Pediatric Sleep Disorders

Pediatric sleep disorders increasingly interfere with daily patient and family functioning. Interest in and treatment of sleep disturbances in youth continues to grow, but research lags. One survey indicated that pediatricians were more likely to prescribe antidepressant medications for insomnia than psychiatrists. ^[1] Further investigation is needed to develop empirically based diagnosis 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. 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.

Major scientific advances have altered the understanding of sleep disorders, which have resulted in major changes moving from Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition Text Revision (DSM-IV-TR) ^[2] to the Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (DSM-5). ^[3] The DSM-IV-TR divided sleep disorders into 3 categories: Dyssomnias, Parasomnias, and Medical Psychiatric Disorders.

These categorical differences were eliminated in the DSM-5 to encourage the understanding that medical disorders and sleep disorders are intertwined and primary causation is usually not important. The entire section has been renamed Sleep-Wake Disorders to highlight that etiology may be based in the inability to maintain alertness during the waking period. The definition of dyssomnia versus parasomnia is provided to highlight the developmental differences of sleep-wake disorders.

Patients with dyssomnias present with difficulty initiating or maintaining sleep or with excessive daytime somnolence. The DSM-IV-TR defined dyssomnias as primary disturbances in the quantity, quality, or timing of sleep. ^[2] These disorders are believed to be a consequence of central nervous system (CNS) abnormalities that alter the sleep process. Adolescents with and without substance use disorders represent a significant proportion of sleep-disordered youths. This is an excellent example how difficult it may be to distinguish a primary sleep disorder from those induced by medical conditions.

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 includes deviated behavioral or physiologic 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 symptoms are characteristic of dyssomnia.

Most parasomnias affect otherwise healthy youths and commonly subside over the course of adolescence. These disorders are typically viewed as transient developmental phenomena, though children with parasomnias have been 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. This category has been eliminated in DSM-5 but should still be considered by the clinician when evaluating sleep disorders. The medical differential should include the following:

• Attention deficit hyperactivity disorder (ADHD)

• Gastroesophageal reflux disease (GERD)

• Pervasive developmental disorders

• Mental retardation

• Down syndrome

• Prader-Willi syndrome

• Smith-Magenis syndrome

• Tourette disorder

• Nocturnal asthma

• Depressive disorders

• Anxiety disorders

• Mania

• Neuromuscular disorders

• Nocturnal seizures

• Kleine-Levin syndrome or periodic hypersomnia

• Chronic fatigue syndrome

• Headaches

• Blindness with associated sleep disorder

Insomnia disorder

Insomnia disorder, classified in DSM-5, which in DSM-IV was described as primary hypersomnia, includes normal sleep efficiency, sleep-wake cycles, and sleep architecture. Patients present with a normal variant sleep pattern except for dissatisfaction with sleep quantity or quality. This may be a lifelong pattern. The problems with sleep are often associated with the following:

• Difficulty initiating sleep: In children, this includes difficult initiating sleep without a caregiver

• Difficulty maintaining sleep: In children, this includes difficulty returning to sleep without caregiver

• Early morning awakening with difficulty returning to sleep

Other criteria for insomnia disorder require significant distress or impairment, occurring 3 nights per week, present for at least 3 months, and occurring despite sufficient time for sleep. The insomnia is not better explained or occurs exclusively in conjunction with another sleep-wake disorder. The insomnia is not due to the physiological effects of a substance, and coexisting mental/medical conditions do not fully explain the insomnia. If an individual reports feeling unrested (nonrestorative sleep) despite adequate duration and no difficulty initiating or maintaining sleep, then a diagnosis of unspecified insomnia disorder is given.

Difficulty initiating sleep means that the subjective sleep latency is greater than 20-30 minutes. Difficulty maintaining sleep is the subjective time awake after sleep onset is longer than 20-30 minutes. There is no standard definition of early morning awakening, but it usually requires awakening 30 minutes before the scheduled time or before total sleep time reaches 6.5 hours. When considering the final awakening time, it is also important to consider when bedtime occurs. For example, a child who initiates sleep at 7 pm versus 9 pm and awakens at 5 am may need to go to bed later.

The pathogenesis of insomnia disorder is poorly defined. First episode often occurs in young adulthood. However, it can also begin in childhood or adolescence. It can be associated with life changes and resolve when the precipitating event subsides. For some, the insomnia can persist because of conditioned arousal from the precipitating event. In children, the conditioned factors include needing a parent to be present to initiate sleep, but they can also include absence of a consistent sleep schedule. In adolescents, insomnia is more often triggered by irregular sleep schedules. Polysomnography (PSG) is of limited value in evaluating insomnia disorder in children. ^[4]

Hypersomnolence disorder

Hypersomnolence disorder as described in DSM-5 is the self-reported excessive need for sleep despite sleeping for at least 7 hours and having at least one of the following symptoms:

• Recurrent periods of sleep or naps within the same day

• A prolonged sleep of more than 9 hours per day that is not refreshing

• Difficulty being fully awake after abrupt awakening

Individuals with hypersomnolence disorder usually fall asleep quickly and have good sleep efficiency (>90%). Despite this, they have sleep inertia/drunkenness, where they have difficulty waking up and appear confused, combative, or ataxic. They can also experience automatic behavior during which they carry out simple routines like driving, have no recall of going several miles, then realize they are several miles from where they thought they were. Naps are not refreshing despite lasting more than 1 hour. Individuals are at risk for autonomic nervous dysfunction such as recurrent vascular-type headaches, Raynaud phenomena, and fainting. The disorder usually begins in late adolescence, at a mean age of 17-24 years.

Hypersomnolence can be increased temporarily by stress and alcohol use. Viral infections have preceded or accompanied hypersomnolence in 10% of cases, sometimes several months after the infection. Head trauma can result in hypersomnolence within 6-18 months after injury. An autosomal dominant mode of inheritance occurs in a subset of familial cases.

Nocturnal PSG findings include normal-to-prolonged sleep duration, short sleep latency (< 8 min), normal-to-increased sleep continuity, and normal distribution of rapid eye movement (REM) sleep but increased amounts of slow-wave sleep. During naps, sleep-onset REM may be present but may occur less than 2 times in 4-5 nap opportunities.

Behaviorally induced insufficient sleep syndrome may produce symptoms of daytime sleepiness and resemble hypersomnolence disorder. Individuals with inadequate sleep "catch up" when they are free from social/academic/occupational demands. After 10-14 days of catch-up sleep, the diagnosis may be clearer.

Narcolepsy

Narcolepsy is defined by DSM-5 as recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping that occurs within the same day. This must occur 3 times per week over 3 months. It also requires one of the following to be present:

• Episodes of cataplexy occurring a few times per month: Cataplexy is defined as (1) in individuals with chronic disease, as having brief (seconds to minutes) episodes of sudden loss of muscle tone with maintained consciousness that are triggered by laughter or joking or (2) in children or individuals within 6 months of onset, spontaneous grimaces or jaw-opening episodes with tongue thrusting or a global hypotonia without any obvious emotional precipitants.

In pediatric patients, excessive daytime sleepiness is the most common first symptom of narcolepsy. ^[5] Symptom onset peaks at 15 years of age. Low hypocretin levels are present, they must occur in the absence of acute brain injury, inflammation, or infection. Nocturnal sleep PSG shows REM sleep latency to be less than or equal to 15 minutes or a multiple sleep latency test shows a mean sleep latency of less than or equal to 8 minutes with 2 or more sleep-onset REM periods.

REM sleep mechanisms are dysregulated in youths with narcolepsy, but evidence also exists of non-REM (NREM) and circadian sleep-wake cycle abnormalities. REM-associated sleep phenomena intrude into the awakened state. Sleep attacks (sleep), cataplexy (abrupt atony precipitated by strong emotions), and 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 or involuntary sleep (sleep attacks) may occur. The roles of the neuropeptide hypocretin and human leukocyte antigen (HLA)-DR2/DBQ1 as a genetic-neuroimmune interaction are being considered in current research on this issue. Narcolepsy is consistent with the polygenic model of development in most human cases. Narcolepsy triggered by streptococcus infections, H1N1 influenza, and H1N1 vaccination in genetically vulnerable individuals has been reported. ^[5]

Specifiers include the following:

• Narcolepsy Without Cataplexy But With Hypocretin Deficiency

• Narcolepsy With Cataplexy But Without Hypocretin Deficiency

• Autosomal Dominant Narcolepsy, Obesity, and Type 2 Diabetes

• Narcolepsy Secondary to Another Medical Condition

Narcolepsy can be diagnosed even when secondary to infections, trauma, or tumor, such as in Whipple disease or sarcoidosis. There is destruction of hypocretin neurons. Individuals who are HLA DQB1*06.02 positive may be more vulnerable to destruction of these neurons from an autoimmune process. Transient decreases in cerebrospinal fluid (CSF) hypocretin levels can occur without cell loss and can complicate the diagnosis. Functional imaging has demonstrated impaired hypothalamic responses.

Breathing-related sleep disorders

The International Classification of Sleep Disorders, 2nd Edition (ICSD-2) identifies 11 types of sleep-related breathing disorders. However, DSM-5 only recognizes 3: Obstructive Sleep Apnea Hypopnea, Central Sleep Apnea, and Sleep-Related Hypoventilation. This simplification is to facilitate the recognition of these sleep problems and referral for further evaluation.

Obstructive sleep apnea hypopnea

The pathophysiology of obstructive sleep apnea syndrome (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. Furthermore, adenotonsillectomy does not appear to resolve OSAS in many children. ^[6] Upper airway neuromotor dysfunction is possible in the initiation of OSAS. Obesity is now recognized as one of leading risk factors for increasing rates of OSAS. ^[7]  Snoring is common in OSAS, but some children with OSAS have no snoring reported by their families. ^[8] Certain medical conditions such as Prader-Willi syndrome or trisomy 21 (Down syndrome) increase the risk for OSAS because of midline deformities such as macroglossia, micrognathia, midface hypoplasia.

Obstructive sleep apnea hypopnea is defined by DSM-5 as evidence from PSG for at least 5 obstructive apnea or hypopneas per hour of sleep and either (1) nocturnal breathing disturbances (snoring, snorting/gasping, breathing pauses during sleep) or (2) daytime sleepiness, fatigue, or nonrefreshing sleep despite sufficient sleep opportunities; these occurrences cannot be explained by another mental disorder or medical condition. Alternatively, it can be diagnosed by PSG evidence of 15 or more obstructive apneas or hypopneas per hour of sleep, regardless of other symptoms. Research criteria used to identify children with OSAS is less stringent, setting the threshold of hypopneas at 1 to 5 events per hour. ^[8]

Central sleep apnea

Central sleep apnea is caused by variability in respiratory effort that results in repeated episodes of apneas and hypopneas during sleep. Central sleep apnea and obstructive sleep apnea hypopnea can coexist. DSM-5 defines central sleep apnea as PSG evidence of 5 or more central apneas per hour of sleep. The disorder is not better explained by another current sleep disorder.

There are 3 subtypes that can be diagnosed: idiopathic central sleep apnea, Cheyne-Stokes breathing, and central sleep apnea comorbid with opioid use. Idiopathic is characterized by variability in respiratory effort without evidence of airway obstruction. Cheyne-Stokes is a pattern of periodic crescendo-decrescendo variation in tidal volume of at least 5 events per hour, accompanied by frequent arousal. This pattern of breathing is associated with heart failure, stroke, or renal failure. Opioids affect the respiratory rhythm generators in the medulla (central area of brain) and the differential effects of hypoxic versus hypercapnic respiratory drive. This can occur even after only a one-time heavy use of the substance.

Sleep-related hypoventilation

In sleep-related hypoventilation, PSG demonstrates episodes of decreased respiration associated with elevated levels of carbon dioxide. In the absence of objective measures of carbon dioxide, persistent low levels of hemoglobin oxygen saturation dissociated from apneic/hypopneic events are also indicative. DSM-5 specifies that in order make this diagnosis, the condition is not better explained by another sleep disorder. In DSM-5, the 3 subtypes are idiopathic hypoventilation, congenital central alveolar hypoventilation, and comorbid sleep-related hypoventilation

Individuals with sleep-related hypoventilation may present with insomnia/sleepiness and/or headaches upon awakening. This disorder can coexist with obstructive sleep apnea hypopnea and central sleep apnea. Patients may have diaphragmatic weakness or ventilatory insufficiency resulting from pulmonary hypertension, cor pulmonale (right-sided heart failure), polycythemia, or neurocognitive dysfunction. Episodes of hypoventilation may be associated with frequent arousals or bradytachycardia. Hypoventilation cannot be present during wakefulness. Other causes of sleep-related hypoventilation include chronic obstructive pulmonary disease (COPD), neuromuscular disorders, and obesity.

Idiopathic and congenital central alveolar hypoventilation are extremely rare. Congenital central alveolar hypoventilation occurs in association with autonomic dysfunction or Hirschsprung disease. Some cases of idiopathic hypoventilation may be cases of late-onset congenital central alveolar hypoventilation.

Circadian sleep disorders

A circadian clock or 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.

In patients with circadian sleep disorders, sleep and associated processes are at opposite phases or periods. These disorders may represent a poor compensatory ability for sleep loss and include failure to adequately synchronize sleep-wake behaviors and adapt to environmental demands, such as school. They are frequently observed in adolescents with delayed sleep phase.

Circadian rhythm sleep-wake disorder as defined by DSM-5 is a persistent or recurrent pattern of sleep disruption that is primarily due to an alteration of the circadian system or to misalignment between the circadian rhythm and the sleep-wake schedule required. This sleep disruption leads to excessive sleepiness and/or insomnia. These symptoms cause significant impairment in functioning. Subtypes to be specified include the following:

• Delayed Sleep Phase Type

• Advanced Sleep Phase Type

• Irregular Sleep-Wake Type

• Non-24-Hour Sleep-Wake Type

• Shift Work Type

• Unspecified Type

The history usually consists of a delay in the timing of onset of sleep by more than 2 hours. When individuals are allowed to set their sleep schedule, sleep is normal in quality and duration. There is an increasing prevalence during adolescence, which may related to physiological and behavioral factors.

Some individuals may be hypersensitive to evening light, which delays their sleep onset. Others are hyposensitive to morning light and do not respond to the phase-advancing effects. There may be familial and sporadic forms involving mutations in circadian genes such as PER3 and CKIe.

Parasomnias

Parasomnias are sleep-related phenomena disrupting normal sleep that result in abnormal behavior, experiential events, or physiological events. Events can take place during sleep-wake transitions, arousal, or REM sleep. The relationship of events to sleep stage and other variables are related to pathogenesis .

NREM sleep arousal disorders

Individuals with NREM sleep arousal disorders, according to DSM-5, report recurrent episodes of incomplete awakening from sleep usually occurring during the first few hours of sleep. During the incomplete awakening, they may sleepwalk (sleep walking type) or panic (sleep terror type). Throughout the episode, the individuals are unresponsive to others who are trying to communicate with or comfort them. Individuals do not recall the events or dreams. The episodes are usually brief (1-10 min) but can last up to an hour.

Two specialized forms of sleepwalking include sleep-related eating and sex. The individuals may even ingest inappropriate foods. In sexsomnia, which occurs more often in males, there are varying degrees of sexual activity, including masturbation, fondling, groping, and sexual intercourse. Again, the individual has no memory of these events.

These disorders occur most frequently in childhood and diminish with age. Onset in adulthood should raise suspicion for other medical causes. These disorders are often familial, with a positive family history in 80% of individuals. "Confusional arousal" disorder is included by the International Classification of Sleep Disorders, 2nd Edition as an NREM sleep arousal disorder. Night terrors is the common name for sleep terror disorder.

Nightmare disorder

Repeated occurrences of extended, unpleasant, and well-remembered dreams that involve avoiding threats to survival, security, or physical integrity that occur during the second half of sleep is defined as nightmare disorder by DSM-5. When awakened, the individual is rapidly alert and oriented. The symptoms must cause clinically significant impairment or distress.

In contrast to NREM sleep arousal disorders, the prevalence of nightmare disorder increases through childhood and adolescence. Nightmares begin between ages 3 and 6 years and peak in late adolescence or early adulthood. Nightmares occur in the second half of sleep, whereas night terrors occur in the first few hours of sleep. Nightmares involve vivid recall, whereas individuals are amnestic for sleep terrors.

REM sleep behavior disorder

REM sleep behavior disorder as defined by DSM-5 involves repeated episodes of arousal during sleep associated with vocalization and/or complex motor behaviors. Since these behaviors arise during REM sleep, they usually occur more than 90 minutes after sleep onset and occur more frequent during the later part of sleep period. It usually does not occur during daytime naps.

Upon awakening from these episodes, the individual is completely awake, alert, and oriented. One of following also needs to be present: REM sleep without atonia on polysomnographic recording or a history if symptoms with an established synucleinopathy diagnosis (Parkinson disease, multiple system atrophy). The vocalizations or complex motor behaviors are usually responses to action-filled or violent dreams and are sometimes termed dream-enacting behaviors.

Nocturnal seizures may mimic REM sleep behavior disorder. However, these behaviors are more stereotyped. Symptoms in young individuals are usually an indication of narcolepsy or medication-induced REM sleep behavior disorder. Symptoms in young females are more likely to be caused by narcolepsy.

Restless legs syndrome (RLS)

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

According to DSM-5, the urge to move the legs must also include all of the following: begins/worsens during periods of rest or inactivity, partially or totally relieved by movement, and is worse in the evening or at night than during the day. The symptoms can delay sleep onset and awaken the individual from sleep. Onset of RLS is usually in the second or third decade of life.

Diagnosis in children may be challenging because children have difficult reporting an "urge." Children and adolescents also report restlessness during the day from prolonged sitting, so a reported increase in restless at night is key to diagnosis. The International Restless Legs Syndrome Study Group published a detailed review regarding the difficulty of diagnosing RLS in the pediatric population. ^[9] They highlighted the need to rule out common mimics such as positional discomfort, sore leg muscles, sprains/strains, positional ischemia, dermatitis, bruises, and growing pains.

RLS may be precipitated by iron deficiency and/or genetic risk. Several genetic markers have been identified to be associated with RLS. African Americans and Asians appear to be less at risk. Serotonergic antidepressants can induce or aggravate RLS.

Other DSM-5 sleep disorders that are not discussed here include Substance/Medication-Induced Sleep Disorder, Other Specified Insomnia Disorder, Unspecified Insomnia Disorder, Other Specified Hypersomnolence Disorder, Unspecified Hypersomnolence Disorder, Other Specified Sleep-Wake Disorder, and Unspecified Sleep-Wake Disorder

Non-DSM-5 diagnoses

Periodic limb movement in sleep

Periodic limb movement in sleep (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 PLMS may be related to dopaminergic dysfunction. Characteristic movements may aid in further understanding of the pathology of PLMS.

PLMS presents as repetitive flexion of lower extremities (more common) or upper extremities in youths; movements last for 0.5–5 seconds and occur 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 as a result of associated sleep disruption or fragmentation. PLMS can occur without RLS.

Limit-setting sleep disorder

Limit-setting sleep disorder is a parent-child transactional model with potentially numerous biopsychosocial variables that influence interactions. It is not simply a failure to set limits; it 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 is observed in ADHD and other neurodevelopmental disorders, or may be a combined medical-behavioral issue.

Insufficient sleep syndrome

Insufficient sleep syndrome is a condition of chronic sleep deprivation without an underlying disease process. Youths with this 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. Patients with this syndrome attempt to decrease sleep debt incurred during the week by sleeping later on the weekends.

Surveys report that 20–25% of youths have some type of sleep problem. The following 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 rates decrease 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 1 to 4% of children ^[8]

• Narcolepsy (0.01–0.20%) may be underestimated in children because a classic tetrad of symptoms is uncommon in this age group; only about 10% of children show all the symptoms: excessive daytime sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis; semipurposeful automatic behavior, disrupted nocturnal sleep, sudden onset of weight gain, obstructive sleep apnea, and, especially, anosmia, should increase clinical suspicion ^[10]

• Bedtime resistance in school-aged children has been reported at 15% and is often associated with limit-setting disorder

The results of a population-based study on schoolchildren in Istanbul found that decreased total sleep duration is more prevalent in boys, older children, and children with higher socioeconomic status; insufficient sleep in these groups may be associated with negative behavioral symptoms and sleep hygiene ^[11]

Restless legs syndrome (RLS) affects 2 to 4% of school-aged children and adolescents. ^[9]

Race-related demographics

Specific racial risk factors may predispose certain individuals to a sleep-wake disorder. African Americans present more often with narcolepsy without cataplexy or with atypical cataplexy. They may be more prone to having advanced sleep phase–type sleep disorder because of having a shorter circadian period and larger magnitude of phase advances to light than whites. Asian Americans may be at increased risk of obstructive sleep apnea hypopnea despite having low body mass index (BMI).

Sex-related demographics

Sex differences in sleep-wake disorders may be associated with sex roles and/or hormonal changes. Insomnia is more common in females and onset is more likely with the birth of a child or with menopause. During the first few years after menarche, females may experience menses associated periodic hypersomnia. In assessing narcolepsy, females may report fatigue instead of sleepiness and underreport snoring.

During NREM sleep arousal disorders, females are more likely to have eating behaviors. During childhood, sleepwalking occurs more often in females but sleep terrors are more common in males. In contrast, in adulthood, sleepwalking occurs more often in males but the sex ratio for sleep terrors is even. Adult females report having nightmares more often than males.

RLS is more common in females without diagnostic differences. The prevalence of RLS during pregnancy is 2–3 times greater than in the general population. It peaks during the third trimester and improves/resolves after delivery. Nulliparous (never pregnant) females are at the same risk for RLS as males. OSAS is, in contrast, more common in boys. ^[8]

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

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 pediatric patients with OSAS. Continuous positive airway pressure (CPAP) is indicated for patients who partially respond to surgery or in whom surgery is contraindicated. A review of available treatments for OSAS in children revealed only a limited evidence base to support their use. Extremely limited data from randomized controlled trials are available to support the effectiveness of adenotonsillectomy, although this represents the current quasi-standard and first-line treatment for OSAS.

The success of therapy for delayed sleep phase syndrome (DSPS) depends to a large extent on the adolescent’s level of motivation. To prevent relapse of DSPS, the new schedule must be rigidly maintained.

Most children with parasomnias outgrow this condition when younger than 10 years or demonstrate a progressive decrease to a prevalence comparable 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.

For sleep disorder related to a general medical condition, the prognosis depends on treatment of the underlying condition. For sleep disorder related to substance use, prognosis depends on treatment of the addiction.

Because human beings spend a third of their time sleeping, it is essential to emphasize the need for good sleep hygiene to children, adolescents, and their families. Treatment of any behavioral problems generally will not not help unless sleep problems are addressed. "Catch-up sleep" is  a misconception as more studies demonstrate the long-term effects of sleep deprivation. 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 television

• 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 patient education resources, see the Sleep Disorders Center, as well as Disorders That Disrupt Sleep (Parasomnias), Night Terrors, Narcolepsy, REM Sleep Behavior Disorder, Periodic Limb Movement Disorder, and Sleeplessness and Circadian Rhythm Disorder.