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Pediatric Sleep Disorders: Assessment and Treatment

NeurologyLive, August 2022, Volume 5, Issue 4

Disease Spotlight | <b>Disease Spotlight: Insomnia</b>

The long-term consequences of untreated—and prevalent—sleep disorders in children and adolescents point to a need for a focus on this field of care.

SLEEP PLAYS A FUNDAMENTAL ROLE in human development and a critical role in the health of children. Unfortunately, sleep problems are often underappreciated and unrecognized in pediatric neurology, despite the pervasive nature of sleep complaints and their high prevalence—estimated at 10% to 46.4% of school-aged children.1-3 Untreated sleep problems result in functional impairment in children and may have long-term consequences.

In this review, we discuss common pediatric sleep disorders and provide epidemiology background, clinical presentation, diagnostic evaluation, and management opportunities.

General Approach in Evaluating Children With Sleep Disturbances

The general assessment of pediatric sleep disorders must, at a minimum, include survey questions about sleep duration and regularity, bedtime resistance and sleep onset delay, night waking, symptoms of sleep-disordered breathing, and signs of increased daytime sleepiness. A sleep diary is of fundamental importance in capturing these data and can be downloaded from a sleep education website endorsed by the American Academy of Sleep Medicine (AASM) or directly from the AASM at sleepeducation.org/ resources/sleep-diary.

Multiple brief sleep screening questionnaires have been developed and validated, including BEARS, a 5-item assessment that is the acronym for the following important areas to screen: bedtime issues, excessive daytime sleepiness, night awakenings, regularity and duration of sleep, and snoring.4

Obstructive Sleep Apnea Syndrome

Pediatric obstructive sleep apnea syndrome (OSAS) is a sleep-related respiratory disorder characterized by intermittent partial or complete upper airway obstruction, which disrupts sleep architecture, impairs ventilation, and impacts brain development.5,6 Its prevalence is estimated to be 1% to 4% of children, although a higher prevalence is seen in certain pediatric populations such as children with trisomy 21, cleft palate, and craniofacial syndromes.7-10

Although pediatric OSAS can occur in all age groups, there are 2 peak periods. The first peak, in preschool-aged children, is associated with adenotonsillar hypertrophy.6 The second peak, in adolescents, is associated with obesity.6 There is no sex difference in the prevalence of pediatric OSAS in prepubertal children, although higher prevalence is seen in adolescent boys than in adolescent girls.6,11 Multiple risk factors are associated with pediatric OSAS (TABLE 16,12,13).

Pediatric OSAS typically presents with frequent snoring, labored respirations, and observed apneic episodes during sleep. Other clinical manifestations include nocturnal enuresis, morning headaches, cyanosis, sleeping in an unusual position such as with the neck hyperextended, and daytime sleepiness. Common physical examination findings include tonsillar hypertrophy, adenoidal facies (long, thin face with malar hypoplasia), allergic shiners (bilateral shadows under the eyes produced by chronic venous congestion), micrognathia, retrognathia, high-arched palate, and failure to thrive.14

The American Academy of Pediatrics recommends polysomnography or referral to sleep medicine specialists or otolaryngologists for further evaluation if there is suspicion for pediatric OSAS.14 The gold-standard test for diagnosis of pediatric OSAS remains the overnight nocturnal polysomnogram (attended in-laboratory sleep study).15 At present time, the AASM does not recommend the use of home sleep apnea tests (portable or in-home studies) in pediatric patients.16 In pediatric populations, the history and physical examination have low sensitivity and specificity for the diagnosis of pediatric OSAS.15 Studies evaluating the accuracy of clinical scoring tools have found that these tools do not accurately predict pediatric OSAS.17 Nocturnal oximetry studies have been found to be inadequate for the diagnosis of pediatric OSAS.15

Treatment depends on the severity of the pediatric OSAS and its etiology. Because adenotonsillar hypertrophy is the most common etiology of OSAS, adenotonsillectomy is often first-line treatment.14 Continuous positive airway pressure therapy may be considered in pediatric patients who are not candidates for adenotonsillectomy or have residual OSAS following adenotonsillectomy.14 Topical intranasal corticosteroids may be considered in select pediatric patients with mild OSA for whom adenotonsillectomy is contraindicated or in pediatric patients with mild OSAS that persists following adenotonsillectomy.14 Weight loss in conjunction with exercise may also be considered in pediatric patients with OSAS who are overweight or obese.14 Left untreated, pediatric OSAS is associated with behavioral, cardiovascular, and neurocognitive consequences, as well as impaired growth and development (TABLE 2).6,15,18

Behavioral Insomnia of Childhood

Insomnia is a sleep disorder characterized by chronic difficulty initiating and maintaining sleep despite adequate opportunity for sleep, resulting in daytime impairment.19 Its prevalence ranges from 19.3% to 41% in children, with the highest prevalence seen in girls aged 11 to 12 years.20,21

Behavioral insomnia of childhood (BIC) is one type of insomnia delineated in the International Classification of Sleep Disorders (2nd ed).22 Within this category of insomnia are 3 subtypes: sleep-onset association type, limit-setting type, and combined type.

  1. BIC sleep-onset association type is characterized by dependence on specific conditions to initiate sleep or return to sleep following nighttime awakenings. In the absence of these specific conditions, sleep onset is delayed. This type may also present with frequent or prolonged nighttime awakenings, which often require caregiver or parental intervention.23
  2. BIC limit-setting type is characterized by bedtime refusal or bedtime stalling and is thought to result from inadequate limit setting by the caregiver or parent. Bedtime refusal presents as refusal to get ready for bed, go to bed, or stay in bed, and bedtime stalling manifests as attempts to delay bedtime. In BIC limit-setting type, sleep onset is often delayed, although there are no frequent or prolonged nighttime awakenings.23
  3. BIC combined type has features of both BIC sleep-onset association type and BIC limit-setting type.23

Diagnosis of BIC is based on parental or caregiver report of symptoms.23 Polysomnography is not typically performed as part of the diagnostic work-up for insomnia, unless it is suspected that part of the stalling to get in bed is associated with leg pain (growing pains mistaken for restless legs syndrome).19 Other useful diagnostic tools include a sleep diary or sleep log and sleep questionnaires.

The AASM recommends behavioral interventions for the treatment of bedtime problems and nighttime awakenings in children younger than 5 years.24-26 The specific therapies recommended include unmodified extinction, extinction with parental presence, graduated extinction, delayed bedtime with removal from bed or positive bedtime routines, scheduled awakenings, and parent education and prevention.24 These behavioral interventions are associated with decreases in bedtime resistance and nighttime awakenings.25

Untreated BIC affects not only children with BIC, but also their caregivers. In children, insufficient sleep and sleep difficulties are associated with attention-deficit/hyperactivity disorder, as well as poorer executive functioning, behavior, and social-emotional functioning.27,28 Parents of infants with BIC sleep-onset association type experience sleep deprivation, depression, and decreased marital intimacy.29

Pediatric Narcolepsy

Narcolepsy is a central disorder of hypersomnolence, with an estimated prevalence ranging from 0.23 per 100,000 in Israel to 160 per 100,000 in Japan.30 The annual incidence in Finnish patients younger than 17 years is approximately 0.12 to 5.3 per 100,000.31 There is a bimodal peak for age of onset, with the first peak occurring at age 15 years and the second peak occurring at age 35 years.30 Diagnosis is often delayed in pediatric patients by 10 to 15 years due to misdiagnosis with other disorders such as depression, hypothyroidism, “laziness,” and conversion disorder.32

Narcolepsy is categorized into 2 phenotypes—narcolepsy type 1 (NT1, previously narcolepsy with cataplexy) and NT2 (previously narcolepsy without cataplexy). Both subtypes are characterized by excessive daytime sleepiness (EDS). EDS commonly presents as inability to maintain alertness and wakefulness during the day and inability to maintain sleep during the night, although in children it may manifest as excessively long sleep duration or need for daytime naps that had previously stopped.33

NT1 is characterized by the presence of cataplexy and hypocretin (orexin) deficiency, which is absent in NT2. Cataplexy presents with brief episodes of abrupt loss of muscle tone without loss of consciousness and is typically triggered by strong emotions such as laughter and surprise. Children may have cataplectic facies, which manifests as mouth opening, tongue protrusion, and ptosis. Other associated features include hypnagogic hallucinations, hypnopompic hallucinations, sleep paralysis, and unexplained excessive weight gain. Hypnagogic and hypnopompic hallucinations typically occur during sleep-wake transitions and usually have visual, auditory, and tactile components. Sleep paralysis presents as a transient inability to move voluntary muscles except for eye movements and breathing. REM sleep behavior disorder (RBD) and REM sleep without atonia are associated with narcolepsy in children and may occur prior to the onset of narcolepsy symptoms. Unlike the adult phenotype of RBD, there is no established risk of phenoconversion to α-synucleinopathy. NT1 is associated with brain hypocretin deficiency (if it is measured). It is also associated with the presence of human leukocyte antigen (HLA) subtype DQB1*0602, although this HLA subtype can be present in up to 30% of individuals without narcolepsy.33

The diagnostic work-up often includes actigraphy or a sleep diary, a nocturnal polysomnogram, and a multiple sleep latency test (MSLT) the day after the polysomnogram. The AASM recommends at least 1 week of actigraphy recording with an accompanying sleep log prior to the MSLT to exclude circadian rhythm disorders, shift work disorder, and insufficient sleep disorder as possible etiologies for EDS.34 Testing must occur after correction of sleep apnea, sleep deprivation, and sleep-wake circadian disorders. The nocturnal polysomnogram should be performed the night prior to the MSLT to confirm sufficient sleep duration and measurement of REM sleep latency.34 Antidepressants and other medications that affect REM sleep must be discontinued for at least 2 weeks prior to the MSLT.33 Additional testing may include HLA typing for HLA DQB1*0602, and measurement of cerebrospinal fluid levels of hypocretin-1.33

Management includes both behavioral and pharmacologic treatment. Planned daytime naps are recommended to improve sleepiness.35 Other nonpharmacologic treatments include adherence to good sleep hygiene, consistent sleep schedule with adequate sleep duration, regular physical activity, and avoidance of emotional triggers for cataplexy.36 A limited number of pharmacologic options are available for pediatric patients. The AASM recommends the use of modafinil (Provigil; Cephalon) or sodium oxybate (Xyrem; Jazz) in pediatric patients with narcolepsy.37 However, the FDA currently lists sodium oxybate for the treatment of excessive sleepiness and cataplexy (for patients aged 7-17 years), oxybate salts (a low-sodium version of sodium oxybate) for the treatment of excessive sleepiness and cataplexy (aged 7-17 years), and traditional stimulants for management of daytime sleepiness associated with narcolepsy.


Parasomnias are abnormal behavioral events or experiences that occur during sleep onset, sleep transitions, or arousals from sleep (TABLE 3).38 They are classified into REM-related parasomnias, non-REM (NREM)- related parasomnias, and other parasomnias. Parasomnias are common occurrences in the pediatric population, with an estimated prevalence as high as 84% among those between 2 and 6 years old.39 The most frequently encountered parasomnia is somniloquy (sleep talking).39 Other commonly encountered pediatric parasomnias are sleep terrors, sleep enuresis, and somnambulism (sleepwalking).39 Confusional arousals, recurrent isolated sleep paralysis, and nightmare disorder are also described in pediatric patients.38

Parasomnias are diagnosed based on clinical history. Although polysomnography is not routinely indicated for evaluation of uncomplicated parasomnias, it may be useful to evaluate for other sleep disorders such as obstructive sleep apnea, identify potential triggers, and rule out disorders with similar clinical manifestations such as nocturnal seizures.38

Treatment is dependent on the specific type of parasomnia involved. General management strategies for NREM-related parasomnias are parental reassurance, promotion of a safe sleep environment (such as avoiding bunk beds for those who sleep walk), appropriate sleep hygiene, and avoidance of potential triggers such as environmental disruptions, sleep deprivation, and stress.40 Caregivers should be counseled to avoid intervention during the parasomnia because this could worsen the event.40 If the NREM-related parasomnias occur frequently and predictably, scheduled awakenings may be considered.41 In this management strategy, the pediatric patient is woken up 15 to 30 minutes prior to the time when the parasomnia typically occurs. This is done nightly for 2 to 4 weeks until resolution. Pharmacologic treatment is not routinely indicated in the management of NREM-related parasomnias unless these events are severe, occur frequently, or may result in injuries. Medications are often used off label and include benzodiazepines and tricyclic antidepressants.41

Sleep-Related Epilepsy

Sleep-related epilepsy encompasses multiple epileptic syndromes that occur predominantly during sleep or following arousals from sleep.42

If there is concern for epilepsy, a standard daytime 16-channel to 20-channel electroencephalogram (EEG) or ambulatory 24-hour EEG monitoring should be considered.42 For nocturnal frontal lobe epilepsy or sleep-related hypermotor epilepsy, nocturnal polysomnogram utilizing expanded EEG montage and high definition video is the gold standard for diagnosis.42

Treatment is dependent on the specific epileptic syndrome diagnosed. General treatment strategies include avoidance of seizure triggers (such as sleep deprivation) and adherence to an antiepileptic drug. Sleep disorders that disrupt sleep should be treated to improve seizure control.43

Circadian Rhythm Sleep-Wake Disorder

Circadian rhythm sleep-wake disorders (CRSWDs) result from disruptions to the intrinsic circadian rhythm. The majority of CRWSDs are a consequence of misalignment of the innate circadian rhythm and the desired sleep-wake schedule. This disturbance in circadian rhythm presents as excessive sleepiness and difficulty with sleep initiation and maintenance, as well as functional impairment.44

The AASM delineates 7 types of CRSWD.44 Of these, the most common CRSWD in pediatrics is delayed sleep-wake phase disorder (DSWPD), with an estimated prevalence of 3.3% to 8.4% in adolescents, with a slight predominance in girls.45,46 DSWPD is characterized by a consistent delay in sleep-onset time relative to conventional time, difficulty with sleep initiation at the conventional bedtime, and difficulty awakening at the conventional wake time.44 The delay in sleep onset is typically 2 hours or more.44 Those with DSWPD who can follow their preferred schedule typically have normal sleep quality and sleep duration, although timing is delayed.44

The diagnostic work-up includes detailed sleep history, sleep log, and actigraphy recording (when possible) for at least 7 days (preferably 14 days).44 Standardized chronotype questionnaires may be considered to assess for morningness and eveningness.44 Laboratory studies demonstrating delay in circadian rhythm may be used to confirm the diagnosis, such as dim-light melatonin onset or urinary 6-sulfatoxymelatonin.44 Polysomnography is not routinely indicated for diagnosis.

Treatment involves both pharmacologic and nonpharmacologic interventions. For pharmacologic interventions, the AASM recommends the use of strategically timed exogenous melatonin administration, although long-term data on melatonin in pediatric patients are lacking.47 For nonpharmacologic treatment, the AASM recommends postawakening light therapy in conjunction with behavioral interventions.47 Left untreated, DSWPD negatively impacts academic performance, social functioning, and caregiver well-being.48

Restless Legs Syndrome

Restless legs syndrome (RLS) is a sleep-related movement disorder seen in 1.9% to 2.0% of pediatric patients.49 This sensorimotor disorder is characterized by an urge to move the legs that is associated with an uncomfortable or unpleasant sensation.50 These symptoms occur primarily at night, worsen during inactivity or rest, and improve with movement.50 Common complaints include disturbed sleep, daytime fatigue, and daytime sleepiness.50 Pediatric RLS is associated with iron deficiency, attention-deficit/hyperactivity disorder, anxiety, depression, oppositional defiant disorder, parasomnias, and chronic kidney disease.49 It is also associated with gene variants of BTBD9, MEIS1, MAP2K5/LBXCOR, and PTPRD.50 The presence of RLS in a first-degree relative is a risk factor for RLS.49

RLS is diagnosed clinically, but it can be challenging to diagnose because it requires pediatric patients to describe their symptoms in their own words.50 Several diagnostic tools have been developed specifically for pediatric RLS including the pediatric Emory RLS diagnostic questionnaire and the RLS questionnaire.51 Severity and quality-of-life questionnaires have also been developed specific to pediatric RLS.51 Polysomnography is not typically indicated in the diagnosis of RLS, but it may demonstrate periodic limb movements of sleep, elevated arousal index, and sleep abnormalities.50

Management of pediatric RLS includes both pharmacologic and nonpharmacologic treatment. Nonpharmacologic interventions include the establishment of good sleep habits, physical activity, and avoidance of RLS exacerbating factors, such as inadequate sleep, irregular sleep schedule, pain, caffeine, nicotine, alcohol, and medications (sedating antihistamines, neuroleptics, and serotonergic antidepressants).52 Pharmacologic treatment options are limited in pediatric RLS and include iron supplementation, clonidine, and gabapentin.52

Sleep and COVID-19

The COVID-19 pandemic has affected many aspects of pediatric health, including sleep. Findings from multiple studies have demonstrated changes in sleep patterns in both preschool-aged children and adolescents, particularly in delayed sleep timing.53-56 During the pandemic, Chinese preschoolers displayed later bedtimes and wake times, shorter nap duration, and longer nocturnal sleep duration.54 Caregivers also reported fewer sleep disturbances.54 Adolescents in the United States were noted to have increased difficulties initiating and maintaining sleep, later bedtimes and wake times, longer school-night sleep duration, and less daytime sleepiness during the pandemic.56 Other study data have demonstrated shifts in sleep timing but have not supported changes in sleep duration.55 Worsening in sleep quality has also been demonstrated in school-aged children during the pandemic.53

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