CHAPTER 22 Sleep and Sleep Disorders in Children
NORMAL SLEEP IN INFANTS, CHILDREN, AND ADOLESCENTS
Although sleep in neonates and infants is quite different from that in adults, the structure of children’s sleep and sleep-wake patterns begin to resemble those of adults as they mature.1 In terms of sleep architecture, there is a dramatic decrease in the proportions of both rapid eye movement (REM) sleep and slow-wave sleep (delta or deep sleep) from birth through childhood to adulthood. Sleep cycles during the nocturnal sleep period (known as the ultradian rhythm of sleep) lengthen, which results in fewer spontaneous arousals. Several general trends in the maturation of sleep patterns over time have also been identified. First, there is a decrease in the 24-hour average total sleep duration from infancy through adolescence, with a less marked and more gradual continued decrease in nocturnal sleep amounts into late adolescence.2 This decline includes a decrease in nocturnal sleep throughout childhood, as well as a significant decline in daytime sleep (scheduled napping) between 18 months and 5 years. There is also a gradual but marked circadian-mediated shift to a later bedtime and sleep onset time that begins in middle childhood and accelerates in early to middle adolescence. Finally, sleep-wake patterns on school nights and nonschool nights become increasingly irregular from middle childhood through adolescence. However, sleep patterns also reflect the complex combined influence of biological, environmental, and cultural factors and thus may differ substantially across different cultures and in different contexts.3 The following section provides a more detailed description of normal sleep behaviors and patterns in different age groups.
Sleep in Newborns
Newborns sleep approximately 16 to 20 hours per day, generally in 1- to 4-hour periods asleep followed by 1- to 2-hour periods awake, and sleep amounts during the day are approximately equal to the amount of nighttime sleep. Sleep-wake cycles are largely dependent on hunger and satiety; for example, bottle-fed babies generally sleep for longer periods (3 to 5 hours) than do breastfed babies (2 to 3 hours). Newborns have two sleep state that are essentially analogous to adult REM and non-REM sleep: active (“REM-like,” characterized by smiling, grimacing, sucking, and body movements; 50% of sleep) and quiet (“non-REM-like”), as well as a third “indeterminate” state. Unlike adults and older children, newborns and infants up to the age of approximately 6 months enter sleep through the active or REM-like state.4
Sleep in Infants (Aged 1 to 12 months)
Infants generally sleep about 14 to 15 hours per 24 hours at age 4 months and 13 to 14 hours total at age 6 months; however, there appears to be a very wide intraindividual variation in parent-reported 24-hour sleep duration in the first year of life.2 Sleep periods last about 3 to 4 hours during the first 3 months and extend to 6 to 8 hours by the age of 4 to 6 months. Most infants between 6 and 12 months of age nap a total of 2 and 4 hours, divided into two naps, per day.5
Two important developmental “milestones” are normally achieved during the first 6 months of life; these are known as sleep consolidation and sleep regulation.6 Sleep consolidation is generally described as an infant’s ability to sleep for a continuous period of time that is concentrated during the nocturnal hours, augmented by shorter periods of daytime sleep (naps). Infants develop the ability to consolidate sleep between ages 6 weeks and 3 months, and approximately 70% to 80% of infants achieve sleep consolidation (i.e., “sleeping through the night”) by age 9 months. Sleep regulation is the infant’s ability to control internal states of arousal in order both to fall asleep at bedtime without parental intervention or assistance and to fall back asleep after normal brief arousals during the night. The capacity to self-soothe begins to develop in the first 12 weeks of life and is a reflection of both neurodevelopmental maturation and learning. However, the developmental goal of independent self-soothing in infants at bedtime and after night awakenings may not be shared by all families, and voluntary or lifestyle sharing of bed or room by infants and parents is a common and accepted practice in many cultures and ethnic groups. Sleep behavior in infancy, in particular, must also be understood in the context of the relationship and interaction between child and caregiver, which greatly affects the quality and quantity of sleep.7,8
Sleep in Toddlers (Aged 12 to 36 months)
Toddlers sleep about 12 hours per 24 hours. Napping patterns generally consist of ½ to 3½ hours per day, and most toddlers give up a second nap by age 18 months. During this stage, both developmental and environmental issues begin to have more of an effect on sleep; examples include the development of imagination, which may result in increased nighttime fears; an increase in separation anxiety, which may lead to bedtime resistance and problematic night awakenings; an increased understanding of the symbolic meaning of objects, which can lead to increased interest in and reliance on transitional objects to allay normal developmental and separation fears; and an increased drive for autonomy and independence, which may result in increased bedtime resistance. Sleep problems in toddlers are very common, occurring in 25% to 30% of this age group; bedtime resistance occurs in 10% to 15% of toddlers, and night awakenings occur in 15% to 20%.9,10
Sleep in Preschoolers (Aged 3 to 5 years)
Preschool-aged children typically sleep about 11 to 12 hours per 24 hours; most children give up napping by 5 years, although approximately 25% of children continue to nap at age 5, and there is some evidence that napping patterns and the preservation of daytime sleep periods into later childhood may be influenced by cultural differences.11 Difficulties falling asleep and night awakenings (15% to 30%) are still common in this age group, in many cases coexisting in the same child.12 Developmental issues affecting sleep include expanded language and cognitive skills, which may lead to increased bedtime resistance, as children become more articulate about their needs and may engage in more limit-testing behavior; a developing capacity to delay gratification and anticipate consequences, which enables preschoolers to respond to positive reinforcement for appropriate bedtime behavior; and increasing interest in developing literacy skills, which reinforces the importance of reading aloud at bedtime as an integral part of the bedtime routine. Bedtime routines and rituals, use of transitional objects, and sleep-wake schedules are all important sleep-related issues at this developmental stage.
Sleep in Middle Childhood (Aged 6 to 12 years)
Most children this age sleep between 10 and 11 hours a night. It is important to note that the presence of daytime sleepiness in an elementary school-aged child is likely to be indicative of significant sleep problems that cause insufficient or poor quality sleep, because of the high level of physiological alertness during the day that is characteristic of school-aged children. Middle childhood is also a critical time for the development of healthy sleep habits. Increasing independence from parental supervision and a shift in responsibility for health habits as children approach adolescence may result in less enforcement of appropriate bedtimes and inadequate sleep duration; parents may also be less aware of sleep problems if they do exist. Although sleep problems were previously believed to be rare in middle childhood, studies have revealed an overall prevalence of significant parent-reported sleep problems of 25% to 40%, ranging from bedtime resistance to significant sleep onset delay and anxiety at bedtime.13,14
Sleep in Adolescents (Aged 12 to 18 years)
Although a number of significant sleep changes occur in adolescence, adolescents’ sleep needs do not differ dramatically from those of preadolescents, and optimal sleep amounts remain at about 9 to 9¼ hours per night. However, a number of studies across different environments and in different cultures have suggested that the average adolescent typically sleeps about 7 hours or less per night15 and that this accumulating sleep debt may have a significant effect on functioning, performance, and quality of life. Biologically based pubertal changes also significantly affect sleep. In particular, around the time of onset of puberty, adolescents develop as much as a 2-hour sleep-wake “phase delay” (later sleep onset and waking times) in relation to sleep-wake cycles in middle childhood.16 Environmental factors and lifestyle/social demands, such as homework, activities, and after-school jobs, also significantly affect sleep amounts in adolescents, and early start times of many high schools may contribute to insufficient sleep. There is significant weekday/weekend variability in sleep-wake patterns in adolescents, often accompanied by weekend oversleep in an attempt to address the chronic sleep debt accumulated during the week; this further contributes to decreased daytime alertness levels. All of these factors often combine to produce significant sleepiness in many adolescents and consequent impairment in mood, attention, memory, behavioral control, and academic performance.17,18
NEUROBEHAVIORAL AND NEUROCOGNITIVE EFFECT OF INADEQUATE AND DISRUPTED SLEEP IN CHILDREN
There is clear evidence from both experimental laboratory-based studies and clinical observations that insufficient and poor quality sleep result in daytime sleepiness and behavioral dysregulation and affect neurocognitive functions in children, especially the functions involving learning and memory consolidation and those associated with the prefrontal cortex (e.g., attention, working memory, and other executive functions).19 Indeed, positron emission tomographic scans of sleep-deprived adults show decreased glucose metabolism in the prefrontal cortex, similar to the changes in neural function seen in attention-deficit/hyperactivity disorder (ADHD). Sleep loss and sleep fragmentation are known to directly affect mood (increased irritability, decreased positive mood, poor affect modulation). Behavioral manifestations of sleepiness in children are varied and range from those that are classically “sleepy,” such as yawning, rubbing eyes, and/or resting the head on a desk, to externalizing behaviors, such as increased impulsivity, hyperactivity, and aggressiveness, to mood lability and inattentiveness.20 Sleepiness may also result in observable neurocognitive performance deficits, including decreased cognitive flexibility and verbal creativity, poor abstract reasoning, impaired motor skills, decreased attention and vigilance, and impaired memory.21,22
Clinical experience, as well as empirical evidence from numerous studies and case reports, have demonstrated that childhood sleep disorders both arising from intrinsic processes, such as obstructive sleep apnea syndrome (OSAS), and those related to extrinsic or environmental factors, such as behavioral insomnia of childhood (sleep onset association type and limit-setting type) and insufficient sleep, may manifest primarily with daytime sleepiness and neurobehavioral symptoms. The pediatric sleep disorders that have been most frequently studied from this perspective include sleep-disordered breathing (SDB) (i.e., OSAS and snoring), and restless legs syndrome (RLS)/periodic limb movement disorder (PLMD). For example, a higher prevalence of parent-reported externalizing behavior problems, including impulsivity, decreased attention span, hyperactivity, aggression, and conduct problems has been frequently reported in studies of children with either polysomnographically diagnosed OSAS or symptoms suggestive of sleep-disordered breathing, such as frequent snoring.23,24 Investigators who have compared neuropsychological functions in children with OSAS have found impairments on tasks involving reaction time and vigilance, attention, executive functions, motor skills, and memory. Although some studies have documented significant short-term improvement in daytime sleepiness, behavior, and academic performance25 after treatment (usually adenotonsillectomy) for OSAS/SDB, other studies have suggested that young children with SDB may continue to be at high risk for poor academic performance several years after the symptoms have resolved.26 Alternatively, the prevalence of SDB symptoms in children with identified behavioral and academic problems has also been examined in several studies; overall, these studies have revealed an increased prevalence of snoring in young children with behavioral and school concerns, which is suggestive of an approximately twofold increased risk of habitual snoring and SDB symptoms in children with high scores on behavior problem scales.27
Significant neurobehavioral consequences may also occur in relation to RLS/PLMD and, as described in several studies, may manifest with a symptom constellation similar to that of ADHD.28,29 A number of studies have revealed an increased prevalence of periodic limb movements on polysomnography in children referred for ADHD; furthermore, treatment of these children with dopamine antagonists has been shown to result not only in improved sleep quality and quantity but also in improvement in “attention deficit/hyperactivity” behaviors previously resistant to treatment with psychostimulants.30
Other postulated health outcomes of inadequate sleep in children include potential deleterious effects on the cardiovascular, immune, and various metabolic systems, including glucose metabolism and endocrine function, and an increase in accidental injuries.31 In addition, studies have documented secondary effects on parents (e.g., maternal depression), as well as on family functioning.32
COMMON SLEEP DISORDERS IN CHILDREN: ETIOLOGY, EPIDEMIOLOGY, PRESENTATION, EVALUATION, AND TREATMENT
Sleep-Disordered Breathing and Obstructive Sleep Apnea Syndrome
SDB in childhood includes a spectrum of disorders that vary in severity, ranging from OSAS to primary snoring (snoring without ventilatory abnormalities).33–35 The prevalence is also variable, from 1% to 3% of children with OSAS to 10% of children with habitual snoring. The basic pathophysiological process of OSAS involves cessation of airflow through the nose and mouth during sleep (pathological duration of an apnea is determined by age-appropriate norms) despite respiratory effort and chest wall movement; this disrupts normal ventilation during sleep, resulting in hypoxemia and/or hypoventilation and a sleep pattern characterized by frequent arousals.36 Common manifestations of SDB in childhood include loud, nightly snoring; choking/gasping arousals; and increased work of breathing characterized by nocturnal diaphoresis, paradoxical chest and abdominal wall movements, and restless sleep. However, as noted previously, SDB may manifest primarily with neurobehavioral symptoms, including inattention and poor academic functioning. Although repeated episodes of nocturnal hypoxia probably constitute an important etiological factor for neurobehavioral deficits in OSAS, sleep fragmentation resulting from frequent nocturnal arousals, which in turn leads to the daytime sleepiness, is also believed to play a key role.
Specific physical examination findings (growth abnormalities such as obesity or failure to thrive, nasal obstruction with hyponasal speech and “adenoidal facies” or mouth breathing, enlarged tonsils) may raise suspicion of OSAS. However, the presence of large tonsils and adenoids does not necessarily mean the patient has OSAS, and there is in fact no constellation of presenting symptoms and physical findings that have reliably been found to differentiate between OSAS and primary snoring in the ambulatory setting.37 Overnight polysomnography remains the “gold standard” for evaluating pediatric SDB; it documents physiological variables during sleep, including sleep stages and arousals (electroencephalographic montage, eye movements, chin muscle tone), cardiorespiratory parameters (air flow, respiratory effort, oxygen saturation, transcutaneous or end-tidal CO2, and heart rate), and limb movements and allows for both confirmation of the diagnosis and assessment of severity of OSAS.
Adenotonsillectomy is generally the first line of treatment for pediatric SDB, although adenoidectomy alone may not be curative when other risk factors such as obesity are present.38 Adenoids may also “grow back” as the result of continued hypertrophy of residual adenoidal tissue after surgery. Reported cure rates after adenotonsillectomy range from 75% to 100% in normal healthy children. Nutrition and exercise counseling should be a routine part of treatment for SDB in obese children. Continuous Positive airway pressure, the most common treatment for OSAS in adults, can be an effective and reasonably well-tolerated treatment option for those children and adolescents for whom surgery is not an option or in children who continue to have OSAS despite surgery.39,40 Little is known about the efficacy of other treatment modalities, such as oral appliances, palatal/pharyngeal surgery, or other noninvasive techniques such as external nasal dilators for OSAS in the pediatric population.
Parasomnias
Parasomnias are defined as episodic, often undesirable nocturnal behaviors that typically involve autonomic and skeletal muscle disturbances, as well as cognitive disorientation and mental confusion.41 Parasomnias may be further categorized as occurring primarily during stage 4 slow-wave or deep (delta) sleep (partial arousal parasomnias), during REM sleep, or at the sleep-wake transition.
PARTIAL AROUSAL PARASOMNIAS
The partial arousal parasomnias, which include sleepwalking and sleep terrors, typically occur in the first third of the night at the transition out of slow-wave sleep and thus share clinical features of both the awake state (ambulation, vocalizations) and the sleeping state (high arousal threshold, unresponsiveness to the environment, amnesia for the event).42 Sleep terrors are typically characterized by a very high level of autonomic arousal, whereas sleepwalking, by definition, usually involves displacement from bed. Both are more common in preschool- and school-aged children and generally disappear in adolescence, at least in part because of the relatively higher amount of slow-wave sleep in younger children. Sleep terrors are considerably less common (1% to 3% incidence) than sleepwalking (40% of the population have had at least one episode). Furthermore, any factors that are associated with an increase in the relative percentage of slow-wave sleep (certain medications, previous sleep deprivation, sleep fragmentation caused by an underlying sleep disorder such as OSAS) may increase the frequency of these events in a predisposed child.43 Finally, there appears to be a genetic predisposition for both sleepwalking and night terrors, and it is not uncommon for individuals to have both types of episodes.
Atypical manifestations of partial arousal parasomnias are sometimes difficult to distinguish from nocturnal seizures; the index of suspicion for a seizure disorder should be higher in the presence of a history of seizures or risk factors for seizures, any unusual or stereotypic movements accompanying the episodes, or postictal phenomena.44
