Insomnia of Childhood

Insomnia may be broadly defined as repeated difficulty initiating and/or maintaining sleep that occurs despite age-appropriate time and opportunity for sleep. These sleep complaints must also result in some degree of impairment in daytime functioning for the child and/or family, which may range from fatigue, irritability, lack of energy, and mild cognitive impairment to effects on mood, school performance, and quality of life. Insomnia complaints may be of a short-term and transient nature (usually related to an acute event), or may be characterized as long-term and chronic. Insomnia is a set of symptoms with a large number of possible etiologies (e.g., pain, medication, medical and psychiatric conditions, learned behaviors) and not as a diagnosis per se. Insomnia, like many behavioral issues in children, is often primarily defined by parental concerns rather than by objective criteria, and therefore should be viewed in the context of family (i.e., maternal depression, stress), child (i.e., temperament, developmental level), and environmental (i.e., cultural practices, sleeping space) considerations.

One of the most common sleep disorders found in infants and toddlers is behavioral insomnia of childhood, sleep onset association type. In this disorder, the child learns to fall asleep only under certain conditions or associations which typically require parental presence, such as being rocked or fed, and does not develop the ability to self-soothe. During the night, when the child experiences the type of brief arousal that normally occurs at the end of a sleep cycle (every 60-90 minutes in infants) or awakens for other reasons, he or she is not able to get back to sleep without those same conditions being present. The infant then “signals” the parent by crying (or coming into the parents’ bedroom, if the child is no longer in a crib) until the necessary associations are provided. The problem is one of prolonged night waking resulting in insufficient sleep (for both child and parent).

Management of night wakings should include establishment of a set sleep schedule and bedtime routine, and implementation of a behavioral program. The treatment approach typically involves a program of rapid withdrawal (extinction) or more gradual withdrawal (graduated extinction) of parental assistance at sleep onset and during the night. Extinction (“cry it out”) involves putting the child to bed at a designated bedtime, “drowsy but awake,” and then systematically ignoring the child until a set time the next morning. Although it has considerable empirical support, extinction is often not an acceptable choice for families. Graduated extinction involves weaning the child from dependence on parental presence with periodic “checks” by the parents at successively longer intervals during the sleep-wake transition; the exact amount of time is determined by the parents’ tolerance for crying and the child’s temperament. The goal is to allow the infant or child to develop skills in self-soothing during the night, as well as at bedtime. In older infants, the introduction of more appropriate sleep associations that will be readily available to the child during the night (transitional objects, such as a blanket or toy), in addition to positive reinforcement (i.e., stickers for remaining in bed), is often beneficial. If the child has become habituated to awaken for nighttime feedings (“learned hunger”), then these feedings should be slowly eliminated. Parents must be consistent in applying behavioral programs to avoid inadvertent, intermittent reinforcement of night wakings; they should also be forewarned that crying behavior often temporarily escalates at the beginning of treatment (“post-extinction burst”).

Bedtime problems, including stalling and refusing to go to bed, are more common in preschool-aged and older children. Sleep disturbances of this type generally fall within the diagnostic category known as behavioral insomnia of childhood, limit setting type, and are often the result of parental difficulties in setting limits and managing behavior, including the inability or unwillingness to set consistent bedtime rules and enforce a regular bedtime, and may be exacerbated by the child’s oppositional behavior. In some cases the child’s resistance at bedtime is due to an underlying problem in falling asleep that is caused by other factors (medical conditions, such as asthma or medication use; a sleep disorder, such as restless legs syndrome; or anxiety) or a mismatch between the child’s intrinsic circadian rhythm (“night owl”) and parental expectations.

Successful treatment of limit setting sleep disorder generally involves a combination of parent education regarding appropriate limit setting, decreased parental attention for bedtime-delaying behavior, establishment of bedtime routines, and positive reinforcement (sticker charts) for appropriate behavior at bedtime; other behavioral management strategies that have empirical support include bedtime fading (temporarily setting the bedtime closer to the actual sleep onset time and then gradually advancing the bedtime to an earlier target bedtime). Older children may benefit from being taught relaxation techniques to help themselves fall asleep more readily. Following the principles of sleep hygiene for children is essential (Table 17-2).

When the insomnia is not primarily a result of parent behavior or secondary to another sleep disturbance, or to a psychiatric or medical problem, it is referred to as psychophysiologic or primary insomnia, also sometimes called “learned insomnia.” Primary insomnia usually occurs largely in adolescents and is characterized by a combination of learned sleep-preventing associations and heightened physiologic arousal resulting in a complaint of sleeplessness and decreased daytime functioning. A hallmark of primary insomnia is excessive worry about sleep and an exaggerated concern of the potential daytime consequences. The physiologic arousal can be in the form of cognitive hypervigilance, such as “racing” thoughts; in many individuals with insomnia an increased baseline level of arousal is further intensified by this secondary anxiety about sleeplessness. Treatment usually involves educating the adolescent about the principles of sleep hygiene (Table 17-3), institution of a consistent sleep-wake schedule, avoidance of daytime napping, instructions to use the bed for sleep only and to get out of bed if unable to fall asleep (stimulus control), restricting time in bed to the actual time asleep (sleep restriction), addressing maladaptive cognitions about sleep, and teaching relaxation techniques to reduce anxiety. Hypnotic medications are rarely needed.

Obstructive Sleep Apnea

Sleep-disordered breathing (SDB) in children encompasses a broad spectrum of respiratory disorders that occur exclusively in or are exacerbated by sleep, and includes primary snoring and upper airway resistance syndrome, as well as apnea of prematurity and central apnea. Obstructive sleep apnea (OSA), the most important clinical entity within the SDB spectrum, is a respiratory disorder that is characterized by repeated episodes of prolonged upper airway obstruction during sleep despite continued or increased respiratory effort, resulting in complete (apnea) or partial (hypopnea; ≥50% reduction in airflow) cessation of airflow at the nose and/or mouth, as well as in disrupted sleep. Both intermittent hypoxia and the multiple arousals resulting from these obstructive events likely contribute to significant metabolic, cardiovascular, and neurocognitive/neurobehavioral morbidity.

Primary snoring is defined as snoring without associated ventilatory abnormalities (e.g., apneas or hypopneas, hypoxemia, hypercapnia) or respiratory-related arousals, and is a manifestation of the vibrations of the oropharyngeal soft tissue walls that occur when an individual attempts to breathe against increased upper airway resistance during sleep. Children with primary snoring may still have subtle breathing abnormalities during sleep, including evidence of increased respiratory effort, which in turn may be associated with adverse neurodevelopmental outcomes.