatr Clin N Am. 1996;6.

18. Schluter B, Buschatz D, Trowitzsch E, Aksu F, et al. Respiratory control in children with Prader-Willi syndrome. Eur J Pediatr. Jan 1997;156(1):65-8. [Medline].

19. Shapiro HL. Sleep disorders. In: Levine MD, Zuckerman BS, eds. Developmental Behavioral Pediatrics. New York, NY:. Harcourt Brace & Co;1999:422-429.

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Keywords

associated problems in select sleep disturbances, dyssomnias, parasomnias, medical-psychiatric disorders, hypersomnia, insomnia, narcolepsy, obstructive sleep apnea syndrome, OSAS, periodic limb movements in sleep, PLMS, sleepwalking, somnambulism, bruxism, teeth grinding, grinding teeth, nightmares, night mares, sleep terrors, primary nocturnal enuresis, rhythmic movement disorders, confusional arousals, delayed sleep phase syndrome, DSPS, sleep disorders, sleep problems, rapid eye movement, REM, nonrapid eye movement, non-REM, NREM, circadian sleep-wake cycle, circadian rhythm

Contributor Information and Disclosures

Author

Dennis A Nutter, Jr, MD, Consulting Staff, Department of Psychiatry, Northeast Georgia Medical Center
Dennis A Nutter, Jr, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry and American Psychiatric Association
Disclosure: Nothing to disclose.

Coauthor(s)

Guy K Palmes, MD, Program Director, Assistant Professor, Department of Psychiatry, Section of Child and Adolescent Psychiatry, Wake Forest University
Disclosure: Nothing to disclose.

Benyam Tegene, MD, Fellow, Department of Psychiatry, Wake Forest University Baptist Medical Center
Benyam Tegene, MD is a member of the following medical societies: American Medical Association and American Psychiatric Association
Disclosure: Nothing to disclose.

Medical Editor

Chet Johnson, MD, Medical Director, Child Development Unit, Department of Pediatrics, Professor, University of Kansas Medical Center
Chet Johnson, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Nothing to disclose.

Managing Editor

Caroly Pataki, MD, Associate Program Director, Clinical Associate Professor, Department of Psychiatry and Biobehavioral Sciences, Division of Child and Adolescent Psychiatry, Neuropsychiatric Institute and Hospital, UCLA
Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry
Disclosure: Nothing to disclose.

CME Editor

Carrie Sylvester, MD, MPH, Director of Education in Child and Adolescent Psychiatry, Professor, Departments of Psychiatry and Pediatrics, Northwestern University Medical School
Carrie Sylvester, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Pediatrics, American Medical Women's Association, American Psychiatric Association, and American Society for Adolescent Psychiatry
Disclosure: Nothing to disclose.

Chief Editor

Murray M Kappelman, MD, Professor, Departments of Pediatrics and Psychiatry, University of Maryland School of Medicine
Murray M Kappelman, MD is a member of the following medical societies: Ambulatory Pediatric Association and American Academy of Child and Adolescent Psychiatry
Disclosure: Nothing to disclose.

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