Pediatric sleep disturbances are very common, with a prevalence of 25% to 37%.1 Most of these involve difficulties initiating and maintaining sleep because of behavioral insomnia of childhood (sleep association and/or limit setting disorder), insufficient sleep, poor sleep hygiene, delayed sleep phase disorder (DSPD) and other circadian rhythm disorders, and obstructive sleep apnea (OSA).2 While pediatricians are taught to search for one unifying diagnosis that explains the symptoms (unlike adults, in whom multiple pathologies often coexist), when it comes to evaluating and treating sleep disorders in a child, it is important to realize that there are often a number of issues simultaneously affecting the quality of sleep, and that without taking a careful history and identifying them, finding a solution to the child’s sleep disturbances can be elusive.


Obstructive Sleep Apnea
OSA affects between 1% and 4% of all children.3 It affects prepubertal boys and girls equally and has two peaks in age distribution. The highest incidence is between the ages of 3 and 6,4 which is when the size of the lymphoid tissue of the upper airway (the tonsils and the adenoids) is largest in proportion to the dimensions of the upper airway itself, but it is also becoming more common in adolescence, with obesity being a major cause in that age group. OSA is recognized as causing deleterious neurocognitive, developmental, and behavioral consequences. Multiple studies have shown a clear-cut connection between OSA and reduction in verbal IQ,5 decreased executive function,6 lower Bailey developmental scores,7 poor school performance,8 and attention deficit and hyperactivity disorder (ADHD).9

Insufficient Sleep
Insufficient sleep is very common among adolescents, with the “Sleep in America Poll” conducted by the National Sleep Foundation in 2006 finding that only 20% of teens get the recommended 9 hours/night.10 It is critical for clinicians to be aware that the breakdown of sleep requirements into nighttime sleep and daytime sleep (naps) varies greatly at different ages.11

Delayed Sleep Phase Disorder
DSPD describes a condition wherein the internal circadian clock is not synchronized with the external clock. It is very common in adolescents, with a prevalence of 5% to 10%.12 The predisposition to develop DSPD may be related to other changes in sleep patterns that parallel structural changes in the brain, known as synaptic pruning, that occur during adolescence.13 Without external cues to entrain their internal circadian body clock, adolescents have been shown to delay their sleep phase and adopt a circadian rhythm that is greater than 24 hours.14 The development of DSPD is brought on by the inherent tendency to put off going to sleep, coupled with the external stimuli to do so, as well as unhealthy sleep habits (struggling on weekdays to awaken for school and “catching up on sleep” on weekends).

Nocturnal Enuresis
Nocturnal enuresis, or bed wetting, is very common in children, occurring three times as often in boys than in girls. It cannot be diagnosed before the age of 5, prior to which bed wetting is considered age appropriate. Bed wetting is present in 15% to 25% of 5 year olds, and 8% of 12-year-old boys.15 Primary enuresis denotes children who have never been dry, whereas secondary enuresis occurs in children who have been dry for at least 6 months. OSA is known to be a cause of secondary nocturnal enuresis.16


“David” was a 12-year-old boy referred for consultation because of concerns of possible obstructive sleep apnea. His mother stated that he was “impossible to wake up” in the mornings, leading to many tardies and absences from school that year. His mother brought up the fact that he had significant snoring, which had been ongoing for years, audible outside his bedroom, and accompanied by night sweats. He usually slept with one pillow, and generally on his side. He also wet the bed three or four times a week, and had never been fully dry at night.

David’s schedule was as follows. During the week, he would typically eat dinner between 4 pm and 6 pm, start getting ready for bed around 9:30 pm, and be in bed with the lights out at 10 pm or later, often closer to midnight. His mother reported that he would generally fall asleep quickly and then sleep through the night without waking. While he was supposed to be out of bed at 6:15 am, it was very difficult to arouse him, and was “always a struggle.” He would straggle out of bed around 6:30 am and eat breakfast in a dimly lit kitchen. Thus, he generally slept between 6:30 and 8:25 hours/night, with most nights being closer to 6:30. While he did not nap during the day, he did doze off in class about twice a week. On weekends, he would generally stay awake until midnight and awaken at 10 am, though he would only get out of bed and turn the lights on at around 11 am, sometimes continuing to lie in bed until as late as 1 pm.

David slept in his own bedroom, which had a television that he would watch at a fairly loud volume as he was trying to fall asleep. Many times he would fall asleep with it on, his mother only turning it off when trying to awaken him the next morning. He also had a 65-pound dog who shared his bed. Because of the enuresis, he slept with plastic sheeting underneath the sheets, which the dog caused to rustle noisily. He did not have his own cell phone or listen to music, and while there was a computer in his bedroom, he did not use it regularly.

David denied symptoms consistent with restless legs or with narcolepsy. He was obese and had mild pervasive developmental disorder. His tonsils and adenoids had been removed “several years ago.” He denied morning headaches. He did have encopresis and complained of constipation. He was on no medication. There was a strong family history of OSA, obesity, hypertension, and diabetes mellitus type 2.


Upon examination, David was an obese young man, cooperative and friendly with no signs of distress. His weight was 96.6 kg, his height 167.1 cm, and his body mass index 34.6. His nasal septum was not deviated, and no polyps were noted. His pharynx was Mallampati 3, and no postnasal drip was noted. He had mild gynecomastia. The remainder of the exam was unremarkable.


1) Likely obstructive sleep apnea. 2) Poor sleep hygiene. 3) Insufficient sleep. 4) Circadian phase delay. 5) Nocturnal enuresis possibly worsened by OSA, chronic constipation.


A sleep study was ordered to diagnose OSA, which was thought likely to be present. In addition, recommendations were made to:

  1. Remove the TV and the dog from the bedroom;
  2. Maintain a regular schedule incorporating fixed bed and wake-up times, not to vary more than a half hour between weekdays and weekends, and allowing for at least 8½ hours sleep/night;
  3. Maintain sleep charts recording daily bedtime, sleep onset, wake-up time, time out of bed, occurrences of enuresis, tardies/absences from school;
  4. Make sure that upon awakening in the morning, he was out of bed, dressed, and exposed to plenty of light (ie, not continuing to lie in bed in a dark bedroom), with no television for the first 2 hours after awakening;
  5. Avoid bright light exposure in the evening for at least 2 hours before going to bed;
  6. Avoid excessive fluid intake in the 3 hours before bedtime; and
  7. Start the use of a laxative, polyethylene glycol, which was prescribed in order to treat the constipation and encopresis, with the hope that there would also be a positive effect upon the nocturnal enuresis.


David had a sleep study done 4 weeks after the initial clinic visit, which demonstrated moderate to severe obstructive sleep apnea, worse in REM, with 64 obstructions associated with desaturation to as low as 86%. He also had an increased arousal index, with many of the arousals being respiratory effort-related arousals. David furthermore presented with higher than normal baseline end-tidal CO2 values, up to 52 mm Hg.


David was started on CPAP, and his obstruction was resolved at a pressure of 7 cm H2O. He returned to the clinic 2 weeks after starting on the CPAP (6 weeks after the initial clinic visit), and both he and his mother reported that he was doing much better. Both the television and the dog were no longer in his room. While his schedule was still not optimal, he was averaging about 8 hours of sleep/night, and he was now sleeping in no later than 8:30 am on the weekends. His constipation and encopresis had improved, and while still wetting the bed occasionally, this was happening much less frequently. He was tolerating the CPAP well, felt that he had more energy during the day, and was no longer falling asleep in school; his mother reported that she no longer had to struggle with him in the mornings to get out of bed, and to school on time in the morning.

Dennis Rosen, MD, is a pediatric pulmonologist and sleep specialist at Children’s Hospital Boston, where he is a member of the Division of Respiratory Diseases, Center for Pediatric Sleep Disorders, and associate medical director of the sleep laboratory. He is an instructor at Harvard Medical School. The author can be reached at


  1. Blader JC, Koplewicz HS, Abikoff H, Foley C. Sleep problems of elementary school children. A community study. Arch Pediatr Adolesc Med. 1997;151:473-480.
  2. Owens JA, Spirito A, McGuinn M, Nobile C. Sleep habits and sleep disturbance in elementary school-aged children. J Dev Behav Pediatr. 2000;21:27-36.
  3. Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc. 2008;5:242-252.
  4. Rosen CL. Obstructive sleep apnea syndrome (OSAS) in children: diagnostic challenges. Sleep. 1996;19(10 Suppl):S274-7.
  5. Halbower AC, Degaonkar M, Barker PB, et al. Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury. PLoS Med. 2006;3(8):e301.
  6. Karpinski AC, Scullin MH, Montgomery-Downs HE. Risk for sleep disordered breathing and executive function in preschoolers. Sleep Med. 2008;9:418.
  7. Montgomery-Downs HE, Gozal D. Snore-associated sleep fragmentation in infancy: mental development effects and contribution of secondhand cigarette smoke exposure. Pediatrics. 2006;117:e496-e502.
  8. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics. 1998;102:616-620.
  9. Chervin RD, Ruzicka DL, Giordani BJ, et al. Sleep-disordered breathing, behavior, and cognition in children before and after adenotonsillectomy. Pediatrics. 2006;117: e769-e778.
  11. Iglowstein I, Jenni OG, Molinari L, Largo RH. Sleep duration from infancy to adolescence: reference values and generational trends. Pediatrics. 2003;111:302–307.
  12. Mindell JA, Owens JA. A Clinical Guide to Pediatric Sleep: Diagnosis and Management of Sleep Problems. Philadelphia: Lippincott, Williams & Williams; 2003.
  13. Feinberg I, Higgins LM, Khaw WY, Campbell IG. The adolescent decline of NREM delta, an indicator of brain maturation, is linked to age and sex but not to pubertal stage. Am J Physiol Regul Integr Comp Physiol. 2006;291:R1724-R1729.
  14. Carskadon M, Labyak SE, Acebo C, Seifer R. Intrinsic circadian period of adolescent humans measured in conditions of forced desynchrony. Neurosci Lett. 1999;269:129-132.
  15. Thiedke CC. Nocturnal enuresis. Am Fam Physician. 2003;67:1499-1506.
  16. Barone JG, Hanson C, DaJusta DG, Gioia K, England SJ, Schneider D. Nocturnal enuresis and overweight are associated with obstructive sleep apnea. Pediatrics. 2009;124:e53-e59.