Circadian Rhythm Sleep Disorders

Chapter 104


image


Circadian Rhythm Sleep Disorders


Deborah M. Brooks, MD, and Lee J. Brooks, MD, FAAP


Introduction


Circadian rhythm basics


Circadian rhythms are the body’s (typically) 24-hour clock, controlled by the suprachiasmatic nucleus (SCN) in the brain.


The circadian clock is regulated or “set” primarily by visual cues of light from the eyes to the SCN (see Figure 104-1). This keeps the clock synchronized to the 24-hour day. Other time cues (zeitgebers) also influence the clock’s timing—for example, meal, social, and exercise schedules.


image


Figure 104-1. The suprachiasmatic nucleus is the body’s “master clock” that uses light and other zeitgebers to control all of the body’s clocks. www.nigms.nih.gov/education/pages/Factsheet_CircadianRhythms.aspx


The SCN regulates release of melatonin by the pineal gland. Melatonin is the main sleep hormone. It is secreted about 2 hours before natural sleep time, and levels are highest in the middle of the night.


Circadian rhythm sleep disorders (CRSDs)


CRSDs are a timing problem with wake and sleep—either a problem with the internal body clock or a mismatch between the internal clock and the environment.


Symptoms include trouble falling asleep, trouble staying asleep, waking up too early, or poor quality of sleep—functioning must be impaired for it to be considered a disorder.


Common to these disorders is inflexibility: Even when physically tired or sleep deprived, sufferers cannot make up for lost sleep outside of their endogenous sleep times.


Types of CRSDs include


Advanced sleep phase


Delayed sleep phase


Jet lag


Shift work


Irregular sleep phase


Non–24-hour sleep-wake rhythm disorder


Advanced Sleep Phase


Basics


Sleep and wake times are habitually early when compared with conventional times, such as in “morning people” or “larks.”


This is more common in older adults.


Etiology


Possibly a shortened circadian rhythm


Symptoms


Extreme sleepiness in the late afternoon or early evening


Involuntary early-morning awakening


Delayed Sleep Phase


Basics


Sleep and wake times are habitually later than conventional times, such as in “evening people” or “owls” (Figure 104-2).


Earlier wake-up times can lead to daytime sleepiness and impaired work and school performance.


image


Figure 104-2. Normal sleep phase and variations.


It is more common among adolescents and young adults, with a reported prevalence of 7%–16%.


Forty percent of affected individuals have a positive family history.


Etiology


An etiologic origin is possibly an exaggerated reaction to the normal shift in the internal clock that is seen in adolescents after puberty.


Because of the delay in falling asleep and yet still needing to get up at the required time for work or school, children or adolescents often experience excessive daytime drowsiness as a result of not getting enough sleep (this is most evident on weekdays). The delayed rhythm is coupled with a delay in the cycle of the night hormone melatonin, which lingers in the morning and makes it harder to wake up.


Symptoms


The patient awakens late.


Inability to fall asleep at the desired time usually manifests as insomnia complaints. It may be exacerbated by the social pressures teenagers feel to stay up late (eg, to do homework or to use the Internet or a cell phone).


Inability to wake up at the desired time and excessive daytime sleepiness are usually the most common complaint because it is more readily evident to parents than the nighttime insomnia.


Jet Lag


Basics


Jet lag occurs when long travel by airplane quickly puts a person in another time zone and the person must sleep and wake at times that are misaligned with his or her body clock.


The body clock is slightly longer than 24 hours. This makes it easier to travel westward than eastward because it is easier to delay sleep than to advance sleep.


Jet lag affects all age groups.


Symptoms


Disturbed sleep


Decreased alertness and impaired daytime function


Occasionally, gastrointestinal distress and general malaise


Depressed mood, irritability, and anxiety


Shift Work


Basics


This occurs when a person’s work hours are scheduled during the normal sleep period.


It is not common in children.


The primary etiologic origin is the opposition of required sleep and wake times to one’s endogenous circadian rhythm of sleep and waking.


Symptoms


Sleepiness during the work shift


Difficulty sleeping while others are awake


Shortened sleep duration by 1–4 hours


Irregular Sleep Phase


Basics


This is characterized by lack of a clearly defined circadian rhythm of sleep and waking.


It is commonly associated with developmental disorders in children and in adults with neurodegenerative diseases and brain tumors or traumatic brain injury.


Etiology


The etiologic origin is likely central degeneration of SCN neurons.


Decreased exposure to or input of external synchronizing agents (zeitgebers), such as light and activity, results in a weakened central circadian rhythm.


Symptoms


Sleep is fragmented into a series of at least 3 naps that occur throughout a 24-hour period.


Total sleep time is usually normal for the patient’s age.


Non–24-Hour Sleep-Wake Disorder


Basics


This disorder is characterized by fluctuating periods of insomnia and/or excessive sleepiness that occur because the intrinsic circadian pacemaker is not entrained to a 24-hour light-dark cycle.


Most individuals with this disorder are totally blind, and the failure to entrain circadian rhythms is related to the lack of light input to the SCN.


Occasionally, the disorder is associated with mental retardation or dementia.


Symptoms


A person’s day length is longer than 24 hours. Sleep times get progressively later and later, so the person is eventually sleeping during the day until he or she cycles back to a nighttime bedtime.


Differential Diagnosis


The presence of sleep disorders, including obstructive sleep apnea (OSA), narcolepsy, and restless legs syndrome, among others, needs to be considered.


In addition to comorbid sleep disorders, psychiatric disorders—particularly depression and anxiety—are common in patients with nearly all types of CRSDs and should be considered in the differential diagnosis.


Children and adolescents with a delayed sleep phase may experience depression and other psychiatric problems, including behavioral problems, as a result of daytime drowsiness and missing school. Daytime drowsiness can also lead to lowered academic performance from missed school days or tardiness and inattention. Dependency on caffeine, sedatives, or alcohol may also be seen.


Diagnostic Considerations


The diagnosis of all CRSDs is based on a careful history and review of a sleep diary with actigraphy.


In addition to the typical symptomatology, diagnosis of irregular sleep phase requires a history of a minimum of 3 irregular sleep-wake cycles in a 24-hour cycle, recorded for 14 days in a sleep diary and/or with actigraphy.


Polysomnography (PSG) is not routinely indicated to establish the diagnosis. However, PSG is indicated to assess the presence of other comorbid sleep disorders, such as OSA syndrome and narcolepsy.


Management


All patients and parents should be encouraged to practice sleep hygiene (see Chapter 96, Sleep Disorders: Evaluation and Prevention).


Non–24-hour sleep-wake disorder


This disorder is treated via timed, exogenous melatonin administration. One method is to give the patient 3 mg of melatonin 1 hour before the desired bedtime. Entrainment typically occurs between 3 and 9 weeks. After entrainment, melatonin must be continued at a lower dose (0.5 mg) nightly to prevent relapse.


Tasimelteon, a melatonin receptor agonist, has been approved for use in adults with non–24-hour sleep disorder.


In patients with some remaining sensitivity to light, morning bright-light therapy (2,500 lux for 2 hours daily on awakening) may be effective.


Irregular sleep phase


Bright-light therapy


Exposure to 3,000–5,000 lux of bright light for 2 hours every morning for 4 weeks has been shown to improve daytime alertness, decrease napping, consolidate nighttime sleep, and reduce nocturnal agitation.


Structured social and physical activity (9:00–10:30 pm and 7:00–8:30 pm daily for 2 weeks)


Minimizing noise and light during the scheduled sleep period and addressing issues such as nocturia (or nocturnal polyuria) and enuresis to reduce sleep disturbances at night


Delayed sleep phase


Good sleep habits


Going to bed and waking up at the same times on weekends as on weekdays


Avoiding caffeinated products; avoiding other stimulants and products that can disrupt sleep (eg, alcohol, sleeping pills, nicotine)


Maintaining a cool, quiet, and comfortable bedroom and avoiding activities before bedtime that are stimulating (eg, computer games and television)


Avoidance of light at night


Shifting the bedtime schedule


Advancing the internal clock simply involves moving the bedtime a bit earlier on each night, until the desired bedtime is reached. For example, set the bedtime at midnight on one night, 11:45 pm on the next night, 11:30 pm on the following night, and so on. This is facilitated by concomitantly moving the waking time to allow this transition to occur with more control. These methods are best individualized with the help of a sleep specialist.


Delaying the internal clock involves moving the bedtime sequentially ≥1–3 hours later on successive nights until the desired bedtime is reached. This requires several days free from social activities and may be best attempted during a long school break or vacation period. The rationale behind this strategy is that it is much easier for the body to adjust to a later bedtime than an earlier one. Again, this is best accomplished with advice from a sleep specialist.


Bright-light therapy


Exposing the child to bright light for approximately half an hour in the morning helps to reset the body’s internal clock. Reduced exposure to bright light in the evening also helps.


Taking melatonin about an hour before the desired bedtime may help shift the circadian clock.


Advanced sleep phase


Sleep-wake scheduling


Time light exposure in the evening and avoid light in early morning hours.


Melatonin or hypnotics may be beneficial for sleep maintenance insomnia.


Jet lag


Melatonin


For greatest effectiveness, melatonin should be taken at the target bedtime, optimally starting 3–4 days before departure.


Light therapy


Strategic exposure and avoidance of exposure to light have been used as an effective treatment approach.


Additional treatment options include maintaining home-based sleep hours for brief travel, short-term use of hypnotics for insomnia, and caffeine to alleviate daytime sleepiness.


Resources for Families


What Is Delayed Sleep Phase Disorder? (National Sleep Foundation). sleepdisorders.sleepfoundation.org/chapter-5-circadian-rhythm-sleep- disorders


What Are Circadian Rhythm Sleep Disorders? (Circadian Sleep Disorders Network). www.circadiansleepdisorders.org/defs.php


Circadian Rhythm Sleep-Wake Disorder Symptoms (PsychCentral). psychcentral.com/disorders/circadian-rhythm-sleep-disorder-symptoms



Part VIII Bibliography


CHAPTER 96: SLEEP DISORDERS: EVALUATION AND PREVENTION


Beebe DW. Cognitive, behavioral, and functional consequences of inadequate sleep in children and adolescents. Pediatr Clin North Am . 2011;58(3):649–665


Galland BC, Taylor BJ, Elder DE, Herbison P. Normal sleep patterns in infants and children: a systematic review of observational studies. Sleep Med Rev. 2012;16(3): 213–222


Magee CA, Gordon R, Caputi P. Distinct developmental trends in sleep duration during early childhood. Pediatrics. 2014;133(6):e1561–e1567


Meltzer L, Crabtree VM. Pediatric Sleep Problems: A Clinician’s Guide to Behavioral Interventions. Washington: APA Books; 2015


Paruthi S, Brooks LJ, D’Ambrosio C, et al. Recommended Amount of Sleep for Pediatric Populations: A Consensus Statement of the American Academy of Sleep Medicine. J Clin Sleep Med. 2016;12(6):785–786


CHAPTER 97: BRIEF, RESOLVED, UNEXPLAINED EVENTS AND SUDDEN INFANT DEATH SYNDROME


Task Force on Sudden Infant Death Syndrome. SIDS and Other Sleep-Related Infant Deaths: Updated 2016 Recommendations for a Safe Infant Sleeping Environment. Pediatrics. 2016;138(5):e20162938


Aminiahidashti H. Infantile apparent life-threatening events, an educational review. Emerg (Tehran). 2015;3(1):8–15


Hymel KP; American Academy of Pediatrics; Committee on Child Abuse and Neglect; National Association of Medical Examiners. Distinguishing sudden infant death syndrome from child abuse fatalities. Pediatrics. 2006;118(1):421–427


Tieder JS, Bonkowsky JL, Etzel RA, et al; Subcommittee on Apparent Life Threatening Events. Brief resolved unexplained events (formerly apparent life-threatening events) and evaluation of lower-risk infants. Pediatrics. 2016;137(5):e20160590


Tieder JS, Altman RL, Bonkowsky JL, et al. Management of apparent life-threatening events in infants: a systematic review. J Pediatr. 2013;163(1):94–99


Weese-Mayer DE, Berry-Kravis EM, Ceccherini I, Rand CM. Congenital central hypoventilation syndrome (CCHS) and sudden infant death syndrome (SIDS): kindred disorders of autonomic regulation. Respir Physiol Neurobiol. 2008;164(1-2):38–48


CHAPTER 98: OBSTRUCTIVE SLEEP APNEA


Alonso-Álvarez ML, Terán-Santos J, Navazo-Egüia AI, et al; Spanish Sleep Network. Treatment outcomes of obstructive sleep apnoea in obese community-dwelling children: the NANOS study. Eur Respir J. 2015;46(3):717–727


Bhattacharjee R, Choi BH, Gozal D, Mokhlesi B. Association of adenotonsillectomy with asthma outcomes in children: a longitudinal database analysis. PLoS Med. 2014;11(11):e1001753


Bonuck K, Freeman K, Chervin RD, Xu L. Sleep-disordered breathing in a population- based cohort: behavioral outcomes at 4 and 7 years. Pediatrics. 2012;129(4);e857–e865


Kheirandish-Gozal L, Dayyat EA, Eid NS, Morton RL, Gozal D. Obstructive sleep apnea in poorly controlled asthmatic children: effect of adenotonsillectomy. Pediatr Pulmonol. 2011;46(9):913–918


Marcus CL, Brooks LJ, Draper KA, et al; American Academy of Pediatrics. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3):576–584


CHAPTER 99: CONGENITAL CENTRAL HYPOVENTILATION SYNDROME


Chen ML, Keens TG. Congenital central hypoventilation syndrome: not just another rare disorder. Paediatr Respir Rev. 2004;5(3):182–189


Gelwane G, Trang H, Carel JC, Dauger S, Léger J. Intermittent hyperglycemia due to autonomic nervous system dysfunction: a new feature in patients with congenital central hypoventilation syndrome. J Pediatr. 2013;162(1):171–176


Low KJ, Turnbull AR, Smith KR, et al. A case of congenital central hypoventilation syndrome in a three-generation family with non-polyalanine repeat PHOX2B mutation. Pediatr Pulmonol. 2014;49(10):E140–E143


Weese-Mayer DE, Berry-Kravis EM, Ceccherini I, Keens TG, Loghmanee DA, Trang H; ATS Congenital Central Hypoventilation Syndrome Subcommittee. An official ATS clinical policy statement: congenital central hypoventilation syndrome: genetic basis, diagnosis, and management. Am J Respir Crit Care Med. 2010;181(6):626–644


Reppucci D, Hamilton J, Yeh EA, Katz S, Al-Saleh S, Narang I. ROHHAD syndrome and evolution of sleep disordered breathing. Orphanet J Rare Dis. 2016;11(1):106 10.1186/ s13023-016-0484-1


Ize-Ludlow D, Gray JA, Sperling MA, et al. Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation presenting in childhood. Pediatrics. 2007;120(1):e179–e188


CHAPTER 100: INSOMNIA


American Academy of Sleep Medicine. International Classification of Sleep Disorders. Chronic Insomnia Disorder. 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014:21–41


Mindell JA, Kuhn B, Lewin DS, Meltzer LJ, Sadeh A; American Academy of Sleep Medicine. Behavioral treatment of bedtime problems and night wakings in infants and young children. Sleep. 2006;29(10):1263–1276


Vriend J, Corkum P. Clinical management of behavioral insomnia of childhood. Psychol Res Behav Manag. 2011;4:69–79


National Sleep Foundation. Sleep in America Poll: summary of findings. 2014. sleepfoundation.org/sites/default/files/2014-NSF-Sleep-in-America-poll-summary-of-findings—FINAL-Updated-3-26-14-.pdf. Accessed October 23, 2017


Paruthi S, Brooks LJ, D’Ambrosio C, et al. Recommended amount of sleep for pediatric populations: a consensus statement of the American Academy of Sleep Medicine. J Clin Sleep Med. 2016;12(6):785–786


CHAPTER 101: EXCESSIVE SOMNOLENCE


American Academy of Sleep Medicine. International Classification of Sleep Disorders. 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014:143–188


Paruthi S, Brooks LJ, D’Ambrosio C, et al. Recommended amount of sleep for pediatric populations: a consensus statement of the American Academy of Sleep Medicine. J Clin Sleep Med. 2016;12(6):785–786


Kallambella K, Hussain N. Approach to a child with excessive daytime sleepiness. Arch Dis Child Educ Pract Ed. 2015;100(6):288–294, discussion 336


CHAPTER 102: NARCOLEPSY


American Academy of Sleep Medicine. International Classification of Sleep Disorders. 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014:143–161


Nevsimalova S. Narcolepsy in childhood. Sleep Med Rev. 2009;13(2):169–180


Aran A, Einen M, Lin L, Plazzi G, Nishino S, Mignot E. Clinical and therapeutic aspects of childhood narcolepsy-cataplexy: a retrospective study of 51 children. Sleep. 2010;33(11):1457–1464


Scammell TE. Narcolepsy. N Engl J Med. 2015;373(27):2654–2662


CHAPTER 103: PARASOMNIAS


American Academy of Sleep Medicine. International Classification of Sleep Disorders. Parasomnias. 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014:225–278


Mason TBA II, Pack AI. Pediatric parasomnias. Sleep. 2007;30(2):141–151


Sheldon SH. Parasomnias in childhood. Pediatr Clin North Am. 2004;51(1):69–88, vi


Kotagal S. Parasomnias in childhood. Sleep Med Rev. 2009;13(2):157–168


CHAPTER 104: CIRCADIAN RHYTHM SLEEP DISORDERS


Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM. Clinical Practice Guideline for the Treatment of Intrinsic Circadian Rhythm Sleep-Wake Disorders: Advanced Sleep-Wake Phase Disorder (ASWPD), Delayed Sleep-Wake Phase Disorder (DSWPD), Non-24-Hour Sleep-Wake Rhythm Disorder (N24SWD), and Irregular Sleep-Wake Rhythm Disorder (ISWRD). An Update for 2015: An American Academy of Sleep Medicine Clinical Practice Guideline. J Clin Sleep Med. 2015;11(10):1199–1236


Zee PC, Attarian H, Videnovic A. Circadian rhythm abnormalities. Continuum (Minneap Minn). 2013;19(1 Sleep Disorders):132–147

Only gold members can continue reading. Log In or Register to continue

Aug 22, 2019 | Posted by in PEDIATRICS | Comments Off on Circadian Rhythm Sleep Disorders
Premium Wordpress Themes by UFO Themes