sleep and its disorders in children

www.medscape.com

Abstract and

Although the physiological mechanisms that underlie sleep disorders in children differ little from those seen in adults, the clinical

manifestations may differ considerably between the two. For example, sleep apnea in adults affects men more than women, is more

prevalent in the obese, and presents with symptoms of snoring and excessive somnolence. In preadolescent children, sleep apnea

affects both sexes equally, is more closely correlated with adenotonsillar enlargement than obesity, and may be more likely to present

with daytime inattention and learning problems rather than frank somnolence. Likewise, the insomnia and associated bedtime struggles

of a 3-year-old bear little resemblance to the insomnia of a mature adult apart from the fact that both individuals are unable to easily fall

asleep. Sleep disorders in children are reviewed with particular focus on age-related changes in normal sleep and on sleep disorders

that primarily or exclusively affect children. Pediatric aspects of other sleep disorders will be reviewed in more limited detail, with

examination of how age, developmental level, and comorbid conditions cause clinical presentation and treatment to differ from that of

adults.

Normal Sleep in Infants and Younger Children

The duration and distribution of normal sleep evolve considerably during the first several years of life. Newborn infants may spend up to

16 to 18 hours per day asleep, usually in the form of 3- to 4-hour sleep periods spanning both daytime and nighttime hours.[1]

Beginning in the first month of life, these sleep periods begin to adapt to a day-night cycle and other environmental cues, with gradual

lengthening of both nighttime sleep period and daytime wakefulness. By 6 months of age, total sleep duration averages 14.2 hours and

the longest period of continuous nighttime sleep lengthens to ~6 hours.[1,2] Between 1 and 2 years of age, total sleep time declines

from an average of 13.9 hours to 13.2 hours while daytime sleep consolidates into a single nap, usually in the afternoon. Most children

give up daytime napping about age 3 and overall sleep time declines gradually to an average of 11.4 hours by 5 years of age.[2,3]

In addition to these considerable changes in sleep duration and distribution during early childhood, important qualitative changes in

sleep stages and architecture also occur. Term newborns exhibit poorly differentiated sleep states on electroencephalography (EEG)

and polysomnography (PSG). Infants spend up to 50% of sleep time in rapid eye movement (REM) sleep, also known as "active

sleep," and usually enter sleep through an initial REM period.[4] REM sleep periods recur in cycles every 50 to 60 minutes, alternating

with periods of non-REM (NREM) sleep, sometimes called "quiet sleep." Sleep-onset REM begins to subside by 3 months of age and

overall REM sleep declines to less than 30% of total daily sleep by 3 years.[1] Sleep cycle length matures more gradually and an adult

cycle length of 90 to 100 minutes is attained only during adolescence.[4]

Typical PSG and EEG markers of specific sleep stages are not fully developed in term neonates but evolve predictably during infancy.

Rapid eye movements may be recorded in even premature infants as young as 28 weeks gestational age, but REM-related muscle

atonia remains quite variable even in term infants.[5-7] Sleep spindles first become evident ~4 weeks of age with development of

mature forms by 8 weeks.[8] K-complexes are first seen by 6 months of age and have mature forms by 2 years.[9]

Sleeplessness in Infants and Younger Children

Nighttime waking is considered to be normal for young infants, influenced in part by the necessity of nighttime feedings for most babies

until 5 or 6 months of age.[10] Although some infants begin to "settle" and sleep through the night as early as 3 months of age, some

degree of brief nighttime waking is normal even during later infancy. Infants between 9 and 24 months of age woke on average twice

nightly during actigraphic monitoring, although many returned independently to sleep without parental intervention or signaling of

distress.[11] There exists no clearly defined threshold age beyond which excessive night waking is automatically considered abnormal.

Instead, parental perception largely governs whether a child's nighttime waking is considered to be a problem. It is estimated that up to

one-third of toddlers and preschoolers awaken at night to a degree considered worrisome by parents.[12]

A substantial number of predisposing or contributory influences have been identified with respect to night waking in infants, toddlers,

and preschoolers. Major influences include:

Persistent Nighttime Feedings. In most healthy infants over 6 months of age, nighttime feeding is more likely to represent a learned

behavior than a biological necessity. This is typically a self-limited behavior that subsides spontaneously as an infant matures. In

situations where persistent nocturnal feedings significantly disrupt the quality and continuity of nighttime sleep, structured schedules for

gradually reducing the quantity and frequency of nighttime feedings are usually highly effective.[12,13]

Separation Issues. Beginning after ~9 months of age, many infants experience distress when separated from their parents or

caregivers. Although separation anxiety is considered a normal element of early childhood development, it can also precipitate

significant distress at bedtime or during nighttime waking. This is typically self-limited and subsides with advancing age. Use of

Timothy F. Hoban, MD

Semin Neurol. 2004;24(3)

http://www.medscape.com/viewarticle/491438_print

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transitional objects such as blankets or stuffed animals may assist children in mastering separation responses that disrupt sleep.[14]

Temperament. There exists limited evidence that intrinsic aspects of child temperament, especially the ability to self-soothe, may

substantially affect sleep during early childhood. Several studies have reported an association between "difficult" temperaments and

disrupted nighttime sleep in young children.[15,16] In addition, lower sensory thresholds have been identified in infants with night waking

compared with those without.[17] When a child's temperament contributes to a problem with sleeplessness, it is the author's experience

that treatment is seldom successful unless this influence is identified and addressed as part of the overall treatment program.

Cosleeping. In the United States, some degree of cosleeping has been noted in about half of families with young children, with

considerable variability of prevalence among different racial and socioeconomic groups.[14,18] In many parts of the world, however,

cosleeping is considered the norm for infants and young children. Several clinical studies have suggested that cosleeping is

associated with increased risk of night waking for young children, although the frequency of sleep disruption and degree to which night

waking is considered problematic by families varies considerably among different ethnic groups.[18,19] Several PSG-based studies

have also reported increased arousals and awakenings during the sleep of infants sleeping with their mothers compared with nights

when sleeping alone.[20,21]

Bedtime resistance is usually seen in conjunction with excessive nighttime waking, although it may occasionally occur as an isolated

problem. Bedtime resistance encompasses a broad variety of child behaviors that occur at or near bedtime. It often takes the form of

"curtain calls," where a child may repeatedly leave the room, sometimes with requests for water, complaints of being unable to fall

asleep, or attempts to engage the parent or spend more time out of bed in other activities. Bedtime resistance may also incorporate

significant degrees of agitation such as protracted crying or oppositional behavior, resulting in significant distress for both child and

parent. Such problems with settling to sleep are common in young children, affecting ~20% of 1- to 3-year-olds and ~10% of 4½-year-

olds.[22]

Although the same associated influences already discussed with respect to night waking may also influence bedtime resistance,

several other factors more directly impact bedtime struggles:

Bedtime Routines and Environment. Consistent, well-structured routines leading to bedtime aid children in transitioning from their

daytime level of activity and alertness to a quiet, relaxed state more conducive to sleep onset. Conversely, irregular schedule or highly

stimulating prebedtime activities often tend to disrupt sleep onset.[23] In a similar fashion, a quiet sleep environment that is dark or only

dimly lit will for most children tend to promote faster and more comfortable sleep onset.

Fears and Anxieties. Childhood fears are common, but for most children they are a mild and self-limited problem. Bedtime is a

common venue for childhood fears and anxieties, which may be either specific (e.g., robbers, monsters, darkness) or ill-defined. In

most instances, bedtime fears can be addressed with gentle reassurance or use of a night-light.

Other Extrinsic Influences That Interfere With Settling at Bedtime. Many chronic medical conditions may be associated with

difficulty settling, particularly neurological conditions such as cerebral palsy, autism, and other developmental disabilities.[24] Many

commonly used medications, including stimulants and some anticonvulsants, are known to cause insomnia in at least some children.

Acute febrile illnesses such as otitis media will often cause short-term disruption of sleep onset or continuity. Finally, extrinsic

psychosocial stressors may have the potential to cause either acute or chronic sleep disruption.[12]

Sleep-onset association disorder is a condition affecting primarily infants and young children in which sleep onset becomes dependent

on an environment or circumstance that cannot be independently recreated by the child without assistance. Potentially problematic

associations for infants include being rocked, nursed, or bottle-fed at sleep onset. For toddlers and preschoolers, requiring parental

presence at sleep onset is a common association. Although providing the specific circumstance desired by the child is usually

perceived by parents to improve sleep onset at bedtime, some children become so reliant on the associated circumstance that they

are unable to fall asleep in its absence. As a result, affected children are unable to settle themselves following the brief physiological

awakenings that are part of normal sleep. The child, reliant upon the parent to provide the circumstance necessary for transition back to

sleep, will cry or otherwise signal the parent, leading to frequent problematic awakenings during the night.

Effective treatment of sleep-onset association disorder generally requires that the child learn a new set of sleep-associated habits that

do not require parental presence or intervention for sleep onset.[12,13] Gradual introduction and progressive reinforcement of the

desired sleep habits (see below) eases this process for both child and parent.

Treatment of Sleeplessness in Infants and Younger Children

Treatment of sleeplessness in younger children usually begins with effective bedtime management—a set of interventions focused on

establishing a regular sleep schedule, an appropriate sleep environment, and consistent limit-setting for dealing with bedtime

struggles:[12]

Bedtime Routine. A regular and well-structured set of prebedtime activities usually helps settle children and promote sleep onset. The

routine for many younger children often includes changing, bathing, stories, and being "tucked in." Stimulating activities (e.g., vigorous

play, watching cartoons) should be avoided due to their potential alerting effect. Keeping the routine quiet and regular helps young


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children achieve a quiet, relaxed state more conducive to sleep onset.

Sleep Schedule. Maintaining a consistent bedtime and waking time 7 nights per week is usually helpful in several respects. Eliminating

late sleeping and any daytime napping that is inappropriate for age may increase the chance that a child will be tired at the usual

bedtime. In addition, regularity of sleep schedule may promote entrainment and stabilization of circadian rhythms as an added impetus

for more rapid sleep onset at the regular bedtime.[25]

Sleep Environment. For most children, a quiet environment is more conducive to sleep than a noisy one. Likewise, a dark or dimly lit

environment promotes settling and sleep onset better than bright lighting, although use of a night-light is appropriate for children who

are afraid of the dark. Finally, it is generally recommended that children be put to sleep without a parent remaining present. This

provides the child with an opportunity to learn to fall asleep comfortably and independently and to minimize dependence upon parental

presence or intervention as a sleep onset association.

Limit Setting. Children who stall, cry, or leave the room at bedtime in an attempt to stay up later will sometimes repeat this behavior to

the point where a parent or caregiver "gives in" and allows the child to stay up. For some children, this pattern of behavior may be

repeated nightly to the point of causing consistent delay and disruption of sleep onset. Setting and enforcing appropriate limits on

inappropriate bedtime behavior are crucial for the effective treatment of limit-setting sleep disorder.[12] Limits must be enforced

consistently by all caregivers, usually for periods of days or weeks, for maladaptive bedtime behaviors to subside. Parents should be

made aware that temperamental and agitated behavior often transiently worsen during the first days of treatment before gradual

improvement becomes evident, making the initials days of treatment the most difficult.

In cases where bedtime management alone is not sufficient in the treatment of a younger child's sleeplessness, a variety of structured

behavioral interventions are available. Although these treatments have been widely utilized, they have received only limited scrutiny in

controlled scientific studies, recently reviewed by Ramchandani and colleagues and by Kuhn and Elliott:[22,26]

Extinction (Systematic Ignoring). This technique involves placing a child in bed and ignoring agitation or inappropriate behavior until

morning except for legitimate concerns regarding illness or safety of the child. Extinction has been found effective in several

large-scale studies and was found by Kuhn and Elliott to represent a well-established intervention.[26]

Graduated Extinction. First described by Douglas and Richman,[27] this technique was popularized by Ferber in his mass-market

book, Solve Your Child's Sleep Problems.[13] Using this technique, parents ignore bedtime tantrums or nighttime waking for a

specified period of time before being allowed to enter the bedroom and briefly calm the child before exiting. The specified interval for

ignoring the child's agitation progressively increases over time, usually over successive nights, and in some versions on successive

checks within the same night. Kuhn and Elliott also considered this to be a well-established intervention, validated by several

well-controlled studies.[26]

Scheduled Awakenings. For young children with nighttime waking occurring at predictable times during the night, this technique

requires that the parent preemptively awaken and then resettle the child 15 to 30 minutes before the usual time of spontaneous

awakening. If effective in eliminating the spontaneous awakenings, the scheduled awakenings are gradually spaced out or delayed

systematically. Kuhn and Elliott classified scheduled awakening as a probably efficacious intervention for excessive night waking.[26]

Bedtime Fading. This technique initially delays a child's bedtime by ~30 minutes. If rapid sleep onset is not observed, a "response

cost procedure" allows the child to be removed from bed and kept awake for 30 to 60 minutes, with the process being repeated as

necessary until the child falls asleep rapidly. On subsequent nights, the initial bedtime is set 30 minutes before the time of rapid sleep

onset was achieved on the night immediately prior, and the response cost procedure repeated if the child does not fall asleep quickly.

The rules are applied on successive nights until the child's sleep onset is "faded" toward a predetermined bedtime goal. Although no

randomized, large-group comparison studies have assessed this intervention, Kuhn and Elliott classified this technique as promising

and deserving of further study.[26]

Drug treatment of sleeplessness in infants and younger children has received limited scientific study despite seemingly common use

of both prescription and nonprescription agents in this population. In one report, one-quarter of firstborn English children had been

given sedatives by 18 months of age.[28] In a German survey of pediatricians, psychiatrists, and primary care providers, sleep

problems were the most common reason for prescribing medicine to infants up to 1 year of age, accounting for 35% of prescriptions in

this age group.[29] Several placebo-controlled trials have suggested short-term efficacy of trimeprazine for treatment of night waking in

children aged 12 through 24 months[30] and 12 through 36 months.[31] Use of nonprescription agents such as melatonin and

diphenhydramine and prescription agents such as short-acting hypnotic agents has not been the subject of controlled studies in healthy

young children. Reports of efficacy using these agents for younger children are largely anecdotal apart from limited experience in the

treatment of youngsters with developmental disabilities.[24,32]

Normal Sleep in Older Children and Adolescents

The sleep of older children continues to evolve with advancing age but at a more modest pace compared with the dramatic changes

seen during the first years of life. During the early school-age and preadolescent years, average nighttime sleep requirements decline

from 11.1 hours at 5 years of age to 10.2 hours by age 9.[2] Sleep architecture continues to mature as well, with gradually declining


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amounts of deep NREM sleep, increasing proportion of stage 2 sleep, and constant proportions of stage REM between the ages of 6

and 11.[33]

Healthy preadolescent children are typically highly alert, with little or no daytime sleepiness as measured by multiple sleep latency

testing (MSLT). Indeed, mean sleep latency on the MSLT for preadolescent children averages 19 ± 1.6 minutes[34,35] in contrast to the

10- to 20-minute range considered normal for healthy adults.[36] Significant daytime sleepiness is highly unusual in healthy

preadolescents, and chronic or recurrent sleepiness at this age is usually strongly indicative of a serious underlying sleep disorder.

During the adolescent years, average nighttime sleep declines from an average of 9.0 hours at age 13 years to 7.9 hours at age 16.[2]

Sleep architecture completes its transition to a mature adult form with a 40% decrease in the amount of slow-wave sleep between the

ages of 10 and 20 years and modest increases in light NREM sleep.[35,37] Daytime sleepiness increases significantly during

adolescence even when total sleep time remains constant, suggesting that the need for sleep does not decline at this age and may in

fact increase.[38] Finally, a tendency toward delayed circadian phase becomes evident during adolescence, with both bedtime and

waking time usually being later on non-school nights compared with school nights.

Insomnia in Older Children and Adolescents

Subjectively reported sleep problems remain common during the school-age and adolescent years. In one large survey studying sleep

problems affecting 5- to 12-year-old children, bedtime resistance was reported in 27%, sleep-onset delays in 11.3%, and excessive

night waking in 6.5%.[39] The high frequency of insomnia in older children and adolescents is accompanied by concerningly high

prevalence of daytime somnolence as well. Several surveys of school-age children have reported excessive sleepiness in 17% to

21% of subjects.[39,40] In a survey of 10- to 13-year-old early adolescents, 13% reported actually falling asleep in school at least once

in the present school year.[35]

Although sleep problems such as cosleeping, night waking, and sleep-onset association disorder become less frequent in older

children and adolescents, bedtime resistance remains common and insomnia becomes common as children grow older. Several

important developmental influences have a direct bearing on these phenomena. First is the fact that children typically gain increasing

autonomy in setting their bedtime as they grow older. This often results in later bedtimes, irregular sleep schedules, and suboptimal

sleep hygiene, which often disrupt sleep onset or sleep quality. In addition, the physiological tendency toward delayed circadian phase

that develops during later childhood may make it difficult for the older child or adolescent to fall asleep at the time necessary to permit

sufficient sleep on school nights, with resultant complaints of nighttime insomnia and daytime tiredness.

Delayed sleep phase syndrome (DSPS) is the most common circadian disorder in adolescents,[41,42] and most adults with the

condition report onset of symptoms during childhood or adolescence.[26] DSPS may be diagnosed when delayed circadian phase is

sufficient to cause sustained and clinically significant impairment of daytime function in the form of oversleeping, somnolence, or

disrupted sleep schedule. Youngsters with DSPS typically present with complaints of insomnia and substantially delayed sleep onset

accompanied by difficulty or inability to wake at an appropriate time the following morning. DSPS is often accompanied by daytime

napping, which further retards timely sleep onset at night, and by late waking on non-school days, which may act to reinforce the

abnormally delayed circadian phase.[37] DSPS can be mimicked or worsened by comorbid problems such as school avoidance or

voluntary participation in stimulating late-night activities.

Psychophysiological insomnia is observed less commonly in older children and adolescents than in adults. When present, the patient's

insomnia is usually accompanied by identifiable rumination or performance anxiety regarding sleep. This emotional state attains

sufficient duration and intensity that wakefulness is maintained for long periods following bedtime, resulting in negative sleep

associations. Insufficient nighttime sleep in older children can be the result of other identifiable sleep disorders or occur as a primary

problem when insufficient time is allotted for nighttime sleep. Only limited data are presently available regarding the neurobehavioral

effects of insufficient sleep. Modest reductions of nighttime sleep from baseline, averaging only 30 minutes for 3 nights, was

accompanied by significant declines in objective measures of neurobehavioral function in one group of elementary school children.

Among a group of older adolescents, restricting sleep to 5 hours nightly for 1 week was accompanied by progressive and substantial

decreases in mean sleep latency, suggesting that consistently insufficient sleep may cause a cumulative impairment of daytime

alertness that may not plateau over time.[38]

Treatment of Insomnia in Older Children and Adolescents

Effective treatment of insomnia in older children and adolescents begins with accurate identification of all pertinent contributory

influences. It is not unusual to identify multiple concurrent predisposing factors, each deserving of treatment. For example, a teenager

who presents with an isolated complaint of insomnia may be found to have simultaneous bedtime resistance, poor sleep hygiene, and

delayed sleep phase.

Treatment of bedtime resistance for the older child differs from the extinction techniques typically used for younger children. Treatment

instead relies on enforcement of a bedtime appropriate for the child's age and individual sleep needs. Appropriate limits must be set

for disruptive behaviors such as stalling or emotional agitation. As in younger children, consistent limit-setting is crucial for effective

treatment of bedtime resistance. Any suboptimal aspects of general sleep hygiene should also be addressed to the extent possible.


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Maintenance of a regular sleep schedule and avoidance of daytime napping should be encouraged. Potentially disruptive influences

such as watching television or listening to music while in bed should be avoided. Use of caffeinated beverages, vigorous exercise, and

excessively stimulating activities should be avoided during the evening time hours. Although a recommendation to maintain a fixed

bedtime and waking time 7 days weekly is usually received less than enthusiastically by an adolescent, it is often possible to improve

compliance by working with patient and parents to implement age-appropriate incentives or by developing a "contract" that offers

increasing flexibility of bedtime schedule on non-school nights after specified milestones are met. Elements of psychophysiological

insomnia may be addressed in the same fashion used for adult patients. Stimulus control techniques, sleep restriction, and

biofeedback have demonstrated some efficacy in adults but have not been rigorously studied in children.[37]

Treatment of DSPS in the older child and adolescent is often challenging due to the normal tendency toward circadian delay that

develops in this age group and the fact that later bedtimes and waking times on non-school nights may additionally reinforce this delay.

Secondary gain may be an additional reinforcing factor in some children, particularly when youngsters intentionally delay bedtime in an

attempt to preclude or limit parental supervision of late-night entertainment or recreational activities. Correction of delayed sleep phase

is usually achieved by gradual realignment of the patient's sleep period in a stepwise fashion toward a desired target schedule

appropriate for the patient's age and school schedule. In some cases, this realignment can be achieved through consistent stepwise

advances of bedtime and waking time by 10 to 15 minutes nightly. In severe or refractory cases, more rapid correction may be

achieved via progressive delays in bedtime and waking time, a process also known as chronotherapy.[37,43] In this process, bedtime

and waking time are delayed by 2 to 3 hours nightly until the target bedtime is reached.

After the target sleep schedule has been achieved, maintaining the desired schedule typically requires additional time and effort.

During the first weeks following schedule correction, even a few days of delayed bedtime and/or waking time may be sufficient to

cause the sleep schedule to revert to its prior pattern. Therefore, rigorous adherence to the target sleep schedule 7 days weekly is

crucial in minimizing the chance of relapse. After several weeks of strict adherence (longer in particularly severe or refractory cases),

some flexibility in bedtime and waking time on non-school nights may be reintroduced, although sleeping beyond 1 or 2 hours after the

usual wake-up time should be avoided.[37]

Light therapy has been reported to be effective in the treatment of DSPS and other circadian rhythm disorders in adults.[44] Use of light

therapy in children has received little formal study, so optimal timing and intensity of light exposure in this age group remains unknown.

The author's practice is to use light therapy as adjunctive treatment for DSPS, beginning with 10,000 lux for 30 minutes on morning

waking with further titration based on clinical response.

Drug treatment of insomnia in older children and adolescents has received little formal study despite seemingly frequent off-label use

of medications for this purpose. In a survey of 671 primary care physicians in the United States, 34.1% had recommended

antihistamines, 24.9% had recommended melatonin, and 22.2% had recommended herbal preparations at least once for teenage

patients within the prior 6 months.[45] In several large French surveys, 10 to 12% of adolescents reported use of medication for

disrupted sleep.[46,47] In the only large, double-blind, placebo-controlled study assessing drug treatment of pediatric insomnia, use of

5 mg of melatonin at 7:00 PM significantly advanced sleep onset by 57 minutes among 62 school-age children with chronic idiopathic

insomnia.[48] In a smaller retrospective survey, prebedtime use of melatonin at an average dosage of 2 mg was associated with partial

to complete improvement of insomnia in 32 children.[49] Most reports of melatonin use in children have consisted of case reports and

uncontrolled clinical trials using doses ranging from 0.3 mg through 20 mg.[32]

Numerous other medications are used off-label for treating insomnia in children despite a significant lack of formal study in this age

group. These range from nonprescription agents such as diphenhydramine and other antihistamines to prescription agents such as

chloral hydrate, benzodiazepines, neuroleptics, tricyclic antidepressants, α-agonists, and the newer short-acting hypnotics. Their routine

use for treating childhood insomnia cannot be recommended until further controlled studies have been performed to document safety

and efficacy in this age group.

NREM Arousal Parasomnias in Children

Sleepwalking, confusional arousals, and night terrors are the major childhood parasomnias that are thought to result from incomplete

arousal from sleep ( ). Such arousals, usually arising from deep NREM sleep, may cause a spectrum of nocturnal behaviors ranging

from quiet sitting or ambulation to violent degrees of agitation. Partial arousal parasomnias tend to occur during the first third of

nighttime sleep, during the time of predominant slow-wave sleep, and may increase in frequency as a result of sleep deprivation or

other stressors. It is usually difficult to alert or awaken a child during these events, and affected children typically demonstrate little or

no independent recollection of these episodes the following day. There is a family history of partial arousals in up to 60% of cases,

suggesting strong genetic influences on this family of parasomnias.[50,51]

Table 1. Table 1. Classification of Common Pediatric Parasomnias


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Episodes of sleepwalking in children usually consist of quiet, nonagitated ambulation lasting several minutes. Sleepwalking is often

difficult to distinguish from drowsy wakefulness, and semipurposeful activity such as voiding next to the toilet is sometimes observed.

Occasional sleepwalking is very common in children, with an overall prevalence of 40% in one large series of 6- to 16-year-olds,

although only 2 to 3% of patients in this series exhibited more than one episode monthly. The prevalence of sleepwalking declines after

age 10, although 3.3% of 13-year-olds still exhibited some degree of sleepwalking in another large series.[52]

Although the terms "confusional arousal" and "night terror" are sometimes used synonymously to describe agitated partial arousals in

children, some authors have suggested a distinction between the two conditions.[50,53] Confusional arousals are most commonly seen

in toddlers and early school-age children. Episodes often evolve gradually, commencing with crying or calling out to parents followed by

overt confusion or inconsolable agitation that may last 30 minutes or more. In contrast, night terrors are characterized by precipitous

onset of screaming or extreme agitation, usually in older children or adolescents. Night terrors typically last only a few minutes, but may

be accompanied by thrashing movements, running, or other potentially hazardous motor activity. Events are usually accompanied by

visible signs of "sympathetic storm" including significant tachycardia or diaphoresis. Agitated arousals of all types are common in

children, affecting 17.3% of children between 3 and 13 years of age in one large recent Canadian study.[52]

Treatment of NREM arousal parasomnias has received little formal study in children. Despite this, the obvious potential for

sleepwalking or night terrors to cause injury necessitates that the families of affected children take measures to safeguard the

sleeper's environment. This can usually be accomplished via a combination of parental watchfulness and other safety measures

designed to limit a sleepwalker's access to balconies, exterior doors, and other potentially hazardous areas inside and outside the

household. Use of alarms or deadbolt locks on exterior doors is sometimes appropriate but must be implemented in a fashion that

does not compromise safety and rapid egress in case of emergencies. Families should also be instructed to maintain a safe

environment when affected children are sleeping away from home. In addition to appropriate safety measures, use of scheduled

awakenings may be an effective treatment for childhood sleepwalking and night terrors.[54,55] In particularly severe cases, use of

low-dose clonazepam or tricyclic antidepressants may be appropriate and effective.[50,56,57]

Other Parasomnias in ChildrenNocturnal Enuresis

Nocturnal enuresis most commonly presents as a primary sleep disorder in otherwise healthy children who are unable to establish

consistent nighttime continence by ~5 years of age. Enuresis is extremely common, affecting 15.7% of children between 3 and 13

years of age in one large study.[52] Enuresis persisted at the age of 13 in only 2.0% of patients, suggesting that the condition remits

spontaneously for most affected children with advancing age. The cause of primary enuresis is unknown, although is has been

postulated that it may result from deficient arousal from sleep, maturational lags, reduced functional bladder capacity, or genetic

influences.[58] Serious underlying neurological and urologic causes are uncommon. Behavioral interventions are often effective,

including scheduled voidings, wetness alarms, and bladder training exercises. Successful use of desmopressin and imipramine have

also been reported, but these agents are ideally used within the context of a comprehensive and closely supervised treatment

program.[59]

Nightmares

Nightmares in children are thought to result from awakening during REM sleep, usually with vivid recall of distressing dream imagery

resulting in agitation. Although nightmares may superficially resemble night terrors, the fact that affected children are awake,

consolable, and can describe dream content usually helps distinguish nightmares from NREM partial arousals. Nightmares most often

occur during the second half of the night, when REM periods are longest and most prevalent. Occasional nightmares in children are

thought to be common, with a prevalence of 57.6% in one large survey studying the sleep of 5- to 7-year old Swedish children.[60]

Although "bad dreams" seldom require medical evaluation for the great majority of affected children, the presence of excessively

frequent nightmares or dreams with particularly violent content may signal a need for further psychological investigation.

Sleep-Related Movement Disorders in Children


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Rhythmic movement disorder (RMD) is characterized by recurrent, well-stereotyped episodes of rhythmic motor activity that are

associated with sleep, usually occurring during drowsiness or light NREM sleep but sometimes during wakefulness as well.[61] The

movements may involve the head, trunk, and limbs either alone or in combination at a typical frequency of 0.5 to 2 Hz (Fig. 1). Several

distinct variations have been described, including head banging (jactatio capitis nocturna) and body rocking, in which affected children

rise upon the hands and knees while vigorously rocking the entire body in an anteroposterior direction.

Figure 1.

Thirty-second polysomnogram epoch documenting rhythmic movement disorder in a 4-year-old girl. Rhythmic activity is clearly evident

on all electroencephalogram (EEG) and electromyogram (EMG) leads during a period of head banging recorded during wakefulness,

as indicated by black arrows. Activity on the snore channel reflects the synchronous vocalizations commonly seen in this condition

rather than snoring. Channels are as follows: electrooculogram (left, right), chin EMG, EEG (left central, right central, left occipital, right

occipital), electrocardiogram (two leads), limb EMG (left arm, right arm, left leg, right leg), snoring, airflow (oral, nasal-oral), respiratory

effort (thoracic, abdominal), nasal pressure, oxygen saturation.

Although rhythmic motor activity during drowsiness and light sleep is observed in a majority of infants, this usually subsides

spontaneously by 5 years of age. Rhythmic movements persisted for 6% of 5-year-olds in one series and body rocking persisted in

3% of 13-year-olds in another series.[52,62] Rhythmic movement disorder most commonly affects otherwise healthy children but may

also be seen in association with autism and other developmental disabilities. For most affected children, RMD is a self-limited condition

that does not require treatment. For youngsters exhibiting particularly violent movements, use of protective padding in the crib or bed is

often helpful. Successful treatment using clonazepam, citalopram, and behavioral modification techniques has also been reported.[61]

Restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) have only recently been identified as affecting children.

The precise prevalence of RLS in children remains uncertain, but several studies suggest that symptoms of RLS may be common in

children. One survey of 138 adults with RLS identified onset of symptoms by age 20 in 43% and by age 10 in 18%, suggesting that

childhood onset may be more common than generally recognized.[63] In a survey completed by parents of 866 children attending

general pediatrics clinics, restlessness of the legs in bed was reported for 17% of children aged 2.0 to 13.9 years.[64] The clinical

features, known comorbidities, and available treatment for RLS and PLMD in children are comparable to those for adults. These are

reviewed by Lesage and Hening elsewhere in this issue. One pediatric aspect of RLS /PLMD that deserves brief elaboration is

emerging evidence of an association between PLMD and neurobehavioral problems in children.[65] Some studies have suggested that

attention-deficit/hyperactivity disorder (ADHD) is overrepresented in children with PLMD, including one retrospective assessment of

129 children with moderate to severe PLMD where 117 (90%) of subjects carried a comorbid diagnosis of ADHD.[66] Conversely, there


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is more limited evidence that PLMD may be more common among children with ADHD. In one study of 14 consecutive children with

newly diagnosed ADHD (DSM-IV criteria), nine patients (64%) exhibited over five PLMs per hour of sleep on PSG, as opposed to no

patients among the age- and sex-matched controls (P < 0.0015).[67] Further research is required to more fully define the potential

relationship between RLS/PLMD and daytime neurobehavioral symptoms.

Sleep-Related Breathing Disorders in Children

The first modern description of obstructive sleep apnea hypoventilation syndrome (OSAHS) in children dates from 1976, in a report of

eight children presenting with snoring and variable daytime symptoms including headache and somnolence.[68] Like obstructive sleep

apnea (OSA) in adults, childhood OSAHS is characterized by recurrent episodes of partial or complete airway obstruction during sleep,

often accompanied by oxyhemoglobin desaturation or hypercarbia. Unlike adults, however, children are more likely to exhibit periods of

prolonged partial airway obstruction rather than discrete events such as apneas and hypopneas.[69-71] Prolonged partial airway

obstruction sometimes takes the form of obstructive hypoventilation, in which pulmonary ventilation falls below the level necessary to

maintain normocapnea, even when normal oxygen saturation is maintained. Upper airway resistance syndrome (UARS), in which

abnormally high upper airway resistance leads to increased respiratory effort and disrupted sleep even in the absence of gas exchange

abnormalities, has also been described in children.[72]

It is estimated that between 10 and 12% of children snore habitually and that between 1 and 3% of children suffer from OSAHS.[73-77]

The prevalence of UARS in children remains unknown. Obstructive sleep apnea hypoventilation syndrome may present at any age

during childhood, with peak incidence between 2 and 5 years of age, when adenotonsillar hyperplasia is most common.[78] Prevalence

of OSAHS is equal in boys and girls until adolescence, when a male preponderance becomes strikingly evident.[73,76,79] Obesity is

less strongly associated with OSAHS in children than in adults. Craniofacial abnormalities (e.g., cleft palate, choanal atresia,

macroglossia) may be associated with increased risk of OSAHS. Other genetic and neurological conditions may also be associated

with increased risk, most notably Down syndrome, in which at least one-third of children are affected.[80,81]

The clinical features of OSAHS in children overlap only partially with those exhibited by adults ( ). Snoring is almost universal in affected

children. Other common nighttime symptoms include prominent mouth breathing, unusual sleeping positions, excessive perspiration,

and refractory enuresis.[82] Symptoms upon waking often include transient grogginess, headache, or sore throat. In contrast to adults,

however, daytime somnolence is seldom a prominent complaint.[83] When present, somnolence is often intermittent or tends to occur

during sedentary activities such as reading or riding in an automobile. Many recent reports support the premise that even childhood

sleep-related breathing disorders (SRBDs) of mild severity may be associated with attentional, behavioral, and learning problems.

Habitual snoring has been reported to be three times as frequent in children with ADHD compared with control groups drawn from child

psychiatry and general pediatrics clinics.[84] In a study of 297 first-grade children with poor academic achievement, 54 (18.1%)

exhibited either significant hypoxemia or hypercapnia during limited overnight monitoring.[85] Of these, the 24 children treated with

adenotonsillectomy exhibited significant academic improvement (P < 0.01) compared with the untreated children.

Table 2. Table 2. Features of Sleep-Related Breathing Disorders in Children Compared with Adults

Physical examination of children with SRBDs is often normal. Tonsillar hypertrophy, although common, is neither necessary nor

sufficient for the diagnosis of SRBDs. Adenoid facies (long face syndrome), daytime mouth breathing, or micrognathia may be

apparent. Elevated blood pressure may be occasionally evident in affected children.[86]

Because full polysomnography in children is both costly and time-consuming, inexpensive and easily administered screening

measures have long been sought. Screening tests such as home audiotapes[87] and overnight oximetry[88] have demonstrated only

limited sensitivity for detection of SRBDs in children. A recently developed Pediatric Sleep Questionnaire has demonstrated sensitivity

of 0.81 to 0.85 and specificity of 0.87 for the prediction of SRBDs in a clinical research environment but has not been validated for use

outside this setting.[89] Polysomnography in children monitors at minimum the same respiratory, cardiac, and neurophysiological data

measured in adult PSGs. End-tidal or transcutaneous CO2 monitoring is sometimes added to augment the sensitivity of the study when

hypoventilation is suspected (Fig. 2). Esophageal pressure monitoring may be used selectively when increased upper airway

resistance or prolonged partial airway obstruction is suspected.[90] Interpretation of the pediatric polysomnogram differs from that of

adults. Although scoring of sleep stages and arousals is performed in the manner used for adult studies,[91] there exist no universally


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accepted pediatric standards for the scoring and interpretation of respiratory disturbances. Some centers score apnea according to

adult criteria, which typically require a minimum duration of 10 seconds. Other centers score apneas that exceed the length of two

respiratory cycles, which is often less than 10 seconds due to the high respiratory rates seen normally in young children. In addition,

there is no consensus on the definition of hypopnea in children.

Figure 2.

Thirty-second epoch from the polysomnogram of a 10-year-old girl with mitochondrial myopathy documenting hypoventilation. Elevated

end-tidal carbon dioxide (ETCO2) levels of 66 to 68 Hg and low oxyhemoglobin saturations of 79 to 81% are demonstrated on adjacent

channels, indicated by arrows. Channels are as follows: electrooculogram (left, right), chin EMG, EEG (left central, right central, left

occipital, right occipital), electrocardiogram, limb EMG (left leg, right leg), snoring, nasal-oral airflow, respiratory effort (thoracic,

abdominal), nasal pressure, capnogram, average ETCO2, oxygen saturation.

Despite the present lack of uniformity regarding how respiratory events are defined and scored for children, it has been convincingly

argued that adult criteria for the diagnosis of OSA frequently fail to identify children with clinically significant obstruction.[92] Alternative

polysomnographic norms for children have been proposed, based on data from 50 normal children, suggesting that more than one

obstructive apnea per hour of sleep is statistically abnormal for healthy children.[93] Norms defining a threshold rate or severity of

respiratory disturbance associated with clinically significant sleep disruption, however, have not been established for children.

Treatment of SRBDs in children has received remarkably little formal study. This is in large part due to the fact that the most common

treatment, adenotonsillectomy, is usually recommended solely on the basis of clinical symptoms without preoperative

polysomnography to document whether sleep-disordered breathing is unequivocally present. Available data suggest that

adenotonsillectomy results in an improved respiratory index for most children with OSAHS, with improvement apparent as soon as the

first postoperative night.[94] In one study of 26 children having a preoperative respiratory disturbance index (RDI) of at least five apneas

per hour, all exhibited a lower RDI upon follow-up polysomnography at least 6 weeks after adenotonsillectomy.[95] Despite this

improvement, four children (15%) continued to have RDIs exceeding five events per hour, suggesting that a substantial minority of

treated patients may still experience residual obstruction. Continuous positive airway pressure (CPAP) is used to treat SRBDs in

children without significant adenotonsillar obstruction and those children having residual upper airway obstruction despite surgery.

Effectiveness of CPAP has been documented for children of all ages,[96-98] although maintaining compliance can be challenging for

parents and medical providers. Uvululopalatopharyngoplasty is performed only occasionally for children[99,100] and tracheostomy is

used as a last resort for the treatment of severe, refractory OSAHS.[101]


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Reprint Address

Timothy F. Hoban, M.D., Department of Pediatrics, L3227 Women's Hospital, 1500 East Medical Center Drive, Ann Arbor, MI48109-0203

Semin Neurol. 2004;24(3) © 2004 Thieme Medical Publishers

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