Insufficient or disrupted sleep in children is now recognized to affect the cognitive development and behavior. Pediatric sleep disorders have unique societal impact; both the child’s and the family’s sleep can be affected when a disorder is present.
The following table gives an idea about the amount of sleep needed by children:
|Age||Average Sleep Duration in 24 Hours (Overnight and naps)|
|Infants (4 to 12 months)||12 to 16 hours|
|Children (1-2 years)||11-14 hours|
|Children (3-5 years)||10–13 hours Most give up naps between 3 and 5 years|
|Children (6-12 years)||9–12 hours|
|Teenagers (> 12 years13-18 years)||8-10 hours|
If the answers to most of the following questions are in the affirmative, your child has sleep disorder.
|Preschool (2–5 Years)||School-age (6–12 Years)||Adolescent (13–18 Years)|
|B edtime problems||Does your child have any problems going to bed? Falling asleep?||Does your child have any problems at bedtime? (P)
Do you have any problems going to bed? (C)
|Do you have any problems falling asleep at bedtime? (C)|
|E xcessive daytime sleepiness||Does your child seem overly tired or sleepy during the day?
Does your child still take naps?
|Does your child have difficulty waking in the morning, seem sleepy during the day, or take naps? (P)
Do you feel tired a lot? (C)
|Do you feel sleepy a lot during the day? In school? While driving? (C)|
|A wakenings during the night||Does your child wake up a lot at night?||Does your child seem to wake up a lot at night? Any sleepwalking or nightmares? (P)
Do you wake up a lot at night? Have trouble getting back to sleep? (C)
|Do you wake up a lot at night?
Have trouble getting back to sleep? (C)
|R egularity and duration of sleep||Does your child have a regular bedtime and wake time? What are they?||What time does your child go to bed and get up on school days? Weekends? Do you think your child is getting enough sleep? (P)||What time do you usually go to bed on school nights?
Weekends? How much sleep do you usually get? (C)
|S leep-disordered breathing||Does your child snore a lot or have difficulty breathing at night?||Does your child have loud or nightly snoring or any breathing difficulties at night? (P)||Does your teenager snore loudly or nightly? (P)|
Common Pediatric Sleep Diagnoses and Treatment
Obstructive Sleep Apnea
The pharynx has many roles, including swallowing, speaking, and maintaining airway patency. Pharyngeal size is determined by the bones and soft tissue. The soft tissue is affected by the size of the tonsils and adenoids, as well as adipose tissue. Airway patency is maintained during wakefulness; a small airway can become vulnerable during sleep resulting in partial or total closure of the airway, hypoxemia, hypercapnia, and an arousal that results in opening of the airway and termination of the obstructive event. This leads to sleep disruption and daytime consequences. OSA in children likely results from a combination of narrowing of the upper airway, abnormal upper airway tone, and genetic factors.
OSA in adults is typically associated with daytime sleepiness. Associations have been made with hypertension, stroke, and metabolic syndrome. In children, OSA may not present with daytime sleepiness. Children may present with daytime inattention and/or neurocognitive and behavioral issues. Symptoms include snoring with or without apneic pauses or gasps. Restless sleep or secondary enuresis may also be noted. Parents may comment on increased work of breathing while sleeping. Other associations include poor growth, obesity, hypertension, and systemic inflammation.
The gold standard for diagnosis of pediatric OSA is an in-laboratory attended PSG by an accredited sleep laboratory. History and physical examination lack sensitivity and specificity in predicting which children with snoring have OSA. However, a history of loud snoring, tonsillar hypertrophy, and abnormal oximetry is strongly suggestive of the diagnosis of OSA (see above). History alone cannot distinguish children with OSA from those with primary snoring. Criteria for the diagnosis of OSA in children are met when there is one or more apnea or hypopnea events per hour identified using scoring criteria by the AASM.
Other forms of sleep-disordered breathing are not as common as OSA. Sleep-related hypoventilation can occur in patients with neuromuscular weakness. Central hypoventilation syndromes are rare, but should be considered in children with persistent gas exchange abnormalities without additional explanation. Sleep-related hypoxemia can be present in pediatric patients with chronic lung disease. Central sleep apnea should be thought of in patients with brainstem abnormalities or Arnold-Chiari malformation. Sleep-related seizures may be difficult to differentiate from OSA in infants and an extended EEG montage may be necessary during their sleep study. Normal breathing patterns of infants and children should also be identified; brief (less than 10 seconds), central respiratory pauses that are self-resolving (and without significant desaturation) are common in normal children in either REM sleep or post-arousal/post-sigh.
Treatment of OSA in most children is adenotonsillectomy. Recent guidelines from the AAP recommend an overnight sleep study in children where the practitioner had a clinical suspicion of OSA before adenotonsillectomy. Children with mild OSA preoperative can be monitored clinically postoperatively. Children with moderate to severe OSA, as well as children with craniofacial abnormalities, neurologic disorders, and obesity, should have a follow-up PSG to demonstrate resolution of OSA after surgery. Children who are not candidates for adenotonsillectomy may be treated with CPAP and use may have an impact on neurobehavioral outcomes. Treatment with CPAP therapy in children requires close follow-up because pressure needs may change with growth.
Difficulty with Sleep Initiation and Night Wakings
Bedtime problems and night wakings occur in up to 30% of children.
The diagnosis of insomnia includes difficulty going to sleep and/or staying asleep, the complaint that sleep is not of good quality, and the report of poor daytime functioning. The sleep complaints of infants and young children are often in the words of their parent or caregiver.
In preschool-age children both bedtime problems and night wakings are common and characterized by two types of behavioral insomnia of childhood: sleep-onset association type and limit-setting type. The definition of the sleep-onset association type , as defined in the ICSD-2, includes the following: sleep initiation is an extended process, associations are demanding, if the associations are not present sleep onset is delayed, and awakenings require caregiver intervention. The limit-setting type involves difficulty initiating or maintaining sleep, there is bedtime stalling or refusal, and the caregiver does not set sufficient and appropriate limits around this behavior. Children with frequent and prolonged night wakings have the sleep-onset association type. They often require an intervention by the caretaker to reinitiate sleep. Both problems can be present at once. Children who have difficulty going to sleep and provide resistance to bedtime have the limit-setting type. Parents of these children may complain of daytime behavioral issues due to the parent’s inability to set limits during the day as well.
Diagnosis is made from the history in the majority of cases. An overnight sleep study may be indicated in cases where another sleep disorder is suspected.
The differential diagnosis of insomnia or behavioral insomnia of childhood includes sleep disorders such as OSA, RLS, or nocturnal seizures. These disorders can prompt nocturnal awakenings or make sleep initiation difficult. If there is clinical suspicion of one of these disorders, an overnight sleep study may be indicated.
Behavioral interventions have been shown to be effective in treating all forms of insomnia. In older children, primary and secondary insomnia can be effectively treated with cognitive-behavioral therapy. This often includes stimulus control and sleep restriction. Stimulus control includes maintaining a regular sleep-wake pattern and using the bed and bedroom only for sleeping. It involves getting out of bed if sleep is not initiated within about 20 minutes. Sleep restriction includes minimizing the time in bed to be only sleeping. It often includes delaying bedtime to the child’s actual sleep onset, and then over time gradually advancing the bedtime. Sleep hygiene should be effectively addressed, including development of a relaxing bedtime routine, maintaining a regular sleep-wake pattern, and eliminating electronic use before bedtime.
There are several treatments of behavioral insomnia of childhood sleep-onset association type. No one treatment has been found to be superior. The goal of all of these methods is for the child to fall asleep in his or her crib or bed on the child’s own. These include extinction (i.e., “cry it out”), which is often not palatable to caregivers. There is the graduated extinction method, which has parents ignoring crying or protests for specified periods of increasingly longer intervals. Some prefer an even more gradual approach of sitting next to the child’s bed in a chair and over several days to weeks moving that chair across the room and out of the room. A consistent bedtime routine should also be implemented. Use of a transitional object can be helpful. Treatment of the limit-setting type includes firm limit setting. Positive reinforcement and limiting negative reinforcement should be used. The use of a reward system can be helpful. Effectively addressing behavioral treatment of sleep issues can be challenging for the primary care provider because of time constraints.
Restless Legs Syndrome/Willis Ekbom Disease
Prevalence rates for pediatric RLS/WED have ranged from 1% to 6%.
Risk factors include a family history and a history of anemia or iron deficiency. Attention-deficit/hyperactivity disorder (ADHD) is associated with RLS.
Decreased dopamine has been suggested in the pathophysiology of RLS/WED. Iron is a cofactor in the synthesis of dopamine and treatment of iron deficiency or low ferritin, if present, may improve symptoms.
Diagnosis of pediatric RLS/WED is a clinical diagnosis. It is made using the adult criteria set forth in the ICSD-3 but with some modification for children due to developmental issues. It consists of the child reporting an urge to move the legs, usually accompanied by an uncomfortable sensation; this urge or sensation worsens during rest or inactivity; the sensations are improved or resolved by movement; the sensations are present or worsen in the evening or night. If a child cannot express a description in his or her own words, diagnosis can be made using two out of the following three criteria: a sleep disturbance for age, a family history of RLS, and a periodic limb movement index on PSG of > 5 per hour. Because of this last criterion, a sleep study can be helpful in children to make this diagnosis. There can be an association with sleep initiation and maintenance difficulties.
Differential diagnosis of RLS should include insomnia, sleep-disordered breathing, or neurologic or musculoskeletal etiologies for the discomfort.
Nonpharmacologic treatment of RLS includes good sleep hygiene, moderate exercise a few hours before bedtime, and avoidance of substances that are associated with worsening of RLS symptoms, including caffeine, alcohol, antihistamines, and antiemetics. A serum ferritin should be drawn in all children with RLS and if < 50 ng/mL, treatment with 6 mg/kg/day of oral elemental iron should be considered. Oral iron absorption is enhanced by vitamin C and impaired by calcium. Gastrointestinal upset and constipation can be common side effects. Compliance can be difficult. A serum ferritin should be rechecked at 3 months to evaluate therapy. Referral to a sleep medicine specialist should be made if lifestyle and oral iron therapy have been unsuccessful. There are no FDA-approved medications for the treatment of RLS in children. Dopamine agonists, gabapentin (Neurontin), 1
1 Not FDA approved for this indication.
Delayed Sleep Phase Syndrome
Delayed sleep phase syndrome (DSPS) occurs most commonly in adolescents and young adults.
Symptoms usually present in adolescents but can occur in younger children. Adolescents with DSPS consistently have sleep onset at a later time, typically after midnight. They have difficulty initiating sleep earlier. They do not have difficulty maintaining sleep. They have difficulty waking in the morning unless able to sleep until their preferred time, which is typically after 10 am . They may have sleepiness during the daytime if forced to rise early (i.e., for school); however, during long vacations or summer breaks when allowed to sleep to preferred wake time they feel refreshed. Children who already have a preferred evening preference may find this exacerbated in adolescence. Poor school performance can be present.
Diagnosis is made from history; actigraphy and sleep logs are also useful. An overnight sleep study may be indicated if another sleep disorder is suspected (e.g., OSA).
The differential diagnosis includes insomnia, poor sleep hygiene, insufficient sleep, mood disorder, OSA, and RLS.
Treatment is typically behavioral and includes good sleep hygiene. Typically either the patient’s sleep-wake schedule is advanced (if there is less than 3 hours between actual and desired bedtime) by 15 minutes every 2 to 3 days until the goal bedtime is achieved. Rise time is advanced as well and if set at the desired wake time initially it should facilitate the advancement of the bedtime by increasing sleep drive. If the desired bedtime of the adolescent is greater than 3 hours from the current bedtime, phase delay can be considered. Bedtime is delayed by 2 to 3 hours each day until the target bedtime is reached. Timing of this therapy should be considered, because it will interfere with school or other daytime activities. Parental or caregiver support is necessary, as well as commitment by the adolescent.
Once the new pattern is established weekends must not differ from weekdays by more than 1 to 2 hours. This is particularly important for the rise time. Relapse is common if strict sleep-wake patterns are not adhered to, a problem common on vacations.
Both bright light exposure and melatonin 7
7 Available as dietary supplement.
have been used to help reset the circadian rhythm. Exposure to bright light in the morning is encouraged and can be as simple as increasing sun exposure in the morning. Light boxes using 2500 to 10,000 lux can be used in the morning for 20 to 30 minutes. Exposure to light in the evening should be limited. A small dose of melatonin (0.5 mg) can be used in the early evening (about 5 hours before desired bedtime) to attempt to physiologically advance sleep onset. If the timing is not optimal for both light and melatonin, the phase delay can be worsened; consultation with a sleep physician should be considered.
Parasomnias can occur out of both non-REM (NREM) and REM sleep. Those occurring out of NREM sleep include sleepwalking, sleep terrors, and confusional arousals. They typically occur in the first one-third of the night, when NREM-3 sleep is most prevalent, and are not recalled the next day. They can be part of normal development, but depending on their nature, they can be distressing to caregiver and child. Parasomnias occurring out of REM sleep include nightmares and REM-sleep behavior disorder (RBD). Nightmares are commonly recalled and have been associated with anxiety in children. Nightmares typically peak in the school-age child. RBD is rare in children but has been reported; it involves the loss of atonia that occurs in REM sleep and consequently dreams are “acted out.”
Poor sleep hygiene, insufficient sleep, irregular sleep-wake patterns, and a positive family history are all risk factors. Sleep disruption from sleep-disordered breathing or periodic limb movements of sleep can exacerbate parasomnias.
The differential diagnosis should include nocturnal seizures. In addition, if another sleep disorder is present, parasomnias can be exacerbated.
Safety is most important in children with parasomnias, and it is important that the child’s sleep environment is kept clear of things that could cause injury. Door alarms can be effective. The child should not be awakened during the episode. The event should not be referred to the next morning because this can cause distress for the child. Maintaining good sleep hygiene and regular sleep-wake patterns is important. If the events occur at a predictable time each night, the caregiver can do planned awakenings 30 minutes before the event typically occurs for several weeks. This may abolish the episodes. It can also have the effect of pushing the episode to later in the night. Pharmacologic treatment with a small dose of a benzodiazepine (e.g., 0.5 mg of clonazepam [Klonopin] 1 at bedtime) may be indicated in severe cases with the drug tapered slowly after episodes are suppressed.
Consideration for a primary hypersomnia should be made in a child who is sleepy after common causes of sleepiness such as insufficient sleep and obstructive sleep apnea have been ruled out. Symptoms of narcolepsy include disrupted nocturnal sleep, hallucinations on going to sleep or waking up, and sleep paralysis. Daytime sleepiness is present with “sleep attacks” both during quiet activities and while active. Cataplexy may also be present and is defined by loss of muscle tone without loss of consciousness. It should be noted that onset of narcolepsy is often in adolescence or as a young adult. Diagnosis is often delayed because the symptoms are attributed to other conditions. Treatment of pediatric hypersomnia is done under the supervision of a sleep specialist and often involves use of stimulants.