A Clinical Guide To Pediatric Sleep

A Clinical Guide to
Pediatric
Sleep
Diagnosis and Management
of Sleep Problems
Se c o n D e Di t i o n
Jodi A. Mindell, Ph.D.
Professor of Psychology
Director, Graduate Program in Psychology
Saint Josephs University
Associate Director, Sleep Center
Childrens Hospital of Philadelphia
Philadelphia, Pennsylvania
Judith A. Owens, M.D., M.P.H.

Associate Professor of Pediatrics
Alpert Medical School at Brown University
Director, Pediatric Sleep Clinic
Hasbro Childrens Hospital
Providence, Rhode Island
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Library of Congress Cataloging-in-Publication Data
Mindell, Jodi A.
A clinical guide to pediatric sleep : diagnosis and management of sleep
problems / Jodi A. Mindell, Judith A. Owens. 2nd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN-13: 978-1-60547-389-5
ISBN-10: 1-60547-389-8
1. Sleep disorders in children. 2. ChildrenHealth and hygiene.
3. Sleep. 4. Sleep disorders in adolescence. I. Owens, Judith A. II. Title.
[DNLM: 1. Sleep Disordersdiagnosis. 2. Adolescent. 3. Child.
4. Sleep Disorderstherapy. WM 188 M663c 2009]
RJ506.5.S55M54 2009
618.92'8498dc22
2009014882
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Table of Contents
Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi

Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .viii
Section i: introduction to Pediatric Sleep

1. Sleep 101 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
2. Sleep in Infancy, Childhood, and Adolescence. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
3. Evaluation of Pediatric Sleep Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
4. Sleep Hygiene: Healthy Sleep Habits for Children and Adolescents . . . . . . . . . . . . . . . . 43
Section ii: Pediatric Sleep Disorders

5. Symptom-Based Algorithms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
6. Bedtime Problems: Behavioral Insomnia of Childhood, Limit-Setting Type . . . . . . . . . . 51
7. Nightwakings: Behavioral Insomnia of Childhood, Sleep Onset Association Type . . . . . 58
8. Nighttime Fears. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
9. Nightmares . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
10. Partial Arousal Parasomnias: Sleepwalking, Sleep Terrors, and
Confusional Arousals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
11. Sleep Related Rhythmic Movements: Head Banging, Body Rocking, and
Head Rolling. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
12. Bruxism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
13. Sleep Enuresis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
14. Sleep-Disordered Breathing and Obstructive Sleep Apnea Syndrome. . . . . . . . . . . . . . 100
15. Restless Legs Syndrome and Periodic Limb Movement Disorder . . . . . . . . . . . . . . . . . 116
16. Excessive Daytime Sleepiness: Narcolepsy and Other Hypersomnias. . . . . . . . . . . . . . 131
17. Delayed Sleep Phase Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
18. Insomnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
Section iii: Sleep and Medications

19. Sleep and Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
Section iV: Sleep in Special Populations

20. Sleep and Neurodevelopmental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 176
21. Sleep and Medical Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
22. Sleep and Psychiatric Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
Appendices
Appendix A Resources for Families . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208
Suggested Readings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211

Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217
TABLE OF CONTENTS v
The following appendices can be found online on the books website:

Appendix B Screening and Evaluation
Appendix B1 Sleep Evaluation Questionnaire
Appendix B2 Sleep Diaries
Appendix B3 Screening Questionnaire for Obstructive Sleep Apnea
Appendix B4 Screening Questionnaire for Restless Legs Syndrome
Appendix C General Sleep Handouts
Appendix C1 Sleep in Newborns
Appendix C2 Sleep in Infants
Appendix C3 Sleep in Toddlers
Appendix C4 Sleep in Preschoolers
Appendix C5 Sleep in School-Aged Children
Appendix C6 Sleep in Adolescents
Appendix C7 Sleep Tips for Children
Appendix C8 Sleep Tips for Adolescents
Appendix D Sleep Disorder Handouts
Appendix D1 Bedtime Problems
Appendix D2 Nightwakings
Appendix D3 Nighttime Fears
Appendix D4 Nightmares
Appendix D5 Sleepwalking
Appendix D6 Sleep Terrors
Appendix D7 Head Banging and Body Rocking
Appendix D8 Bruxism
Appendix D9 Bedwetting
Appendix D10 Obstructive Sleep Apnea
Appendix D11 Your Childs Sleep Study
Appendix D12 Restless Legs Syndrome
Appendix D13 Periodic Limb Movement Disorder
Appendix D14 Narcolepsy
Appendix D15 Delayed Sleep Phase Disorder
Appendix D16 Insomnia
Preface to the Second Edition
Sleep affects every aspect of a childs health, daily functioning, and well-being. Thus, it is not
surprising that inadequate, disrupted, poor-quality, and, at times, elusive sleep constitutes one of
the most common complaints raised by parents to pediatric and family medicine practitioners, as
well as to child mental health providers. Approximately 25% of children overall experience some
type of sleep problem, ranging from diff culty falling asleep and nightwakings, to more serious
primary sleep disorders, such as sleep apnea or narcolepsy; more than one-third of elementary
school-aged children and 40% of adolescents have signif cant sleep complaints. Although many
sleep problems in infants and children are transient and self-limited, the common wisdom that
children grow out of sleep problems is not an accurate perception, and certain intrinsic and
extrinsic risk factors (e.g., diff cult temperament, chronic illness, neurodevelopmental delays,
maternal depression, family stress) may predispose a given child to develop a more chronic sleep
disturbance.
Furthermore, there are few pediatric health issues that have a more signif cant impact on
health and well-being than childhood sleep disorders. Sleep affects every aspect of a childs phys-
ical, emotional, cognitive, and social development, and the consequences of sleep disorders in
children range from cardiovascular problems and failure to thrive, to signif cant mood and behav-
ioral concerns and academic failure. Sleep problems in children also have a major impact on the
family, often resulting in signif cant caregiver stress, fatigue, mood disturbances, and a decreased
level of effective parenting. In addition, the coexistence of sleep problems exacerbates virtually
every medical, psychiatric, developmental, and psychosocial problem in childhood. Given that
virtually all sleep disorders are highly treatable with effective medical and behavioral interven-
tions, sleep disorders in children and adolescents are particularly important for the primary care
healthcare provider to recognize and diagnose.
Sleep is also an important health education issue. Not only are sleep problems treatable, but
many are preventable. The pediatric encounter provides an ideal opportunity to educate parents
about normal sleep in children and to teach them strategies to prevent sleep problems from either
developing in the f rst place (primary prevention) or becoming chronic when problems already
exist (secondary prevention). Primary care providers are in the optimal position to identify sleep
concerns because of their regular access to children and families during well-child encounters,
especially prior to school entry, and because of the inherently biopsychosocial orientation of
primary care practice. However, while pediatric providers have become more vigilant in moni-
toring and providing education about virtually every aspect of childrens health and well-being,
survey studies suggest that sleep issues in both primary care and mental health clinical settings
are commonly inadequately addressed. Unfortunately, given the expanding number of competing
demands for increasingly smaller amounts of time and the information overload that the average
busy pediatric practitioner faces on a daily basis, sleep issues in clinical practice may not always
receive the attention that they deserve.
The purpose of this updated and expanded edition of A Clinical Guide to Pediatric Sleep: Di-
agnosis and Management of Sleep Problems in Children and Adolescents, therefore, is threefold:
1. To provide the practitioner with an appreciation for the pervasive effect that sleep problems
have on childrens and families lives and the multiple ways in which they impact clinical pe-
diatric practice.
2. To synthesize new state-of-the-art information about the etiology, clinical assessment tools,
and management of sleep disorders in children and adolescents in the form of a comprehen-
sive but accessible resource for practitioners.
vi
PREFACE TO THE SECOND EDITION vii
3. To provide the basic knowledge and practical tools with which to recognize, evaluate, and treat
sleep issues in children and adolescents in primary care, as well as mental health settings.
Other features of this second edition of A Clinical Guide to Pediatric Sleep include updated
diagnostic criteria (International Classif cation of Sleep Disorders ICSD-2, 2005), inclusion of
revised and new American Academy of Sleep Medicine Standards of Practice guidelines, and
updated parent handouts on sleep within each age group and for every common pediatric sleep
disorder.
A Clinical Guide to Pediatric Sleep is divided into four sections, with extensive appendices
of handouts for healthcare practitioners to give parents, now available online: Please see inside
cover of your book for online access information.
Section I addresses basic sleep issues in pediatric practice, including an overview of sleep
regulation and core features of sleep physiology relevant to clinical practice. This section also
presents information on developmental aspects of sleep, including normal sleep parameters and
commonly experienced sleep problems for each age group, as well as updated data regarding epi-
demiology of pediatric sleep disorders. Finally, basic approaches to evaluation of sleep problems,
including the use and interpretation of sleep diagnostic tools, are discussed.
Section II provides extensively updated, comprehensive information on the etiology, evalu-
ation, treatment, management, and prognosis for each of the most common pediatric sleep dis-
orders. Section II also contains symptom-based algorithms based on the three most common
presentations of sleep problems in the clinical setting (i.e., diff culty falling asleep, nightwakings,
and daytime sleepiness). Since there are multiple sleep problems that can account for each of
these presenting symptoms, the algorithms enable the healthcare provider to evaluate sleep com-
plaints in a step-wise fashion with the goal of developing the most appropriate treatment plan.
Section III discusses sleep pharmacology, including sedatives and hypnotics in children and
medication effects on sleep. New hypnotics, use of over-the-counter medications in pediatrics,
especially melatonin, and misuse of stimulants (e.g., medications such as methylphenidate, caf-
feine) to manage fatigue in the adolescent population are also covered.
Section IV presents updated and expanded information on sleep problems in special popula-
tions, including children with neurodevelopmental disorders and pediatric patients with a comor-
bid medical or psychiatric problem.
Furthermore, an updated national listing of clinical resources and other informational re-
sources (e.g., foundations, Internet sites) is included. Finally, the updated online Appendices (see
inside cover of your book for online information) provide comprehensive resources for pediatric
providers, including intake and screening questionnaires, as well as parent education handouts
for each age group and each sleep disorder.
Our goal is to make it possible for all children and families to get the sleep they need in order
to optimize their health and well-being. It is our hope is that this book will provide primary care
and mental health providers with a state-of-the-art, comprehensive, accessible, and user-friendly
resource on pediatric sleep to help us move closer to achieving that goal.
Acknowledgments
No project of this magnitude is ever developed without the enthusiasm and support of others.
We would like to extend our thanks to the many individuals who supported this work with their
advice and feedback, to the clinicians with whom we have had the privilege of working, and to
the families who shared their experiences (and sleepless nights!) to help further our knowledge
of pediatric sleep.
We also would like to acknowledge the incredible work of the non-prof t organization Sleeping
Children Around the World, whose mission is to provide children in the poorest nations around
the globe with the comfort of a good nights sleep. Each donation to this all-volunteer organiza-
tion provides a bed-kit (mattress, mosquito netting, blanket, clothing, and school supplies) to a
child living in poverty. For more information, please visit www.scaw.org.
Finally, our deepest appreciation to those who have supported this project: particularly Sonya
Seigafuse of Lippincott Williams & Wilkins for her enthusiasm and sage advice and Kerry Bar-
rett, Managing Editor, who shepherded this book through the publishing process. We are also
grateful to our many colleagues in sleep medicine, past, present, and future, who continue to
inspire and educate us.
And, most importantly, to our families, for their unwavering support, enthusiasm, good humor,
and endless patience.
viii
Sleep 101
1
It is estimated that by the age of 2 years the average child has spent about 9,500 hours (or a total
of 13 months) sleeping, in contrast to 8,000 hours for all waking activities combined. Sleep is the
primary activity of the brain during early development. Between the ages of 2 and 5 years old,
children spend equal amounts of time awake and asleep. And throughout childhood and adoles-
cence, sleep continues to account for about 40% of a childs average day.
The organization and regulation of sleep and wakefulness are complex, highly active physi-
ologic processes that involve the interaction of multiple central nervous system components. A
detailed description of the neuroanatomy and neurophysiology of sleep, which may be found
in a number of excellent reviews (see Suggested Readings), is beyond the scope of this book.
However, some understanding of the function of sleep, the impact of inadequate sleep, the basic
structure or architecture of sleep, and familiarity with the basic mechanisms that regulate sleep
and wakefulness are necessary in order for the primary care practitioner to fully appreciate the
causes and effects of both sleep disturbances and inadequate sleep in children and adolescents.
Def nition of Sleep

Sleep may be def ned as a behavioral state characterized by the following:
Reduced motor activity
Decreased interaction with and responsivity to the environment
Specif c postures (e.g., lying down, eyes closed)
Easy reversibility
Fun c t io n S o F Sl eeP
Despite the virtual explosion of knowledge in the past half-century regarding the structure, neu-
roanatomy, and neurophysiology of sleep (e.g., the discovery of REM sleep occurred just over
50 years ago), the basic function of sleep largely remains a mystery. Most of what we under-
stand about the function of sleep has evolved from studies that have examined the impact of
experimentally induced sleep loss or pathologic sleep conditions on a host of physiologic and
neurobehavioral systems in both animal models and humans. What we do know is that adequate
sleep is a biological imperative that appears necessary for sustaining life, as well as for optimal
functioning. For example, slow-wave sleep (SWS) appears to be the most restorative form of
sleep and rapid eye movement (REM) sleep (see below) appears not only to be involved in vital
cognitive functions, such as the consolidation of memory, but also to be an integral component in
the growth and development of the central nervous system. Recent studies indicate that adequate
amounts of both of these sleep stages are necessary for optimal learning. In addition, the release
of growth hormone during SWS clearly links sleep to the regulation of somatic growth as well
as many other neuroendocrine functions. Sleep may also functionally ref ect a neurobiological
need to limit time in the awake state, thereby protecting the individual, especially the developing
organism, from being bombarded by information and environmental stimulation that cannot be
adequately processed. Finally, studies have clearly demonstrated that rest is not a substitute
for sleep and, furthermore, that wakefulness-promoting agents (e.g., psychostimulants, caffeine)
1
2 SECTION I INTRODUCTION TO PEDIATRIC SLEEP
used to combat sleepiness induced by insuff cient sleep do not restore the physiologic benef ts of
sleep itself.
Insuff cient Sleep

Insuff cient sleep is the most common cause of excessive daytime sleepiness. The resulting
chronic sleep loss impacts daytime functioning, including mood disturbances, daytime behav-
ior problems, cognitive impairment, and increased risk-taking behavior.
in SuFFic ien t Sl eeP

A basic principle of sleep physiology relates to the consequences of the failure to meet basic sleep
needs, termed insuff cient or inadequate sleep or sleep loss. Most of the studies conducted have
examined the effects of total sleep loss, rather than the more real-world scenario of partial sleep
loss (sleep restriction). However, more recent studies have demonstrated that partial sleep loss
on a chronic basis accumulates in what is termed a sleep debt and produces def cits equivalent
to those seen under conditions of total sleep deprivation. If the sleep debt becomes large enough
and is not voluntarily paid back (by obtaining adequate recovery sleep), the body may respond by
overriding voluntary control of wakefulness, resulting in periods of decreased alertness, dozing
off, and napping that is excessive daytime sleepiness. In addition, the sleep-deprived individual
may experience very brief (several seconds) repeated daytime microsleeps of which he or she
may be completely unaware, but which nonetheless may result in signif cant lapses in attention
and vigilance. There also appears to be a relationship between the amount of sleep restriction
and performance, with decreased performance correlating with decreased sleep. Furthermore,
subjective perception of sleepiness and the degree of associated performance impairment tend to
be poorly correlated with actual impairment, commonly leading individuals to overestimate their
ability to function adequately in the face of sleep loss.
What is Sleepiness?
Sleepiness is def ned as a state of decreased ability to maintain wakefulness or an increased
propensity to fall asleep; this is in contrast to fatigue, which typically does not include this
sleep tendency. Sleepiness, like hunger or thirst, is a normal biologic need; sleep is to sleepi-
ness as food is to hunger. Furthermore, the only thing that replaces sleep is sleep (i.e., not
rest). Excessive sleepiness is a symptom characterized by diff culty maintaining wakeful-
ness and an increased propensity to fall asleep, even in inappropriate circumstances and situ-
ations, that interferes with activities of daily living.
Chronic sleep loss impacts daytime functioning and causes excessive daytime sleepiness, which
can be manifested in a number of ways in children and adolescents (e.g., dozing off while en-
gaged in activities, overactivity, behavior problems). Falling asleep at an unintended time, espe-
cially in school, is a common manifestation, as well as unplanned naps and planned naps past
an age when napping is appropriate. Insuff cient sleep, however, can also be manifested as the
following:
n Mood disturbance, including complaints of moodiness, irritability, emotional lability, de-
pression, and anger.
n Fatigue and daytime lethargy, including increased somatic complaints (headaches, muscle
aches).
n Cognitive impairment, including problems with memory, attention, concentration, decision-
making, and problem solving.
n Daytime behavior problems, including overactivity, impulsivity, and noncompliance.
SLEEP 101 3
n Risk-taking behaviors, especially in adolescents.

n Academic problems, including chronic tardiness related to insuff cient sleep and school fail-
ure resulting from chronic daytime sleepiness.
n Use of stimulant medications, and other alertness enhancers such as caffeine and nicotine, to
artif cially maintain wakefulness and combat daytime fatigue.
Functions of Sleep: Cognition

Sleep is needed to:
Remember what we learned
Organize our thoughts, predict outcomes and avoid consequences, be goal-directed (execu-
tive functions)
React quickly
Work accurately and eff ciently
Think abstractly
Be creative
There are multiple causes of insuff cient sleep, including the result of a primary sleep disorder
(e.g., insomnia, obstructive sleep apnea); however, the predominant reasons are environmental:
n Academic and extracurricular demands can result in delayed bedtimes.
n Social activities, such as late-night socializing (including on the internet), often delay bedtime
in older children and adolescents.
n Television viewing time and playing computer and video games, particularly if there is a
television set and/or computer in the childs bedroom, may take priority over bedtime in some
families.
n Part-time employment, especially if over 20 hours per week, is associated with inadequate
sleep in teenagers.
n Early school start times are a major risk factor for inadequate sleep in older children and ado-
lescents. Given the need for 9 to 10 hours of sleep in adolescents, coupled with a delayed shift
in circadian rhythm, early school start times do not enable most adolescents to obtain adequate
sleep on a nightly basis.
Sl eeP Ar c h it ec t ur e
The framework or architecture of sleep is based on recognition of two distinct sleep stages: non-
REM (NREM) sleep and REM sleep (rapid eye movement or dream sleep). These stages are
def ned by distinct polysomnographic features of electroencephalographic (EEG) patterns, eye
movements, and muscle tone.
n NREM sleep may be viewed as a period of relatively low brain activity during which the regu-
latory capacity of the brain is actively ongoing and in which body movements are preserved.
Respiratory and cardiovascular parameters are regular in NREM sleep. After about the age of
6 months, NREM may be further divided as follows:
n Stage 1 (N1) sleep occurs at the sleepwake transition. Initial stage 1 typically lasts from
30 seconds to 5 minutes. Recall of fragmented visual imagery (hypnogogic hallucinations)

may occur as well as brief involuntary muscle contractions (hypnic jerks), both of which are
considered to be normal phenomena in most cases.
n Stage 2 (N2) sleep is usually considered the initiation of true sleep. It is characterized by
bursts of rhythmic rapid EEG activity called sleep spindles (f uctuating episodes of fast ac-
tivity, occurring after 4 weeks of age) and high-amplitude slow-wave spikes called K com-
plexes (f rst occurring at 6 months). The initial stage 2 period lasts from 5 to 25 minutes.
n Stage 3 (N3) is also known as deep sleep, SWS, or delta sleep (note that slow-wave sleep
is no longer divided into Stage 3 and 4). This stage of sleep is dominated by delta waves,
characterized by high-voltage, low-frequency activity. Respiration is slowest and most regu-
lar during SWS, and parasympathetic activity is high. The highest arousal threshold (the
period during which it is most diff cult to awaken) also occurs during SWS; the lowest
arousal threshold (the period during which it is easiest to awaken) is in stage 1. The initial
SWS period is about 30 to 45 minutes and is followed by a brief arousal (i.e., transition to
wakefulness or to a lighter sleep stage).
n REM sleep is characterized by desynchronized cortical activity (low-voltage, high-frequency
EEG) and the highest brain metabolic rate, dreaming, absence of skeletal muscle tone (except
for diaphragm, middle ear, and erectile muscles), lack of normal thermoregulation, and epi-
sodic bursts of phasic eye movements that are the hallmark of REM sleep. Several of these
characteristics of REM sleep (e.g., muscle atonia, dream mentation) have direct clinical rel-
evance to symptoms of REM-associated sleep disorders such as narcolepsy (e.g., cataplexy,
hypnogogic hallucinations). In young infants, REM sleep is termed active sleep and is char-
acterized by frequent muscle twitches and grimaces that parents may interpret as abnormal.
Until age 3 months, infants also enter sleep through REM. REM-associated alterations in
autonomic parameters (increased sympathetic tone) and changes in control of breathing not
only result in irregular respiration and heart rate, but also typically increase the severity of
sleep-disordered breathing during this stage of sleep. The f rst REM sleep period occurs about
70 to 100 minutes after sleep onset (REM onset latency) and lasts about 5 minutes.
Sleep Stage Percentages in Healthy Young Adults

Non-REM 75%80% (total)
Stage 1 2%5%
Stage 2 45%55%
Stage 3 3%23%
REM 20%25%
Sleep c ycles
NREM and REM sleep alternate throughout the night in cycles (ultradian cycles or rhythm) of
about 90 to 110 minutes (50 minutes in infancy and gradually lengthening to adult levels at about
school age); this typical pattern of nocturnal sleep is illustrated in a hypnogram (Figure 1.1).
Brief arousals normally followed by a rapid return to sleep often occur at the end of each sleep
cycle (4 to 6 times per night); this pattern of normal arousals plays an important role in the etiol-
ogy of problematic nightwakings in infancy and childhood (see Chapter 7). The relative propor-
tion of REM and NREM sleep per cycle changes across the night, such that SWS predominates
in the f rst third of the night and REM sleep in the last third. That is, REM sleep percentage
increases and SWS percentage declines over the course of the night. The potential clinical sig-
nif cance of this timing of sleep stages is apparent. For example, partial arousal parasomnias that
occur during NREM sleep primarily occur at the beginning of the night. In addition, there is a
signif cant reduction in REM sleep that occurs when the average adolescent has to awaken for an
early school start time.
The amount and timing of each sleep stage are also affected by a multitude of extrinsic factors.
For example, the amount and depth of SWS is determined by prior sleep loss, as well as the time
of sleep onset and the length of prior wakefulness. SWS is relatively protected by its appear-
ance early on in the nocturnal sleep period and is also preserved at the expense of other sleep
stages when total sleep amounts are restricted. There is also typically a dramatic increase in SWS
(rebound) during nights of recovery sleep following sleep restriction. REM sleep also demon-
strates this rebound phenomenon in recovery sleep, further highlighting the physiologic impor-
SLEEP 101 5
FIG 1.1. Hypnogram: Normal distribution of sleep stages in healthy children, adults, and the elderly.
tance of these two sleep stages. With an increase of REM sleep, there may be reports of increased
and/or more vivid dreams. REM sleep is also intimately linked to circadian body temperature
rhythms. The relative percentage of sleep stages on a given night is also a ref ection of other fac-
tors, such as circadian rhythm disruption associated with shift work or jet lag (causes disruption
of timing of REM sleep), stress (may increase REM sleep need), and medications, which have
both direct effects and withdrawal effects, especially on SWS and REM sleep (see Chapter 20).
Sleep also changes as a function of age (see Table 1.1). Both the emergence of def ned sleep
stages and the proportion of sleep that each occupies have a distinct ontogenic and developmental
pattern. Although a more detailed discussion of the development of sleep patterns and behaviors
across infancy and childhood is found in Chapter 2, several general trends in normal sleep pat-
terns across childhood are listed below; these may be summarized as the gradual assumption of
more adult sleep patterns as children mature. These trends ref ect the physiologic and chronobio-
logic, developmental, and social and environmental changes that are occurring across childhood
and include:
n A decline in the average 24-hour sleep duration from infancy through adolescence, which
involves a decrease in both diurnal and nocturnal sleep amounts. In particular, there is a dra-
matic decline in daytime sleep (scheduled napping) by age 5 years, with a less marked and
more gradual continued decrease in nocturnal sleep amounts into late adolescence.
t ABl e 1.1. Normal developmental changes in childrens sleep architecture
Age Category Sleep Physiology

Newborns 3 sleep states: active (REM-like; 50% of sleep) quiet (non-REM-
like), and indeterminate
Enter sleep through active state
Infants (01 yrs) Amount of active/REM sleep declines
Development of 4 stages of non-REM sleep
Sleep cycles every 50 minutes
Enter sleep through non-REM
Toddlers (13 yrs) REM sleep amounts continue to decline
Pre-school (36 yrs) REM sleep amounts continue to decline
Sleep cycles every 90 minutes
High levels of slow-wave sleep (SWS)
Middle Childhood (612 yrs) Latency from sleep onset to REM sleep increases
High sleep eff ciency (time asleep/time in bed)
Adolescence (>12 yrs) 40% decline in SWS
REM sleep at adult levels (25%30%)
n A dramatic decrease in the proportion of REM sleep from birth (50% of sleep) through
early childhood into adulthood (25% to 30%), and a similar initial predominance of SWS
that peaks in early childhood, drops off abruptly after puberty (40% to 60% decline), and
then further decreases over the life span. This SWS preponderance in early life has clinical sig-
nif cance; for example, the high prevalence of partial arousal parasomnias (sleepwalking and
sleep terrors) in preschool and early school-aged children is related to the relative increased
proportion of SWS in this age group.
n Due to the lengthening of the ultradian sleep cycle, a concomitant decrease in the number of
end-of-cycle arousals across the nocturnal sleep period occurs.
n A gradual shift to a later bedtime and sleep onset time that begins in middle childhood and
accelerates in early to mid-adolescence.
n Irregularity of sleepwake patterns characterized by increasingly larger discrepancies be-
tween school night and non-school night bedtimes and wake times and increased weekend
oversleep that typically begin in middle childhood and peaks in adolescence.
n eur o An At o My An D Ph ySio l o g y o F Sl eeP

Although it shares many features with the awake state, sleep is not merely the absence of wake-
fulness and vice versa. There are many highly complex neural networks and related processes that
actively control the three distinct states of wakefulness, NREM sleep, and REM sleep. Further-
more, sleep is an active process during which many physiologic, metabolic, and neurobehavioral
functions are ongoing.
Wakefulness is promoted by ascending projections that originate in neurons located in the
brainstem (reticular formation) as well as hypothalamic pathways (Figure 1.2). These largely ex-
citatory neurons relay sensory input to the thalamus, hypothalamus, and basal forebrain (BF) and
activate vast areas of the cortex to increase wakefulness; their activity is suppressed during sleep.
Cholinergic neurons of the dorsal midbrain and pons (pedunculopontine nucleus [PPT] and the
laterodorsal tegmental nucleus [LDT]) also demonstrate increased activity during wakefulness
and REM sleep and decreased activity during NREM sleep; they send excitatory projections to
SLEEP 101 7
FIG 1.2. Ascending arousal systems in the brainstem and posterior hypothalamus. Pedunculopontine and
laterodorsal tegmental areas (PPT/LDT), locus coeruleus (LC), tuberomammillary nucleus (TMN), substan-
tia nigra and ventral tegmental area (SN/VTA), basal forebrain (BF). ACh, acetylcholine; HA, histamine;
DA, dopamine; 5-HT, serotonin; NE, norepinephrine. From Espaa, RA; Scammell TE. Sleep neurobiology
for the clinician. Sleep 2004;27(4):811820.
the thalamus, where they then regulate cortical activity and allow the f ow of information through
the thalamus to and from the cortex (thalamocortical activation). Cholinergic neurons located in
the BF also send projections throughout the cortex, hippocampus, and amygdala; their activity is
high during wakefulness and REM sleep and low during NREM sleep.
A number of neurotransmitters and of neuropeptides actively modulate and inf uence wake-
fulness promotion. These include acetylcholine (increased in wakefulness and REM sleep) and
a number of aminergic neurotransmitters (increased in wakefulness and very low in REM; see
Figure 1.2), including histamine in the tuberomammillary nucleus (posterior hypothalamus); do-
pamine in the ventral tegmental area, substantia nigra, posterior hypothalamus and brainstem;
serotonin in the median and dorsal raphe; and norepinephrine (NE) in the locus coeruleus (mid-
brain). While coordinated activity across these arousal systems is necessary for complete and
sustained wake states, each aminergic pathway may mediate different functions of wakefulness.
For example, histamine appears to be the major arousal-promoting neurotransmitter at wake on-
set; NE increases cortical activation, particularly under conditions of stress and in the presence
of novel stimuli; and dopamine may be more likely to promote wakefulness under conditions
of motivation or physical activity. Finally, neurons in the lateral or posterior hypothalamus that
produce hypocretin and orexin are also active during the wake state (Figure 1.3); a def ciency of
hypocretin or orexin has been shown to be the primary etiology of both the excessive daytime
sleepiness and cataplexy in narcolepsy. Hypocretin and orexin function also appears to be linked
to control of feeding behaviors, locomotion, and autonomic functions.
The ventrolateral preoptic area in the anterior hypothalamus (VLPO) is a major sleep-promot-
ing area of the brain (Figure 1.4); most likely distinct sub-regions of the VLPO control NREM
and REM sleep. During sleep, especially SWS, VLPO neurons are active and exhibit high f ring
rates. VLPO neurons send projections to all major wake-promoting regions, including the tuber-
omamillary nucleus (TMN), locus ceruleus (LC), and LDT and PPT. These inhibitory neurons
are believed to induce sleep by coordinating the inhibition of all the wake-promoting cholinergic
and aminergic regions. Most VLPO neurons release the inhibitory neurotransmitter gamma ami-
nobutryic acid (GABA) at their sites of projection, while some utilize the inhibitory neurotrans-
FIG 1.3. Ascending arousal systems in the brainstem and hypothalamus: role of orexin/hypocretin. From
Espaa RA & Scammell TE. Sleep neurobiology for the clinician. Sleep 2004;27(4):811820.
FIG 1.4. Control of non-REM sleep. From Espaa RA & Scammell TE. Sleep neurobiology for the clini-
cian. Sleep 2004;27(4):811820.
FIG 1.5. Control of REM sleep. From Espaa RA & Scammell TE. Sleep neurobiology for the clinician.
Sleep 2004;27(4):811820.
SLEEP 101 9
mitter galaninin. The control of REM sleep involves the interaction of brainstem cholinergic and
aminergic neurons in a complex feedback loop; neurons releasing acetylcholine (LDT/PPT re-
gion) are disinhibited by the suppression of aminergic neurons [e.g., NE, histamine] during REM
(Figure 1.5). REM-associated muscle atonia is linked to inhibition or loss of excitation of motor
neurons in the brainstem and spinal cord via the medulla; these pathways originate in the LDT
and PPT and involve neurotransmitters including acetylcholine (Ach), glutamate, and glycine.
These complex relationships help to explain the powerful sleep effects of drugs that alter the
balance in these complex and inter-related systems. For example, sleep-promoting benzodiaz-
epines and antihistamines enhance GABA signaling and block histamine receptors, respectively.
Tricyclic antidepressants and serotonin reuptake inhibitors act as REM suppressants due to their
enhancement of aminergic signals and the resultant inhibition of REM-promoting neurons. Psy-
chostimulants promote wakefulness by increasing dopamine and NE signals.
Sl eeP r eg ul At io n
Sleep and wakefulness are regulated by two basic, highly coupled processes operating simultane-
ously (the two process sleep system [Figure 1.6]):
n Homeostatic process (process S): This process primarily regulates the length and depth of
sleep. The homeostatic drive may be related to the accumulation of adenosine and other sleep-
promoting chemicals (somnogens), such as cytokines, during prolonged periods of wakeful-
ness; caffeine most likely exerts its wake-promoting effect by blocking adenosine receptors.
This sleep pressure appears to build more quickly in infants and young children, thus limiting
the duration of sustained wakefulness during the day and necessitating periods of daytime
sleep (i.e., naps).
n Endogenous circadian rhythm (process C): This process inf uences the internal organi-
zation of sleep and timing and the duration of daily sleepwake cycles. It also governs pre-
dictable patterns of alertness throughout the 24-hour day. The master circadian clock that
controls sleepwake patterns is located in the suprachiasmatic nucleus (SCN) in the ventral
hypothalamus; other circadian clocks govern the timing of multiple other physiologic sys-
tems in the body (e.g., cardiovascular reactivity, hormone levels, renal and pulmonary func-
FIG 1.6. Normal distribution of sleep stages in healthy children, adults, and the elderly. (From Dement
WC & Vaughan C. The promise of sleep: a pioneer in sleep medicine explores the vital connection between
health, happiness, and a good nights sleep. New York: Delacorte Press, 1999.)
tions). Circadian rhythms are generated by the expression of specif c clock genes. The cir-
cadian timing system develops rapidly in the f rst 6 months of life as a result of the combined
inf uence of neurodevelopmental maturation and social and environmental cues (especially
lightdark cycles).
The relative level of sleepiness (sleep propensity) or alertness existing at any given time during
a 24-hour period is partially determined by the duration and quality of previous sleep as well as
time awake since the last sleep period (the homeostatic drive or sleep drive). Interacting with
this sleep homeostat is the 24-hour cyclic pattern or rhythm characterized by clock-dependent
periods of maximum sleepiness (circadian troughs) and maximum alertness (circadian na-
dirs). There are two periods of maximum sleepiness, one in the late afternoon (3:00 to 5:00
p.m.) and one towards the end of the night (3:00 to 5:00 a.m.) and two periods of maximum alert-
ness, one in mid-morning and one in the evening, just prior to sleep onset (the so-called second
wind). In addition, relative sleepiness and wakefulness are inf uenced by many other variables,
including individual factors (e.g., age and individual variations in sleep needs and tolerance to the
effects of inadequate sleep); the nature of the task being performed (e.g., type, length, complex-
ity); and environmental and physiologic factors (e.g., noise, light, ambient temperature, satiety)
that may unmask but do not cause sleepiness. Finally, a phenomenon known as sleep inertia,
def ned as a period of incomplete arousal characterized by confusion, impaired judgment, and
poor memory consolidation occurring immediately upon waking from sleep, may further com-
promise alertness levels (particularly in the early morning).
Because the human circadian clock is actually slightly longer than 24 hours, intrinsic circa-
dian rhythms must are synchronized or entrained to the 24-hour-day cycle by environmental
cues called zeitgebers. In the absence of zeitgebers, circadian rhythms are desynchronized or
uncoupled from one another (what is termed the free-running state). The most powerful of
these zeitgebers is the lightdark cycle; light signals are transmitted to the SCN via the circadian
photoreceptor system within the retina (functionally and anatomically separate from the visual
system), which switch the bodys production of the hormone melatonin off (light) or on (dark)
by the pineal gland. Circadian rhythms are also synchronized by other external time cues, such
as timing of meals and alarm clocks. Thus, daytime schedules that are not consistently regulated
may further exacerbate circadian disturbances such as delayed sleep phase disorder. Finally, re-
cent research also supports an important role for genetics in determining intrinsic circadian clock
periodicities and, thus, inf uencing individual circadian preference for sleepwake cycle timing
(night owl versus morning lark).
The Importance of Morning Light Exposure

Morning light exposure is one of the most powerful inf uences on a persons sleepwake
schedule. Early morning light exposures basically sets a persons internal clock for the day. For
example, research has shown that morning light inf uences sleep consolidation in newborns
and infants, and it is critical for keeping an adolescents schedule on track. So families should
be encouraged to expose their child to bright light in the morning, whether that is heading out
for a walk or a trip to the playground in the morning, eating breakfast in the sunniest place in
the house, or having adolescents open their bedroom shades and avoid wearing sunglasses on
their way to school.
Sl eeP AS An in t r in Sic Bio l o g ic Al Pr o c eSS An D Sl eeP AS A

l eAr n eD Beh AVio r
Despite the seemingly contradictory nature of this statement, it is important for the pediatric
practitioner to understand the implications of both of these concepts in approaching sleep and
sleep problems in children. Few clinical paradigms in pediatrics are a better example of the need
SLEEP 101 11
for a biopsychosocial approach than sleep. While our scientif c understanding of the structure,
organization, regulation, and development of sleep has advanced signif cantly in the past decade
and has elucidated much regarding the genetics and neurobiology of sleep, it is clear that sleep is
also impacted by multiple psychosocial factors, ranging from exposure to environmental toxins,
such as lead; to cultural variables, such as co-sleeping practices; and to community standards
such as school start times. While much of the chronobiological hard-wiring of sleep is immu-
table, the plasticity of the developing brain makes it likely that sleep and its relationship to other
neural systems in the brain are also highly susceptible to environmental inf uences. Furthermore,
the construct that much of sleep behavior is learned behavior not only underscores the impor-
tance of developing health-promoting sleep behaviors early in childhood but also emphasizes the
role that parents and healthcare providers may play in shaping and modifying sleep behaviors in
children.
2 Sleep in Infancy, Childhood,
and Adolescence
g en er Al c o n SiDer At io n S
The evaluation of pediatric sleep problems f rst and foremost requires a basic understanding of
what constitutes normal sleep in infants, children, and adolescents. Sleep disturbances, as well
as many characteristics of sleep itself, have some distinctly different features in children from
those in adults. As outlined in Chapter 1, normal sleep architecture changes signif cantly over the
f rst two decades of life. In addition, sleep patterns and sleep behaviors also evolve and are modi-
f ed by both intrinsic (e.g., normal development) and extrinsic (e.g., environment, parenting
practices) processes as children progress from infancy to middle childhood through adolescence.
Appreciation and understanding of these changes are needed to provide parents with anticipa-
tory guidance regarding normal sleep and sleep patterns at different developmental stages. For
example, two important developmental milestones are normally achieved during the f rst 6
months of life; these are known as sleep consolidation and sleep regulation. Sleep consolida-
tion is generally described as an infants ability to sleep for a continuous period of time that is
concentrated during the nocturnal hours, augmented by shorter periods of daytime sleep (naps).
Because this developmental progression occurs over the f rst few months of life, parents should
be counseled not to expect their infant to sleep through the night until about 3 months of age.
Sleep regulation refers to the infants ability to be able to control internal states of arousal (e.g.,
self-soothe) in order to both fall asleep at bedtime without parental intervention or assistance,
and to fall back to sleep following normal brief arousals during the night. Thus, anticipatory
Educacin guidance counseling to put a baby to sleep drowsy but awake is most appropriately initiated at
preventiva
the 2-month visit, so that parents can begin to establish the conditions under which their baby can
more readily learn to self-soothe. Studies indicate that sleep at 3 months is an important predic-
tor of future sleep habits, as the ability to fall asleep independently at this age is associated with
los trastornos de
sueno
fewer nightwakings at 6 and 12 months. Thus, preventive education is essential.
estan relacionados
con
The relative prevalence and the various types of sleep problems that occur throughout child-
procesos fisicos,
cognitivos
hood must also be understood in the context of normal physical and cognitive/emotional phenom-
y emocionales
situaciones
ena that are occurring at different developmental stages. For example, normal separation anxiety
in older infants may be associated with increased bedtime problems; development of normal
La relacion entre
la creencia de los
fears in toddlers may result in nighttime fears and problematic nightwakings; and the prevalence
padres sobre los
trastornos del
of obstructive sleep apnea in preschoolers is linked to the relative prominence of lymphoid tissue
sueno y el
pensamiento de
(adenotonsillar hypertrophy) in early childhood. Parental identif cation and reporting of sleep
los ninos problems in children also varies across childhood, with parents of infants and toddlers more
likely to be aware of sleep concerns than those of school-aged children and adolescents. For
example, a poll by the National Sleep Foundation found that just 7% of parents thought that their
adolescent had a sleep problem, whereas 16% of adolescents themselves thought so. One-third
of these adolescents had not told anyone about their sleep issues. Finally, the very def nition of a
sleep problem by parents is often highly subjective and is commonly determined by the amount
of disruption caused to parents sleep.
In addition to considering sleep disturbances in a developmental context, it is important for
the clinician to recognize that a number of other important child, parental, and environmental
variables affect the type, relative prevalence, chronicity, and severity of sleep problems. Child
variables that may signif cantly impact sleep include temperament and behavioral style, indi-
12
SLEEP IN INFANCy, CHILDHOOD, AND ADOLESCENCE 13
vidual variations in circadian preference, medical problems, delays in development, and acute
and chronic stress. Parental variables include parenting styles, parents educational level and
knowledge of child development, mental health issues, family stress, quality and quantity of par-
ents sleep, and fatigue level. Environmental variables include the physical environment (space,
sleeping arrangements), family composition (number, ages, and health status of siblings and
extended family members), lifestyle issues (working parents, regularity of daily schedule), and
cultural issues and family values (importance and meaning of sleep, acceptance of co-sleeping).
La siesta
deoende de Finally, recent research including over 30,000 children ages 0 to 3 years indicates great variabil-
lo biologico
mientras que ity in sleep amounts and sleep behaviors across cultures, with children in different countries and
el
comportamie regions obtaining signif cantly more or less overall sleep at night. Interestingly, there are almost
nto nocturno
depende de no differences in daytime sleep, indicating that napping likely has a strong biological context,
factores,
culturales, whereas nighttime sleep is inf uenced by environmental and cultural factors, as well as potentially
geneticos
etc by biologic and genetic factors. Other studies also indicate that the amount of daytime sleep is
strongly negatively correlated with age and that the inf uence of environment is relatively limited.
Nature vs. Nurture

Sleep habits, in general, may be viewed as learned behaviors superimposed on fundamental
processes of circadian and sleep biology that, in turn, may be modif ed by genetic factors and
developmental changes.
A description of normal sleep patterns, developmental issues, common parental sleep concerns,
prevalence and types of common sleep problems, and other sleep issues in different age groups is
provided below, followed by general sleep hygiene tips. Suggested specif c anticipatory guidance
points to emphasize during well-child visits are provided in Table 2.1.
What Is Enough Sleep?

The simple answer to the question is the amount of sleep that a child needs to feel well
rested. Parents are generally quite good at acknowledging behaviors that are associated with
being overtired (whininess, moodiness, having a short fuse, hyperactivity) at the end of
the day but may need help in recognizing that these signs may be evidence of chronically
inadequate sleep.
The numbers given below for average sleep duration at different ages represent the best
information that is currently available. Recent research in adults and some preliminary data
in children suggest, however, that there are individual variations in both sleep needs and toler-
ance levels to inadequate sleep, within certain basic parameters of human sleep needs. Indi-
vidual variations in sleep times are highest in the f rst 3 years, especially in the f rst 12 months.
If parents are uncertain as to the amount of sleep their child needs to function optimally,
monitoring sleep amounts and mood while allowing a child to sleep until he or she awakens
spontaneously in the morning for at least 3 days (during vacation, for example) may help in
sorting out this issue.
n ew Bo r n S (0 t o 2 Mo n t h S)
n ormal Sleeping Patterns
n Hours of sleep:
n Total sleep: 10 to 19 hours per 24 hours (average = 13 to 14 1/2 hours), may be higher in
premature babies.
n Bottle-fed babies generally sleep for longer periods (2-hour to 5-hour bouts) than breast-fed
babies (1 to 3 hours).
n Sleep periods are separated by 1 to 2 hours awake.
n No established nocturnal or diurnal pattern in the f rst few weeks; sleep is evenly distributed
throughout the day and night, averaging 8 1/2 hours at night and 5 3/4 hours during the day.
Developmental issues t hat May impact Sleep

n Sleepwake cycles are largely dependent on hunger and satiety; circadian rhythms and en-
vironmental cues play a much smaller role in newborns than in older infants. Immaturity of
the circadian sleepwake system and melatonin production results in limited rhythmicity and
predictability of sleep.
c ommon Sleep issues

n Day/night reversal: Day/night reversal is common in the f rst few weeks; increasing the in-
fants activity during the day and promoting dim lights at night will help align sleep with
nighttime. Studies indicate that newborns often have limited bright light exposure; however,
increased natural light exposure, especially in the morning, is associated with improved sleep
at night.
n Irregular sleep patterns: Regular rhythm of periods of sleepiness and alertness will emerge
by 2 to 3 months.
n Active vs. quiet sleep: The smiling, grimacing, sucking, snuff ing, and body movements such
as twitches and jerks that are typical of active sleep (equivalent to REM sleep) in infants may
be misinterpreted by parents as restless or disturbed sleep.
n Sleeping environment: Options include a bassinet or crib in a siblings or babys own room or
a bassinet or crib in the parents room. Sleeping in the parental bed may pose a risk of acciden-
tal suffocation or strangulation, particularly under unsafe sleeping conditions (e.g., maternal
smoking, obesity, or use of alcohol or sedating medications; sleeping on a couch or with mul-
tiple family members). The American Academy of Pediatrics (AAP) issued a formal recom-
mendation in 2005 advocating against bed-sharing in the f rst year of life, instead encouraging
proximate but separate sleeping surfaces for mother and infant. The infants bedroom and sur-
rounding environment (e.g., lighting) should be the same at bedtime as it will be throughout
the night in order to avoid the development of inappropriate sleep onset associations.
n Sleeping surface: Safety and prevention of accidental suffocation and strangulation are key
considerations. Crib mattresses should provide a f rm sleeping surface and f t tightly in the
crib, and no pillows or comforters should be used. The distance between crib slats should be
no greater than 2 38 inches.
n Sleeping position: Empirical studies have clearly demonstrated that sleeping in the prone po-
sition (back to sleep) signif cantly reduces the risk of sudden infant death syndrome (SIDS).
Safe Sleep Practices for Infants

Place the baby on his or her back to sleep at night and during naptimes.
Place the baby on a f rm mattress with a well-f tting sheet in a safety-approved crib.
Do not use pillows or comforters
Cribs should not have corner posts over 1116 inch high or decorative cut-outs.
Make sure the babys face and head stay uncovered and clear of blankets and other coverings
during sleep. If a blanket is used, make sure the baby is placed feet to foot (feet at the bot-
tom of the crib, blanket no higher than chest level, blanket tucked in around mattress) in the
crib. Consider using a sleeper rather than a blanket.
Create a smoke-free zone around the baby.
Avoid overheating during sleep by maintaining the babys bedroom at a temperature com-
fortable for an average adult.
Remove all mobiles and hanging crib toys by age 5 months, when the baby begins to pull up
in the crib.
Crib bumpers may prevent minor injuries but have been under recent scrutiny related to
deaths due to strangulation and suffocation.
n Parental sleep: Parental sleep also needs to be a priority; sleep deprivation is associated with
maternal mood changes and is a risk factor for postpartum depression.
Prevalence of Sleep Problems

Most sleep issues that are perceived as problematic at this stage represent a discrepancy between
parental expectations and developmentally appropriate sleep behaviors. Newborns who are noted
by parents to be extremely fussy and persistently diff cult to console are more likely to have un-
derlying medical issues, such as colic, gastroesophageal ref ux, and formula intolerance.
o ther important c oncepts

n Parents should be encouraged to learn to recognize both their newborns intrinsic sleepwake
rhythms and signs of drowsiness (e.g., eye rubbing, irritability, yawning); delaying the oppor-
tunity to sleep when these signs occur may result in more diff culty settling.
in FAn t S (2 t o 12 Mo n t h S)
n Hours of sleep:
n Nighttime: average is 9 to 10 hours
n Naps: average is 3 to 4 hours
n Total sleep: average is 12 to 13 hours (note that there is great individual variability in sleep
times during infancy)

n Naps: Decrease from 4 to 1, with fewer as infants get older, each lasting from 30 minutes to
2 hours. Although most infants move to a longer morning/afternoon nap schedule by 6 months
of age, many infants continue to take several short naps of 30 to 45 minute duration until the
age of even 9 or 10 months, with naps typically following 1 1/2 to 2 hours of awake time.

n Issues of attachment and social interaction are felt to play an important role in shaping sleep
behaviors. For example, infants who are insecurely attached have been reported to have more
sleep problems, although sleep problems do not necessarily imply attachment concerns. On
the other hand, studies have shown that infants who are more socially engaged with their care-
taker may be more reluctant to interrupt social interactions at bedtime for sleep.
n Acquisition of gross motor developmental milestones (e.g., rolling over, pulling to standing,
crawling) and other such events may temporarily disrupt sleep, with one study indicating sleep
disruption occurring in the weeks prior to walking.
n As object permanence develops in the second half of the f rst year, separation anxiety may
result in increased bedtime resistance and problematic nightwakings.
Sleep as a Social Behavior

Sleep behavior in infancy, in particular, must be understood in the context of the relationship
and interaction between child and caregiver, which impacts greatly on the quality and quantity
of sleep.

n Sleep regulation or self-soothing involves the infants ability to negotiate the sleepwake
transition both at sleep onset and following normal awakenings throughout the night. The ca-
pacity to self-soothe begins to develop in the f rst 12 weeks of life, and is a ref ection of both
neurodevelopmental maturation and learning.
n Sleep consolidation or sleeping through the night, although operationally def ned by some
researchers as a period of sleep without waking from 12:00 a.m. to 5:00 a.m., is typically
def ned by parents as a continuous sleep episode without the need for parental intervention
(e.g., feeding, soothing) from the childs bedtime through the early morning. Infants develop
the ability to consolidate sleep between 6 weeks and 3 months, and studies suggest that about
50% to 80% of infants sleep through the night on a regular basis by 9 months.
n Sleep onset associations are those conditions that are present at the time of sleep onset and to
which the infant becomes conditioned in order to fall asleep; these may include being rocked
or fed or sucking on f ngers or a pacif er. These same conditions may be required again during
the night in order for the infant to fall back asleep following normal nighttime arousals; in-
appropriate or problematic sleep onset associations are typically those that require parental
intervention (see Chapter 7).
n Nighttime arousals are a consequence of the normal ultradian rhythm of 90-minute to
120-minute sleep cycles. Most infants and children arouse brief y on average 2 to 6 times
throughout the night. Characterization of these nighttime arousals include the following
considerations:
n Self-soothers vs. non-self-soothers: Babies who soothe themselves back to sleep
generally experience brief arousals rather than prolonged nightwakings. This capacity to
self-soothe is associated with the practice of being put to bed while drowsy but still awake
and without sleep onset associations that will be unavailable during the night. It may be
benef cial to suggest to parents that they help their infant develop appropriate sleep onset
associations by 3 to 6 months that will be readily available to the infant during the night
without the need for parental intervention (e.g., falling asleep independently in crib, thumb-
sucking, use of a transitional object).
n Signalers vs. nonsignalers: During nighttime arousals or awakenings, infants may
alert (signal) parents by crying or may return to sleep without disrupting parental sleep
(nonsignalers). Not surprisingly, signalers are more likely to be labeled by parents as having
problematic sleep. It has been estimated that 20% to 30% of 1-year-olds are considered to
be signalers.
n Parental intervention vs. nonintervention: Parents can choose whether or not to respond,
how quickly to respond, and the type of response (e.g., verbal soothing, rocking, or feed-
ing) to a signaled or nonsignaled nighttime arousal or awakening. The practice of parents
responding immediately to signaled nightwakings, particularly if the social or feeding inter-
action becomes reinforcing for the infant, may result in a trained night crier.
n Night-to-night variability: It should be noted that there is often considerable night-to-
night and week-to-week variability in all of these behaviors, and neither infants nor parents
are always consistent in the way they behave and interact. However, it is clear that a pattern
of persistent diff culty in self-soothing is associated with frequent and problematic night-
wakings in infants.
n Transitional objects, such as a pacif er or a blanket, become important during infancy. Pro-
viding the same object at naptime may strengthen attachment to a transitional object. A televi-
sion set is not a transitional object and should not be in the room where the baby sleeps or play
a role in the regular bedtime routine. Some infants respond positively to the use of a mothers
well-worn, knotted (to prevent accidental suffocation or strangulation) tee-shirt with her scent
as a comfort object.
n Night feedings do not improve the quality or quantity of sleep and, in most cases, are not
physiologically necessary after 6 months of age. If the bedtime transition to sleep onset rou-
tinely occurs in the context of feeding (breast or bottle), night feeding may become a necessary
component of the infants returning to sleep following nightwakings. The need for feedings
during the night may also become a learned behavior (learned hunger), which leads to more
frequent and prolonged nightwakings. Frequent night feedings may also disrupt sleep by re-
sulting in bladder distention and discomfort from soaked diapers. Finally, being put down to
sleep with a nighttime bottle may increase the risk of dental (baby bottle) caries and otitis
media. Breast-fed babies are likely to have more nighttime awakenings than bottle-fed babies.
In younger infants this may be related to hunger, but in older infants it is likely related to the
development of the habit of feeding to sleep.
Parents should be encouraged to wean their infant from middle-of-the-night feedings by 6
months and to avoid putting him or her to sleep with a bottle.
Pacif ers
Pacif er use during infancy is somewhat controversial. Concerns have been raised regarding its
potential negative impact on establishment of breastfeeding, the possible risk of it becoming a
prolonged habit, and the need for parental intervention to replace the pacif er during the night
in young infants, thus creating an inappropriate sleep onset association (after the age of 6 to
8 months, most infants are physically capable of f nding a displaced pacif er during the night;
some parents scatter several in one corner of the crib to increase this likelihood). However,
based on a number of epidemiologic studies of SIDS risk and preventive factors, the AAP
now recommends the use of pacif ers at bedtime to reduce the risk of SIDS in infants (2005).

Many sleep problems that occur before the age of 6 months are def ned as such because of a
discrepancy between unrealistic parental expectations in regards to meeting developmental sleep
milestones (e.g., sleeping through the night, settling at bedtime) and normal maturation of
the infant; thus, these problems are likely to be transient in nature. Others are the result of a
mismatch between infant behavior and parental expectation. Temporary sleep disturbances that
occur in conjunction with developmental milestones, as well as acute illnesses, also tend to be
self-limited if parents avoid engaging in behaviors that reinforce diff culty settling or nightwak-
ings, such as resorting to rocking to sleep. However, not all infant sleep problems are transient,
and certain factors appear to be associated with an increased risk of chronicity. These include
inability to self-soothe, diff cult temperament, maternal depression, and bed-sharing.
It is estimated that about 25% to 50% of 6- to 12-month-olds and 30% of 1-year-olds have
problematic nightwakings and about 50% have sleep onset or settling diff culties at 12 months.
c ommon Sleep Disorders

n Nightwakings/behavioral insomnia of childhoodsleep onset association type (see Chapter 7)
n Sleep related rhythmic movements (head banging, body rocking, body rolling) commonly
present in the f rst year of life (see Chapter 11)

n Most infants benef t from a set sleep schedule with regular naptimes and bedtime that ref ects
the infants natural preferences for sleep and waking patterns as well as family lifestyle issues.
n At the 2-month visit, parents should be encouraged to start putting the infant to bed drowsy but
awake within the next 4 to 8 weeks.
n A consistent and enjoyable bedtime routine leading up to sleep onset should be established
by the age of 3 months. Studies indicate that a bedtime routine results in reduced sleep onset
diff culties and nightwakings. The bedtime routine may include any of the following: feeding,
bath, story, music, massage, and rocking.
n Parents should be encouraged to take the opportunity to nap or rest when the infant is sleeping.
n It is important to discuss the possibility with parents that their previously great sleeper may
develop transitory problems with nightwakings and bedtime resistance during times of stress
or in association with achievement of developmental milestones. Avoidance of parental rein-
forcement (e.g., attention, night feedings) often prevents a small, temporary sleep problem
from becoming a large and chronic one.
To Co-sleep or Not to Co-sleep

Co-sleeping, which may be broadly def ned as including room-sharing but more typically
refers specif cally to bed-sharing, is a topic that has generated a considerable amount of con-
troversy and discussion among pediatric practitioners, parent advocacy organizations, and the
general public. The issues that have been raised in defending or decrying the practice of co-
sleeping are myriad, ranging from the effects on the health of the co-sleeping infant (the AAP
recommends against the practice in the f rst year of life to prevent accidental suffocation,
while breastfeeding advocates cite the association between co-sleeping and reinforcement of
nursing practices) to both positive and negative psychosocial and developmental effects (indi-
viduation vs. intimacy, sexual attitudes, attachment) to sociologic and anthropologic consider-
ations as viewed in a family context (cultural and ethnic values).
The decision to co-sleep is made by families for a variety of reasons, which are important
to explore in addressing this issue in the healthcare setting. It is important to differentiate
between lifestyle or cultural co-sleeping, in which caregivers make a conscious decision
to have a family bed, and reactive co-sleeping, which is typically initiated by caregivers in
response to the childs sleep diff culties (e.g., bedtime resistance or nightwakings). Potential
safety concerns and other issues, such as parental sexual activity or the birth of a new sibling,
are appropriate to discuss with caregivers in the former situation, whereas working with par-
ents to develop workable solutions for sleep problems that do not involve bed-sharing is more
likely to be helpful for the latter circumstance.
Parents should be encouraged to share their practices and feelings; all too often, parents
are reluctant to be honest about the practice of co-sleeping for fear of disapproval from the
medical profession. It may be more useful to consider the strengths and vulnerabilities of the
individual child, parent, and parentchild dyad in assessing the potential risks of co-sleeping
in a given situation rather than adopting a one-size-f ts-all approach. Counseling parents on
this issue requires a sensitive, open, and nondogmatic approach, the goal of which is to more
effectively guide parents in making informed choices that are in their childs and familys best
interest.
t o DDl er S (12 Mo n t h S t o 3 yeAr S)

n ormal Sleep Patterns
n Hours of sleep:
n Nighttime: average is 9 1/2 to 10 1/2 hours
n Naps: average is 2 to 3 hours
n Total sleep: average is 11 to 13 hours (note that there is individual variability in sleep times
for toddlers)
n Naps decrease from two naps to one at an average age of 18 months. Overall, almost 100% of
1-year-olds and 81% of 2-year-olds take a nap, decreasing to just over half of 3-year-olds.

Gross motor:
n Independent locomotion and increased mobility makes it easier for the child to engage in
limit-testing behaviors (e.g., getting out of bed, coming into the parents bedroom) at bedtime
and during the night.
Cognitive:
n Drive to learn and rapid acquisition of skills may result in diff culty settling at bedtime.
n Comprehension of cause and effect enables the child to respond to simple behavioral
interventions.
n Understanding of the symbolic meaning of objects leads to increased interest in and reliance
on transitional objects.
n Development of imagination and fantasy may result in increased nighttime fears.
Language:
n Expressive language development lags behind receptive, which may limit verbal expression of
nighttime fears and concerns.
Social/emotional:
n The drive for autonomy and independence may lead to increased bedtime resistance.
n Separation anxiety is often associated with bedtime diff culties and increased nightwakings.
n Regression in behavior is a common stress response and may increase the likelihood of
co-sleeping.

n Naps: There are many components that can raise concerns with naps, including number, dura-
tion, timing, location, giving up, and need for naps. Restricting naps will not help a child sleep
better at night; however, placement of naps too close to the scheduled bedtime may interfere
with sleep onset.
n Transition from crib to bed: This step is usually taken between 2 and 3 years of age, or when
safety concerns related to falling while climbing out of the crib become an issue. In the latter
situation, a mesh crib tent is recommended to alleviate safety concerns while maintaining the
child in a crib. The transition to a bed at too young an age can often result in the development
of sleep problems because young children often do not have the cognitive development or
behavioral control to stay within the essentially imaginary boundaries of a bed. Waiting until
closer to age 3 to make the change is recommended. Similar to recommendations regarding
premature attempts at toilet training before the child is developmentally ready, parents should
be encouraged to temporarily switch back to a crib if the transition does not go smoothly, and
to wait and make the transition at a later age.
n Bedtime bottles and night feedings: As noted in the section on infants, the bedtime transi-
tion to sleep onset ideally occurs without a feeding in order to facilitate independent settling.
The same issues as described in infants in terms of learned hunger, arousals related to bladder
distention, dental caries, and increased risk of otitis media associated with nighttime bottles
apply to toddlers as well.
n Bedtime routines: These are an important daily ritual for parents to develop and maintain in
order to help ease the transition from high levels of activity during the day to sleep onset. The
events of the bedtime routine should be consistent, occur in the same temporal order, and be
of an increasingly relaxing nature for that particular child as bedtime nears. As with infants,
a recent study found that the institution of a consistent bedtime routine in toddlers reduced
latency to sleep onset and improved nighttime sleep.
n Transitional objects: Introducing these, such as blankets, dolls, and stuffed animals, at bed-
time and naptime becomes increasingly important at this stage and helps to foster independent
settling and self-soothing. The practice of thumbsucking and use of pacif ers, especially if lim-
ited to nighttime, is unlikely to result in signif cant orthodontic problems before age 4 years,
and should not be discouraged.

Sleep problems in toddlers are very common, occurring in 25% to 30% of this age group. Bed-
time resistance and stalling at bedtime, found in 25% to 30% of toddlers, and nightwakings
in up to 50%, are the two most common concerns of parents, followed by nighttime fears and
nightmares. Sleep problems may also be persistent, especially in children with daytime behavior
problems. Conversely, daytime behavior problems are more common in poor sleepers (45%).

n Bedtime problems/behavioral insomnia of childhoodlimit setting type (see Chapter 6)
n Sleep related rhythmic movements (head banging, body rocking, body rolling) may continue
into the preschool years (see Chapter 11)

n Secondary prevention involves avoiding reinforcement of transitory sleep problems and pre-
venting a sleep disturbance from becoming a sleep disorder.
n Sleep disturbances are often manifested in daytime behavior as a result of the bidirectional
effects of sleep on behavior.
n It should be noted that in children with nightwaking problems, there may be a golden win-
dow of opportunity to initiate a behavioral intervention, such as a graduated extinction pro-
gram (see Chapter 7) before the child is transitioned to a bed and is, thus, easily able to come
into the parents bedroom during the night.
Cultural and Family Context of Sleep

It is important to always consider the cultural and family context within which sleep problems
in children occur. How we sleep, where we sleep, with whom, and for how long we sleep are
all molded by culture and customs. For example, co-sleeping of infants and parents is a com-
mon and accepted practice in many ethnic groups, including African-American, Hispanic,
and Asian families. Therefore, the goal of independent self-soothing in young infants may not
be shared by these families. The relative importance of sleep as a health behavior, normal
sleep practices such as napping patterns and bedtime rituals, the sleeping environment, and the
relative acceptability of various treatment strategies for sleep problems (e.g., the cry-it-out
approach) are just a few additional examples of sleep issues that are inf uenced by cultural
and family values and practices. Furthermore, not only is the range of sleep behaviors that
may be considered normal or pathologic wide, but the very def nition of what constitutes
a problem is often quite subjective and highly dependent on culturally determined factors.
These factors include parents awareness of, expectations for, and tolerance of sleep behaviors
and the perceived societal impact of sleep problems and insuff cient sleep on childrens health,
behavior, and learning. Figure 2.1 summarizes the myriad inf uences that help to determine
optimal sleep in children.
Pr eSc h o o l - Ag eD c h il Dr en (3 t o 5 yeAr S)
n ormal Sleep Patterns
n Hours of sleep:
n Nighttime: average is 9 to 10 hours
n Naps decrease from 1 nap to no nap. Overall, 26% of 4-year-olds and just 15% of 5-year-olds
nap. However, one study found that African-American children were more likely to continue
to take daytime naps until a later age compared to Caucasian children, with no difference in
total sleep time across the groups (i.e., the Caucasian children had earlier bedtimes and slept
longer at night).

n Expanded language and cognitive skills may lead to increased bedtime resistance, as children
become more articulate about their needs and may engage in more limit-testing behavior.
Macro Sleep Micro Sleep

Environment Environment
(temp, noise, light, toxins, (sleep surface, bedding,
safety) position)
Sleep Practices Health Issues

(schedules, feeding, Optimal Sleep (illness, meds,
napping) nutrition)
Socio-Emotional
Socio-Cultural Context
Context Developmental
(attachment, Context
(values, temperament,
parenting practices) (sleep, cognitive)
maternal mental
health/stress
FIG 2.1. Factors that play a role in determining optimal sleep in children.
n A developing capacity to delay gratif cation and anticipate consequences enables preschoolers
to respond to positive reinforcement (e.g., sticker charts) for appropriate bedtime behavior.
n Further development of imagination and fantasy may heighten nighttime fears.
n Increasing interest in developing literacy skills reinforces the importance of reading aloud at
bedtime as an integral part of the bedtime routine.

n Co-sleeping and parent presence: Persistent co-sleeping tends to be highly associated with
sleep problems in this age group. Almost 50% of preschoolers have a parent present when
falling asleep at bedtime, which may result in diff culty sleeping independently and prolonged
nightwakings.
n Sleep schedules: Preschoolers need a set, consistent bedtime and waketime. A regular and
consistent daytime routine (e.g., meals, playtimes) also helps to regularize the sleepwake
schedule. Children who are not in morning school or daycare settings may do f ne with a rela-
tively later bedtime and waketime but may need to readjust their schedule once school starts.
Parents should be encouraged to start this gradual process several weeks in advance of the
anticipated change in morning schedule.
n Second wind or forbidden zone: The normal evening circadian-mediated surge in alertness
and activity levels that occurs in everyone may have an exaggerated behavioral component in
some children; it also may occur relatively later in children who are natural night owls. Thus,
if (attempted) bedtime coincides with the timing of this circadian drive towards wakefulness,
the likely result is bedtime resistance. Temporarily delaying the bedtime to coincide with the
preferred sleep onset time and then moving it gradually earlier often successfully addresses the
problem of a child being consistently wide awake at bedtime.
Los casos de Prevalence of Sleep Problems

chicos que Diff culties falling asleep and nightwakings are still common in this age group (15% to 30%), in
comienzan con many cases coexisting in the same child (average time to fall asleep in this age group is around 15
desordenes minutes). A number of studies have suggested that sleep problems in this age group may become
continuan con
chronic; in one study, 84% of children aged 15 months to 48 months with bedtime struggles and/
este problema
or nightwakings continued to have signif cant sleep disturbance at their 3-year follow-up.
al menos 3
anos mas
n Nighttime fears and nightmares (see Chapters 8 and 9)
n Bedtime problems/behavioral insomnia of childhoodlimit setting type (see Chapter 6)
n Obstructive sleep apnea and sleep disordered breathing (see Chapter 14)
n Partial arousal parasomnias (sleepwalking, sleep terrors) (see Chapter 10)

n The association between inadequate or disturbed sleep and behavioral problems tends to be-
come more evident at this age.
n Parents should be encouraged to make reading an integral part of the bedtime routine. In one
study, children for whom reading was part of their bedtime routine obtained more total sleep
and had fewer sleep disturbances.
Sc h o o l - Ag eD c h il Dr en (6 t o 12 yeAr S)
n Hours of sleep: Average is 9 to 10 hours over 24 hours
Wake-up Call
Because school-aged children are normally highly alert, behaviors such as napping, dozing off
during short car rides or while watching TV, and persistent complaints or behavioral manifes-
tation of daytime sleepiness reported by parents or teachers in school-aged children are a red
f ag and should be taken seriously. These symptoms suggest signif cant problems with sleep
quality and/or quantity or, less frequently, a primary disorder of excessive daytime sleepiness,
and require prompt evaluation by the primary care provider for the root cause(s).

Cognitive:
n Comprehension of existence of real dangers (e.g., burglars) may increase nighttime fears.
Social/emotional:
n Increasing independence from parental supervision and a shift in responsibility for health hab-
its 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.
n Involvement in academic, social, athletic, and family activities as well as parent work sched-
ules may conf ict with time for sleep.
n Increasing reliance on peer relationships can compete for sleep time.
n Social anxiety and need for academic achievement may result in nighttime worrying, interfer-
ing with sleep onset.
n Media and electronics, such as television, computer, video games, and the Internet, all com-
pete increasingly for sleep time (see Chapter 19).
Healthy Sleep/Healthy Child

Middle childhood is a critical time for the development of health habits in general and healthy
sleep habits in particular. Practitioners have a real opportunity in the context of well-child care
to introduce concepts of sleep health promotion (good sleep habits) and disease prevention
(impact of inadequate sleep) to children at this stage, and studies suggest that middle school
aged children may be particularly receptive to counseling and education about sleep from their
primary care provider.
The Electronic Sandman

Television viewing at bedtime and the presence of a television set in the childs bedroom in
particular have been found to be associated with diff culties in falling and staying asleep in
children, as well as reduced total sleep times. Television may also play a role in increasing the
likelihood of nightmares and nighttime anxiety. Other screens (desk and laptop comput-
ers, handheld devices, electronic gaming systems, cell phones) not only provide cognitive
and sometimes psychological and physical stimulation that interfere with the relaxed state re-
quired for sleep initiation but may provide enough light exposure to suppress the normal eve-
ning surge in melatonin and thus further delay sleep onset. Parents should be strongly encour-
aged to keep electronic devices out of (or remove them from) the childs sleeping environment.

n Irregularity of sleepwake schedules ref ects increasing discrepancy between school-night
and nonschool-night bedtimes and waketimes.
n Later bedtimes have been shown to be consistently linked to shorter, and frequently insuf-
f cient, sleep amounts in school-aged children. Several studies have suggested that lower in-
come and minority children, especially boys, are at increased risk for both later bedtimes and
inadequate sleep.
n Decreased nighttime sleep has been shown to be associated with impairments in daytime
functioning. Two studies have found that restricting sleep in school-aged children by just 30
to 60 minutes for several nights led to daytime behavior problems, including inattention and
other cognitive effects. Inadequate sleep has also been linked on both cross-sectional and lon-
gitudinal studies to the development of obesity in children (see Chapter 21).
n Increased caffeine intake may interfere with sleep onset and quality of sleep. Approximately
40% of school-aged children have a daily caffeinated beverage, which is associated with less
total sleep time.
n Parental presence at bedtime is still quite common with school-aged children, occurring in
about 30% of families. The requirement to have a caregiver present at sleep onset is associated
with a six-fold increase in nighttime awakenings.
n Daytime sleepiness is rare in this age group; therefore, parents should be questioned about
and encouraged to report any evidence of recurrent daytime sleepiness (e.g., napping, dozing
off in school).

Although conventional wisdom has previously indicated that sleep problems are rare in middle
childhood, recent studies have reported an overall prevalence of signif cant parent-reported sleep
problems of 37% in this age group, with a 15% to 25% prevalence of bedtime resistance, a 10%
prevalence of signif cant sleep onset delay and anxiety at bedtime, and a 10% prevalence of
teacher-reported and parent-reported daytime sleepiness. Another study found that almost one-
third of school-aged children report diff culty waking in the morning and 10% feel tired during
the day. It should also be noted that these f gures might underestimate the magnitude of sleep
problems because parents may be unaware of and, thus, underreport sleep concerns at this age.

n Sleepwalking and sleep terrors (see Chapter 10)
n Bruxism (see Chapter 12)
n Enuresis (see Chapter 13)
n Insuff cient sleep (see Chapter 14)
n Inadequate sleep hygiene (see Chapter 14)
n Restless legs syndrome/periodic limb movement disorder (see Chapter 15)

n Maturational issues: Many of the developmental sleep changes associated with puberty de-
scribed in the following section on adolescent sleep may be applicable to the early-maturing
middle schoolaged child.
n Circadian preference: Recent data suggest that individuals may begin to manifest an inherent
relative lifelong circadian sleep phase preference (morningnesseveningness, night owl
vs. morning lark) in childhood. Children who are relatively phase delayed (e.g., prefer a later
bedtime and rise time) may display sleep onset problems and associated bedtime resistance
when given a bedtime that is signif cantly earlier than their preferred sleep onset time but
fall asleep easily and quickly when given a later bedtime. Allowing a child to sleep on a self-
selected sleep schedule for several days (e.g., during vacation) may help to clarify the issue of
circadian preference.
n Encouragement of healthy sleep habits and an emphasis on the importance of adequate sleep
by parents, teachers, and health care practitioners is particularly important in the middle child-
hood years and may set the stage for development of continued positive sleep behaviors in
adolescence and adulthood.
Owls and Larks

Parents and providers should be sensitive to circadian preference, particularly for a delayed
(later) sleep phase as a possible cause of bedtime struggles. Sleep schedules for these children
may need to be adjusted accordingly to reduce sleep onset delay while preserving adequate
sleep amounts.
ADo l eSc en t S (12 t o 18 yeAr S)

n Hours of sleep: The vast majority of adolescents are not getting adequate sleep. Average sleep
duration across adolescence is 7 to 7 1/2 hours; only 20% of adolescents overall get the recom-
mended 9 to 9 1/4 hours of sleep. This situation typically results in a 2-hour sleep debt per
night, which accumulates over the school week, precisely when teens need to be at their most
alert. Sleep amounts steadily decrease with age, with 6th graders averaging approximately 8 1/2
hours of sleep on school nights, compared to just under 7 hours in 12th graders. Average sleep
times even on non-school nights is only 9 hours; thus the attempt on weekends to make up
for chronically inadequate sleep during the week still falls short of even normal daily sleep
requirements. Compounding the situation, the majority of parents polled (70%) think their
teens are getting adequate sleep.
n Bedtime: Bedtimes become steadily later on school nights, from an average of 9:30 p.m. in
6th grade to 11:00 p.m. in 12th grade, with average waketimes consistent at approximately
6:30 a.m. Bedtimes on non-school nights also steadily become later with age, with an average
of 10:30 p.m. in 6th graders to 12:45 a.m. in 12th graders.

n Circadian factors: Around the time of puberty onset, adolescents develop an approximately
2-hour physiologically based phase delay (later sleep onset and wake times), relative to sleep
wake cycles in middle childhood. This is a result of pubertal and hormonal inf uences on
circadian sleepwake cycles and melatonin secretion, and is linked to Tanner stage rather than
chronological age. This shift to a later sleepwake cycle is accompanied by a similar delay in
timing of other circadian clock-driven events; for example, the second wind phenomenon
of increased alertness just before sleep onset is shifted to a later time in the evening, and the
nocturnal circadian wakedrive trough (3:005:00 a.m.) is also shifted, often coinciding
with the rise time required by early school-start schedules. In addition, some researchers have
suggested that adolescents are relatively more sensitive to the melatonin-suppressing effects
of evening light exposure, further delaying sleep onset.
Another sleep development in adolescence that relates to circadian timing is the increas-
ingly large discrepancies between bedtimes and waketimes on school nights versus non-school
nights. Sleep onset and morning (or afternoon) waking times may differ by 3 to 4 hours or
more, creating an eastward-direction jet laglike situation by the end of the weekend (or
vacation). In other words, on Sunday evening, the adolescent is attempting to shift sleep onset
time earlier by 3 to 4 hours, an almost impossible task for even the most seasoned traveler!
n Sleep drive: Studies suggest that adolescents may accumulate their sleep drive more slowly
during periods of prolonged wakefulness compared to younger children. This results in an
increased ability to voluntarily delay sleep onset and more diff culty in falling asleep at an
earlier time. However, the rate of dissipation of the sleep drive during the night, and thus the
amount of sleep required to restore normal alertness levels, does not change signif cantly in
adolescence; therefore, adolescent sleep needs do not differ dramatically from sleep needs of
preadolescents. Optimal sleep amounts in teens remain at about 9 to 9 1/4 hours per night.
Given that the majority of adolescents are only obtaining 7 hours on average, this situation has
created a whole generation of profoundly sleepy individuals.

n Environmental and lifestyle factors: Environmental factors and lifestyle and social demands,
such as homework, after-school jobs, and social activities, impact signif cantly on sleep cycles
in adolescents, frequently resulting in delayed sleep onset.
n Sleepwake variability: There is signif cant variability in sleepwake patterns in adolescents
from weekday to weekend.
n Early high school start times: The early start times of many high schools, as well as some
middle and junior high schools, often require that students wake up not only before they have
had suff cient sleep, but also at the time of their lowest daily level of alertness. Not only do
schools with earlier start times report signif cant negative consequences, such as higher rates
of tardiness and decreased concentration in their students, but research has documented posi-
tive outcomes in school districts that have delayed their school times. These benef ts have in-
cluded increased attendance, better grades, improvements in SAT scores, and decreased drop-
out rates. Overall satisfaction with the change by adolescents, parents, and teachers has also
been high. Of note, students attending schools that have adopted delayed start times report
increased sleep amounts; in other words, these students go to bed at the same time (i.e., do not
stay up later) but, on average, sleep in an additional hour per day.
n Signif cant daytime sleepiness: All of the above factors often combine to produce signif cant
sleepiness in many adolescents and consequent impairment in mood, attention, memory, be-
havioral control, and academic performance. Overall, more than half (56%) of adolescents say
they get less sleep than they think they need to feel their best, and 51% say they feel too tired
or sleepy during the day. Over 25% of adolescents report falling asleep in school at least once
a week, and more than 1 in 5 fall asleep while doing homework. Perhaps most alarmingly, over
one-half of adolescent drivers report having driven while drowsy in the past year and 15%
drive while sleepy at least once a week. Therefore, parents of teenagers should be strongly
encouraged to monitor their adolescents sleep and possible negative consequences of sleep
deprivation and to actively intervene if sleep is chronically inadequate.
n Risk-taking behavior: As with all adolescent risk-taking behavior, parents should be encour-
aged to maintain a level of open communication with their teenagers regarding the impact of
inadequate sleep and poor sleep habits on social and emotional functioning, school perfor-
mance, and health. Studies indicate that inadequate sleep is associated with other health-risk
behaviors, such as excessive caffeine intake and stimulant use, poor nutrition, and decreased
physical activity.
Sleep and School

Many high-achieving college-bound high school students state that they have to stay up late
in order to complete homework assignments, participate in extracurricular and athletic activi-
ties, and get involved in community service projects as well as the myriad of other activities
that look good on college applications. While there is clearly a great deal of very real pres-
sure on adolescents to perform and succeed, this reasoning has some fundamental f aws. Stud-
ies, in fact, have repeatedly shown that students who get better grades sleep more, not less.
Furthermore, sleep-deprived individuals are less eff cient in completing cognitive tasks, thus
establishing a cycle in which the student takes longer to complete the same amount of work,
necessitating staying up later, and the cycle continues. Thus, helping high school students to
understand the repercussions of insuff cient sleep and to prioritize tasks to allow for adequate
sleep opportunity are important components of anticipatory guidance in adolescence.
Sleepy, Dopey, and Grumpy

There is now substantial evidence to suggest that, as a group, adolescents in the United States
are chronically sleep deprived. Studies suggest that many teens function for a good part of the
day in the twilight zone, which is a level of sleepiness equivalent to that in individuals with
narcolepsy! Practitioners should be aware of this epidemic of insuff cient sleep and carefully
assess adolescent patients for chronic sleepiness and the accompanying effects on mood, be-
havior, and school performance.

Data suggest that chronic partial sleep deprivation is a serious problem in this age group and that
particular groups, including high achievers who are engaged in many extracurricular activities,
may be at a relatively higher risk. Chronic sleep restriction in adolescents can lead to signif -
cant neurobehavioral consequences, including a negative impact on mood, vigilance and reaction
time, attention, memory, behavioral control, and motivation.
Adolescents may also suffer from a number of sleep disorders. A number of studies have sug-
gested that the prevalence of signif cant sleep problems in adolescents is high (at least 20%) and
that particular groups of adolescents, such as those with chronic medical or psychiatric problems
(e.g., depression), may be at increased risk.

n Insuff cient sleep (see Chapter 14)
n Inadequate sleep hygiene (see Chapter 14)
n Insomnia (see Chapter 18)
n Delayed sleep phase disorder (see Chapter 17)
n Restless legs syndrome/periodic limb movement disorder (see Chapter 15)
n Narcolepsy (see Chapter 16)

Chronic insuff cient sleep in adolescents may be associated with:
n signif cant declines in school and work and occupational performance;
n use of potentially harmful alertness-promoting agents, such as caffeine and stimulant medica-
tions; and
n increased risk-taking behaviors (e.g., use of alcohol, illicit drugs), injuries, including occupa-
tional and sports injuries, and motor vehicle crashes.
Asleep at the Wheel

Older adolescent boys are among the highest risk group for drowsy drivingrelated accidents
because of a combination of risk factors (decreased sleep amounts and increased sleepiness,
driving inexperience, greater willingness to engage in risk-taking behavior, combined with
drugs, marijuana, and/or alcohol). However, all adolescents with insuff cient sleep are at risk.
Many teens assume that ingesting caffeinated beverages (e.g., Red Bull) will counteract the ef-
fects of both sleepiness and alcohol, unfortunately sometimes with fatal results. In fact, stud-
ies have shown that individuals who consume alcohol plus energy drinks show equivalent
levels of objective impairment (i.e., decreased vigilance on computerized tests) compared to
alcohol alone, but rate themselves as more alert and less impaired. The most common drowsy
driving accident scenario involves a single motor vehicle and driver who drifts off the highway
late at night. Many sleepiness-related accidents are fatal, because the driver (who is asleep)
makes no effort to avoid the crash.
t ABl e 2.1. Anticipatory Guidance for Sleep Issues in Infants, Children, and Adolescents
Prenatal Visit
Discuss normal newborn sleep patterns (day/night reversal, sleep amounts per 24 hours, average
sleepwake periods).
Discuss plans for sleeping arrangements.
Newborn Visit
Discuss normal newborn sleep patterns (day/night reversal, sleep amounts per 24 hours, average
sleepwake periods, irregularity).
Discuss specif c safe sleep practices (sleeping position, surface, environment).
Breast-fed baby: Discuss shorter sleep periods, avoidance of caffeine.
Highlight importance of parental sleep needs.
2-Week Visit
Review normal newborn sleep patterns (day/night reversal, normal range of total sleep per 24 hours,
average sleepwake periods, irregularity).
Review safe sleep practices (sleeping position, surface, environment).
2-Month Visit
Discuss normal development of infant sleep patterns (normal range of total sleep per 24 hours,
sleeping through the night, self-soothing, appropriate sleep onset associations).
Encourage parents to put their baby to sleep drowsy but awake starting at about 3 months of age to
avoid the development of inappropriate sleep associations.
Encourage parents to make the transition to f nal sleeping arrangements (e.g., bassinet to crib; par-
ents room to babys room) by 3 months.
Explain to parents that periodic, brief arousals during the night are part of a babys normal sleep
pattern, which may help to avoid unnecessary parental intervention and subsequent reinforcement of
nightwaking.
Encourage establishment of a bedtime routine.
4-Month Visit
Discuss normal development of infant sleep patterns.
Encourage parents to put their baby to sleep drowsy but awake.
Discuss importance of a daily schedule with consistent feeding times and sleep times.
Suggest that during-the-night feedings should be discouraged after about 6 months, as they may
contribute to inappropriate learned sleep behaviors and are no longer physiologically necessary for
most healthy babies.
Encourage establishment of a bedtime routine.
6-Month Visit
Discuss normal development of infant sleep and napping patterns.
Encourage parents to put their baby to sleep drowsy but awake.
Suggest that during-the-night feedings should be discouraged after about 6 months, as they may
contribute to inappropriate learned sleep behaviors and are no longer physiologically necessary for
most healthy babies.
Encourage establishment of a bedtime routine and consistent sleep schedule.
Anticipate possible temporary regression in sleep behaviors with developmental milestones, illness,
and changes in routine.
Invite discussion of co-sleeping.
(continued)
t ABl e 2.1. Anticipatory Guidance for Sleep Issues in Infants, Children, and Adolescents
9-Month Visit
Discuss normal development of infant sleep and napping patterns.
Anticipate recurrence of nightwakings at 9 to 12 months; discourage parental reinforcement of
nightwakings.
Encourage establishment of a bedtime routine and consistent sleep schedule.
Invite discussion of co-sleeping.
1-Year Visit
Discuss normal development of toddler sleep and napping patterns.
Encourage use of transitional objects.
Discuss transition to single daily nap period.
Encourage bedtime routine and regular bedtime.
Discourage bedtime bottles.
15-Month Visit
Encourage use of transitional objects.
Discuss transition to single daily nap period.
18-Month Visit
Encourage transitional objects.
Discuss nighttime developmental fears (especially separation).
Discourage television viewing at bedtime.
2-Year Visit
Discuss effects of inadequate sleep on daytime behavior.
Discuss transition from crib to bed.
Discuss parental limit setting.
Discourage television viewing at bedtime.
3-Year to 5-Year Visits
Discuss normal development of sleep and napping patterns in preschoolers.
Discuss effects of inadequate sleep on daytime behavior and review signs of sleepiness.
Discuss development of good sleep habits.
Discuss parental limit setting.
Discourage TV viewing at bedtime and suggest no TV set in the childs bedroom.
6-Year to 12-Year Visits
Discuss normal range sleep amounts in school-aged children.
Encourage obtaining adequate sleep and appropriate bedtime.
Discuss impact of inadequate sleep on school performance.
Discuss development of good sleep habits.
Discourage TV at bedtime and suggest no TV set in the childs bedroom.
Discourage caffeine use.
Adolescent Visits
Discuss average sleep needs (9 to 9 1/4 hours) in teenagers.
Encourage obtaining adequate sleep and appropriate bedtime.
Discuss avoiding discrepant weekday and weekend schedules.
Review pubertal inf uences on sleep (phase delay).
Review healthy sleep habits (regular bedtimes and waketimes, avoidance of caffeine, avoidance of
TV set/computers in bedroom).
Discuss dangers of drowsy driving.
3 Evaluation of Pediatric
Sleep Disorders
As is the case with other medical and psychiatric disorders, a key issue in the evaluation and
management of pediatric sleep disorders is differential diagnosis. Because many sleep disorders
present with similar symptomatology (e.g., excessive daytime sleepiness) and sleep complaints
can arise from multiple possible causes (e.g., delayed sleep onset may be associated with restless
legs syndrome, delayed sleep phase disorder, or behavioral insomnia of childhood), differential
diagnosis is especially critical in the assessment of sleep complaints. Differentiation between a
sleep disorder and other medical or mental health concerns that may present with similar symp-
toms is also important. For example, a child with apparent sleep terror symptoms may actually
have a nocturnal seizure disorder. Similarly, what appears to be delayed sleep onset related to
normal developmental nighttime fears may be a manifestation in some children of a more serious
generalized anxiety disorder.
Furthermore, in many cases, two or more sleep disturbances may coexist, and medical and be-
havioral sleep disorders are frequently comorbid. For example, a child may have both obstructive
sleep apnea and behavioral issues with bedtime refusal. Thus, treating the sleep apnea alone will
alleviate the nighttime arousals associated with sleep-disordered breathing but will not eliminate
bedtime resistance. In addition, the presence of one sleep problem may exacerbate another; for
example, partial arousal parasomnias may be triggered by inadequate sleep in susceptible chil-
dren. Finally, because sleep disorders can be secondary to physical illness or another psychologi-
cal disorder, it is essential to evaluate for possible contributing factors to the sleep problem with
a comprehensive and thorough history.
Dual Diagnoses in Sleep

There are a number of sleep disorders that are often related and commonly coexist:
Obstructive sleep apnea and secondary enuresis
Obstructive sleep apnea and partial arousal parasomnias (e.g., sleepwalking, sleep terrors)
Chronic inadequate sleep and partial arousal parasomnias
Insomnia and inadequate sleep hygiene
Bedtime problems and nightwakings
Restless legs syndrome and periodic limb movement disorder
c onceptual Framework of Sleep Disturbances in c hildren

Most sleep problems in children may be broadly conceptualized as involving one or more basic
mechanisms: inadequate duration of sleep for age (insuff cient sleep quantity), disruption and
fragmentation of sleep (poor sleep quality), inappropriate timing of the sleep period (as occurs
in circadian rhythm disturbances), or primary disorders of excessive daytime sleepiness (central
hypersomnias such as narcolepsy) (Figure 3.1). Insuff cient sleep is usually the result of diff culty
initiating (delayed sleep onset) and/or maintaining sleep (prolonged nightwakings), whereas
sleep fragmentation most often results from frequent, repetitive, and brief arousals during sleep.
Inadequate sleep duration, especially in older children and adolescents, may also represent a
conscious lifestyle decision to sacrif ce sleep in favor of competing priorities, such as homework
and social activities.
30
EvALUATION OF PEDIATRIC SLEEP DISORDERS 31
Insufficient Sleep Fragmented Sleep

(Sleep Restriction) (Sleep Disruption)
Daytime Sleepiness
Primary Sleep Circadian Rhythm

Disorders of EDS Disorders
Fig 3.1. Conceptual framework of sleep disturbances in children. EDS = excessive daytime sleepiness.
c o MPo n en t S o F t h e PeDiAt r ic Sl eeP eVAl uAt io n

Sleep complaints in primary care, as well as mental health settings, may be identif ed with the use
of routine screening by the practitioner or may be spontaneously offered by the caregiver (or less
frequently by the patient) during the health encounter. In addition, although concerns about sleep
are commonly raised with health care providers by parents of infants and toddlers, caregivers may
be less aware of and less attuned to sleep issues beyond the early childhood period. Furthermore,
it should be emphasized that caregivers may not regard some sleep symptoms as problematic
(e.g., snoring), thus a systematic approach to screening for sleep disorders needs to be a key
component of routine well-child care. The sleep questions presented below outline a screening
strategy that is appropriate, with some age-related modif cations, across most age groups from
infancy through adolescence.
Key Sleep Screening Questions

1. Does your child maintain a regular sleep schedule (school and non-school days)?
2. Does your child have any problems at bedtime?
3. Does your child have any problems falling asleep?
4. Does your child wake up during the night?
5. Does your child snore or have any problems breathing during the night?
6. Does your child have any unusual behaviors during the night?
7. Does your child need assistance (e.g., alarm clock, parent) to wake up in the morning
(school and non-school days)?
8. Does your child seem sleepy or overtired during the day?
Once a sleep problem has been identif ed, a step-wise approach to gathering information in
the clinical setting regarding the presenting sleep complaint; daytime sequelae; and related sleep,
medical, and psychiatric problems is obviously needed to both generate an appropriate differen-
tial diagnosis and to begin the process of treatment planning.
An initial assessment of pediatric sleep disturbances typically includes:
n Sleep history
n Review of medical history
n Developmental history/assessment of school functioning
n Family history
n Psychosocial history
n Behavioral assessment
n Physical examination.
Further evaluation may include the completion of sleep diaries and/or an overnight polysom-
nogram or other diagnostic tests as appropriate. The sleep questions presented below outline a
diagnostic approach that is generally appropriate across all age groups, from newborn through
adolescence. Focused questions pertaining to specif c sleep disorders, such as obstructive sleep
apnea and sleepwalking, are presented in the appropriate corresponding chapters. Symptom-
based algorithms also are provided in Chapter 5 to facilitate a basic approach to diagnosis and
subsequent treatment. In addition, a sleep evaluation intake questionnaire is provided in Appen-
dix B1.
Sl eeP h iSt o r y
The f rst step in evaluating a child or adolescent for a sleep disorder is the completion of a
thorough sleep history (including presenting complaint, sleep patterns and schedules, bedtime,
nocturnal behaviors, and daytime behaviors).
Presenting c omplaint
It is important to elicit a description of the presenting complaint from as many family members
as possible, especially the child or adolescent (if appropriate). Often differences in perception of
the issues between parents emerge, as well as discrepancies between child and parent perspective.
For example, parents may attribute sleep onset delay following lights out to noncompliance,
whereas the child may state that he or she is not sleepy at the regular bedtime (but can fall
asleep easily an hour later, suggesting a delayed sleep phase or an inappropriately early bedtime
for age). Included in the description of the presenting complaint should be a detailed review of
the onset, duration, severity, and night-to-night variability of the current sleep problem. This is
particularly important because, as is the case with many behavioral problems in childhood, the ul-
timate determinant of what constitutes a sleep problem is highly subjective and dependent upon
the context in which it occurs, including caregiver tolerance for the behaviors. Thus, nightwak-
ings that occur twice a week may be def ned as problematic for one family, but not for another.
A history of events that seem to have immediately preceded the onset of the sleep problem should
also be elicited. It is also often helpful to ask parents what prompted them to address the sleep
complaint at this particular time (e.g., imminent birth of a sibling, school problems). In addition,
parents should be questioned in regards to current and past attempts to manage the sleep problem;
for example, it is not uncommon for parents to state that they have already tried everything to
address nightwakings but with further questioning it becomes apparent that interventions were
instituted inconsistently or for inadequate periods. Finally, clarifying parental expectations in
regards to treatment outcomes assists in the development of mutually acceptable treatment goals
and active exploration of opportunities and obstacles as well as allowing ongoing communication
of issues and concerns.
Sleep Patterns, Sleep Schedules, and Sleep h abits

No matter what the presenting sleep complaint, it is important to have a general sense of sleep
patterns and behaviors. A review of sleep habits will often shed considerable light on the nature,
duration, and cause of the presenting sleep complaint, and may also illuminate the presence of
coexisting sleep problems and maladaptive sleep behaviors (inadequate sleep hygiene; see Chap-
ter 4). General sleep behaviors over the previous several weeks (or over an average week, if the
most recent weeks have been atypical) should be reviewed. Review of sleep schedules during the
school year compared to the summer or holidays can also help evaluate for factors such as circa-
dian preference and sleep need in school-aged children and adolescents. Note that is not unusual
for parents to state that their child has never slept well, but the identif cation of specif c triggers
or exacerbating factors may be helpful.
Bedtime
It is often easiest to have the family describe events from dinnertime until sleep onset in order
to obtain a complete picture of evening and bedtime behaviors. Specif c information that may
be helpful in elucidating the causes of and contributing factors to sleep problems include the
following.
Bedtime schedule
n Presence of a set bedtime, as some parents do not establish a regular bedtime and allow their
child to go to bed whenever (and wherever) they fall asleep.
n Actual bedtime (e.g., 8:00 p.m.) appropriateness for age and developmental level, and con-
sistency of bedtime, night-to-night, particularly weekday/weekend discrepancies. The impact
of environmental demands (e.g., homework, after-school employment) on sleep schedule
should also be considered.
n Parental supervision of bedtime indicates whether parents are monitoring and enforcing
bedtime. Many parents, especially of adolescents, do not enforce bedtime limits because they
go to bed before their child does, and thus have little idea what time their child actually goes
to sleep. Furthermore, some children will only go to bed for one parent, suggesting the pos-
sibility of limit-setting issues, separation issues, or family conf ict. Other children may wait
up for a parent to return from a third shift job.
Bedtime routines
n Evening activities, particularly the childs involvement in stimulating evening activities, in-
cluding television viewing, outside play, and video games. Engaging in evening extracurricu-
lar activities (e.g., sports) can also impinge on an appropriate bedtime, contributing to inad-
equate sleep and daytime consequences.
n Presence of a bedtime routine, that is, a series of consistent nighttime activities set up by
parent and child leading to bedtime.
n Time of initiating the bedtime routine, the time the child or adolescent begins to get ready
for bed and duration of the bedtime routine, because extended or elaborate routines lasting
longer than 30 minutes may indicate a limit-setting problem.
n Specif c nature of the bedtime routine activities, appropriateness for age, and supervision
of activities by parents. Also assess if these activities are likely to be stimulating for that child
(e.g., baths are not relaxing for all children; in addition, the activity closest to bedtime should
be the most soothing).
n Location of the bedtime routine, such as in the childs room versus the parents room.
n Electronics, including the prominence of television viewing or computer or video games in
the bedtime routine and presence of a television set or computer in the childs bedroom.
Sleep associations
Sleep associations are behaviors that occur at the time of sleep initiation (e.g., nursing, rocking).
Inappropriate sleep associations can contribute to bedtime diff culties and nightwakings since
behaviors that occur at bedtime (e.g., nursing, rocking) may be required to reinitiate sleep fol-
lowing normal nighttime arousals.
Bedtime stalling or refusal behaviors

A review of noncompliant behaviors should be conducted, including types of behaviors (e.g.,
crying, climbing out of crib, leaving room); intensity of the behaviors (e.g., calling out versus
tantrums); frequency (how often they occur in a week period), and duration (how long they typi-
cally last) as well as the presence of bedtime fears. It is also important to assess any discrepancy
between the childs behavior with one parent versus the other, and/or with other caretakers as well
as the parental reaction to the childs behavior at bedtime, including appropriateness of parents
response to bedtime behaviors (see also Chapter 6).
Falling asleep
n Time of lights out in relation to sleep onset, that is, the time the child actually falls asleep.
Specifying these time periods may narrow down the sleep problem and help differentiate be-
tween bedtime resistance and diff culty falling asleep. In children who are primarily having
diff culty falling asleep, factors that may contribute to delayed sleep onset should be evalu-
ated, including nighttime anxiety and potential symptoms of RLS (e.g., leg discomfort, urge to
move). In these cases, direct questioning of the child or adolescent is particularly important.
n The level of sleepiness (readiness for bed), of the child at the typical bedtime. Children and
adolescents who fall asleep easily at a later bedtime (e.g., on weekends) may have a delayed
sleep phase.
n Sleep onset location, particularly where sleep onset typically occurs (e.g., living room) and
the childs activity at the time (e.g., on the couch watching television), and variability in loca-
tion of sleep onset from night to night.
n Transfers after sleep onset, that is whether the child falls asleep elsewhere and is subse-
quently transferred to his or her own bed.
Sleeping environment
n Bedroom space and location, including bedroom-sharing with a parent, sibling, or other
household member (some research indicates increased nightwakings in infants and toddlers
who share a room with parents), and location of childs bedroom in relation to parents room
(e.g., childs anxiety may be increased if the bedroom is far away or on a different f oor). For
children who frequently sleep in different households besides their primary residence (e.g.,
non-custodial parent, grandparents), the sleeping arrangements and environment, as well as
the sleep schedule in each, should be described.
n Light, including use of nightlights and other lights in the room (childs need for bright light-
ing may be indicative of anxiety issues). Other sources of ambient light (e.g., streetlights,
screens [television, computer]) in the evening may interfere with nighttime melatonin secre-
tion and normal circadian rhythm patterns, while early morning light exposure (northern and
eastern locations) may prematurely suppress melatonin and result in waking too early.
n Noise, including amount and type of noise, from other family members and outdoor noise, as
well as sound levels at bedtime, during the night, and in the early morning.
n Temperature, including availability of adequate temperature control (e.g., heat,
air-conditioning).
n Bed type, as a crib provides natural limits to bedtime behaviors, while a bed allows unlimited
movement. Moving a child from a crib to a bed prematurely sometimes initiates or exacerbates
sleep problems. Young children commonly do not have the cognitive development or behav-
ioral control to stay within the imaginary boundaries of a bed. If sleep is problematic with the
switch to a bed, returning to a crib until the child is more developmentally ready is appropriate
and often resolves the sleep issue.
n Bedding, including different sleeping surfaces (e.g., mattress, futon) and personal preference
(e.g., hard versus soft mattress). Although there are no data on the relative advantage of dif-
ferent sleeping surfaces in regards to sleep quality in children, safety concerns (e.g., pillows
for young infants) and medical issues (e.g., environmental allergies) may be considerations
in some cases. Research, however, continues to indicate that infants who sleep on couches
and other soft surfaces are at increased risk for suffocation and sudden infant death syndrome
(SIDS).
n Co-sleeping, including assessment of type (room-sharing, bed-sharing, other), persons in-
volved (siblings, parents, grandparents), intensity (all-night versus part-night co-sleeping),
timing (starts out in own bed versus parents bed), frequency (nightly versus intermittently),
reasons for co-sleeping (lifestyle choice versus reactive co-sleeping in response to a sleep
problem), and parents reaction to co-sleeping (discrepancies in parent response, displacement
of one parent from the marital bed).
Daytime Sleep
Naps, including timing, duration, and consistency of napping patterns, as well as ease or diff -
culty of falling asleep at naptime. It should be emphasized that unplanned napping (e.g., dozing
off in the car, while engaged in sedentary activities) at all ages and the need for planned naps in a
child after the age of 5 years is suggestive of inadequate sleep or an underlying sleep-disrupting
factor.
n octurnal Behaviors
Nighttime behaviors are important to review in order to obtain a complete picture of the sleep
problem. These include a complete evaluation of nightwakings (see Chapter 7), including approx-
imate date of initial presentation; frequency per week, number per night, timing, and duration of
nightwaking episodes; identif able triggers (e.g., getting up to void, respiratory disturbance, par-
ent coming home from third-shift work); behaviors that occur upon waking (calling out, coming
into parents bed); type and consistency of parental response to nightwaking (ignoring, intermit-
tent reinforcement); and what assistance the child needs to return to sleep (parental soothing,
breastfeeding or bottle feeding). In addition, the presence and nature of episodic nocturnal events
such as partial arousal parasomnias (see Chapter 10) and nightmares (see Chapter 9) as well as
symptoms possibly suggestive of sleep-disordered breathing (see Chapter 14) and periodic limb
movement disorder (PLMD [see Chapter 15]) should be elicited.
Daytime Behaviors
It is critical that daytime behaviors be assessed, particularly those that may be contributing to
or indicative of signif cant daytime sleepiness (morning waking, daytime sleepiness and/or low
functioning, and fatigue), in order to quantify the impact of the sleep disturbance on the child and
family. In addition, the daily schedule, including timing of meals (e.g., too close to bedtime) and
the regularity and structure of daytime activities (e.g., lack of exercise during the day or timing
vigorous exercise periods, stimulating activities too close to bedtime, lack of a consistent daily
schedule).
Morning awakening
n Time of awakening, including weekday versus weekend waketime. Children with a delayed
circadian sleepwake rhythm may drift to their preferred later waketime on weekends and
school vacations. In addition, it is particularly important in older children and adolescents
to note the presence of weekend oversleep, i.e., sleeping in for 2 or more hours on weekend
mornings to catch up, because this practice suggests that the weekday sleep duration is
inadequate.
n Mood and cognitive functioning upon awakening, such as irritable and groggy versus alert
and ready to start the day. Extreme confusion, grogginess, and diff culty in awakening on
school days may occur in adolescents with delayed sleep phase, both as a result of inadequate
sleep duration and because they are attempting to wake up during their circadian trough of
alertness (i.e., 6:008:00 a.m.).
n Diff culty waking in the morning, including need for multiple attempts at waking by parents,
siblings, or others. The time that the child spontaneously awakens, or would spontaneously
awaken if allowed, is also important to note, especially during prolonged periods of a self-
selected sleepwake schedule such as Christmas or summer vacation. This helps identify both
the childs intrinsic preferred timing of sleep as well as average sleep need. Diff culty
waking in the morning despite what appears to be an adequate sleep quantity suggests that the
quality of sleep may be compromised by an underlying sleep disorder (e.g., sleep disordered
breathing, PLMD).
n Consequences of diff culty waking, including habitual tardiness or school absences.
You Snooze, You Lose

In general, the habitual need for an alarm clock in order to awaken in the morning, especially
multiple snooze alarm hits, strongly suggests insuff cient sleep. This is particularly true in
school-aged children, who should awaken spontaneously in the morning if adequately rested.
Daytime sleepiness
Falling asleep in school, while riding in a car, and during passive, or in particular, stimulating
(e.g., in conversation, at mealtime) activities is indicative of inadequate sleep or an underlying
sleep disruption. In younger children, daytime sleepiness may be manifested as overtiredness,
which may be described by parents as irritability, aggressive, oppositional or acting-out behavior,
disinhibition and silliness, or hyperactivity and impulsivity.
Daytime functioning
Inadequate or poor sleep may have negative consequences on a host of functional domains, in-
cluding mood, behavior, attention, learning, school performance, social relationships, and health.
Fatigue/tiredness
Sleepiness is the tendency to doze off or fall asleep, often in inappropriate settings, and gener-
ally implies insuff cient and/or disrupted sleep. Complaints of fatigue or being tired, on the other
hand, are often indicative of subjective feelings of low energy and low motivation, which may or
may not be primarily a result of poor sleep. Fatigue is def ned as lethargy without sleep initiation
and tends to be associated with medical (e.g., thyroid function) or psychiatric (e.g., depression)
disorders. However, a distinction between sleepiness and fatigue is not always possible, as there
may be considerable overlap in descriptions of these two states by parents and/or older children
and adolescents.
MeDic Al h iSt o r y
A standard pediatric medical history and review of systems should be elicited, with particular
emphasis on past and current medical conditions, prior hospitalizations and surgeries (especially
prior history of adenotonsillectomy for symptoms of sleep-disordered breathing), and medica-
tions (see Chapter 21 for a detailed discussion on the interaction between sleep and medical is-
sues and Chapter 19 for a complete review of the effects of specif c medications on sleep).
DeVel o PMen t Al /Sc h o o l h iSt o r y

A developmental history is important, including a history of developmental delays, prematurity,
and impaired neurologic functioning, as there is often an increased prevalence of sleep problems
in children with neurodevelopmental disorders (see Chapter 20). Furthermore, academic prob-
lems are one of the most important sequelae of insuff cient and/or disrupted sleep, and provide
an indication of the daytime impact of sleep disturbances.
FAMil y h iSt o r y
A family history of sleep problems can be helpful in conf rming the diagnosis of certain sleep dis-
orders, especially for those disorders that may have a genetic component. Such diagnoses include
partial arousal parasomnias (sleep terrors and sleepwalking), RLS, obstructive sleep apnea, and
narcolepsy. In many cases, these disorders have not been formally diagnosed in family members,
but symptoms are clearly present if directly questioned (e.g., His father snores so loudly, he has
to sleep in another room!). In addition, parental experience with sleep problems, such as chronic
insomnia, may impact on parental attitudes toward and management of similar sleep problems
in the child.
Like Father, Like Son

One of the most rewarding aspects of diagnosing and treating pediatric sleep disorders is the
potential to impact the whole family. Not only does successful treatment of a childs sleep
problem result in everyone getting a better nights sleep, but it may encourage adult family
members to obtain needed help for their own sleep problems. Parents may be much more will-
ing to seek medical attention for loud snoring, daytime sleepiness, or symptoms of restless
legs when their child is also being evaluated and treated for a similar symptom.
PSyc h o So c iAl h iSt o r y

A complete psychosocial history is appropriate, including the following:
n Family functioning, including overall family functioning, effectiveness of parenting skills (in-
cluding limit setting), family structure (e.g., siblings, extended family members in household,
one-parent versus two-parent household), parental psychological functioning (e.g., parental
depression), and family discord. Some caregivers may have their own issues (e.g., mental ill-
ness, long work hours) that interfere with their ability to set clear limits both during the day
and at bedtime. In other cases, there is a mismatch between parental expectations regarding
sleep behaviors and the normal developmental trajectory.
n Parental separation or divorce, including time elapsed since the separation or divorce, visita-
tion schedules and level of involvement of noncustodial parent, consistency of sleep patterns
and habits across households, discrepancies in parenting styles, and stress on the child.
n Signif cant life events, such as death of a family member, change in school, or a recent move,
that may result in adjustment sleep problems.
n Family and cultural context, including cultural inf uences on sleep behaviors, family values
regarding health priorities, and family beliefs about sleep and the importance of sleep.
n Impact on family of the sleep problem, including the effect of the childs sleep on the parents
sleep, impact on parents daytime functioning, and impact on marital and family satisfaction.
Beh AVio r Al ASSeSSMen t

A behavioral and psychological assessment is important because sleep disturbances can result in
psychiatric symptoms, such as mood changes and oppositional behavior; conversely, psychiatric
disorders can result in sleep disturbances. Thus, particularly in older children and adolescents, it
is important to elicit possible symptoms of depression, anxiety, and other psychiatric disorders.
In younger children, bedtime problems are also often associated with child temperament. For ex-
ample, fussy children may insist on a particular type of soothing or sleep-inducing technique,
resisting any alternative that is less dependent on the caregiver.
Ph ySic Al ex AMin At io n
A physical examination should be conducted on all children and adolescents being evaluated for
sleep complaints. The presence of specif c symptoms (e.g., snoring, severe sleepiness) should
prompt more detailed examination according to the systems affected; more detailed aspects of
the physical examination in various specif c sleep disorders (e.g., obstructive sleep apnea) may be
found in the respective chapters. Although the physical examination is normal in many children
with sleep disorders, careful attention should be paid to the following points:
n Growth parameters, including height, weight, and age- and gender-adjusted body mass in-
dex. For example, growth failure and obesity are both associated with sleep-disordered breath-
ing. Assessment of pubertal status (Tanner stage) may be helpful in identifying a circadian
component in patients presenting with recent onset of sleep initiation insomnia, because the
onset of puberty is associated with a normal biological shift (delay) in sleep-wake cycles.
n General appearance, including activity level and evidence of fatigue and/or sleepiness. Chil-
dren with severe obstructive sleep apnea or inadequate sleep may actually doze off during the
evaluation. Conversely, sleepy children may appear hyperactive, irritable, or disinhibited in
the off ce. Developmental milestones and concerns about development should also be elicited,
as signif cant sleep disruption and inability to settle or self-soothe in a young child may be an
early indication of a developmental delay.
n Otolaryngologic examination, including examination of the nose, mouth, and throat for pos-
sible risk factors (e.g., adenotonsillar hypertrophy) for suspected obstructive sleep apnea (see
Chapter 14). The HEENT (head, eyes, ears, nose, throat) examination may also suggest evi-
dence of atopic disease (e.g., allergic shiners, bogginess of the nasal mucosa, cobblestoning
of the soft palate) contributing to sleep fragmentation and as a risk factor for sleep-disordered
breathing.
n Neurologic assessment, particularly in cases where the concern is excessive sleepiness or
where there is a possibility of nocturnal seizures.
Observation of Family Interactions

The obtaining of a sleep history and exam of a child also affords the practitioner the oppor-
tunity to observe family interactions. For example, lack of limit-setting in the off ce can be
an indication of similar issues in the home, which can contribute to bedtime problems and
nightwakings.
DiAg n o St ic t o o l S
Sleep Diaries
An important step in the evaluation of many sleep problems is the collection of sleep diaries or
logs. A typical sleep diary collects information on bedtime (lights out), latency to sleep onset,
number and duration of nighttime awakenings, time of morning waking, total sleep time, sleep
eff ciency (time asleep and time in bed), and duration and time of naps. Two weeks of baseline
sleep diaries is usually adequate to delineate sleep patterns (samples of different styles of sleep
diaries are provided in Appendix B2). Parents typically complete these diaries; however, in older
school-aged children and adolescents, more accurate information may be obtained by having the
patient complete the sleep log.
o vernight Polysomnography
Once basic information regarding the sleep history as well as a review of medical, developmental,
and behavioral issues have been obtained, it is important to determine whether an overnight sleep
study (i.e., polysomnography [PSG]) is needed. A PSG is a diagnostic test typically performed in
a sleep laboratory that yields detailed information regarding sleep architecture (distribution and
percentage of sleep stages), cardiorespiratory parameters, body movements, and arousals during
sleep. Many sleep disorders centers require an initial evaluation in a sleep clinic before a sleep
study can be scheduled, whereas other sleep laboratories will take direct referrals from primary
care physicians if adequate documentation of the problem and the need for a sleep study is made
available.
When Is an Overnight Sleep Study Appropriate?

In children and adolescents, overnight polysomnography (PSG) is indicated primarily to:
Diagnose sleep-disordered breathing.
Determine optimal treatment for sleep-disordered breathing (e.g., continuous positive air-
way pressure).
Document the presence of periodic limb movements (PLMs).
Investigate sleep-related causes of excessive daytime sleepiness, including narcolepsy (with
multiple sleep latency test).
Occasionally to delineate the etiology of atypical or unusual episodic nocturnal phenomena
(e.g., parasomnias versus nocturnal seizures).
A polysomnogram is typically not indicated in the routine assessment of insomnia (i.e., dif-
f culty initiating or maintaining sleep), circadian rhythm disorders, restless legs syndrome (ex-
cept to document associated PLMs), or most parasomnias. However, the primary care physi-
cian should maintain a high index of suspicion and a low threshold for requesting a sleep study
in children who present with possible symptoms of sleep-disordered breathing, fragmented
sleep, and/or unexplained daytime sleepiness. This is particularly true in pediatric populations
at high risk for particular sleep disorders (e.g., Down syndrome, neuromuscular disorders,
craniofacial anomalies, obstructive sleep apnea, iron def ciency anemia, and periodic limb
movement disorder).
Indications for ordering an overnight PSG include the following:

n Suspected sleep disordered breathing: PSG is currently considered the diagnostic gold
standard to document the presence and severity of sleep-disordered breathing (obstructive
sleep apnea [OSA]). It can also be helpful in the delineation of the severity of OSA in preop-
erative and post-operative planning for adenotonsillectomy. In addition, repeat PSG to assess
for residual OSA following treatment (i.e., adenotonsillectomy) may be necessary with severe
preoperative OSA, or if symptoms (e.g., snoring) and/or risk factors (e.g., obesity) persist
post-treatment (see Chapter 14).
n Titration of continuous positive airway pressure (CPAP) or bilevel positive airway pres-
sure (BiPAP): Once OSA has been diagnosed on overnight PSG, a repeat sleep study is re-
quired if CPAP or BiPAP is to be included in the treatment plan in order to f t the patient with
the appropriate interface (e.g., full face or nasal mask, nasal pillows) and titrate to optimal
pressure(s) (see Chapter 14). Although split-night studies (i.e., f rst half of the night base-
line level of sleep-disordered breathing and second half CPAP/BiPAP titration) are sometimes
conducted in adults, these are rarely appropriate in children because of the preparation and
education required prior to initiation of positive airway pressure.
n Periodic limb movements (PLMs): To assess for the presence of PLMs, both as a potential
cause of sleep fragmentation in the patient with signif cantly restless sleep and/or observed
kicking movements during sleep, and occasionally to provide supportive evidence for the di-
agnosis of RLS (see Chapter 15). A sleep study may be helpful.
n Unexplained daytime sleepiness: Even in the absence of symptoms suggestive of sleep-dis-
ordered breathing (e.g., loud snoring) or PLMD, an overnight sleep study should be strongly
considered in patients with signif cant daytime sleepiness despite apparently adequate sleep
duration to assess for sources of sleep fragmentation. Disruptions in sleep architecture may
also ref ect abnormalities that are part of a primary sleep disorder of excessive daytime sleepi-
ness (narcolepsy). It is also important to conduct an overnight sleep study prior to a multiple
sleep latency test (MSLT) to be able to appropriately interpret the f ndings of this daytime
study.
n Episodic nocturnal phenomena: To evaluate episodic nocturnal phenomena, such as para-

somnias, that are frequent, violent, atypical, prolonged, or resistant to treatment, a PSG may
be appropriate. However, given the sporadic nature of many parasomnias, it should be kept in
mind that a single overnight sleep study may fail to capture an event. In this situation, asking
the parent to videotape an event in the home setting may yield more information and be more
cost effective.
The standard overnight PSG involves recording a number of different parameters during sleep
with close monitoring by a qualif ed technician. The following parameters are usually recorded:
sleep staging (electroencephalogram [EEG], electromyogram [EMG] of chin, and electro-ocu-
logram [EOG]), respiratory rate and effort (chest wall and abdominal motion using inductance
plethysmography), airf ow (oral and nasal thermal sensors and/or air pressure transducers), he-
moglobin oxygen saturation (pulse oximeter), heart rate (ECG), arousals spontaneous, associ-
ated with respiratory events or leg or body movements (EEG), leg movements (anterior tibialis
EMG), body position and movements (video recording), and snoring (microphone); many labs
also include measures of ventilation (end-tidal PCO2 sampled at the nose and/or mouth or trans-
cutaneous CO2). Select labs may also include specialized respiratory monitoring, such as bal-
loon esophageal manometry (see Chapter 14) or an extended EEG montage to detect nocturnal
seizures in addition to the standard central and occipital EEG channels. A sample PSG montage
and 30-second epoch is presented in Figure 3.2, which is representative of a standard pediatric
recording montage used by most sleep laboratories.
Most pediatric overnight studies are done in a hospital or free-standing sleep laboratory set-
ting. Although both attended and unattended home studies are increasingly used in adults, their
utility and feasibility in children are still largely unexplored. Laboratory studies have the benef t
Fig 3.2. Pediatric polysomnography montage. C4A1, O2A1, C3A2, O1A2: EEG leads; ROC: right eye;
LOC: left eye; FLOW: nasal airf ow; THOR: thoracic movement; ABDM: abdominal movement; ECO2:
end-tidal CO2; SAO2: oxygen saturation; BPOS: body position.
of increased validity and inclusion of behavioral observation. In addition, both home and nap
studies have a high false-negative rate for sleep-disordered breathing, frequently necessitating a
repeat in-lab study.
An overnight PSG can be performed in a child of any age and in children with an underlying
medical illness or neurodevelopmental or psychiatric disorder if adequately trained staff, ap-
propriate equipment, and adequate preparation of the child and family are in place. Many sleep
laboratories service both adults and children; however, a child-friendly environment and techni-
cians who are comfortable working with children are key components needed in order to facili-
tate a good nights sleep and to minimize the anxiety associated with an unfamiliar environment.
In preparation for the study, it may be preferable, especially for anxious children, to arrange an
in-person tour of the sleep laboratory. Most laboratories require that children under a specif c age
(typically 1416 years old, if no developmental delays) are accompanied by a parent throughout
the sleep study; sleeping arrangements for caregivers are generally a fold-out chair or cot in the
same bedroom. Sedation is not recommended for a sleep study, as many sedating agents are
also respiratory depressants; consultation with sleep laboratory personnel regarding medication
management is recommended for children who are already being treated with hypnotics at home
or who are on other psychotropic medications that may affect sleep. It is particularly important
to notify the sleep laboratory of any special considerations involved with the children being
evaluated, such as anxiety, fears, behavioral issues, and developmental considerations. Because in
many areas of the country there is still a shortage of facilities that perform pediatric studies and
interpret studies using age-appropriate criteria, the primary care practitioner should familiarize
him or herself with the local community facilities in terms of accredited labs conducting pediatric
sleep studies; the American Academy of Sleep Medicine (AASM) has developed some excellent
resource materials to enable sleep labs to develop more child-friendly policies and procedures.
Pediatric sleep studies should be scored and interpreted by technicians and physicians who
have specif c training in pediatric sleep medicine, according to the Rechtschaffen and Kales
(R&K) scoring manual rules and the recent 2007 changes to R&K described in the new AASM
scoring manual. Details of these changes are beyond the scope of this book, but include addi-
tional EEG leads (frontal), new scoring rules for PLMs and bruxism as well as for apneas and
hypopneas, and optional respiratory effort-related arousals. Updated guidelines for the visual
scoring of sleep and arousal in infants and children were published in 2007 (Journal of Clinical
Sleep Medicine, Vol 3 [2]; 201-240).
Multiple Sleep l atency t est (MSl t )

As an adjunct to a nocturnal PSG, a multiple sleep latency test may be conducted to objectively
evaluate an individual for pathologic levels of daytime sleepiness, particularly if narcolepsy or
other central hypersomnias are suspected. The MSLT is conducted in a sleep laboratory on the
morning and afternoon following an overnight sleep study, and consists of f ve 20-minute nap
opportunities given at 2-hour intervals. A more detailed discussion of MSLT interpretation is
found in Chapter 16; consultation with a sleep specialist is recommended for interpretation of
the MSLT.
Actigraphy
Actigraphy is a diagnostic procedure that utilizes a portable wristwatch-like device to record and
store information regarding body movements over a period of time (typically 1 to 2 weeks). The
data collected by the actigraph, in conjunction with a sleep diary, is then analyzed with computer
software, using preset activity thresholds to generate a printout of approximate sleepwake pat-
terns. This enables a more objective assessment of sleepwake behavior in the naturalistic
home setting compared to sleep diaries or self-report alone. Although largely still a research tool,
practice parameters for the clinical use of actigraphy in adults and in infants and children have
been published; actigraphy appears to be most useful in delineating sleep patterns and to diag-
nose circadian rhythm disorders (advanced or delayed sleep phase). Actigraphy may also be used
to more accurately document sleep duration, nightwakings, and, less reliably, sleep onset latency
in patients for whom there appears to be a discrepancy between subjective sleep complaints and
daytime consequences (e.g., an adolescent who reports sleeping less than 4 hours per night but
has no complaints of daytime sleepiness). Actigraphy can also be helpful in determining sleep
amounts in families in which the parents are unable to provide adequate information regarding
nighttime awakenings (e.g., child gets up to watch television during the night and the parents
are unaware of these behaviors). Actigraphy is becoming more common in clinical assessment,
although some challenges continue to exist regarding insurance compensation.
Sleep Hygiene: Healthy
Sleep Habits for Children
and Adolescents
4
Basic good sleep hygiene and habits, or positive sleep practices, are essential for healthy sleep.
Unfortunately, poor sleep hygiene practices are very common and often contribute to inadequate
and disrupted sleep. While poor sleep hygiene can contribute signif cantly to the development of
insomnia (see Chapter 18), patients with pre-existing insomnia frequently engage in maladaptive
sleep hygiene practices in an attempt to address their sleep problems.
Inadequate sleep hygiene includes two categories of sleep-related behaviors:
n Practices that increase arousal:
n Caffeine: Caffeine and its related sister chemicals, theophylline and theobromine (which
are also found in varying amounts in beverages like coffee, tea, and colas), increase alert-
ness by blocking the sedative effects of the neuromodulator adenosine and increasing excit-
atory neurotransmitter release. Increased consumption is also associated with a temporary
decrease in daytime sleepiness and an increase in alertness. Although caffeine reduces some
of the def cits associated with sleep loss, it is not a substitute for sleep; caffeine also does not
counteract the effects of alcohol. Furthermore, there are negative effects on subsequent noc-
turnal sleep after caffeine ingestion (increased sleep onset latency and fragmented sleep).
Its elimination half-life is approximately 6 hours. However, the degree of impact on sleep is
also dose-dependent, and sensitivity to these effects likely varies across individuals. Typical
withdrawal symptoms associated with caffeine are irritability, fatigue, diff culty concentrat-
ing, nausea, muscle pain, and headache. This headache, well known among coffee drink-
ers, usually lasts from 1 to 5 days. Caffeine also may exacerbate symptoms of restless legs
syndrome and periodic limb movements and acts as a diuretic, further compromising sleep
quality.
Many beverages and products contain caffeine, including a number of over-the-counter
cold remedies, pain relievers, and weight loss preparations. There are a number of herbal
stimulants that also contain caffeine as the active ingredient. However, because many bever-
ages containing caffeine (e.g., energy drinks) do not list the amount on the label, parents and
providers may need to conduct some detective work to accurately assess daily caffeine
consumption; see Table 4.1 for a list of common caffeinated products. Finally, adolescents
may have access to super-caffeinated beverages, syrups, and other products (e.g., candy,
gum, pills) through the Internet (e.g., at Web sites like Thinkgeek.com).
n Nicotine: Cigarette smoking is associated with increased sleep onset latency and disrupted
nonrestorative sleep. It also increases restless legs symptoms and increases the risk of sleep-
disordered breathing. Withdrawal from nicotine may result in disrupted sleep and daytime
somnolence.
n Evening television viewing: Watching television and using other electronics is one of the
most common poor sleep practices for children and adolescents. A recent national survey
found that 30% of preschoolers and 43% of school-aged children have a television in their
bedroom. Furthermore, multiple studies have found a relationship between television view-
ing in the evening, especially having a television in the bedroom, and more sleep problems
and insuff cient sleep. Television viewing not only is mentally activating but it also increas-
es bright light exposure and, thus may suppress melatonin production. Furthermore, some
children can easily develop the bad habit of needing the television to fall asleep. It is also
much more diff cult to control a childs television viewing if the set is in the bedroom.
43
t ABl e 4.1 Caffeine intake
Serving Content Caffeine Content

Product Size (total mg) (mg/ounce) Caffeine
Sodas and energy drinks
Jolt Energy 23.5 oz 280 11.91
Red Bull 8.3 oz 80 9.64
Rockstar Energy 16 oz 150 9.38
Vault Zero * 12 oz 74 6.17
Diet SunDrop * 12 oz 72 6.00
Pepsi One * 12 oz 57 4.75
Diet Mountain Dew * 12 oz 55 4.58
Mountain Dew * 12 oz 55 4.58
Tab * 12 oz 48 4.00
Diet Coke * 12 oz 46 3.83
Diet Dr. Pepper * 12 oz 44 3.67
Dr. Pepper * 12 oz 43 3.58
Diet Sunkist * 12 oz 42 3.50
Sunkist * 12 oz 41 3.42
Pepsi * 12 oz 39 3.25
Diet Pepsi * 12 oz 37 3.08
Coca-Cola * 12 oz 34 2.83
Big Red * 12 oz 34 2.83
Barqs Root Beer * 12 oz 22 1.83
Yoo-hoo Chocolate 8 oz 0 0.00
Coffee and tea
Starbucks coffee, tall 12 oz 260 21.67
Starbucks coffee, grande 16 oz 330 20.63
Dunkin Donuts coffee 16 oz 206 12.88
Arizona Green Tea Energy 16 oz 200 12.50
McDonalds coffee 12 oz 109 9.08
Tazo chai 8 oz 47 5.88
Snapple iced tea (all kinds) 16 oz 42 2.63
Coffee, decaf 8 oz 5 0.63
Other
Dark chocolate bar 1.45 oz 31 21.38
Milk chocolate bar 1.55 oz 9 5.81
Hot chocolate 8 oz 9 1.13
Chocolate milk 8 oz 5 0.62
Frozen desserts
Ben & Jerrys Coffee Heath Bar Crunch 8 oz 84 10.50
Ben & Jerrys Coffee ice cream 8 oz 68 8.50
Haagan-Dazs Coffee ice cream 8 oz 58 7.25
Over-the-counter drugs
Anacin 2 tablets 64
Dexatrim 1 tablet 200
Excedrin, maximum strength 2 tablets 130
No Doz, maximum strength 1 tablet 200
No Doz, regular strength 1 tablet 100
*Chou KH, Bell LN. Caffeine content of prepackaged national-brand and private-label carbonated beverages.
J Food Science 2007;72:C337342.
HEALTHy SLEEP HABITS FOR CHILDREN AND ADOLESCENTS 45
Get rid of the electronics in the bedroom

Families should be encouraged to remove all electronics from the bedroom, including televi-
sions, computers, hand-held video games, and cell phones.
n Stimulating play at bedtime: Playing can increase arousal and make it diff cult to fall
asleep.
n Cognitive activation: Feeling stressed, or excited, or engaging in any demanding mental
activities can result in insomnia.

n Bright light in the bedroom during the night or in the early morning: Nightlights are
f ne and some children f nd them comforting; however, bright light from indoor lighting,
streetlights, or early morning sunlight can disrupt sleep.
n Noise: Household noise and street noise can lead to diff culties falling asleep and frag-
mented sleep.
n Practices that are inconsistent with sleep organization:
n Napping late in the day: In toddlers, children, and adolescents, late daytime napping may
not allow for adequate time to suff ciently increase the sleep homeostatic drive before bed-
time and results in delayed sleep onset.
n Maintaining a disorganized or inconsistent sleepwake cycle: This practice will impede
sleepwake regulation.
n Spending more awake time in bed (reading, talking on the phone) in relation to sleep
time: Doing so may lead to an association between being in bed and being awake (versus
being asleep), which may result in associating the bed with wakefulness rather than sleep.
BeSt Sl eeP Pr Ac t ic eS
Given the above considerations, the following best sleep practices are recommended for children
and adolescents. Handouts for families on positive sleep practices are provided in Appendices
C7 and C8.
n Appropriate sleep schedule: A sleep schedule that factors in both individual sleep need and
lifestyle issues should be developed with the child or adolescent and the parents.
Individual Sleep Needs

Individual sleep needs are dependent on a number of factors, including age. Recent research
also indicates that tolerance for inadequate sleep appears to vary across individuals. That is,
some individuals appear to function better or worse following sleep deprivation than do others.
Although the general prof le of performance def cits following sleep loss is fairly consistent in
human beings (e.g., compromise of eff ciency, deterioration of performance over time), there
may also be individual variation in relative susceptibility to the effects of inadequate sleep
across domains (e.g., memory, attention, mood).
n Consistent sleep schedule: A schedule should be followed, including a set bedtime and con-
sistent naptimes if age appropriate. There should also be a consistent morning waketime re-
gardless of the prior nights sleep so as to regulate the internal clock and synchronize the
sleepwake cycle. Schedules on weekdays and weekends should be similar.
n Naps: Naps should be geared to the childs age and developmental need. However, very long
naps or too many naps should be avoided, as too much daytime sleep can result in less night-
time sleep.
n Bedtime routine: A routine should be implemented that involves the same three to four activi-
ties every night, and is relaxing and calming. Appropriate bedtime activities include taking a
bath or shower, reading or being read to, singing lullabies, listening to soft music, and discuss-
ing the childs day.
n Snack: Children should not go to bed hungry; thus, having a light snack before bed can be
benef cial. Heavy meals within an hour or two of bedtime, however, may interfere with sleep.
n Quiet evening activities: Especially in the hour before bed, high-energy activities, such as
playing outside, and stimulating activities such as computer games should be avoided.
n Sunlight exposure: Getting exposure to the sun, especially in the morning, will help regulate
the internal clock (see Chapter 1).
n Exercise: Exercise can decrease diff culties falling asleep and may lead to better quality sleep.
n Sleep-conducive environment: Create an environment that is conducive to sleep, including
a bedroom that is cool, dark, quiet, and comfortable. A nightlight may be comforting to some
children, but bright bedroom light should be avoided. A child also needs an appropriate sleep-
ing surface, such as a crib or a bed.
n Avoidance of caffeine, nicotine, and alcohol: These substances are disruptive to sleep.
Symptom-Based Algorithms 5
The following algorithms present a clinical framework for evaluating three of the most com-
monly presenting sleep complaints in pediatric patients (bedtime resistance or prolonged sleep
onset, nightwakings, and daytime sleepiness in adolescents). The major diagnostic categories to
consider for each presenting complaint are printed in bold; important differentiating features are
outlined in italics; and suggested diagnostic tests are underlined. It is important to keep in mind
that there may be more than one etiology for a sleep complaint in any given child or adolescent;
thus, several diagnostic categories may need to be considered. In addition, children may present
with more than one sleep complaint (e.g., delayed sleep onset and nightwakings). Finally, these
algorithms represent only a guideline for clinical evaluation. Specif c assessment, diagnostic, and
treatment recommendations for each disorder are found within the individual chapters.
47
48 SECTION II PEDIATRIC SLEEP DISORDERS
Bedtime Resistance/Prolonged Sleep Onset
Assess for inadequate sleep hygiene (e.g., Assess for chronic medical or
inappropriate napping, inconsistent sleep psychiatric conditions related to
schedule, lack of bedtime routine, excessive sleep disturbance (e.g., pain,
caffeine, environmental factors) medications, ADHD)
Anxiety symptoms Anxiety symptoms Assess sleep onset in relation

(primarily bedtime-related) (daytime and bedtime) to bedtime
Anxiety Dream- Develop- Falls Consistent

regarding related mentally asleep prolonged
Anxiety
falling or anxiety appropriate easily at sleep
Disorder
staying Nightmares fears later onset
asleep Nighttime bedtime
Psycho- Fears
physiologic
Insomnia
younger older
Develop- Circadian Delayed

mentally preference Sleep
inapprop- Phase
riate Syndrome
bedtime
Assess
parent-child
interactions,
child
behavior
Leg sensations
relieved by Needs Bedtime
movement, +FH parental refusal,
Restless Legs presence to delaying
Syndrome fall asleep; tactics;
associated no or few
with nightwakings
nightwakings Behavioral
Behavioral Insomnia of
Insomnia of Childhood
Childhood- Limit
Sleep Onset
Fig . 5.1. Bedtime resistance/prolonged sleep onset. ADHD = attention def cit hyperactivity disorder; FH
= family history.
SymPTOm-BASED ALGORITHmS 49
As s e s s for in a d e q u a te s le e p
h yg ie n e (e .g., ina ppropria te As s e s s for chronic m e d ic a l o r
p s yc h ia tric c o n d itio n s re la te d
na pping, incons is te nt s le e p Nightwa kings to s le e p dis turba nce (e .g., pa in,
s che dule , e xce s s ive ca ffe ine ,
e nvironme nta l fa ctors ) me dica tions , a s thma , ADHD)
Nightly brie f a rous a ls , Fre que nt prolonge d Epis odic, dis cre te
fra gme nte d s le e p night wa kings e ve nts
+ S noring S noring Timing: firs t Timing: Timing: la s t

(a pne ic pa us e s , 1/3 night; va ria ble ; 1/3 night;
mouth Re ca ll Re ca ll Re ca ll +
bre a thing, S le e p wa lkin g (s te re otype d Nig h tm a re s
e nla rge d tons ils ) S le e p Te rro rs move me nts ,
PSG ne urologica l
Ob s tru c tive ris k fa ctors )
s le e p a p n e a P rofound Mode ra te to
e xce s s ive EEG
mild da ytime No c tu rn a l
da ytime s le e pine s s ; s e izu re s
s le e pine s s kicking
(s le e p pa ra lys is , move me nts ,
ca ta ple xy, pos s ible
hypna gogic uncomforta ble
ha llucina tions ) le g s e ns a tions
P S G/MS LT PSG
Na rc o le p s y P e rio d ic Lim b
Mo ve m e n t
As s e s s pa re nt-child
inte ra ctions , child be ha vior
Ne e ds pa re nta l Be dtime re fus a l, Anxie ty Anxie ty

pre s e nce +/ fe e ding de la ying ta ctics Nig h ttim e re ga rding fa lling
to fa ll a s le e p Be h a vio ra l Fe a rs or s ta ying a s le e p
Be h a vio ra l In s o m n ia o f An xie ty P s yc h o p h ys io -
In s o m n ia o f Ch ild h o o d - Dis o rd e r lo g ic In s o m n ia
Ch ild h o o d - S le e p Lim it S e ttin g
On s e t As s o c ia tio n S le e p Typ e
Typ e
younge r a ge olde r a ge
Fig 5.2. Nightwakings. Note: The etiology of sleep disturbances in children is frequently multifactorial.
Therefore, any evaluation of nightwakings should take into consideration all of the factors listed above. PSG
= polysomnography; MSLT = multiple sleep latency test; EEG = electroencephalogram; ADHD = attention
def cit hyperactivity disorder.
As s e s s for chronic m e d ic a l
(e .g., pa in, me dica tions ) o r
Da ytime S le e pine s s p s yc h ia tric (e .g.,
(Adole s ce nts ) de pre s s ion, a nxie ty)
c o n d itio n s re la te d to s le e p
dis turba nce
As s e s s s e ve rity of As s e s s tota l
e xce s s ive da ytime s le e p time
s le e pine s s a nd
impa ct on da ytime
functioning
Tota l s le e p time Tota l s le e p time

>8-9 hours on <8-9 hours on
s chool nights s chool nights
Uncontrolla ble , s e ve re ,
fre que nt
+ S noring S noring + Difficulty Difficulty

(a pne ic fa lling fa lling
pa us e s , mouth a s le e p a s le e p
Continuous , bre a thing,
chronic e nla rge d
P S G/MS LT tons ils ) Kicking
PSG move me nts ,
Ob s tru c tive le g dis comfort
S le e p Ap n e a PSG Ina ppro-
Re s tle s s pria te
Le g s s le e p
S le e p Id io p a th ic S yn d ro m e / s che dule
pa ra lys is , Hyp e r- Epis odic P e rio d ic Lim b In s u ffic ie n t
ca ta ple xy, s o m n o le n c e Kle in - Mo ve m e n t S le e p
hypnogogic Le vin e Dis o rd e r
ha llucina tions S yn d ro m e
P S G/MS LT
Na rc o le p s y
As s e s s s le e p
Tre a tme nt-
re s is ta nt ons e t in re la tion
to be dtime
De la ye d
S le e p
Phas e
S yn d ro m e
Fa lls Cons is te nt
Tre a tme nt-
a s le e p prolonge d
re s pons ive
e a s ily a t s le e p
Circ a d ia n
la te r ons e t
P re fe re n c e be dtime
Anxie ty re ga rding
fa lling a s le e p
P s yc h o p h ys io lo g ic + Anxie ty Anxie ty
In s o m n ia
+ Da ytime a nxie ty
An xie ty Dis o rd e r Ina ppropria te na pping,
incons is te nt s le e p s che dule ,
e xce s s ive ca ffe ine , drug/a lcohol
us e
In a d e q u a te S le e p Hyg ie n e
Fig 5.3. Daytime sleepiness (adolescents). PSG = polysomnography; MSLT = multiple sleep latency test.
Bedtime Problems: Behavioral
Insomnia of Childhood,
Limit-Setting Type
6
Bedtime problems, including stalling and refusing to go to bed, are often the result of parental
diff culties in setting limits and managing behavior. Sleep disturbances of this type generally fall
within the diagnostic category known as behavioral insomnia of childhood, limit-setting type.
These sleep problems typically begin after the age of 2 years, when children are either able to
climb out of the crib or have been moved to a bed. Bedtime stalling behaviors include attempts to
delay bedtime (e.g., by watching additional television) and the bedtime routine (e.g., by reading
another story) or occur following lights out (curtain calls, such as requests for a drink of water
or an additional hug). Typically, the requests are based on what the child has learned will elicit
a parental response, for example a trip to the bathroom or being afraid of monsters under the
bed. Bedtime refusal includes behaviors such as the child refusing to get ready for bed and to
remain in the bed or the bedroom, often following the parent(s) back to the living room or other
rooms of the house.
Bedtime Problems: Behavioral Insomnia of Childhood, Limit-Setting Type

Behavioral insomnia of childhood, limit-setting type is characterized by the inadequate en-
forcement of bedtime limits by a parent or caregiver, resulting in the child stalling or refusing
to go to bed at an appropriate time. When limits are not set and enforced, or are enforced only
sporadically, sleep will be delayed, and total sleep may not be enough to meet the childs sleep
needs.
Another type of limit-setting problem occurs when there are few or no limits instituted by par-
ents around sleep behaviors; examples include allowing the child to fall asleep while watching
television in the living room and allowing an older child to play computer games in his or her
bedroom. Parents may also institute limits in an unpredictable or inconsistent way (e.g., inter-
mittently allowing the child to fall asleep in the parents bed). This type of inconsistent parental
response provides intermittent reinforcement, which maintains the childs inappropriate behavior.
Limit-setting sleep problems may also affect parental response to nightwakings, as in the case of
the child who is allowed to join the parents in their bed during the night. Parental limit-setting is
also likely to be the problem if the child goes to bed and falls asleep quickly for other caregivers
(e.g., babysitter, other parent) or has no diff culty falling asleep at the desired bedtime in other
situations (e.g., allowed to stay in living room and falls asleep on couch watching television).
The environment may also contribute to limit-setting problems. For example, limits may be
diff cult to set in homes in which the child shares a bedroom with his or her parents or siblings
or in which a grandparent resides. Parents of children with a current or past history of medical
problems may also have diff culty setting limits because of guilt, a sense that the child is vul-
nerable, or concerns about doing psychological harm (see Chapter 22 for more information on
children with medical problems).
Impact on the Family

Successful behavioral intervention for bedtime resistance will not only result in improvement
in the childs sleep problems but has also been shown to alleviate parental stress and improve
parental sleep. Implementation of behavioral management strategies for sleep may also lead
to improvements in parenting skills and management of daytime behaviors.
51
ePiDeMio l o g y
Bedtime resistance, found in 10% to 30% of toddlers and preschoolers, is one of the most com-
mon concerns of parents and may coexist with nightwakings. Not only are bedtime problems
common, but this behaviorally based sleep problem often becomes chronic; in one study, 84%
of children aged 15 to 48 months with bedtime struggles and/or nightwaking continued to have
signif cant sleep disturbance at the 3-year follow-up. School-aged children may also have signif -
cant limit-setting sleep issues; in one study, 15% of children aged 4 to 10 years had problematic
bedtime resistance reported by parents.
et io l o g y An D r iSk FAc t o r S
There are both precipitating and perpetuating factors that contribute to bedtime diff culties and
include both extrinsic factors (e.g., environment, parental issues) and intrinsic factors (e.g., tem-
perament, circadian rhythm).
n Permissive parenting style, in which there is minimal limit-setting regarding most discipline
issues. This ineffective parenting may be related to parenting style or may ref ect caregiver
problems, such as depression or substance use.
n Conf icting parental discipline styles, especially when parents frequently disagree about how
to handle behavioral issues. In this situation, one parent is often the authoritarian, whereas
the other is more lenient (good cop versus bad cop). Children often sense (and sometimes
exploit) this ambivalence, leading to increased noncompliant behavior.
n Parent expectations, which may contribute to bedtime issues. Parents may not have realistic
expectations regarding sleep behaviors and normal developmental.
n Age, as toddlers and preschool-aged children are more likely to assert their independence
and refuse to comply with parental requests. As children get older, they typically require less
parental interaction at bedtime.
n Temperament, especially diff cult and unpredictable temperament styles.
n Oppositional behavior during the day, which makes noncompliance at bedtime more likely.
n Environments, which inhibit limit setting, such as parents and child sharing a bedroom or
living with grandparents.
n Circadian timing, which can also play a role in bedtime struggles. When a relatively early
bedtime is set to coincide with the normal early evening circadian-mediated surge (i.e., na-
dir) in alertness, often referred to as the second wind, a child may have signif cantly more
diff culty settling, which can result in bedtime resistance. Children with an owl circadian
preference for later sleep onset and wake times also tend to have a later circadian nadir and are,
thus, particularly likely to have a settling problem if bedtime is set too early. These children
may also resist going to bed because they are not ready to fall asleep at the parent-determined
bedtime. On the other side, a late bedtime can lead to a child being overtired and taking longer
to fall asleep. One study found that a bedtime after 9:00 p.m. resulted in children actually tak-
ing longer to fall asleep. These situations are not primarily caused by parental failure to set
limits, but the resulting sleep onset problems may be compounded by parental management.
Pr eSen t At io n An D SyMPt o MS
n Noncompliant behavior, in response to parental requests to get ready for bed (e.g., change
into pajamas, brush teeth).
n Bedtime resistance, including refusal to go to bed or requiring a parent to be present at
bedtime.
n Curtain calls, characterized by frequent requests for parental attention (e.g., drinks, kisses)
after lights out.
n Delayed sleep onset, of 30 minutes or more following lights out.
BEHAvIORAL INSOmNIA OF CHILDHOOD, LImIT-SETTING TyPE 53
Diagnostic c riteria
See Table 6.1.
Associated Features
n Nightwakings: Many children with bedtime struggles also present with frequent nightwak-
ings, resulting from similar limit-setting issues or as a result of negative sleep associations
(e.g., parental presence required to fall asleep) that have developed at bedtime (see Chapter 7).
n Fearful behaviors: Some children present with nighttime fears characterized by fearful
behaviors (e.g., crying, clinging, leaving bedroom to seek parental reassurance) that are a
manifestation of bedtime stalling rather than being anxiety based.
n Daytime behavior problems: Daytime behavior problems appear to be more common in
poor sleepers. This relationship may ref ect an increase in behavior problems because of
inadequate sleep or may be related to the fact that children with daytime behavior problems
are more likely to have similar problems at night, or a combination of both.
n Family tension: Bedtime resistance often results in signif cant family tension, including argu-
ments between the child and the parents and marital discord. This tension may contribute to
heightened arousal in the child, making sleep onset even more diff cult. Parents also may focus
more attention on the childs behavior at bedtime to avoid dealing with underlying marital
conf icts.
eVAl uAt io n
n Medical history: Children with medical conditions may be more likely to have bedtime strug-
gles, related to a number of physical (pain, medication) and behavioral issues (see Chapter 21);
however, the history is typically benign.
t ABl e 6.1. Diagnostic criteria: Behavioral insomnia of childhood (V69.5)
A. A childs symptoms meet the criteria for insomnia based upon reports of parents or other adult
caregivers.
B. The child shows a pattern consistent with either the sleep-onset association or limit-setting type of
insomnia described below.
1. Sleep-onset association type includes each of the following:
a. Falling asleep is an extended process that requires special conditions.
b. Sleep-onset associations are highly problematic or demanding.
c. In the absence of the associated conditions, sleep onset is signif cantly delayed or sleep is
otherwise disrupted.
d. Nighttime awakenings require caregiver intervention for the child to return to sleep.
2. Limit-setting type includes each of the following:
a. The individual has diff culty initiating or maintaining sleep.
b. The individual stalls or refuses to go to bed at an appropriate time or refuses to return to bed
following a nighttime awakening.
c. The caregiver demonstrates insuff cient or inappropriate limit setting to establish appropriate
sleeping behavior in the child.
C. The sleep disturbance is not better explained by another sleep disorder, medical or neurological
disorder, mental disorder, or medication use.
American Academy of Sleep Medicine. International classif cation of sleep disorders, 2nd ed.: Diagnostic and cod-
ing manual. Westchester, IL: American Academy of Sleep Medicine, 2005:23.
n Developmental history: Developmentally delayed children, especially those with sensory in-
tegration issues, may have more diff culty with self-soothing at bedtime.
n Family history: The history should include an evaluation of parenting skills and limit-setting
abilities.
n Behavioral assessment: A history of more global behavior problems, especially noncompli-
ance and oppositional def ant disorder (ODD), may be present. Children with attention def cit
hyperactivity disorder (ADHD) often have more diff culty settling at bedtime (see Chapter 22).
n Physical examination: Physical symptoms are usually noncontributory.
n Diagnostic tests: Such tests are not indicated.
DiFFer en t iAl DiAg n o SiS

Bedtime struggles may be the result of a more global problem with noncompliance, including
ODD. In addition, alternative reasons for delayed sleep onset should be considered:
n Inappropriate sleep schedules, which may contribute to delayed sleep onset. Naps, includ-
ing napping past 4:00 p.m. or continued napping in an older preschooler, may result in a later
sleep onset. In addition, an irregular sleep schedule (inconsistent bedtime and waketime) may
conf ict with the circadian sleepwake rhythm and contribute to diff culties in falling asleep.
Similarly, signif cant discrepancies between weekday and weekend sleep schedules can result
in problems falling asleep on Sunday evenings, especially if the child or adolescent is sleeping
in late on weekend mornings. Finally, parents may not be attentive to the childs natural sleep
onset time, which may be later than the desired bedtime.
n Delayed sleep phase, related to a night-owl tendency or, in some cases, delayed sleep phase
syndrome (see Chapter 17). In both situations, sleep onset occurs at a consistent time each
night, and no problems are noted if bedtime is set closer to the usual fall-asleep time.
n Nighttime fears and separation anxiety, in which anxiety is a signif cant component of the
childs bedtime behavior. Typically, if the parent remains with an anxious child at bedtime or
lets the child sleep in a room with another person present, resistance disappears and sleep
onset is not delayed.
n Transient or adjustment insomnia, which is likely to present in children with previously
normal sleep. Transient insomnia can be the result of sleeping in an unfamiliar or noncondu-
cive (e.g., too noisy, too hot) sleep environment, stressful life event, disruption of sleep sched-
ule (e.g., trip, jet lag), or illness.
n Restless legs syndrome, which often presents with diff culty falling asleep at bedtime. Rest-
less legs syndrome is characterized by uncomfortable sensations and increased movements in
the legs that interfere with sleep onset (see Chapter 15).
n Medication effects, including stimulant medications for ADHD, may result in delayed sleep
onset (see Chapter 19 for more information on medication effects).
MAn Ag eMen t
w hen to r efer
Children or adolescents with persistent or severe bedtime issues that are not responsive to simple
behavioral measures or that are extremely disruptive should be referred to a mental health profes-
sional for evaluation and treatment. Collaboration with a behavioral therapist in designing and
implementing treatment plans may be prudent (1) if there is anxiety; (2) if there are complex,
chronic, or multiple sleep problems; or (3) if initial behavioral strategies have failed.
t reatment
Treatment for limit-setting sleep problems should include the institution of appropriate sleep hab-
its, development of an appropriate sleep schedule that coincides with the childs natural circadian
rhythm, and appropriate and consistent parental limit-setting. A summary of recent standards of
practice for bedtime problems and night wakenings can be found in Chapter 7.
Sleep Habits
n Establish a set bedtime, one that coincides with the childs natural sleep onset time. A con-
sistent nightly bedtime will help to set the circadian clock and enable the child to fall asleep
more easily. If, however, the attempted bedtime coincides with the late-day circadian peak in
alertness, the likely result is bedtime resistance. In this case, delaying the bedtime or moving
the bedtime earlier, when the child is more physiologically ready for sleep, may be warranted.
With children who have an evening circadian preference, temporarily delaying the bedtime to
coincide with the natural sleep onset time and then gradually advancing the bedtime over a pe-
riod of several weeks may be a reasonable approach (see discussion of bedtime fading, below).
n Institute bedtime fading, which involves temporarily setting the bedtime at the current sleep
onset time and then gradually advancing it to the desired bedtime. This has the advantage of
temporarily eliminating the struggles that occur between bedtime and sleep onset, thus reduc-
ing tension in the household. In addition, children usually view this procedure positively (be-
ing allowed to stay up later), which increases the likelihood of compliance with the rest of
the behavioral program.
n Evaluate daytime sleep habits, particularly in older children, that may be interfering with
sleep onset such as napping. Preschoolers often continue to require a daytime nap, but daytime
sleep past 3:00 or 4:00 in the afternoon interferes with an early bedtime. In these cases, bed-
times need to be moved later and parental expectations need to be adjusted.
Nap Problems
Parents of young children often struggle with naptime issues. Similar to bedtime problems
and nightwakings (see Chapter 7), nap problems are often related to scheduling problems and/
or poor sleep associations. To deal with naptime problems, the following strategies can be
benef cial:
Set naptimes that are either based on the same time each day (e.g., 9:00 a.m. and 2:00 p.m.)
or occur within 2 to 3 hours after the last awakening. Up to the age of 6 to 9 months, most
babies are ready to take a nap exactly 2 hours after awakening.
Set a consistent naptime routine that is similar to, but shorter than, the bedtime routine. For
children who are taking only one nap per day, have the nap occur immediately following
lunch so that there is a clear routine to the day.
Develop positive sleep habits, including self-soothing skills. As with nightwakings, an in-
fant or toddler who develops negative sleep associations (e.g., being rocked to sleep) will
require this to occur at the onset of the nap and will be unable to return to sleep following a
brief arousal. Negative sleep associations often account for short nap periods, e.g., 20 to 45
minutes.
Establish clear naptime rules, especially with toddlers.
n Establish a consistent bedtime routine, one that is approximately 20 to 45 minutes and in-
cludes three or four soothing activities (e.g., bath, pajamas, stories) rather than high-energy
or stimulating activities (e.g., playing outside, watching television). The f nal activity (e.g.,
stories) should be a preferred one to motivate compliance with prior activities (e.g., brushing
teeth). A chart of the bedtime routine can be highly benef cial.
n Provide a transitional object, such as a blanket, doll, or stuffed animal.
n Exposure to morning bright light, as well as avoidance of light in the evening, can help set
the circadian clock for the day and increase sleepiness at bedtime.
n Maintain good sleep hygiene practices, including avoiding caffeine and getting regular
exercise.
Behavior Management Strategies

Bedtime problems are similar to any other behavioral issue and, thus, respond to general be-
havior management strategies. Suggestions for parents include the following:
Use positive reinforcement to increase appropriate behaviors.
Avoid punishment to decrease inappropriate behaviors, as punishment is not an effective
way to change a childs behavior.
Focus on increasing positive behaviors rather than decreasing negative behaviors.
Be consistent in responding, as this is the key to behavior change.
Do not ask questions (e.g., Ready for bed?) when the intention is to state a fact (e.g., Its
time for bed).
Set clear limits and follow through.
Provide acceptable choices (e.g., Do you want to go to bed now or in 5 minutes?) to give
the child some control but within reasonable limits.
Limit Setting: Guidelines for Parents

n Establish clear bedtime rules, including activities involved in getting ready for bed (e.g.,
change into pajamas, brush teeth). Parents should also identify specif c appropriate behaviors
(e.g., staying in bed) and inappropriate bedtime behaviors (e.g., calling for parents).
n Ignore any complaints or protests about bedtime, such as Im not tired, or I dont want to
go to bed. Parents should also avoid discussing or arguing about bedtime as this will lead to
a struggle, often reinforcing bedtime problems with increased attention. Parents should f rmly
and calmly let their child know that it is time for bed and continue with the established routine.
n Put the child to bed drowsy but awake, as it is benef cial for children to learn to fall asleep
independently.
n Check on the child, especially if he or she is upset or crying. The visits should be brief (1
minute) and nonstimulating and occur at a frequency that is comfortable for both parents and
child. These check-ins provide reassurance, but at the same time should be structured to
reinforce limits.
n Return child to bed or room, being f rm and calm if he or she comes out of the bedroom. For
some children, simply returning them to bed multiple times works. For others, establishing a
system in which the bedroom door is closed for a brief period (1 minute) if the child gets out
of bed can be helpful. The time can be increased by 1 minute for each successive time out of
bed. In addition, parents should praise their child for positive behaviors (e.g., staying in bed,
not calling).
n Use positive reinforcement, including sticker charts and reward systems. Small rewards
should be given contingent on positive behaviors and, especially in younger children, rewards
should be presented immediately (f rst thing in the morning). Larger rewards can be offered
for continued positive behaviors, such as three nights of going to bed without protest. The
specif c behaviors and number of days and nights required to earn a reward should be based
on the childs developmental level (younger children need more frequent rewards) and should
be based on the number of successes rather than on number of consecutive nights of success
(e.g., three stickers obtain a trip to the playground, not three consecutive stickers). The reward
schedule should also be set up initially to ensure a reasonable expectation of immediate suc-
cess, which is likely to increase the childs investment in the process.
n Stick to f rm bedtime limits, once clear rules have been established. Parents must follow
through on their expectations and not inadvertently reinforce inappropriate behaviors.
n Be persistent and consistent, in responding to the child. Consistency is the key to any be-
havior change. It is very important to explain to parents that intermittent reinforcement of an
undesired behavior (occasionally allowing the child to fall asleep in the parents bed) actually
makes it more diff cult to extinguish or eliminate the behavior. The analogy of playing a slot
machine may help parents understand this important behavioral concept; that is, the more un-
predictable the reward is (winning the jackpot or getting to stay in Moms bed), the more
likely the individual is to persist in the behavior (pulling the slot machine lever or coming
into the bedroom).
n Expect an extinction burst, after initiation of a behavioral program. It is very important to
warn parents that the behavior will often become worse (intensify in severity and frequency)
for several days before signif cant improvement occurs. Anticipating this often prevents par-
ents from immediately abandoning the behavioral program. An extinction burst can also occur
days or weeks later, so parents should be prepared for future testing of limits.
Bedtime Pass
A bedtime pass can help parents set limits and can be extremely helpful with children who
make multiple requests after lights out. Parents can provide their child with one or two bed-
time passes, which can be as simple as an index card that has been decorated. The child must
turn in a card for each request made. No more passes means no more requests. This simple
system allows children a way to make a reasonable request while setting clear limits. Another
aspect that parents can add is providing a reward (e.g., trip to the library) for any pass that the
child still has in the morning to discourage requests. Research shows that the bedtime pass can
be highly effective in reducing problematic bedtime behaviors. It may be especially helpful for
anxious children, for whom just having the option to seek out parents if they really need it
is often suff ciently reassuring.
Pr o g n o SiS
Bedtime struggles can usually be well controlled with behavioral interventions.
Tips for Talking to Parents

Explain the role of limit-setting in bedtime stalling and bedtime refusal.
Discuss developmentally appropriate parental responses to and strategies for handling
noncompliant bedtime behaviors.
Develop an appropriate sleep schedule that ensures adequate sleep and avoids sleep de-
privation. Be sure the set bedtime is appropriate given the childs circadian rhythm and
preference.
Develop a behavior management plan that incorporates all potential pitfalls.
Establish a reward system to reinforce positive behaviors.
Refer for behavioral management if the bedtime problems are indicative of more global
parenting limit-setting issues or the bedtime problems are unresponsive to simple behavioral
interventions.
See Appendix D1 for a parent handout on bedtime problems.
Nightwakings: Behavioral
7 Insomnia of Childhood, Sleep
Onset Association Type
Nightwakings are one of the most common sleep problems experienced by infants and tod-
dlers. By 3 months of age, most healthy full-term babies are physiologically capable of sleeping
through the night (i.e., sleep consolidation) and by 6 months of age no longer require nighttime
feedings. However, 25% to 50% continue to awaken during the night at 9 to 12 months. Studies
also indicate that problematic nightwakings are likely to persist, as young children often do not
outgrow the problem.
Diff culties with sleep maintenance occur for many different reasons, but persistent and pro-
longed nightwakings are most commonly related to inappropriate sleep onset associations (also
referred to as behavioral insomnia of childhood, sleep onset association type). Sleep onset asso-
ciations are conditions that the child learns to need in order to fall asleep at bedtime. These same
sleep onset associations are also typically needed in order to fall back to sleep after arousals or
awakenings during the night. Thus, when a child develops bedtime sleep onset associations that
are not readily available during the night (being rocked or held, having a parent present), pro-
longed nightwakings may occur. As infants and children typically arouse brief y on average 2 to 6
times throughout the night as a result of the normal ultradian rhythm of sleep cycles, these night-
wakings (or, more accurately, these failures to fall back to sleep) may occur as often as every 90
to 120 minutes. One study found that parental presence at bedtime was the strongest predictor of
disrupted sleep patterns and was associated with increased nightwakings and reduced total sleep
time. For example, in infants, parental presence was associated with a decreased sleep duration of
1.7 hours. Furthermore, approximately 30% of school-aged children were reported to fall asleep
with a parent present, and this practice was associated with a six-fold increase in the likelihood
of nightwakings.
Children who are able to soothe themselves back to sleep without parental intervention (self-
soothers) generally experience brief arousals rather than prolonged nightwakings. Thus, parents
are generally unaware of these brief arousals. In contrast, signalers are those children who alert
their parents by crying or going into the parents bedroom upon awakening. Whether an infant or
child is a self-soother or a signaler is highly inf uenced by the appropriateness of the bedtime
sleep onset associations provided (i.e., those that will also be readily available to the child during
the night and do not require parental intervention). Thus, the capacity to self-soothe is clearly as-
sociated with the practice of being put to bed while drowsy but still awake (avoiding associating
sleep onset with being held or rocked). In addition, parents, especially with infants and toddlers,
then choose whether or not to respond to the signaled arousal or waking with such reinforcing
Sleep Associations
Sleep associations are those conditions that are habitually present at the time of sleep onset
and in the presence of which the infant or child has learned to fall asleep. These same condi-
tions are then required in order for the infant or child to fall back to sleep following periodic
normal nighttime arousals. These sleep associations can be appropriate (e.g., thumbsucking)
or inappropriate (e.g., rocking, nursing, swinging). Inappropriate, or problematic, sleep asso-
ciations are those that require parental intervention and thus cannot be reestablished indepen-
dently by the child upon awakening during the night. Inappropriate sleep associations are the
primary cause of frequent nightwakings.
58
NIGHTwAkINGS 59
behaviors as verbal soothing, rocking, or feeding. The practice of parents both responding im-
mediately to and providing social reinforcement for nightwakings further increases the likelihood
that they will occur and may eventually result in a trained night crier. Finally, although there
is often considerable night-to-night and week-to-week variability in all of these behaviors, and
neither infants nor parents are always consistent in the way they behave and interact, it is clear
that a persistent pattern of diff culty in self-soothing and parental reinforcement of nightwakings
is associated with sleep disruption in infants and children.
ePiDeMio l o g y
Overall, studies indicate that 25% to 50% of 6- to 12-month-olds and 30% of 1-year-olds have
problematic nightwakings. In toddlers (aged 13 years), 15% to 20% continue to have nightwak-
ings. However, some studies indicate prevalence rates of nightwakings as high as 70% in infants
and 50% in toddlers. In preschoolers and school-aged children, prevalence of nightwakings is
approximately 15% to 20%; thus, this is not an issue exclusive to very young children.
As presented in Chapter 6, nightwakings are often the result of both extrinsic factors (e.g., envi-
ronmental issues, parent behavior) and intrinsic factors (e.g., temperament). These intrinsic fac-
tors include a complex combination of biological, circadian, and neurodevelopmental factors that
are then inf uenced by and interact with environmental and behavioral variables. The inability to
self-soothe may represent a delay in the emergence of or a regression in behavior associated with
the neurodevelopmental processes of sleep consolidation and sleep regulation that occur over the
f rst few years of life. Developmental maturation typically governs the emergence of these sleep
milestones, but they are also inf uenced by the context and environment in which they occur;
thus, these are learned behaviors and amenable to modif cation by behavioral strategies.
In addition, the genesis of nightwakings typically involves predisposing, precipitating, and
perpetuating factors. Multiple studies have found that frequent nightwakings are associated with
a number of factors, including parent presence while falling asleep, room-sharing and bed-shar-
ing, feeding to sleep and to go back to sleep during the night, and not having a consistent bedtime
routine. Thus, the overriding factor, as discussed above, is negative sleep associations. An addi-
tional consideration intertwined with negative sleep associations is that children who experience
more frequent arousals or disruptions during sleep, such as related to sleep apnea, also have more
opportunities to have prolonged nightwakings that require parental intervention. Conditions that
may increase the likelihood of nocturnal arousals and sleep fragmentation include:
n Co-sleeping, as studies have found that babies who either share a room or share a bed with
their parent(s) are highly likely to awaken during the night and seek interaction with a parent.
n Breast feeding, given that breast milk is more easily digested and breast-fed babies need to
be fed more frequently. Breast-fed babies are also more likely to be nursed to sleep at bedtime
and thus, to become dependent upon nursing to fall back to sleep during the night. Further-
more, one study found that nursing back to sleep following a nightwaking is associated with
decreased sleep consolidation and increased nightwakings in breast-fed babies.
n Acquisition of normal developmental milestones, both motor (e.g., pulling to stand, crawl-
ing) and cognitive milestones (e.g., separation anxiety), often coincide with an exacerbation or
resurgence of nightwakings, especially between the ages of 9 and 12 months.
n Sleep-disrupting events, such as illness, vacations, and scheduling changes, can result in
fragmented sleep and increased nightwakings.
n Colic or other medical conditions, such as otitis media, may result in more frequent night-
time arousals. In addition, in those conditions that typically require nighttime parental inter-
vention (e.g., colic), it may be diff cult for parents to differentiate between nightwakings due
to ongoing physical symptoms and those related to learned behaviors (parental attention to
crying).
Other risk factors for problematic nightwakings include:
n Diff cult temperament, which has been noted to be related to sleep diff culties, especially
nightwakings, likely due to the childs inability to self-soothe. In addition, children who are
fussy or diff cult may insist on specif c behaviors at bedtime and resist any attempts by parents
to initiate more independent settling.
n Insecure maternalchild attachment, as infants who are insecurely attached are reported to
have more sleep problems, although the presence of sleep problems does not necessarily imply
that there should be concerns about attachment.
n Parental anxiety, especially common in f rst-time parents, as these parents are more likely
to respond immediately to their baby throughout the night, often interfering with the childs
learning to return to sleep independently. In addition, negative emotional states and heightened
arousal in parents are likely to increase arousal levels in the infant as well, making settling
more diff cult.
n Maternal depression, as longitudinal studies indicate an increased risk of sleep disturbances
in children of mothers who have previously been identif ed as depressed. However, infant and
toddler sleep disturbances clearly contribute to maternal depression.
Nightwakings, which require parental intervention for the child to return to sleep, are the pre-
senting symptom. It should be noted that research, clinical, and individual parental def nitions
of problematic nightwakings in terms of frequency, length, and chronicity of the wakings may
differ substantially. In clinical practice, however, it is the parents def nition of a problem that
warrants further assessment and possibly intervention.
See Table 7.1.
Associated Features
n Diff culties at naptime, also related to the development of negative sleep associations.
n Delayed sleep onset, as the transition to sleep may be prolonged if the association requires
continued effort, such as a parent continuously rubbing the childs back or a child sucking on
a pacif er without letting it fall out of the mouth. Furthermore, many parents who rock or hold
their child to sleep f nd it diff cult to make the transition to putting their child down asleep in
the crib without waking their child and, thus, needing to start the pattern again.
It should also be noted that delayed sleep onset in children with nightwakings may be pri-
marily due to caregivers diff culties with setting limits at bedtime (i.e., behavioral insomnia
of childhoodlimit setting type; see Chapter 6). Although these two subtypes of behavioral
insomnia of childhood are def ned as separate entities for classif cation purposes, in reality,
they often co-exist, and many children present with both bedtime delays and nightwakings.
n Daytime behavior problems, such as irritability and an increase in temper tantrums, associ-
ated with the sleep fragmentation resulting from nighttime awakenings.
n Family stress, including parental sleep disruption, psychiatric symptomatology (including
postpartum depression), marital discord, and overall family tension, often results from night-
time sleep disturbances in infants and children. Studies indicate that successful behavioral in-
tervention not only results in fewer sleep problems for the child, but may also alleviate parental
stress, improve parental sleep, and lead to improvements in parenting skills and management
of daytime behaviors.
NIGHTwAkINGS 61
t ABl e 7.1. Diagnostic criteria: Behavioral insomnia of childhood (V69.5)
A. A childs symptoms meet the criteria for insomnia based upon reports of parents or other adult
caregivers.
B. The child shows a pattern consistent with either the sleep-onset association or limit-setting type of
insomnia described below.
1. Sleep onset association type includes each of the following:
a. Falling asleep is an extended process that requires special conditions.
b. Sleep-onset associations are highly problematic or demanding.
c. In the absence of the associated conditions, sleep onset is signif cantly delayed or sleep is
otherwise disrupted.
d. Nighttime awakenings require caregiver intervention for the child to return to sleep.
2. Limit-setting type includes each of the following:
a. The individual has diff culty initiating or maintaining sleep.
b. The individual stalls or refuses to go to bed at an appropriate time or refuses to return to bed
following a nighttime awakening.
c. The caregiver demonstrates insuff cient or inappropriate limit setting to establish appropriate
sleeping behavior in the child.
C. The sleep disturbance is not better explained by another sleep disorder, medical or neurological
disorder, mental disorder, or medication use.
American Academy of Sleep Medicine. International classif cation of sleep disorders, 2nd ed.: Diagnostic and cod-
Early Risers
There are two groups of young children who awaken too early in the morning (usually de-
termined by parental def nition). The f rst group includes those children who have a relative
advance in their circadian sleepwake pattern (i.e., morning larks). In these children, both
sleep onset and morning waking time are shifted relatively earlier, and they typically have
adequate sleep duration if allowed to sleep on their preferred schedule. The second group
involves those children who often get up for the day before they have had enough sleep. These
early-morning awakenings in actuality represent the f nal arousal of the night, after which
the child fails to return to sleep for the remainder of the nocturnal sleep period. This may be
due to inappropriate sleep associations (e.g., nursing, rocking) and an inability to self-soothe,
poor limit setting (e.g., parent allows child to join him or her in the parents bed) or inadvertent
reinforcement of the waking (e.g., the child is allowed to watch early-morning television).
These children typically return to sleep within an hour or so of getting up for what seems to
be an early morning nap or may appear tired and irritable during the day. Once behavioral
interventions are instituted, these children begin to sleep until a more appropriate waketime.
eVAl uAt io n
n Medical history: Although generally benign, the presence of medical issues in a history may
predispose a child to nightwakings and may also increase the likelihood that parents will inter-
vene during the night. Comorbid medical problems may also make behavioral strategies that
involve extinction procedures (see below) and distress on the part of the child more chal-
lenging for parents to successfully implement.
n Developmental history: Developmentally delayed children often have sleep problems that
ref ect the childs developmental (younger) age rather than chronological age.
n Family history: The history may be positive for psychopathology, especially maternal
depression.
n Behavioral assessment: Children with a diff cult temperament are at increased risk for sleep
disturbances related to dysregulation.
n Nightwaking history: Parents often identify sleep associations as the trick that gets the
child to fall asleep or return to sleep (e.g., nursing, bottle feeding, rocking). Many of these
children have not learned to self-soothe and have never slept through the night.
n Diagnostic tests: Tests are not indicated, although medical evaluations such as a pH probe to
assess for gastroesophageal ref ux or an overnight sleep study to diagnose obstructive sleep
apnea may be considered if there are symptoms suggestive of an underlying medical or sleep
disorder.

The diagnosis of behaviorally based nightwakings is usually straightforward. However, other
causes of nighttime awakenings need to be considered:
n Medical concerns, including ref ux and pain (especially related to otitis media), which often
result in prolonged nighttime awakenings, delayed return to sleep, and parental inability to
console the child. However, continued parental reinforcement of these nightwakings after the
medical condition has resolved may contribute to maintaining them.
n Underlying sleep disrupter, such as periodic limb movement disorder (see Chapter 15) or
obstructive sleep apnea (see Chapter 14), that contributes to increased nighttime arousals and
awakenings.
n Poor limit setting, which is usually characterized by the parents failure to set limits during the
night (e.g., allowing the child to watch television in the middle of the night) or reinforcement
of inappropriate nighttime behaviors (e.g., bringing the child to the parents bed on a nightly
basis).
n Inadequate sleep, which may increase arousals during sleep. Insuff cient sleep can be the
result of poor napping or premature discontinuation of naps by parents, an inappropriately late
bedtime, inadequate time in bed, or the result of another sleep disorder. Conversely, develop-
mentally excessive time in bed may lead to poor sleep consolidation.
n Transient sleep disturbances, which usually occur in a child with previous normal sleep.
Transient nightwakings (i.e., adjustment insomnia) can be the result of a stressful life event,
disruption of sleep schedule (e.g., trip, jet lag), or an illness. Short-term sleep disturbances,
however, can become chronic if parents respond in a way (e.g., reinforcement of the nightwak-
ings) that fosters inappropriate sleep habits.
n Inadequate sleep hygiene, including maintaining an erratic sleep schedule, use of caffeine or
other substances, and inadequate sleep may contribute to disturbed sleep and nightwakings.
n Environmental contributors, such as a bedroom that is not conducive to sleep (e.g., noisy,
hot) or disruption of sleep by others (e.g., parent waking in early morning for work) can cause
an increase in the number and duration of awakenings.
MAn Ag eMen t
w hen to r efer
Children or adolescents with persistent nightwakings that are not responsive to simple behavioral
measures or that are extremely disruptive to the family should be referred to a sleep specialist or
a professional who specializes in behavior management. If there is a concern about the existence
of an underlying sleep disorder or a medical problem, appropriate referral is warranted.
NIGHTwAkINGS 63
Standards of Practice
In 2006, the American Academy of Sleep Medicine released a standards of practice for the
treatment of bedtime problems and nightwakings in young children. An overall review of the
literature found that 94% of studies report that treatment was eff cacious and 80% of treated
children demonstrate clinically signif cant improvement. These results were maintained at 3-
to 6-month follow-up. Empirical evidence from controlled group studies utilizing Sackett cri-
teria for evidence-based treatments provide strong support for unmodif ed extinction and pre-
ventive parent education. Furthermore, there is support for graduated extinction and bedtime
fading and other positive routines. Note that given these guidelines and considering parental
acceptance of treatment recommendations, as well as overall child response, we recommend
the use of graduated extinction in the treatment of bedtime problems and nightwakings.
t reatment
Management of nightwakings should include establishment of a set sleep schedule and bedtime
routine. In addition, an intervention strategy should be chosen based on the temperament of
the child and parental tolerance, as well as the parenting style of the family. Thus, behavioral
interventions that are tailored to the needs and special circumstances of the individual child and
family have a higher likelihood of success. For example, some families are likely to accept and
tolerate prolonged crying at bedtime. Other families will require a more moderate approach in
which they gradually make changes (e.g., f rst 3 nights establish a bedtime routine only, next 3
nights rock baby to sleep while gradually weaning off bottle).
n Sleep Habits
n Sleep schedule, one that ensures a developmentally appropriate amount of sleep, as both
inadequate sleep and excessive time in bed may result in increased nighttime arousals. A
consistent nightly bedtime will also help to reinforce the circadian sleepwake rhythm and
enable the child to fall asleep more easily.
n Consistent bedtime routine, one that is approximately 20 to 45 minutes and includes three
to four soothing activities (e.g., bath, pajamas, stories). Research shows that simply insti-
tuting a nightly bedtime routine signif cantly improves both bedtime diff culties and night-
time awakenings. The mechanism is unknown, but it may be due to an overall decrease in
arousal.
n Maintenance of daytime sleep (naps), at least through the age of 3 to 3.5 years, as insuf-
f cient sleep in a young child will increase nighttime arousals and, thus, increase sleep
problems.
n Transitional objects, such as a blanket, doll, or stuffed animal.
n Wait and see approach, in which parents avoid responding immediately to a babys move-
ments or sounds during the night. This allows the baby a chance to return to sleep indepen-
dently, without parental interference, and avoids reinforcement of nightwakings.
Drowsy But Awake

The key to a successful transition from relying on parental intervention to self-soothing to
fall asleep is to put the child to bed drowsy but awake at bedtime. This will encourage the
development of self-soothing skills, which will lead to self-soothing back to sleep following
normal nighttime arousals. Anticipatory guidance during well-child visits should begin to in-
troduce this concept at the 2-week and 2-month visits, encouraging parents to implement this
strategy by about 12 weeks.
n Extinction (crying it out) involves putting the child to bed at a designated bedtime and
then systematically ignoring the child until a set time the next morning. Extinction has been
documented to be a successful treatment (see Standards of Practice); however, it is often not an

acceptable choice for families. Parents are often concerned about the effects of the treatment
on their childs emotional development and are, thus, less likely to be compliant.
Will Sleep Training Harm My Child?

Parents are often concerned that any sleep training that involves crying will result in psycho-
logical harm to their child. There is no research that supports this belief. Rather, research indi-
cates that following sleep interventions, infants are found to be more secure, more predictable,
and less irritable and to cry less following treatment. No negative impact on breastfeeding
has been found. Furthermore, there are often signif cant improvements in daytime behaviors,
likely as a result of increased sleep time and improved sleep quality.
n Graduated extinction involves putting the child to bed drowsy but awake and waiting pro-
gressively longer periods of time, usually in 5-minute increments, before checking on the
child. On each subsequent night, the initial waiting period before checking is increased by
5 minutes. Clinical experience indicates that there is no recommended optimal period of
time between checks, and that the exact amount of time should be determined by the parents
tolerance for crying and the childs temperament (e.g., some children become more agitated
with brief parental checks). Since the key to this treatment is to allow the child to fall asleep
independently and, thus, develop self-soothing skills, parents can choose how frequently or
infrequently they check. When parents check on their child, they should reassure the child
but keep contact brief (12 minutes) and neutral (e.g., pat on shoulder rather than pick up and
cuddle). Research has also indicated that graduated extinction is effective even if instituted ini-
tially only at bedtime rather than throughout the night, as generalization of self-soothing skills
to nighttime arousals will typically occur within 1 to 2 weeks of the childs falling asleep easily
and quickly at bedtime. Thus, parents can institute checking at bedtime only, responding to
their child in their usual manner throughout the night (e.g., nursing, bringing child to parents
bed). A similar checking routine during the night may need to be instituted several weeks later
if nightwakings persist.
The success of graduated extinction is usually based on the parents ability to be consistent
and follow through. Thus, proactive problem-solving with the family, including discuss-
ing potential pitfalls (e.g., child becoming so upset that he or she vomits) and anticipation of
problems (e.g., waking an older sibling), greatly increases the likelihood of success. Parents
should be also warned that the f rst few nights of intervention are often more diff cult because
Sleep Training Steps

Step 1. Establish a set bedtime and regular sleep schedule.
Step 2. Develop a consistent bedtime routine in which the activities occurring closest to
lights out take place in the room where your child sleeps. Avoid making bedtime feedings
part of the routine after 6 months.
Step 3. Make the bedroom environment the same at bedtime as it is throughout the night
(e.g., lighting, music).
Step 4. Put your child to bed drowsy but awake.
Step 5. Check on your child on a preestablished schedule that takes into account the childs
temperament and your tolerance for crying. The goal is to allow your child to fall asleep
independently.
Step 6. Respond to your baby as usual (rocking, soothing) following nighttime awakenings.
The self-soothing skills (falling asleep easily and quickly) that the baby develops at bedtime
are highly likely to lead to self-soothing during the night within 2 weeks.
NIGHTwAkINGS 65
of a so-called extinction burst (increase in intensity and duration of crying), so it is critical

to encourage them to anticipate this and to persevere with the intervention. In general, parents
may expect signif cant improvement in nightwakings within 3 to 7 days.
Good Morning Light

A good morning light is a simple strategy to combat early morning awakenings or continued
nighttime awakenings that are perpetuated by parents bringing their child to their bed in the
early morning hours or in other ways reinforcing awakenings (e.g., parent brings child to bed
once it is 5:00 a.m.). A good morning light involves attaching a nightlight to a timer that
is set for a reasonable morning time (e.g., 6:00 a.m.). The child is told that s/he may get out
of bed or go to the parents bed once her good morning light turns on. Clinically, it has been
found to be highly effective.
n More gradual fading of adult intervention is appropriate for families who are unable to
tolerate the above extinction approaches or consider them to be unacceptable. A plan should
be developed that gradually fades (eliminates) adult intervention. In order to develop such a
strategy, the end goal should be identif ed (e.g., falling asleep independently at bedtime) and
successive steps to achieving that goal specif cally outlined (e.g., 3 nights of establishing a
bedtime routine and setting bedtime; 3 nights of parent sitting with baby while baby falls
asleep in crib; 3 nights of parents sitting 3 feet from crib while baby falls asleep; 3 nights of
sitting in doorway; 3 nights of sitting outside doorway; and so forth). Similar strategies can
be implemented during the night. Again, initially parents can start with instituting treatment
at bedtime only and responding to their child in their usual manner throughout the night, as
generalization to a decrease in nightwakings often occurs (although nighttime intervention
may be required 23 weeks later). However, some parents may decide to respond to their
childs nightwakings in the exact same manner as at bedtime (e.g., if sitting 3 feet from crib at
bedtime, will sit 3 feet from crib when child awakens) to provide a consistent response at all
sleep times.
n Discontinuing nighttime feedings is appropriate for a baby older than 6 months to avoid
inappropriate sleep associations and reinforcement of nightwakings. There is no evidence that
night feedings increase the quality or quantity of sleep and, in most cases, are not physiologi-
cally necessary after 6 months of age. A signal that an infant no longer requires night feedings
is a very rapid return to sleep after feeding is initiated (e.g., taking 1 ounce or less, or nursing
for only 13 minutes before falling back to sleep). The need for feedings during the night may
also become a learned behavior (learned hunger), which leads to more frequent and pro-
longed nightwakings. Nighttime feedings can be weaned abruptly (cold turkey approach) or
can be decreased gradually by volume (e.g., 1 ounce every few days) in bottle-fed babies or
duration (e.g., decrease by 1 minute per night) in breast-fed infants.
n Reinforcement strategies (e.g., sticker charts) can be benef cial with preschoolers and older
children. In devising such a system, note that it is most effective if rewards are given imme-
diately (e.g., applying sticker to chart f rst thing in the morning with an immediate reward)
and obtainable goals are established (e.g., sticker may be earned initially just for sleeping in
own bed all night, even in the face of frequent calls to parents) to reinforce success. With time,
more challenging goals can be implemented (e.g., sticker obtained for sleeping in bed all night
without calling to parents), with less frequent rewards (e.g., 5 stickers per week instead of 3
required to obtain a reward).
n Collaboration with a behavioral therapist in designing and implementing treatment plans,
collaboration with a specialist may be prudent if there are complex, chronic, or multiple sleep
problems or if initial behavioral strategies have failed.
Family Bed versus Ferber Method

There is a great deal of public debate by family bed advocates (e.g., Sears) against graduated-
extinction approaches (dubbed the Ferber method or cry-it-out approaches). Family bed
advocates claim that co-sleeping (typically bed-sharing) is more natural and promotes attach-
ment. In contrast, family bed proponents feel that allowing a child to cry it out at bedtime
or during the night will result in psychological damage and will interfere with parentchild
attachment and prolonged breast feeding. At this time, there are no research studies that have
provided support for better parentchild attachment related to the family bed or for negative
repercussions of behavioral interventions (nor have they conf rmed any long-term psycho-
logical sequelae resulting from prolonged co-sleeping). In actuality, research has indicated
improved attachment and mood in children, as well as improved family well-being, following
behavioral treatment.
Overall, there is no correct response to this age-old debate; rather, it is an individually
based family decision. The choice will depend on parenting style, parental tolerance, and child
temperament. However, there are two caveats that should be noted. The f rst is the American
Academy of Pediatricians recommendation against bed-sharing in the f rst year of life due to
its role as a potential risk factor for sudden infant death syndrome. The second is the distinc-
tion between voluntary lifestyle (i.e., family bed) co-sleeping and reactive co-sleeping,
in which the parent institutes bed-sharing as a behavioral strategy for nightwakings; the latter
is associated with signif cant sleep disruption and is often diff cult to reverse without specif c
behavioral intervention.
Pr o g n o SiS
Studies indicate that nightwakings are likely to persist without intervention, although negative
sleep associations that are established during infancy often taper off following the age of 3 or 4
years, when these behaviors markedly decrease (e.g., bottles/pacif ers/nursing; rocking, holding).
However, if the child requires parental presence to fall asleep, the sleep disturbance may continue
through middle childhood.

Explain that the nighttime arousals are part of the normal sleep pattern and that the
nightwakings per se are not problematic. The concern is rather that the child fails to return to
sleep independently (has not learned to self-soothe) and, thus, requires parental intervention
to go back to sleep.
Discuss sleep associations at bedtime and their role in perpetuating nightwakings.
Develop an appropriate sleep schedule that ensures adequate sleep and avoids sleep
deprivation.
nightwakings.
Institute sleep training at bedtime only to start, with the goal of developing self-sooth-
ing skills and more appropriate sleep associations that will likely generalize to nighttime
arousals.
Refer for behavioral management if the nightwakings are severe and unresponsive to
simple behavioral interventions.
See Appendix D2 for a parent handout on nightwakings.
Nighttime Fears 8
Nighttime fears are common and typically both normal and benign. Most children experience
bedtime or middle-of-the-night fears at some point during childhood, and these are usually con-
sidered a normal aspect of development. These fears characteristically begin to occur during the
preschool years as children develop the cognitive capacity to understand that they can get hurt or
be harmed. The types of fears that children typically have vary at different developmental stages;
while young children are often afraid of monsters and other imaginary creatures, older children
are more likely to fear being harmed or hurt by more realistic dangers, such as burglars or natural
disasters.
Nighttime fears, however, can become persistent and intense, resulting in interference in daily
functioning. Severe nighttime fears can result in refusal to go to bed, sleep with the lights off,
or enter dark places. Some children and adolescents even refuse to be left alone or sleep in a
separate room.
Nighttime Fears
Nighttime fears are highly prevalent in children and adolescents, paralleling cognitive devel-
opment. Fears are usually short-lived and benign but must be differentiated from pathologic
fears, nightmares, and anxiety disorders.
ePiDeMio l o g y
Studies indicate that the majority of children experience nighttime fears. A study of nighttime
fears in children ages 4 to 12 years found that 59% of 4- to 6-year-olds, 85% of 7- to 9-year-olds,
and 80% of 10- to 12-year-olds reported nighttime fears. A more recent study of children ages
8 to 16 years found that 64% reported nighttime fears, with fear of intruders and home invasion
the most commonly reported concern. Report of fears decreased with age, with 79% of children
reporting nighttime fears compared to 49% of adolescents.
Severe nighttime fears are less common, occurring in 20% to 30% of children and accounting
for 15% of referrals for the treatment of childhood phobias.
Anxiety, stress, and traumatic events have been linked to nighttime fears. Parental anxiety and
family conf ict may also play a role in exacerbating nighttime fears in children by increasing
the level of emotional arousal in the child. The most common anxiety disorders associated with
nighttime fears are separation anxiety, overanxious disorder, and specif c phobias (including ani-
mal and environmental phobias). Overall, girls (73%) report more fears than do boys (55%).
As stated above, it is important to note that the onset of nighttime fears is developmentally
normal, coinciding with cognitive development and representational capabilities of children. The
types of fears also progress with age, with fears of scary dreams and imaginary creatures decreas-
ing with age and fears of personal harm increasing with age. However, fears of darkness and wor-
rying about the security of family and friends and about daily events are universal across the ages.
67
Common Fears at Different Ages

Infants: stimuli in the immediate environment (loud noises, sudden moves)
Toddlers: strangers, separation, lack of physical support, strange places, heights
Preschoolers: being alone, the dark, imaginary creatures, animals, bad dreams, thunder,
bodily injury, blood, needles
School-aged children: personal harm (home intruders), threats to self-esteem, social or
testing situations, bodily injury, illness, supernatural phenomenon, natural disasters
Adolescents: future events, the unknown, performance failure
Children express their fears in many ways. Note, however, that reports indicate that parents typi-
cally under-report nighttime fears. Thus, it is important to ask children directly about their night-
time fears.
n Fearful behaviors, such as crying, clinging, and leaving the bedroom to seek parental reassur-
ance, at bedtime or in the middle of the night.
n Bedtime resistance, including refusal to go to bed or requiring a parent to be present at
bedtime.
n Curtain calls, characterized by frequent requests of parents (e.g., drinks, kisses) after lights
out.
n Partial or complete alleviation of fears, in the context of sharing a room with a sibling or
other household member.
Associated Features
n Daytime fears, which may involve similar or different fears.
n Somatic complaints at bedtime, including headaches and stomachaches.
n Family distress, as nighttime fears can be disturbing to the entire family.
eVAl uAt io n
n Medical history: The history is generally benign.
n Developmental history: Types of fears experienced by developmentally delayed children gen-
erally ref ect the childs developmental age rather than chronological age.
n Family history: Anxiety disorders in the family suggest the potential for more global anxiety
problems in the child.
n Behavioral assessment: Th presence of daytime anxiety symptoms or oppositional behavior
may suggest more global behavioral problems. It is also important to elicit a detailed descrip-
tion of the typical parental response to the fearful behavior.
n Diagnostic tests: Tests are not indicated.

Diagnosis of nighttime fears is usually straightforward; however, other disorders should be
considered:
n Bedtime resistance: Some children learn that expressing fears is an effective stalling tactic
or a way to avoid bedtime, especially because parents may respond more positively to fearful
behaviors than they do to oppositional behavior. These parental responses may then serve to
NIGHTTImE FEARS 69
reinforce fearful behaviors. The bedtime resistance, in turn, may be related to any number of
different sleep problems, including limit-setting sleep disorder (see Chapter 6) and sleep phase
delay (see Chapter 17).
n Noncompliance or oppositional behavior: The presentation of bedtime diff culties and pre-
sentation of fears may be indicative of more global noncompliant behavior that is also pres-
ent throughout the day. Overall daytime behavior and parental management skills should be
assessed.
n Nightmares: Frightening dreams that awaken a child during the night may contribute to the
development of a conditioned fear as well as avoidance of bedtime and falling asleep (see
Chapter 9).
n Phobias: Phobias are conditioned, persistent, and often quite dramatic fear responses to spe-
cif c stimuli (dogs) or circumstances (riding on elevators) that typically occur during the day,
as well and signif cantly impact on daytime functioning.
n Anxiety disorders: Children and adolescents with anxiety disorders, including separation
anxiety disorder, generalized anxiety disorder, and posttraumatic stress disorder, frequently
present with nighttime fears. The fearful behavior is usually present concomitantly during the
day, and functioning is impacted. In addition, the degree, duration, and pervasiveness of the
symptoms help differentiate situational and transient nighttime anxiety from a more chronic
and global anxiety disorder.
n Child abuse: Children who have experienced physical, sexual, or emotional abuse may have
nighttime fears, but these are generally severe and persistent and are accompanied by sig-
nif cant physiologic arousal. Many of these children also have signif cant daytime symptoms,
including anxiety, withdrawal, and depressive symptomatology.
MAn Ag eMen t
Most children are able to cope effectively with nighttime fears. The most commonly reported
coping mechanisms include distraction (thinking of other things) and social support (talking to
parents about their fears). Less frequently reported management activities include turning on a
light or f ashlight, hugging an inanimate object (stuffed animal), or interacting with others (e.g.,
asking for a drink). Adolescents are much more likely to cope independently with their fears,
whereas children are more likely to engage their parents.
w hen to r efer
Children or adolescents with persistent or severe bedtime fears that are not responsive to simple
behavioral measures should be referred to a mental health professional.
t reatment
An important aspect in counseling parents on how to respond to nighttime fears is to have the
parents maintain a balance between reassuring the child and avoiding reinforcement of the fears.
If a child or adolescent is reassured too much, the parents may be subtly providing positive at-
tention for the fearful behavior, thus increasing the likelihood that it will recur. In addition, some
children may interpret their parents concern about the fears as tacit proof that the fears are well
founded. In general, strategies aimed at younger children more often involve parental reassur-
ance while older children typically benef t from an approach that includes teaching and positive
reinforcement for independent coping skills.
Following are suggestions for ways parents can respond to their childs nighttime fears.
n Reassure and communicate the idea of safety: For example, have parents repeatedly tell the
child that he or she is safe and that they are always nearby and will make sure that nothing bad
happens (e.g., Mommy and Daddy are right downstairs and well always make sure that you
are safe).
n Teach the child developmentally appropriate coping skills: Discuss alternative ways to
respond to nighttime fears, such as being brave and making positive self-statements (e.g.,
Monsters are just pretend, I can take care of myself, and The dark is fun). Practicing
these self-statements well before bedtime can be helpful. Another strategy is to provide ex-
amples of coping role models by reading stories about children who are afraid and conquer
their fears.
n Implement a gradual exposure to fears: The establishment of a step-wise approach to expo-
sure to specif c fears can be developed. For example, if a child is afraid of the dark, spending
increasing amounts of time in dark places (starting with 30 seconds and increasing in 1-minute
increments) or gradually diminishing nighttime lighting can be benef cial.
n Develop creative solutions: The use of monster spray (parent f lls a spray bottle with water
and sprays the childs room and closet at bedtime), for example, can be effective, although it
should be noted that some young children might view this as evidence that a monster actually
exists. Having a pet as a nighttime companion or having siblings share a bedroom are alterna-
tive strategies that work for some families. Whenever possible, the child should be actively
involved in generating solutions to foster a sense of mastery and control.
n Encourage the use of security objects: Blankets and stuffed animals, for example, can be
comforting to the child.
n Use a nightlight: Having a light on can decrease a childs fear of the dark or monsters.
n Leave the bedroom door open: Children can feel isolated behind a closed door.
n Avoid television shows and movies: Scary movies can exacerbate fears or may be overstimu-
lating, particularly just before bedtime.
n Teach the child relaxation strategies: Implementing strategies such as deep breathing or vi-
sual imagery (e.g., imagining a beach or other favorite scene) can help a child relax at bedtime
and fall asleep more easily.
n Discuss the childs fears: Explore alternative ways to respond to the fears during the day
rather than in the evening, as this is less likely to provoke anxiety.
n Set appropriate, f rm, and consistent limits: Set limits on bedtime behavior to avoid rein-
forcing the childs being scared. For example, a parent might say, Remember, no crying and
no calling at bedtime.
n Institute a checking system at bedtime: Provide the child with a predictable schedule
(e.g., every 10 minutes) of parental reassurance. This has the benef t of making parental con-
tact noncontingent on the childs behavior (e.g., calling out).
n Encourage the child to remain in bed or in the bedroom: If parental presence is temporarily
required to alleviate the childs fears, it is generally better for parents to stay in the childs room
rather than to have the child join the parents in their room, so that he or she does not become
conditioned to avoid the bedroom.
n Develop a reward system for appropriate bedtime behavior: Use rewards for appropriate
bedtime behavior (stickers for being a big boy) rather than reinforcing (with attention) the
learned fearful behavior (e.g., saying, Im scared). Appropriate behaviors that are required
for positive reinforcement should be as specif c as possible (staying in bed all night, not call-
ing out after lights out), and the reward schedule should be set up to offer a high likelihood
of the childs being successful (e.g., nightly reward). Parents can reinforce for progressively
appropriate behaviors, such as lower illumination levels or staying in room for longer periods.
Pr o g n o SiS
Nighttime fears that are part of normal developmental and are usually short lived and disappear
by age 5 or 6 years. Fears may become more chronic in a child or adolescent with an anxiety
disorder.
NIGHTTImE FEARS 71

Distinguish between normal and pathologic fears.
Explain that normal nighttime fears are part of normal cognitive development.
Discuss treatment options and parents response to fearful behavior.
Develop a plan of gradual exposure to fears and use of coping skills.
Reinforce establishment of appropriate sleep habits and parental limit-setting.
See Appendix D3 for a parent handout on nighttime fears.
9 Nightmares
Nightmares are frightening dreams that usually awaken a child or adolescent, leaving the child
upset and in need of comfort. Other terms synonymous with nightmares include bad dreams,
scary dreams, and anxiety dreams. Although some individuals distinguish between nightmares,
which awaken the sleeper, and bad dreams, which do not, this distinction is arbitrary. When the
nightmare involves awakening, most children are afraid to return to sleep and seek comfort.
Given that very young children often cannot distinguish between a dream and reality, they may
insist that something fearful continues to exist.
Nightmares
Nightmares are frightening dreams, occurring during REM sleep, that usually result in an
awakening from sleep.
Nightmares usually involve fear or anxiety but can also include other negative emotions, such as
anger, sadness, embarrassment, or disgust. They also typically involve imminent physical harm to
the child. The content of nightmares usually differs across the ages and ref ects common develop-
mental issues. Most young toddlers have concerns about being separated from their parents. By
age 2 years, nightmares typically begin to incorporate monsters and other frightening imaginary
creatures. For young children, nightmares may also involve a recent traumatic event (e.g., getting
lost, being immunized, being barked at by a large dog). Older children often have nightmares
related to frightening or upsetting movies, television programs, stories, or a disturbing daytime
experience. Nightmares may also coincide with a stressor or traumatic event (e.g., being away
overnight, starting a new school).
ePiDeMio l o g y
Studies indicate that approximately 75% of children report experiencing at least one nightmare
in their lifetime, and 10% to 50% of young children have nightmares that result in parental in-
teraction during the night. Although experiencing infrequent nightmares is quite common, the
prevalence of frequent nightmares is much less common. One study reported prevalence rates
for chronic nightmares, def ned as a nightmare problem lasting longer than 3 months, as 24% for
ages 2 to 5 years and 41% for ages 6 to 10 years. Peak nightmare prevalence is between 6 and 10
years of age, with surprisingly few parents of preschool children reporting frequent nightmares
(1.9% to 3.9%).
Nightmares are equally experienced by boys and girls before the age of 12 years. After age
12 years, girls are more likely to have nightmares. Twin studies have found support for a genetic
basis to frequent nightmares.
n Prior nightmares, as having bad dreams appears to be a somewhat stable characteristic.
n Stress and/or traumatic events, including child abuse.
72
NIGHTmARES 73
n Anxiety and anxiety disorders, which can lead to both increased frequency and severity of
nightmares. Separation anxiety is commonly associated with nightmares or bad dreams.
n Sleep deprivation, which can result in intense and vivid dreams due to increased rebound
REM sleep.
n Insomnia, which is often comorbid with nightmares.
n Medications, particularly those that have a direct effect on REM sleep. These may be medica-
tions that increase the amount of density of REM or drugs that suppress REM and thus result
in REM rebound when discontinued (see Chapter 19).
Children or adolescents with nightmares will usually recall at least fragmented and often detailed
scary dream content and will awaken frightened but coherent. In addition, if awakening occurs,
the child or adolescent is afraid to return to sleep and will often seek parental reassurance.
See Table 9.1.
Associated Features
n Daytime fears: Many children with nightmares also report nighttime fears (see Chapter 8).
Some may also have symptoms of a more global anxiety disorder that includes daytime fears.
n Bedtime resistance: Some children develop a conditioned aversion to their bed or bedtime
because they associate sleep with nightmares.
eVAl uAt io n
n Nightmare history: In evaluating nightmares, both chronicity and severity should be carefully
assessed, as nightmare severity is more likely to be related to psychopathology.
n Developmental history: Developmentally delayed children may be less able to verbalize con-
cerns about nightmares.
n Family history: The ubiquitous nature of nightmares in the general population makes a posi-
tive family history nonspecif c. However, parents who have themselves experienced frequent
or troublesome frightening dreams may respond differently to their childs nightmares (e.g.,
more attention, anxiety).
n Behavioral assessment: A history of more global anxiety, regression in behavior, or extreme
arousal in association with nightmares should raise concerns about the possibility of abuse or
trauma.
t ABl e 9.1. Diagnostic criteria: Nightmare disorder (307.47)
A. Recurrent episodes of awakenings from sleep with recall of intensely disturbing dream mentation,
usually involving fear or anxiety, but also anger, sadness, disgust, and other dysphoric emotions.
B. Full alertness on awakening, with little confusion or disorientation; recall of sleep mentation is im-
mediate and clear.
C. At least one of the following associated features is present:
1. Delayed return to sleep after the episodes
2. Occurrence of episodes in the latter half of the habitual sleep period
American Academy of Sleep Medicine. International classif cation of sleep disorders, 2nd ed.: diagnostic and cod-

n Diagnostic tests: A sleep diary that documents the frequency of nightmares over a period of
several weeks and the duration of associated night wakings may be helpful.

n Sleep terrors and sleepwalking: Parents often have a diff cult time distinguishing between
nightmares and partial arousal parasomnias, such as sleep terrors and sleepwalking (see Chap-
ter 10); it should be noted that many children with sleep terrors or sleepwalking will also have
nightmares. Nightmares, in comparison to partial arousal parasomnias, usually have the fol-
lowing features:
n Occurrence in the latter half of the night, when REM sleep predominates
n Complete or partial recollection of dream content
n Total recall for the event
n No confusion or disorientation
n Delayed return to sleep
n Other episodic nocturnal phenomena: Nocturnal seizures, for example, are occasionally
confused with nightmares, but typically have associated motor and sensory features and of-
ten include stereotypic characteristics (see chart in Chapter 10 for a comparison of clinical
features).
n Psychiatric disorder: Frequent nightmares may be associated with a psychiatric disorder,
including anxiety disorders, bipolar disorder, schizophrenia, and, most notably, posttraumatic
stress disorder.
n REM behavior disorder (RBD): RBD is an unusual sleep disorder characterized by loss
of muscle atonia (e.g., paralysis) that normally occurs during REM sleep. The consequent
acting out of vivid, disturbing, and frequently violent dreams can result in severe injury to
the sleeper and also to any bed partner. This disorder is associated with neurodegenerative
processes, such as Parkinsons disease, in older adults, and although reported in children in
association with neurological disorders, is considered extremely rare in childhood.
MAn Ag eMen t
w hen to r efer
Children or adolescents with persistent or severe nightmares that are not responsive to simple
behavioral measures or whose nightmares are extremely disruptive should be referred to a mental
health professional for evaluation and treatment.
t reatment
In general, as with other anxiety-associated behavioral issues, strategies for dealing with night-
mares aimed at younger children more often involve active parental reassurance, whereas older
children may benef t more from an approach that includes teaching and positive reinforcement
for independent coping skills.
Suggestions for ways parents can manage their childs nightmares follow.
Reduce the Likelihood of Nightmares

n Avoid exposure to frightening or overstimulating images, especially just before bedtime,
including frightening stories, movies, and television shows.
n Reduce stressors, as persistent nightmares may indicate stress or an ongoing concern.
n Ensure adequate sleep, as sleep deprivation contributes to increased nightmare frequency.
NIGHTmARES 75
Parental Response to Nightmares

n Reassurance by parents that It was only a dream. It is important that parents remain calm
and matter of fact and strike a balance between reassuring the child and not providing exces-
sive attention. If the child gets out of bed, the parent can calmly escort the child back to bed
and brief y provide reassurance there. Further discussion of the nightmare should be postponed
until the following day, when alternative coping strategies for the future may be discussed.
n Security objects can be comforting and facilitate a faster return to sleep. Some children f nd
the presence of a family pet reassuring.
n Dim, low-level nightlight can be helpful.
n Encouragement of verbal children to use their imagination may help alleviate nightmares.
Effective strategies may include drawing a picture that represents the bad dreams and then
crumpling it up and throwing it away, devising a positive ending to the dream, or hanging a
dream catcher over the bed.
Additional Treatment Strategies

n Relaxation strategies, including progressive muscle relaxation and guided imagery. Relax-
ation tapes can be obtained through the Child Anxiety Network (www.childanxiety.net). Other
resources are available at the Anxiety Disorder Association of America ([ADAA]; www.adaa.
org).
n Systematic desensitization, combined with relaxation strategies, can be used to countercon-
dition the anxiety response. Systematic desensitization involves developing a hierarchy of
fear-invoking activities or thoughts from least to most frightening with the child (e.g., looking
at a picture of a dog, watching a friend play with a puppy, petting a large dog). These activities
or thoughts are paired with a relaxing activity (deep breathing, progressive muscle relaxation)
that counters the fear response. This technique may be particularly helpful with nightmares
that have a recurrent specif c theme.
n See Chapter 8 (Nighttime Fears) for additional treatment strategies.
Pr o g n o SiS
Nightmares are usually short lived but may persist in some children or adolescents, especially if
the nightmares are related to a traumatic event.

Explain that nightmares are virtually universal and are part of normal cognitive develop-
ment, usually peaking between 6 and 10 years of age.
nightmares.
Develop an appropriate sleep schedule that ensures adequate sleep and avoids sleep
deprivation.
Discuss any recent stressors or traumatic events that may be contributory, while reas-
suring parents that the vast majority of the time nightmares are isolated events.
Refer for psychological evaluation if the nightmares are highly persistent or severe and
unresponsive to simple behavioral interventions.
See Appendix D4 for a parent handout on nightmares.
Partial Arousal Parasomnias:
10 Sleepwalking, Sleep Terrors,
and Confusional Arousals
Parasomnias are def ned as episodic, often undesirable behaviors that accompany sleep. Para-
somnias may be further characterized as occurring primarily during non-REM (NREM) sleep
(partial arousal parasomnias) or in association with REM sleep, including nightmares (see
Chapter 9), hypnogogic hallucinations and sleep paralysis (see Chapter 16), and REM be-
havior disorder. Other sleep related behaviors include sleep starts, sleep inertia (see below),
sleeptalking, and those that are movement related (e.g., sleep related rhythmic movements; see
Chapter 11).
This chapter will discuss the clinical presentation and management of the partial arousal
parasomnias, which include sleepwalking (somnambulism), sleep terrors (pavor nocturnus),
and confusional arousals. These are related sleep disorders that share a common underlying
pathophysiology, have similar clinical features, and commonly co-occur in children. The partial
arousal parasomnias share characteristics of both the waking and deep sleep states, and involve
autonomic or skeletal muscle disturbances, autonomic behaviors, and disorientation. Sleepwalk-
ing, sleep terrors, and confusional arousals occur almost exclusively during slow-wave sleep
(SWS); (stage N3 of NREM sleep), although episodes can also occur during a nap if SWS is
present. These usually occur within a few hours after sleep onset, last from a few minutes to an
hour, and are characterized by amnesia for the event. During an episode, children or adolescents
have the appearance of being awake, and most children actively avoid comfort or soothing, which
may be disturbing to parents. Although they may be triggered by stress, these disorders do not
indicate the presence of a primary underlying psychological problem or trauma. Finally, because
the relative percentage of SWS is highest in childhood and drops fairly dramatically in the second
decade of life, partial arousal parasomnias are most common in young children and their preva-
lence declines with increasing age.
Common Characteristics of Partial Arousal Parasomnias

Occurrence within the f rst few hours of the night
Agitation, confusion, and disorientation
Avoidance of, or increased agitation with, comforting by parents or attempts at awakening
Amnesia for the event
Precipitation by forced awakening from slow-wave sleep in susceptible individuals
Positive family history
Exacerbation by insuff cient sleep and/or sleep fragmentation
Sl eePw Al kin g
Sleepwalking is a common and generally benign sleep behavior, although potential safety con-
cerns (see below) should be taken into consideration. During sleepwalking episodes, the child ap-
pears confused or dazed, the eyes are usually open, and he or she may mumble or give inappropri-
ate answers to questions. Occasionally, a sleepwalking child may appear agitated. A sleepwalker
is typically clumsy and may perform bizarre or strange actions such as urinating in a closet. The
sleepwalking may range from walking calmly to a parents bedroom, to walking downstairs, to
76
SLEEPwALkING, SLEEP TERRORS, AND CONFUSIONAL AROUSALS 77
leaving the house or stepping out onto a balcony or rooftop. Sleepwalking can occur infrequently
or on a nightly basis.
Sleepwalking
Sleepwalking is a common parasomnia in children, occurring during the f rst few hours of the
night when slow-wave sleep is predominant. Although usually benign and self-limited (typi-
cally disappearing by adolescence), there are often associated safety concerns (e.g., falling out
of windows, wandering outside) that should be addressed.
Sl eeP t er r o r S
Sleep terrors, or night terrors, are dramatic events and, as such, can be distressing to parents or
caregivers (these episodes are referred to as sleep terrors rather than night terrors because
they can occur during any sleep period, including naps). As disturbing and frightening as these
events appear to the observer, the child is totally unaware of his or her behavior. Paradoxically,
sleep terrors are much worse to watch than to experience, and much less traumatic to the child
than a nightmare or bad dream.
Sleep Terrors
Sleep terrors are characterized by a sudden arousal from slow-wave sleep, accompanied by
autonomic and behavioral manifestations of intense fear.
c o n FuSio n Al Ar o uSAl S
Confusional arousals (sometimes referred to as sleep drunkenness) have many features simi-
lar to the other partial arousal parasomniasthat is, origination during SWS, disorientation and
unresponsiveness to the environment, and amnesia for the event. They are often triggered by
forced awakening, particularly early in the night or upon attempting to awaken in the morning.
Children typically arise more gradually from sleep with them compared to with sleep terrors, may
involve thrashing around in, but usually not displacement from bed, and are often accompanied
by agitation and combative behavior. A prominent feature is sleep inertia, a period of extreme
grogginess and confusion after awakening SWS, lasting from 15 to 30 minutes up to an hour.
Although exacerbated by stress and anxiety, comorbid psychiatric conditions are rarely present
in confusional arousals; there have been rare reports of associated central nervous system lesions
occurring in these children.
Confusional Arousals
Confusional arousals are nocturnal episodes characterized by confusion, disorientation, grog-
giness, and, at times, signif cant agitation upon awakening from slow-wave sleep or following
forced awakenings.
ePiDeMio l o g y
There appears to be no difference between boys and girls in the occurrence of these behaviors.
n Sleepwalking: Many children (15% to 40%) sleepwalk on at least one occasion, with studies
indicating a prevalence of approximately 17% of children regularly sleepwalking, and 3% to
4% with frequent episodes. Sleepwalking may persist into adulthood, with the prevalence in
adults of about 4%. The prevalence is approximately 10 times greater in children with a family
history of sleepwalking. It should be noted that the prevalence of sleepwalking reported may
be an underestimate because episodes may be unobserved or misinterpreted as nightwakings.
Onset of episodes is usually between ages 4 and 6 years, and peak occurrence is between ages
8 and 12 years. About one-third of sleepwalkers have episodes over a 5-year span; about 10%
will continue to sleep walk for 10 years. Most children who sleepwalk had confusional arous-
als at an earlier age.
n Sleep terrors: Approximately 1% to 6% of children experience sleep terrors, primarily during
the preschool and elementary school years, and the age of onset is usually between ages 4 and
12 years. The frequency of episodes is often highest at the onset and tends to be higher with
younger age of onset. Because of the common genetic predisposition, the prevalence of sleep
terrors in children who sleepwalk is about 10%. Although sleep terrors can occur at any age
from infancy through adulthood, most individuals outgrow sleep terrors by adolescence.
n Confusional arousals: Because confusional arousals may not be recognized or brought to
medical attention, the prevalence is diff cult to determine but one study indicated a prevalence
rate of approximately 17% in children ages 3 to 13 years. Confusional arousals commonly
co-occur with sleepwalking and sleep terrors. Onset is typically before age 5 years, and the
duration is described as ranging from 6 months to 13 years.
n Positive family history: There is often a genetic component in partial arousal parasomnias.
Twin studies indicate genetics are involved in 50% to 65% of cases of sleepwalking. The
likelihood of sleepwalking is 22% if neither parent has the disorder, 45% if one parent has the
disorder, and 60% if both parents are affected.
n Other associated conditions: Partial arousal parasomnias appear to be more common in in-
dividuals with migraine headaches and Tourette syndrome, possibly related to alterations in
serotonin metabolism.
n Factors that exacerbate parasomnias: Partial arousal parasomnias occur almost exclusively
in SWS. Inadequate sleep and sleep disruption often result in a rebound compensatory in-
crease in SWS. Therefore, in general, any condition that disrupts sleep or reduces sleep dura-
tion tends to increase the likelihood that a partial arousal parasomnia episode will occur in
a susceptible individual. Environmental conditions (e.g., noise) that increase arousals, espe-
cially during SWS, may also trigger events. Some conditions may also increase the likelihood
of partial arousal episodes by decreasing the arousal threshold.
Exacerbating and trigger factors include:

n Inadequate sleep (acute or chronic)
n Irregular sleep schedule
n Change in sleep schedule, such as discontinuing daytime naps, beginning attending daycare,
or start of school
n Sleep disrupters, including sleep-disordered breathing (see Chapter 14) and periodic limb
movement disorder (see Chapter 15)

n Fever and illness
n Medications that increase SWS (e.g., lithium) or result in rebound SWS upon withdrawal
(e.g., benzodiazepines, tricyclic antidepressants)

n Caffeine
n Sleeping with a full bladder
n Sleeping in a different environment
n Noise and light
n Stress and anxiety

Partial arousal parasomnias usually occur in the f rst few hours after sleep onset and last a few
minutes to half an hour. Frequency ranges from a one-time event to a nightly occurrence; some
children may have multiple episodes in a single night. In addition, occurrences may be epi-
sodic, happening in nightly cycles of for several nights to a few weeks followed by periods of no
episodes.
Injury Risk
Sleepwalking in particular can lead to physical harm, resulting from falling down stairs, walk-
ing into traff c, or going outside in cold weather without adequate clothing. Although sleep
terrors and confusional arousals do not typically involve displacement from bed, children may
injure themselves by f ailing around, falling out of bed, or actively trying to resist attempts at
restraint or comforting by the parent. Ensuring safety should be one of the primary concerns
of healthcare practitioners when dealing with partial arousal parasomnias.
Sleepwalking
Parents are generally able to identify an event as sleepwalking; occasionally, the presenting com-
plaint is nocturnal episodes that involve unusual or bizarre behaviors (going to a siblings room
in the middle of the night, wandering around downstairs), confusion, agitation, and incoherent
responses to questions. Parents, however, are not always able to tell whether their child is awake
or asleep at the time.
Sleep t errors
Sleep terrors usually have a sudden onset, and the childs appearance during one of these epi-
sodes is that of extreme agitation, fright, and confusion, often involving crying and/or screaming.
Extreme physiologic arousal (e.g., hyperventilation, tachycardia, diaphoresis, dilated pupils) is
common. However, sleep terrors may be much milder (sometimes described as a confusional
arousal), with the child simply appearing agitated. A child having a sleep terror is often clumsy
and may f ail, push a parent away, or behave in other strange ways. Because of the dramatic nature
of these episodes, parents may be concerned that their child has experienced some emotional or
physical trauma; alternatively, parents may also assume that the events themselves result in psy-
chological damage to the child. The presentation may be atypical in very young children, with
prolonged episodes (3045 minutes) that are less dramatic (whimpering, rocking).
c onfusional Arousals
Clinical characteristics of confusional arousals include: agitation, crying or moaning (no, no!),
disorientation, and, particularly, slow mentation on arousal from sleep (sleep inertia). The dura-
tion of episodes is typically 5 to 15 minutes but may last up to several hours.
o ther c onditions
Sleep-related eating disorder is considered to be a unique variant of sleepwalking, which rarely
presents in childhood. This disorder is more common in female patients than in male patients
(2:1). Symptoms include nightly out-of-control eating of which the patient is not or only par-
tially aware, morning anorexia, abdominal distension, unexplained weight gain, and injuries sus-
tained while preparing foods (e.g., knife lacerations, burns). High-calorie, odd food combina-
tions and nonnutritive substances are typically consumed. The diagnosis requires the absence
of evidence of eating disorder symptoms, such as daytime bingeing, purging, and body image
distortions. This disorder has been associated with hypnotic use.
See Tables 10.1 through 10.3.
Associated Features
n Impact on social functioning: Because of the potential embarrassment and the high likeli-
hood of harm, many children and adolescents with parasomnias avoid social situations such as
overnight visits to friends and summer camp.
t ABl e 10.1. Diagnostic criteria: Sleepwalking (307.46)
A. Ambulation occurs during sleep.

B. Persistence of sleep, an altered state of consciousness, or impaired judgment during ambulation is
demonstrated by at least one of the following:
1. Diff culty in arousing the person.
2. Mental confusion when awakened from an episode.
3. Amnesia (complete or partial) for the episode.
4. Routine behaviors that occur at inappropriate times.
5. Inappropriate or nonsensical behaviors.
6. Dangerous or potentially dangerous behaviors.
C. The disturbance is not better explained by another sleep disorder, medical or neurological disorder,
medication use, or substance use disorder.
t ABl e 10.2. Diagnostic criteria: Sleep terrors (307.46)
A. A sudden episode of terror occurs during sleep, usually initiated by a cry or loud scream that is ac-
companied by autonomic nervous system and behavioral manifestations of intense fear.
B. At least one of the following associated features is present:
1. Diff culty in arousing the person.
2. Mental confusion when awakened from an episode.
3. Amnesia (complete or partial) for the episode.
4. Dangerous or potentially dangerous behaviors.
C. The disturbance is not better explained by another sleep disorder, medical or neurological disorder,
t ABl e 10.3. Diagnostic criteria: Confusional arrousals (307.46)
A. Recurrent mental confusion or confusional behavior occurs during an arousal or awakening from
nocturnal sleep or a daytime nap.
B. The disturbance is not better explained by another sleep disorder, medical or neurological disorder,
n Parental anxiety: Because of the unusual nature of these events, parents are often highly anx-
ious about whether there is an underlying meaning to the episodes as well as how to respond
to the events, and are often concerned about not being present during an event (e.g., avoid use
of babysitters, discourage sleepovers).
eVAl uAt io n
n Medical history: The history is generally benign. However, it may reveal evidence sugges-
tive of a sleep disorder that results in disrupted and/or insuff cient sleep, including obstructive
sleep apnea and restless legs syndrome or periodic limb movement disorder (PLMD). The
medical history may also (see below) suggest the need to rule out a seizure disorder. Possible
risk factors for seizures include a history of seizures as well as unusual characteristics of the
episodes themselves, such as stereotypic features, multiple nightly occurrences, and late onset
(adolescence).
n Developmental and school history: The history is usually normal. The presence of develop-
mental delay may increase suspicion for seizures.
n Family history: The family history is often positive for sleeptalking, sleepwalking, or sleep
terrors.
n Behavioral assessment: Most children do not have signif cant behavioral concerns. Because
individuals with partial arousal parasomnias are actually asleep during the episodes, sleep
disruption and associated evidence of daytime sleepiness are unusual.
n Physical examination: The physical examination is generally unremarkable.
n Diagnostic tests:
n Overnight polysomnography (PSG) is not a routine part of the evaluation for partial
arousal parasomnias. Because these are episodic events, they may not be captured on a
single-night study. However, if there is a concern about another underlying sleep disrupter
(e.g., sleep disordered breathing, PLMD), an overnight sleep study is appropriate. PSG may
also be warranted to differentiate between a parasomnia and a seizure disorder (note that
only some sleep centers have the capability of a full seizure montage).
n Home videotaping of nocturnal episodes by parents can be a more eff cient way of captur-
ing and recording events that occur infrequently. Reviewing the tapes may be helpful in
distinguishing parasomnias from other nocturnal behaviors, especially seizures.
n Sleep diaries can help the assessment for contributing factors, such as sleep deprivation
and irregular sleep schedules.

n Partial arousal parasomnia (sleep terrors, sleepwalking, confusional arousal) versus
nightmare seizure disorder: It may be very diff cult to differentiate nocturnal seizures from
partial arousal parasomnia, particularly if atypical features are present. Major characteristics
of the episodes that are more likely to indicate the presence of a seizure disorder are summa-
rized in Table 10.4; these include stereotypic behaviors and tonic-clonic movements, multiple
events per night, occurrence at sleepwake transitions or after the f rst third of the night, and
associated daytime sleepiness. Enuresis may occur during or after partial arousal parasomnias,
particularly confusional arousals, but more commonly indicates seizure activity. The presence
of developmental delays or neurological disorders, daytime seizures, or a family history of
seizures increases the risk of nocturnal seizures (see also Chapter 22).
n Nocturnal panic attacks: The patient typically has similar episodes that occur in the daytime,
and there is recall of the episode the next morning.
t ABl e 10.4. Differentiation of episodic nocturnal phenomenon
Sleepwalking/
Sleep Terrors/
Confusional
Characteristics Arousals Nightmares Nocturnal Seizures
Timing during night First third Last third Variable; often at sleep
wake transition
Sleep stage Slow-wave sleep REM Non-REM>Wake>REM
Age of onset
Autonomic arousal Low/high/medium Mild to high Variable
Arousal threshold High Low Low
Daytime sleepiness None +/ Often
Increased by sleep deprivation Yes Sometimes +/
Incontinence, tongue-biting, No No Yes
drooling, stereotypic,
repetitive behavior
Recall of event None or fragmentary Vivid Not usual
Multiple episodes per night Rare Occasional More common
Family history Common Rare Variable
Polysomnography Indicated if atypical Not indicated Indicated if atypical
features features; requires
extended EEG
montage
MAn Ag eMen t
w hen t o r efer
Children or adolescents with parasomnias who also present with symptoms of another underlying
sleep disrupter (e.g., sleep-disordered breathing) should be referred to a sleep specialist. If phar-
macologic treatment is being considered, it is also best to consult with a pediatric sleep specialist.
Where there are concerns regarding stress or other psychological issues, a referral to a mental
health specialist is warranted.
t reatment
Management of partial arousal parasomnias should f rst include reassurance and education of
the child and family regarding the benign and self-limited nature of the disorder. Parents may
be told that most children stop having sleepwalking episodes or sleep terrors by adolescence.
Interim management should include institution of appropriate safety measures and discussion
of trigger and exacerbating factors. Sleep hygiene and behavioral management of the episodes
should be reviewed. However, the decision about whether to actively treat the parasomnias is
based on the frequency and severity of the episodes and can involve medication management or
scheduled awakenings.
n Safety
n Safety measures, including use of gates (doorways, top of staircases), locking of outside
doors and windows, lighting of hallways, and ensuring the safety of the sleeping environ-
ment (e.g., removing clutter on f oors).
n Parent notif cation measures, such as alarm systems or a bell attached to the bedroom
door.
n Managing sleep-overs away from home, including informing other caregivers of potential
sleepwalking behavior.
n Sleep hygiene
n Ensure adequate sleep and maintain regular sleepwake schedule, as sleep deprivation
is the primary contributor to parasomnias.

n Avoid caffeine, as caffeine can increase sleep disruption, decrease sleep eff ciency, and
contribute to sleep deprivation.

n Address behaviorally based nightwakings or bedtime refusal, which may be contributing
to sleep deprivation.
n Parental response during an event
n Avoid awakening, as attempts to awaken a child during a parasomnia will typically increase
agitation and prolong the event.

n Guide the child back to bed, to encourage return to normal sleep.
n Avoid interfering, as this can prolong the event. The normal response of parents is to try
and comfort their child during one of these episodes, which may increase the childs agita-
tion. It is best for a parent to quietly stand nearby to ensure safety, but not to interact.
n Avoid next-day discussions, as this is likely to worry the child and may lead to bedtime
resistance and sleep deprivation.

n Additional treatment
n Pharmacologic treatment may be indicated in cases of frequent or severe episodes, high
risk of injury, violent behavior, or serious disruption to the family. The primary pharma-
cologic agents used are potent SWS suppressants, primarily benzodiazepines and tricyclic
antidepressants.
Short-acting benzodiazepines: Benzodiazepines (e.g., diazepam, 12 mg) given as a
single small dose at bedtime for 3 to 6 months (until episodes are totally suppressed).
Small doses of longer-acting benzodiazepines (e.g., lorazepam, clonazepam) may also be
effective, although more likely to result in morning grogginess. Intermittent drug therapy
has also been used in patients who have a pattern of events that occur in clusters of days
or weeks separated by parasomnia-free periods. Abrupt discontinuation often results in
signif cant increased SWS (rebound), so it is important to taper medication slowly over
several weeks.
Antidepressants: Tricyclic antidepressants (clomipramine, desipramine, imipramine) at
bedtime have also been used in patients who are nonresponsive to benzodiazepines. Al-
though selective serotonin reuptake inhibitors are also potent SWS suppressants, they are
rarely used to treat parasomnias.
n Scheduled awakening is a behavioral technique that is most likely to be successful in situ-
ations in which partial arousal episodes occur on a nightly basis. Studies have indicated
that in children with frequent parasomnias that occur at a highly predictive time, scheduled
awakening can be highly effective. Scheduled awakening involves having the parent wake
the child approximately 15 to 30 minutes prior to the time of night that the f rst parasomnia
episode typically occurs. Thus, parents f rst need to keep a sleep diary that includes the
exact time of each episode. The parent then begins awakening the child on a nightly ba-
sis, approximately 30 minutes before a usual event, just to the point of arousal (e.g., child
changes position or mumbles). For example, if the child usually falls asleep at 8:30 p.m. and
sleepwalks at 10:00 p.m., then the parent should institute scheduled awakenings at 9:30 p.m.
These nightly awakenings should be continued for 2 to 4 weeks. If the parasomnias recur
following discontinuation of the scheduled awakenings, they may be reinstituted for several
weeks.
Pr o g n o SiS
Most children naturally stop sleepwalking or experiencing sleep terrors in childhood. By age 8
years, 50% of children with sleepwalking or sleep terrors no longer experience parasomnias, and
most cases resolve spontaneously following puberty as a result of the dramatic decrease in SWS.
However, about 10% of individuals continue to experience sleepwalking episodes for 10 or more
years, and thus persistence into young adulthood does occur. This is particularly relevant for col-
lege students, who are more likely to have trigger factors for partial arousal parasomnias, includ-
ing inadequate and/or disrupted sleep and excessive caffeine consumption. Patients should be
encouraged to share this information with college health services and roommates, and to request
a f rst-f oor living space in dormitories.

Explain that sleepwalking and sleep terrors are a neurodevelopmental phenomenon, as
they are neither indicative of an underlying psychological issue nor result in psychological
harm. Help parents understand that sleep terrors in particular are far more upsetting for the
observing caregiver than for the child experiencing them.
Ensure safety measures, including locking of all outside doors and windows and installing
an alarm system to notify parents that the child has left the bedroom.
Encourage parents to share information about sleepwalking with other caregivers, es-
pecially if the child is sleeping away from home.
Suggest an appropriate sleep schedule, which will ensure adequate sleep.
Discourage parental intervention during an episode, as this is likely to increase agitation
and prolong the event.
Discuss potential trigger and exacerbating factors, including sleep deprivation, sleeping
in an unfamiliar environment, and caffeine.
Discuss the risks and benef ts of treatment options, including medications and scheduled
awakening in more problematic cases.
Discuss prognosis, including the likelihood of disappearance by adolescence. If episodes
do persist, discuss safety measures in regards to living away from home (e.g., avoidance of
bedrooms on upper f oors).
See Appendix D5 for a parent handout on sleepwalking and D6 on sleep terrors.
Sleep Related Rhythmic
movements: Head
Banging, Body Rocking,
and Head Rolling
11
Head banging (jactatio capitis nocturna), body rocking, and head rolling are specif c sleep-
related phenomena that fall under the diagnostic category of sleep related movement disorders.
This diagnostic category includes restless legs syndrome (RLS), periodic limb movement dis-
order (PLMD), and bruxism. Sleep related rhythmic movements are characterized by repetitive,
stereotyped, and rhythmic movements or behaviors that involve large muscle groups. These be-
haviors typically occur with the transition to sleep at bedtime, but also at naptimes and following
nighttime arousals. They can also occur during sleep, usually in stages 1 and 2 sleep, occasionally
in slow-wave sleep, and rarely in REM sleep. Children typically engage in these behaviors as a
means of soothing themselves to (or back to) sleep, and the duration of these behaviors can be
from minutes to several hours.
In most instances, rhythmic movement behaviors are benign. Sleep is not signif cantly dis-
rupted as a result of these movements, and, although sometimes distressing to caregivers, associ-
ated signif cant injury is rare. These behaviors typically occur in normally developing children,
and in the vast majority of cases their presence does not indicate that there is some underlying
neurological or psychological problem. However, in situations that involve children with psychi-
atric or neurologic disorders, such as developmental delays, autism, or blindness, there may be
a risk of potential injury due to the intensity and frequency of the behaviors. These children are
much more likely to also engage in these behaviors while awake.
Because rhythmic movement behaviors are considered to be benign in typically developing
children, the most recent International Classif cation of Sleep Disorders (2nd ed.) has not clas-
sif ed these behaviors as pathological unless there are signif cant consequences, such as interfer-
ence with normal sleep, resulting in signif cant impairment in daytime function, or resulting in
injury. For the practitioner, however, note that these behaviors are often of signif cant concern to
parents, even though they may not be considered a disorder per se.
Sleep Related Rhythmic Movements

Rhythmic movements, including head banging, body rocking, and head rolling, are common
in young children and often function as self-soothing behaviors. They can occur at sleep onset,
following normal nighttime arousals, and while sleeping.
ePiDeMio l o g y
n Prevalence and age of onset: Studies indicate that approximately two-thirds (59%) of all
infants engage in some type of rhythmic behavior. Body rocking is most common (43%), fol-
lowed by head rolling (24%), and head banging (22%). By 18 months of age, the prevalence
has decreased to 33% and to only 5% at 5 years of age; rarely do these behaviors persist into
adulthood. Onset of rhythmic movement behaviors is typically prior to 1 year of age, with
body rocking starting at an earlier age than head banging.
n Gender: Some studies report sleep related rhythmic movements to be found equally in boys
and girls, whereas others report a higher prevalence in boys.
85
n Vestibular stimulation: An increased need for kinesthetic stimulation may be related to rhyth-
mic behaviors, as these rhythmic behaviors are reported to be soothing.
n Nighttime arousals: Any factor that increases nighttime arousals or awakenings, such as
sleep-disordered breathing, pain, or gastroesophageal ref ux, may provide increased opportu-
nities for the behavior to occur. Environmental sleep disrupters, such as noise from within or
outside the household, can also lead to increased arousals.
n Parental attention: Caregivers can inadvertently reinforce rhythmic behaviors by providing
attention.
n Developmental disabilities: It should be emphasized that the majority of children who en-
gage in rhythmic behaviors are developmentally normal and healthy. However, sleep related
rhythmic movements, especially when persistent or also occurring during the day, can be as-
sociated with mental retardation, pervasive developmental disorders (including autism), and
psychopathology.
n Additional factors: Other associated conditions include environmental stress, lack of envi-
ronmental stimulation, and self-stimulation. Some studies have suggested that there is a famil-
ial predisposition.
Children and adolescents with rhythmic movements typically present with one of the following:
n Body rocking (shuttling) presents as rocking forward and back, without head banging,
usually while on the hands and knees. Body rocking usually begins earliest, at about 6 months
of age.
n Head banging, starting around 9 months, can occur in multiple forms:
n Lying prone and lifting the head to bang down into a pillow or the mattress.
n Rocking on hands or knees and banging head into the headboard or wall.
n Sitting upright and banging head back into the headboard or wall.
n Head rolling involves side-to-side movements of the head, usually in the supine position, with
an average age of onset of 10 months.
n Body rolling is less common than the other behaviors, and involves rolling of the entire body
in a lateral manner (side to side).
See Table 11.1.
Associated Features
n Rhythmic humming or chanting: These and other sounds may accompany the movements.
n Disruption to parental sleep (and that of other family members): This may occur if the
rhythmic behavior is loud and especially if it occurs throughout the night.
n Parental anxiety: Parents may feel anxiety because they are commonly concerned about the
risk of injury, especially head trauma. They may also associate these behaviors with mental
retardation and/or autism, and, thus, may have concerns about their childs development.
eVAl uAt io n
n Medical history: The history is generally unremarkable. It should include a complete review
for additional factors that may result in increased arousals, including sleep-disordered breath-
ing, ref ux, and pain (e.g., ear infection, headaches).
n Developmental history: The history is usually normal. However, further evaluation for de-
velopmental delays in a child with persistent rhythmic behaviors, especially if they also occur
HEAD BANGING, BODy ROCkING, AND HEAD ROLLING 87
t ABl e 11.1. Diagnostic criteria: Sleep related rhythmic movement disorder (327.5)
A. The patient exhibits repetitive, stereotyped, and rhythmic motor behaviors.

B. The movements involve large muscle groups.
C. The movements are predominantly sleep related, occurring near nap or bedtime, or when the indi-
vidual appears drowsy or asleep.
D. The behaviors result in a signif cant complaint as manifested by at least one of the following:
1. Interference with normal sleep.
2. Signif cant impairment in daytime function.
3. Self-inf icted bodily injury that requires medical treatment (or would result in injury if prevent-
able measures were not used).
E. The rhythmic movements are not better explained by another current sleep disorder, medical or
neurological disorder, medication use, or substance use disorder.
during the day, may be warranted. Because sensory deprivation can contribute to the etiology
of rhythmic movement behaviors, in severe or persistent cases the possibility of child neglect
or abuse should be considered.
n Family history: The history may be positive, as there appears to be a genetic component.
n Behavioral assessment: An assessment usually does not indicate the existence of behavioral
problems, but parental response to the behavior (reinforcement) should be explored. Children
who have other self-stimulatory behaviors (e.g., rumination) may be more likely to have expe-
rienced neglect.
n Physical examination: The examination is usually unremarkable. Occasionally, children may
have minor contusions or calluses at the point of impact, but serious injury is rare.

n Developmental delay, as children with developmental delay may engage in self-injurious be-
havior or self-stimulatory behaviors, usually also seen during the day.
n Medical disorders, including neurologic disorders, blindness, ear infections, pain, and gastro-
esophageal ref ux, may result in head banging or body rocking.
n Seizures, although usually these can be easily differentiated by clinical history. One distin-
guishing feature is that children have voluntary control over rhythmic movements.
n Other movement disorders, including sleep starts (hypnic jerks), excessive fragmentary my-
oclonus, RLS or PLMD (see Chapter 15), and benign sleep myoclonus of infancy.
MAn Ag eMen t
w hen to r efer
If symptoms of other underlying sleep disrupters (e.g., obstructive sleep apnea) are present, the
patient should be referred to a sleep specialist. Where there are concerns regarding similar be-
haviors during the daytime, a referral for a developmental assessment is warranted. Referral to a
pediatric neurologist is seldom warranted except in the case of persistent or severe behaviors or
if there is a concern regarding possible seizure disorder.
t reatment
Typically, little needs to be done if a child engages in rhythmic movements at sleep times, al-
though parents should be instructed about safety, behavioral management, and, occasionally,
alternative treatments. Usually, the most important aspect in management of head banging or
body rocking is reassurance to the family that this behavior is normal, common, benign, and self-
limited; most children outgrow it by age 2 or 3 years.
Safety
All parents should be instructed to regularly tighten all screws and bolts on their childs crib or
bed and to install guardrails on beds.
Behavioral management
n Discontinue attempts to protect the child: Even if the child engages in vigorous head bang-
ing, it is unlikely that injury will occur. Installing extra bumpers on the crib or placing pillows
in strategic places is usually not needed and is rarely effective, although parents may be reas-
sured by these measures.
n Avoid reinforcement of the behavior: If the parents respond to the child, they may be inad-
vertently reinforcing the behavior. In these cases, it may be best for the parents to ignore the
behavior both at bedtime and throughout the night.
n Dampen the noise: Moving the crib or bed away from the wall and oiling screws and bolts can
dampen noise.
n Increase sleep: Increasing naptimes and moving bedtime earlier may result in diminished
sleep deprivation, minimizing the rhythmic behaviors related to increased nighttime arousals.
Additional treatments
n Treat underlying sleep disrupters (e.g., sleep-disordered breathing), which may signif -
cantly decrease the frequency and duration of the rhythmic behavior.
n Treat concurrent medical problems, e.g., ear infections.
n Reduce environmental sleep disrupters, such as household noise that may arouse the child
during the night. Installing a noisy fan or white noise machine in the childs room can be
helpful.
n Consider pharmacologic treatment, as, in severe or extremely persistent cases, treatment
with a benzodiazepine may be appropriate, especially in combination with extinction if there
is an attentional component. Studies have found clonazepam to be effective. Hydroxyzine and
tricyclic antidepressants have also been used for severe cases. At times, a short course of 2 to
3 weeks may be enough to disrupt the habit basis of these behaviors.
n Sleep restriction, as one study found that a 3-week mild sleep restriction regimen, in combi-
nation with a hypnotic, was effective for school-aged children. Patients were sleep restricted
by 1 hour at night for 1 week, with the use of a low-dose hypnotic, followed by 1 week of just 1
hour of sleep restriction, and then sleep time was gradually returned to baseline by 10-minute
increments nightly.
Pr o g n o SiS
Most young children outgrow rhythmic behaviors by age 3 years (they disappear in 90% of chil-
dren by age 4 years), although some children continue to engage in these behaviors throughout
childhood, adolescence, and even into adulthood.
HEAD BANGING, BODy ROCkING, AND HEAD ROLLING 89

Explain the nature of rhythmic behaviors, emphasizing that these are soothing behaviors
for the child, similar to thumbsucking.
Emphasize the benign nature of these behaviors, which neither indicate an underlying
neurodevelopmental or psychological condition nor result in injury (brain damage) to the
child.
Review any factors that may be increasing diff culty falling asleep and/or nighttime
arousals, including parental attention, sleep disrupters (e.g., sleep-disordered breathing,
ref ux, pain), or environmental factors (e.g., noise, room temperature).
Encourage parents to ignore the behavior, so that the behavior is not reinforced and per-
petuated by parental attention.
Review safety issues, including tightening of crib or bed bolts.
Discuss measures to reduce impact on other family members sleep, such as moving the
crib or bed away from the wall and using white noise in family members rooms to mask
sound.
Discuss the risks and benef ts of treatment options, if medication is being considered.
See Appendix D7 for a parent handout on head banging and body rocking.
12 Sleep Related Rhythmic
movements: Bruxism
Bruxism, a sleep related movement disorder, is def ned as the involuntary nonfunctional repeti-
tive grinding or clenching of the teeth during sleep. The sound of the teeth grinding, although not
always audible, can be disturbing to others and is often the reason for parental concern. Brux-
ism can eventually lead to dental erosion, jaw and/or facial pain, and tissue damage over time,
although these are unlikely to be the presenting complaints in children and adolescents. Bruxism
typically occurs during stages 1 and 2 non-REM sleep and infrequently in REM sleep. It can also
occur during sleep stage transitions. It can be associated with brief sleep arousals, although it
infrequently leads to prolonged awakenings or signif cant sleep disruption.
Bruxism
Bruxism is the repetitive grinding or clenching of teeth during sleep.
ePiDeMio l o g y
Although occasional teeth grinding is common in the general population, the repetitive and per-
sistent teeth grinding characteristic of bruxism occurs with a much lower frequency. Several
studies have been conducted on the prevalence of bruxism in children based on parental report.
Prevalence rates have ranged from several studies reporting 14% to 20% in children under the
age of 11 years, to another study f nding an overall lifetime prevalence of 38% in children and
adolescents. In this latter study, the mean age of onset was 3.6 years and bruxism ceased at a
mean age of 6 years. The prevalence of bruxism typically increases in middle childhood, then
often resolves with the eruption of the secondary dentition. Across the lifespan, the prevalence of
bruxism decreases from approximately 8% in middle-aged adults to 3% in older persons.
In addition, bruxism during infancy is common, typically following eruption of the deciduous
incisors. This type of bruxism during infancy, with a median age of onset at 10.5 months, is not
considered to be clinically signif cant.
Bruxism appears to occur with similar frequency in boys and girls.
Recent studies have shed light on the underlying pathophysiology of bruxism. Voluntary chewing
appears to involve fairly complex serotonergic and dopaminergic pathways in the midbrain and
prefrontal cortex; bruxism has been linked in several studies to dysfunction in the dopaminergic
system in particular.
n Anxiety, stress, and depression have been linked to bruxism.
n Occlusal misalignments due to malocclusion or dental trauma may increase the risk of
bruxism.
n Allergies and nasal obstruction have been reported to be associated with bruxism.
n Gastroesophageal ref ux has been linked to bruxism in adults.
n Patients with cerebral palsy and mental retardation show increased risk for bruxism.
n Alcohol and stimulant medications (e.g., amphetamines) can also exacerbate bruxism.
90
BRUxISm 91
n Nicotine has also been reported to exacerbate symptoms in adults.

n Selective serotonin reuptake inhibitors (SSRIs) have been reported to increase the risk of
bruxism.
n Primary sleep disturbances (e.g., obstructive sleep apnea) may trigger bruxism.
n Family history increases the risk of bruxism in a child. Sleep bruxism tends to occur in family
members, with 20% to 50% of individuals with bruxism having at least one family member
with a history of teeth grinding. Children with a parent with a history of bruxism are almost
twice as likely to grind their teeth.
n Attention def cit hyperactive disorder, autism spectrum disorders, and Down syndrome
have all been associated with increased rates of bruxism.
Bruxism is characterized by clenching, gnashing, or grinding of the teeth during the night, which
may be observed and/or heard by parents or others, especially those who share a bedroom with
the child or adolescent. Most children with bruxism are not aware of the behavior.
See Table 12.1.
Associated Features
n Muscle pain: Children may complain of painful and swollen jaw (masseter and temporal)
muscles, limited jaw opening, or a clicking jaw. Bruxism can also lead to temporomandibu-
lar joint (TMJ) dysfunction.
n Headache: Children or adolescents with bruxism may complain of neck and shoulder pain, or
bitemporal headache in the morning (TMJ syndrome).
n Sensitive teeth: Patients may complain of tooth discomfort associated with extremes in food
temperature.
n Daytime bruxism: Children and adolescents may also grind their teeth during the day, al-
though these two behaviors appear to be etiologically different.
n Dental damage: Dental damage can include erosion of the teeth, damage to the tissues sur-
rounding the teeth (recession and inf ammation of the gums), and resorption of the alveolar
bone.
n Daytime behavior problems: Bruxism can be associated with increased arousals from sleep,
resulting in sleep deprivation and concomitant daytime behavior problems, such as inattention
and oppositional behavior.
t ABl e 12.1. Diagnostic criteria: Sleep related bruxism (327.53)
Diagnostic criteria:
A. The patient reports or is aware of tooth-grinding sounds or tooth clenching during sleep.
B. One or more of the following is present:
1. Abnormal wear of the teeth
2. Jaw muscle discomfort, fatigue, or pain and jaw-lock upon awakening
3. Masseter muscle hypertrophy upon voluntary forceful clenching
C. The jaw muscle activity is not better explained by another current sleep disorder, medical or neuro-
logical disorder, medication use, or substance use disorder.
eVAl uAt io n
n Medical history: The history is generally unremarkable, but may include symptoms of head
and jaw pain and dental problems.
n Developmental and school history: The history is usually normal.
n Family history: The history may be positive for other family members with bruxism.
n Behavioral assessment: An assessment may show possible contributory factors, such as anxi-
ety and stress.
n Physical examination: Evaluation for dental erosion and tissue damage should be conducted.
There may be tenderness over the maxillary and temporal areas.
n Diagnostic tests: Tests are not indicated.

Diagnosis of bruxism is usually straightforward. Differential diagnosis includes:
n Dental disorders and other TMJ disorders.
n Seizure disorder. In rare cases, abnormal jaw movements may be associated with partial com-
plex or generalized seizures.
MAn Ag eMen t
w hen to r efer
Children or adolescents with bruxism who also have signif cant psychiatric or behavioral issues
should be referred to a mental health professional. In addition, referral to a dentist is appropriate
if there are any dental concerns.
t reatment
Because bruxism is usually self-limited, treatment in children and adolescents is rarely war-
ranted. However, since stress is a major contributing factor in many cases, possible sources of
stress should be explored and eliminated if possible. Specif c stress management techniques that
have been shown to be helpful include the introduction of relaxing bedtime rituals, progressive
relaxation exercises, hypnotherapy, and biofeedback. In more problematic cases, additional man-
agement strategies may include the following.
n Sleeping position: Lying in the supine position with support for the neck may alleviate muscle
strain on the jaw and neck.
n Pain relief: Nonsteroidal anti-inf ammatory medications are occasionally indicated to relieve
jaw pain. Local application of heat may be helpful.
n Dental appliances: For children and adolescents with dental damage or persistent complaints
of jaw pain, referral to a dentist for a nighttime intraoral appliance may be warranted.
n Pharmacotherapy: Although REM-suppressing medications, such as benzodiazepines and
muscle relaxants, have been shown to be effective for severe bruxism in adults, their use is
rarely indicated in the pediatric population. It should be noted that serotonergic drugs such as
SSRIs may cause or worsen symptoms of bruxism.
n Psychological treatment: If an underlying anxiety disorder is suspected, psychological treat-
ment may be warranted.
Pr o g n o SiS
Bruxism, although most often self-limited in children, may be chronic and is likely to be exac-
erbated by stress.
BRUxISm 93

Explain what bruxism is in simple terms, including that this behavior is usually self-lim-
ited and benign in infants and children, although there is a possibility of dental damage in
older children and adolescents.
Explain risk factors for bruxism, primarily stress.
Discuss treatment options (if warranted), including stress management and/or psychologi-
cal treatment.
Refer for a dental examination in older children and adolescents.
See Appendix D8 for a parent handout on bruxism.
13 Sleep Enuresis
Sleep enuresis (bedwetting) is characterized by recurrent involuntary voiding during sleep. For
a diagnosis, it must occur a minimum of twice a week after the age of 5 years. Enuresis is consid-
ered primary if the child has never had a dry period of 6 months, and secondary if the child had
previously been consistently dry for 6 months but bedwetting is now occurring at least twice a
week for 3 months. Monosymptomatic enuresis (uncomplicated enuresis) involves normal void-
ing during the night without any associated urogenital or gastrointestinal problems, including
lower urinary tract infections (UTIs) or bladder dysfunction. Non-monosymptomatic enuresis
(polysymptomatic enuresis; complicated enuresis) is associated with daytime symptoms, includ-
ing severe urgency, daytime incontinence, increased or decreased voiding frequency, chronic
constipation, and encopresis. Enuresis can occur in any stage of sleep, with most episodes occur-
ring in the f rst half of the night.
Enuresis
Enuresis involves involuntary voiding during sleep, at least twice a week beyond the age of
5 years.
It is important to note that becoming consistently dry at night is a developmental maturation

process. Children with primary enuresis typically fail to wake from sleep in response to blad-
der sensations or fail to inhibit bladder contractions during sleep. These skills are acquired with
development, with some children taking much longer to achieve the skill of being dry at night
compared to daytime continence. Thus, enuresis is not even diagnosed until age 5 years and typi-
cally not treated until after age 7 years.
Although enuresis is not problematic per se, it can have a signif cant impact on children and
their families. Many children feel extremely embarrassed by their bedwetting and parents often
punish children for something that they are unable to control.
ePiDeMio l o g y
Primary enuresis steadily decreases by age with a spontaneous remission rate of approximately
15% per year. It is experienced by about 30% of 4-year-olds, 10% of 6-year-olds, 7% of 7-year-
olds, 5% of 10-year-olds, 3% of 12-year-olds, and 1% to 2% of 18-year-olds. Boys are 1.5 to 2
times more likely to experience enuresis than girls. Secondary enuresis accounts for less than
25% of cases. Cross-cultural studies indicate quite consistent f ndings.
Infrequent bedwetting, ranging from less than twice a week to less than once a month, is even
more common. The more severe the bedwetting, in terms of frequency, the more likely it is to
persist.
Primary enuresis
n Maturational delay: Maintaining bladder control throughout the night is a maturational pro-
cess, with enuresis related to central nervous system maturational delays.
94
SLEEP ENURESIS 95
n Lowered arousal threshold: A child with enuresis may have decreased arousability and fails
to awaken in response to a full bladder. This may be associated with sleep-disordered breath-
ing, possibly due to fragmented sleep or another mechanism.
n Positive family history: There is commonly a genetic component in primary enuresis. Studies
indicate a 74% prevalence rate if both parents were enuretic during childhood and 44% if one
parent had enuresis as a child, in comparison to 15% if neither parent had a history of enuresis.
Genetic linkage of sleep enuresis is autosomal dominant and has been noted for chromosomes
22q, 13q, and 12q.
n Psychiatric and neurodevelopmental conditions: Enuresis is more prevalent in children
with attention def cit hyperactivity disorder (ADHD, with an almost three-fold increase in
prevalence) and neurodevelopmental disorders, such as developmental delays and mental
retardation.
n Reduced nocturnal bladder capacity: Enuresis can be due to decreased functional bladder
capacity and an inability to hold urine at night. Bladder capacity increases with age from ap-
proximately 6 ounces at age 5 years to 11 ounces at age 10 years. Any condition that further
reduces bladder capacity, such as constipation or cystitis, will result in increased enuresis.
n Decreased vasopressin production during sleep: Some children do not have the typical in-
crease in vasopressin during sleep, resulting in polyuria (high urinary volume) that exceeds
bladder capacity. If the child does not arouse in response to the sensation of a full bladder,
sleep enuresis will occur.
Secondary enuresis
n Inability to concentrate urine: Enuresis can be the result of diabetes mellitus, diabetes in-
sipidus, or sickle cell disease.
n Increased urinary production: Enuresis can result from intake of caffeine or diuretics.
n Urinary tract pathology: A child with enuresis may have other symptoms, including urinary
tract infections (UTIs), irritable bladder, or a malformation of the genitourinary tract.
n Chronic constipation and encopresis: Constipation occurs in over 50% of children with
secondary nocturnal enuresis.
n Neurologic pathology: There may be a neurologic component to enuresis in some children,
including nocturnal epilepsy.
n Sleep disorders: Sleep disorders, primarily obstructive sleep apnea (OSA), has been associ-
ated with both primary and secondary enuresis. Studies indicate that 8% to 47% of children
with OSA have sleep enuresis; the mechanism has been postulated to involve disruption of the
normal nocturnal pattern of secretion of the anti-diuretic hormone vasopressin by OSA-related
sleep fragmentation. Resolution of enuresis following adenotonsillectomy in these children
occurs in 55% to 77% of cases. Enuresis may also occur in conjunction with a partial arousal
parasomnia (sleepwalking).
n Psychosocial stressor: Enuresis may result from a psychosocial stressor, such as parental
divorce or death in the family.
Bedwetting occurs at least twice a week. Some children have enuresis on a nightly basis, and may
even have multiple episodes per night, whereas in other children it is much less frequent.
See Tables 13.1 and 13.2.
Associated Features
n Daytime enuresis: Involuntary voiding during wakefulness, together with nighttime enuresis,
is more likely to be associated with an organic cause.
t ABl e 13.1. Diagnostic criteria (ICSD-2): Sleep enuresis (307.6)
A. Primary Sleep Enuresis

1. The patient is older than age 5 years.
2. The patient exhibits recurrent involuntary voiding during sleep, occurring at least twice a week.
3. The patient has never been consistently dry during sleep.
B. Secondary Sleep Enuresis
1. The patient is older than age 5 years.
2. The patient exhibits recurrent involuntary voiding during sleep, occurring at least twice a week.
3. The patient has previously been consistently dry during sleep for at least 6 months.
t ABl e 13.2. Diagnostic criteria (DSM-IV): Enuresis (307.6)
A. Repeated voiding of urine into bed or clothes (whether involuntary or intentional).

B. The behavior is clinically signif cant as manifested by either a frequency of twice a week for at
least 3 consecutive months or the presence of clinically signif cant distress or impairment in social,
academic (occupational), or other important areas of functioning.
C. Chronological age is at least 5 years (or equivalent developmental level).
D. The behavior is not due exclusively to the direct physiological effect of a substance (e.g., a diuretic)
or a general medical condition (e.g., diabetes, spina bif da, a seizure disorder).
Specify type:
Nocturnal Only
Diurnal Only
Nocturnal and Diurnal
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, fourth edition (DSM-IV).
Washington, DC: American Psychiatric Press, 1994:557.
n Constipation: Enuresis is often associated with constipation.

n Impact on social functioning: Because of potential embarrassment, many children and ado-
lescents with sleep enuresis avoid social situations, such as overnight visits to friends or sum-
mer camp. Studies also indicate increased vulnerability to victimization.
n Emotional toll: Children and adolescents with enuresis may have negative self-thoughts, in-
cluding lowered self-esteem, guilt, shame, and embarrassment. There is often a fear of being
found out.
n Increased psychological problems: Children who wet the bed are more likely to have both
internalizing and externalizing problems, especially oppositional behaviors and conduct
problems.
Enuresis is Expensive
The cost of coping with a child with enuresis should not be underestimated; neither should its
f nancial impact on families, especially low-income families. Overnight diapers are expensive
($250$300 per year), as is the cost of extra loads of laundry, especially for those who need to
go to a laundromat ($500$700 per year). Some families literally cannot afford the expense of
having a child who wets the bed.
SLEEP ENURESIS 97
eVAl uAt io n
n Enuresis history: The age of onset, duration, and severity of enuresis and the duration of
continence should be determined for secondary enuresis.
n Medical history: The history is generally benign. Presence of daytime wetting, constipation,
and genitourinary symptoms should be assessed, as well as other symptoms related to second-
ary causes.
n Developmental and school history: The history is usually normal, although enuresis can be
related to developmental delays.
n Family history: The history is commonly positive for childhood enuresis.
n Behavioral assessment: Behavioral concerns are uncommon in children with primary enure-
sis, but are common in children with secondary enuresis. Behavioral concerns include depres-
sion, anxiety, conduct disorders, and ADHD.
n Physical examination: The examination is generally unremarkable, although should include a
urinalysis. If daytime enuresis is also present, then evaluation of urinary abnormalities should
be considered. Evaluation for diabetes, urinary tract infection (UTI), seizure disorder, sickle
cell disease, and neurologic disorders may be considered.
n Diagnostic tests:
n Urinalysis and urine culture to assess for glucosuria and UTI, particularly in secondary
enuresis.
n Enuresis diary that documents frequency of bedwetting events.
n Overnight polysomnography may be warranted if there is a suspicion of OSA, but is not a
routine part of the evaluation for enuresis.

n Secondary causes of enuresis need to be considered.
n Nocturnal seizures may result in incontinence, but typically are accompanied by other fea-
tures suggestive of a seizure disorder (e.g., stereotypical movements, altered consciousness).
MAn Ag eMen t
w hen t o r efer
Children or adolescents with persistent enuresis, daytime wetting, genital abnormalities, or a his-
tory of UTIs should be referred for a urology consult. If other potentially contributing medical
disorders exist, such as diabetes, a seizure disorder, or OSA, a referral is warranted. A specialist
in treating behaviorally based issues can be benef cial in the implementation of behavioral treat-
ments. Finally, where there are concerns regarding stress or other psychological issues, a referral
to a mental health specialist is warranted.
t reatment
Reassurance and education of the child and family is the f rst step in management of sleep
enuresis, followed by treatment of secondary causes, including urologic and neurologic is-
sues. The prevalence of this condition and the fact that it often resolves spontaneously should be
reviewed.
If the enuresis is not distressing to the child, treatment is not warranted, especially given the
high spontaneous remission rate. For young children (ages 5 to 7 years), treatment is typically not
warranted or recommended. Normalization of the behavior (as well as use of overnight training
pants) is often the best option.
In cases in which the enuresis is distressing (i.e., in older children and adolescents) or is
impacting functioning (e.g., social functioning), the following treatments should be considered.
Overall, treatment is considered successful with 14 consecutive dry nights. Lack of success is
def ned as less than a 50% decrease in enuresis, with partial success indicated by a 50% to 90%
decrease.
n Overall good bladder health: Bladder health can improve sleep enuresis. Children should
be encouraged to void regularly (every 23 hours) and avoid urgency. Many children avoid
urinating at school, and thus voiding should be encouraged. Increased f uid intake during the
day can also be benef cial, both for bladder health and to reduce constipation.
n Behavioral treatments: The following treatments can be effective.
n Enuresis alarms are the f rst-line treatment and the most effective for sleep enuresis, al-
though it is important to note that they require signif cant effort and motivation by the child
and family as well as persistence over time. There are many different types of enuresis
alarms, including pads that go on the bed or alarms that attach to a childs underwear, but
all are based on the premise of a moisture sensor that gets triggered by wetting. It eventually
conditions a child to respond to the sensation of a full bladder. Treatment may take months
before success is attained; typical treatment is 6 to 16 weeks. The initial response rate is
approximately 60%, with a cure rate of approximately 40%. The benef ts of alarm treatment
are the short-term and long-term eff cacy and that it is non-invasive. The negatives are the
relative cost of treatment ($70$90) and the amount of motivation required by the family.
n Awakening the child at times that enuresis typically occurs or prior to parents going to bed
can decrease events. Parents, however, may f nd that it is diff cult to waken their child or
that their child resists middle-of-the night trips to the bathroom. Thus, parents may f nd this
treatment frustrating.
n Implement sticker charts and other reward systems for dry nights.
n Minimize f uids in the evening after dinner.
n Avoid caffeine.
n Bladder training, which involves having the child drink increasing amounts of f uid and
progressively waiting longer to void.

n Involve the child in changing the bed by having him or her help remove wet sheets and
remake the bed.

n Pharmacologic treatment: Using drugs is not curative but can temporarily resolve enuretic
events. Medication is typically not given to children under the age of 7 years, and should be
used if behavioral treatments fail. Some children benef t from nightly medication use, whereas
others use it on a night-to-night basis, such as for sleepovers or overnight camp.
n Imipramine (Tofranil) is FDA-approved for the treatment of enuresis in children. Doses
range from 25 mg for children older than 6 years (20 kg to 25 kg) to 50 mg to 75 mg in

children older than age 11 years. A starting dose of 25 mg 1 hour prior to bedtime for 1 week
is recommended, increasing the dose as needed. Relapse typically occurs with discontinua-
tion. The mode of action is unclear but can be effective with refractory enuresis. Side effects
can include lethargy, drowsiness, agitation, and gastrointestinal upset. Because of the risk
of cardiotoxicity in accidental overdose, parents should be cautioned to carefully monitor
medication.
n Desmopressin (DDAVP) is the only other medication that is FDAapproved for enuresis.
Desmopressin, an analogue of vasopressin, reduces urine volume. Oral preparations and

nasal spray formulations are available. Studies indicate that 60% to 70% of children respond
to treatment, with 80% relapse following discontinuation. Desmopressin is most effective in
children with normal bladder capacity and requires nightly administration.
n Anticholinergics (Detrol, Ditropan) reduce muscle spasms in the bladder and are most
effective for those children and adolescents with an overactive bladder and small functional
bladder capacity.
SLEEP ENURESIS 99
Pr o g n o SiS
Most children naturally stop bedwetting, with a spontaneous remittance rate of 15% per year.

Educate parents and child about enuresis, including lack of volition of the behavior and
eliminating punishment and negative consequences of nighttime episodes.
Discuss whether treatment is necessary, given that most children outgrow enuresis at a
rate of 15% per year.
Discuss good bladder health, including frequent voiding during the day and increased f uid
intake during the day (to prevent constipation), while decreasing f uid intake in the evening.
Consider bedwetting alarms, for those children over the age of 7 years and for those for
whom enuresis is having a signif cant impact on functioning or family stress.
Review medication alternatives, especially for occasional use such as sleep-overs.
See Appendix D9 for a parent handout on enuresis.
Sleep-Disordered Breathing
14 and Obstructive Sleep
Apnea Syndrome
Sleep-disordered breathing (SDB) in children encompasses a broad spectrum of respiratory

disorders that occur exclusively in or are exacerbated by sleep, and includes apnea of prematurity
and central apnea. Disorders of obstructive SDB, which are discussed in this chapter, include
pathology ranging from primary snoring (snoring without observable ventilatory abnormalities)
to obstructive hypoventilation to frank apneas with complete cessation of airf ow. Obstructive
sleep apnea syndrome (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
or partial cessation of airf ow at the nose and/or mouth as well as in disrupted sleep. Both inter-
mittent hypoxia and multiple arousals resulting from these obstructive events contribute to the
signif cant medical (e.g., increased blood pressure, insulin resistance) and neurocognitive and
neurobehavioral (e.g., def cits in attention, executive functions) morbidity associated with OSA
in the pediatric population. General etiologic factors include reduced upper airway patency and
increased collapsibility related to obstruction, reduced muscle tone, and upper airway anatomi-
cal features; specif c risk factors include adenotonsillar hypertrophy, chronic nasal obstruction,
craniofacial abnormalities, and obesity.
c l in ic Al PAt t er n S o F Sl eeP- DiSo r Der eD Br eAt h in g

It is important to understand that OSA is at one end of a clinical spectrum of SDB that includes
the following clinical conditions:
n Snoring: The most common symptom of SDB, snoring, 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.
n Primary snoring: Snoring without associated ventilatory abnormalities (e.g., apneas or hy-
popneas, hypoxemia, hypercapnia) or respiratory-related arousals is def ned as primary snor-
ing. However, children with primary snoring may still have subtle breathing abnormalities dur-
ing sleep, including evidence of increased respiratory effort, which in turn may be associated
with adverse neurodevelopmental outcomes.
Snoring: No Laughing Matter

While clearly a common symptom of obstructive sleep apnea syndrome, snoring itself may
also be associated with adverse neurobehavioral and neurocognitive outcomes in children.
Furthermore, chronic nasal obstruction and mouth breathing in the f rst 4 years of life may
itself lead to impairments in maxillomandibular growth, further increasing the risk of sleep-
disordered breathing.
n Obstructive hypoventilation: This condition is characterized by snoring, increased respira-

tory effort, and hypercapnea, without apneas or hypopneas or respiratory arousals.
n Upper airway resistance syndrome: This condition is characterized by increasing negative
intrathoracic pressure during inspiration, as measured by balloon esophageal manometry.
100
SLEEP-DISORDERED BREATHING AND OBSTRUCTIvE SLEEP APNEA SyNDROmE 101
Brief, repetitive respiratory arousals terminate the negative pressure swings, which results in
sleep fragmentation and daytime evidence of sleepiness. Symptoms of upper airway resistance
syndrome include snoring and increased respiratory effort (including paradoxical inward rib
cage movements) without a signif cant decrease in airf ow or ventilatory abnormalities.
n OSA: This condition is characterized by snoring, apneas and hypopneas, and arousals with
ventilatory abnormalities resulting from the complete cessation of airf ow, resulting in sleep
disturbance and daytime symptoms.
American Academy of Pediatrics Clinical Practice Guidelines

for Obstructive Sleep Apnea Syndrome (April 2002)
1. All children should be screened for snoring.
2. Complex high-risk patients should be referred to a specialist.
3. Patients with cardiorespiratory failure cannot await elective evaluation.
4. Diagnostic evaluation is useful in discriminating between primary snoring and obstructive
sleep apnea syndrome, the gold standard being polysomnography.
5. Adenotonsillectomy is the f rst line of treatment for most children, and continuous positive
airway pressure is an option for those who are not candidates for surgery or do not respond
to surgery.
6. High-risk patients should be monitored as inpatients postoperatively.
7. Patients should be reevaluated postoperatively to determine whether additional treatment is
required.
ePiDeMio l o g y
Data regarding the prevalence of pediatric SDB are available largely for primary snoring and
OSA; the prevalence rates of upper airway resistance syndrome and obstructive hypoventilation
in children have not been studied. It should also be noted that SDB prevalence rates may vary
according to the diagnostic def nition used (e.g., apnea-hypopnea threshold for OSA, habitual
snoring as occurring often versus specif ed number of times per week) and the methods em-
ployed (parent report of symptoms versus PSGdocumented symptoms).
n Primary snoring: Overall prevalence of parent-reported snoring in the pediatric population is

about 8%; always snoring is reported in 1.5% to 6%, and often snoring in 3% to 15%. A
recent study suggested a habitual snoring prevalence of 5% in infants.
n Apneic events: The prevalence of parent reported breathing pauses is in the 0.2% to 4% range.
n OSA: When def ned by parent-reported symptoms, the prevalence of OSA is between 4% and
11%. The prevalence of pediatric OSA as documented by overnight sleep studies utilizing
ventilatory monitoring procedures (e.g., in-lab PSG, home studies) is 1% to 4% overall, with
a reported range of 0.1% to 13%. Prevalence is also affected by the following demographic
characteristics.
n Age: It is important to note that OSA occurs in all ages, including infants, but is particu-
larly prevalent between the ages of 2 and 8 years, coinciding with the peak age of lymphoid
hyperplasia and adenotonsillar hypertrophy. As being overweight and obesity have become
more prominent risk factors for OSA in the pediatric population, the age distribution has
shifted somewhat to older children and adolescents.
n Gender: There is now a reasonable preponderance of evidence suggesting that OSA is more
common in boys, especially after puberty.

n Ethnicity: Some data suggest that African-American and Asian children may have a higher
risk for OSA compared to Caucasians, even after controlling for body mass index (BMI).
There are a number of factors that put a child at risk for OSA, although the primary risk factor
in many children remains adenotonsillar hypertrophy. In general terms, OSA results from an
anatomically or functionally narrowed upper airway; this typically involves some combination
of decreased upper airway patency (upper airway obstruction and/or decreased upper airway
diameter), increased upper airway collapsibility (reduced pharyngeal muscle tone), and de-
creased drive to breathe in the face of reduced upper airway patency (reduced central ventila-
tory drive). Upper airway muscle tone is also inf uenced by sleep state, as the activity of the
pharyngeal dilator muscles is diminished in REM sleep.
Adenotonsillar hypertrophy
Adenotonsillar hypertrophy is the most common cause of obstructive sleep apnea.
Specif c factors related to these underlying mechanisms include the following.
upper Airway o bstruction

Upper airway obstruction often ref ects an interaction between anatomically reduced upper air-
way size and soft tissue structures encroaching upon the upper airway. Underlying obstruction
varies in degree and level (i.e., nose, nasopharynx, oropharynx, hypopharynx) and may be due to:
n Adenotonsillar hypertrophy, although tonsillar size does not necessarily correlate with de-
gree of obstruction, especially in older children.
n Allergies, associated with chronic rhinitis or nasal obstruction.
n Craniofacial abnormalities, including hypoplasia or displacement of the maxilla and
mandible.
n Gastroesophageal ref ux, due to pharyngeal reactive edema.
n Nasal septal deviation.
n Obesity or being overweight.
n Velopharyngeal f ap cleft palate repair.
n Chronic nasal obstruction and mouth breathing, especially in the f rst 4 years of life,
which may itself lead to impairments in maxillomandibular growth, further increasing the
risk of SDB. Conversely, these skeletal abnormalities may be at least partially reversible with
treatment.
upper Airway r educed Muscle t one

Also known as a f oppy airway, upper airway reduced muscle tone also has an important role
in the underlying pathophysiology of OSA. Factors that may inf uence patency of the upper air-
way include:
n Neuromuscular disease, including hypotonic cerebral palsy and muscular dystrophies.
n Hypothyroidism, as it may be related to reduced upper airway patency or reduced central
ventilatory drive.
r educed c entral Ventilatory Drive

Reduced central ventilatory drive may be present in some children with OSA; central apneas are
also very common in these children. Conditions that may be associated with reduction in ventila-
tory drive include:
n Arnold-Chiari malformation, types I and II.
n Myelomeningocele.
n Brainstem injury or masses.
Medical c onditions
A number of specif c medical conditions signif cantly increase the risk for OSA in children. In
many of these disorders, a combination of risk factors is present. For example, children with
Down syndrome often have multiple risk factors for OSA, including hypotonia, glossoptosis
(posterior tongue displacement), obesity, midface hypoplasia, and hypothyroidism. Table 14.1
lists the most common medical conditions in children that are associated with increased risk for
OSA.
environment
Passive exposure to cigarette smoking has been associated with both snoring and OSA in chil-
dren, including in infants as young as 8 months old. Studies suggest that environmental tobacco
exposure in infants may be associated with snoring-related sleep fragmentation, which in turn
may be negatively correlated with developmental measures.
o besity
Although many children with OSA are of normal weight, an increasingly large percentage are
overweight or obese, and many of these children are school-aged and younger. Multiple studies
have found a signif cant correlation between weight and SDB (habitual snoring, OSA, central
apneas) in a variety of pediatric samples. While adenotonsillar hypertrophy also plays an im-
portant etiologic role in overweight and obese children with OSA, mechanical factors related to
an increase in the amount of adipose tissue in the throat (pharyngeal fat pads), neck (increased
neck circumference), and chest wall and abdomen can create increased upper airway resistance,
worsen gas exchange, and increase the work of breathing, particularly in the supine position and
during REM sleep. There may be a component of blunted central ventilatory drive in response
to hypoxia, hypercapnia, and hypoventilation as well, particularly in children with morbid or
syndrome-based (e.g., Prader-Willi) obesity. Overweight and obese children and adolescents are
at a particularly high risk for metabolic and cardiovascular complications of SDB, such as insulin
resistance and systemic hypertension; morbidly obese children may also be at increased risk for
postoperative complications following adenotonsillectomy.
The Obesity Epidemic and Obstructive Sleep Apnea

As the prevalence of childhood obesity increases, weight has become more of a relative risk
factor for pediatric obstructive sleep apnea (OSA). Both overweight and obese children and
adolescents are at a particularly high risk for metabolic and cardiovascular complications of
OSA, such as insulin resistance and systemic hypertension. Practitioners should systemati-
cally screen for sleep-disordered breathing symptoms in children who are considered over-
weight or obese according to the guidelines of the Centers for Disease Control for age and
gender body mass index percentiles.
Family h istory
Positive family history of OSA or disruptive snoring is found in a signif cant percentage of chil-
dren with OSA symptoms.
underlying Pathophysiology
Recent studies have yielded important new information regarding the underlying pathophysiol-
ogy of OSA in children, including mechanisms through which OSA may increase cardiovascular
and neurocognitive morbidity. In regards to cardiovascular risk, upregulation of inf ammatory
pathways, as indicated by an increase in peripheral markers of inf ammation, such as C-reactive
protein (CRP), appear to be linked to metabolic dysfunction (e.g., insulin resistance, dyslipid-
emia) in both obese and non-obese children with OSA. It has been postulated that both systemic
t ABl e 14.1. Medical conditions associated with obstructive sleep apnea in children
Craniofacial syndromes: Miscellaneous disorders and syndromes:

Apert syndrome Achondroplasia
Crouzon syndrome Beckwith-Wiedemann syndrome
Pfeiffer syndrome Choanal stenosis
Pierre Robin syndrome Down syndrome
Treacher-Collins Goldenhar syndrome
Neurological disorders: Hallerman-Streiff syndrome
Arnold-Chiari malformation (I and II) Hypothyroidism
Cerebral palsy Klippel-Feil syndrome
Meningomyelocele Marfan syndrome
Mobius syndrome Mucopolysaccaridoses
Myasthenia gravis Obesity
Prader-Willi syndrome
Sickle cell disease
Subglottic stenosis
inf ammation and arousal-mediated increases in sympathetic autonomic nervous system activity
with altered vasomotor tone are key contributors to increased cardiovascular risk in both adults
and children with OSA. Studies utilizing measures of heart rate variability or peripheral arterial
tonometry, a new noninvasive technique that measures sympathetic tone, have demonstrated that
children with OSA have alterations in vascular reactivity that may eventually increase the risk of
systemic hypertension and ischemic heart disease. Another potential mechanism that may medi-
ate cardiovascular sequelae in both adults and children with OSA is altered endothelial function,
as indicated by elevations in circulating adhesion molecules, such as the CD40 ligand, and by
blunted reperfusion following occlusion tests; both of these measures of endothelial dysfunction
have been demonstrated to be reversible following treatment for OSA in children. Finally, new
data regarding pathophysiologic mechanisms in pediatric OSA have also led to a potential expan-
sion of therapeutic options in these children. For example, it is postulated that mechanical stress
on the upper airway induced by chronic snoring may result in both local mucosal inf ammation
of adenotonsillar tissues and subsequent upregulation of inf ammatory molecules, most notably
leukotrienes. This has led to speculation that leukotriene inhibitors such as montelukast may be
a therapeutic alternative in children with mild or residual OSA (see Treatment section below).
Similarly, targeting glucocorticoid expression in upper airway lymphoid tissues with intranasal
steroids has also been shown to reduce residual OSA in children post-adenotonsillectomy.
The most common presenting complaints in childhood OSA are those associated with nocturnal
symptomsfrequent loud snoring, observed breathing pauses, restless sleep, and chronic mouth
breathing with nasal obstruction. OSA is unlikely in the absence of at least occasional snoring, al-
though obviously many children who snore do not have OSA. It should be noted that parents may
not recognize, and thus may not spontaneously volunteer, information about OSA symptoms,
such as snoring, and the history may only be elicited on direct questioning (a screening question-
naire for OSA is provided in Appendix B). Behavior and academic problems, as well as concerns
about inattention, hyperactivity, impulsivity, and irritability, may also be the primary presenting
complaints in children with OSA. Because parents do not necessarily associate these problems
with OSA, a high index of suspicion should be maintained by the clinician in these situations.
Thus, children presenting with behavioral, mood, attentional, or academic concerns should be
systematically screened for symptoms of and risk factors for OSA.
Symptoms of Obstructive Sleep Apnea Vary By Age

The presenting symptoms of obstructive sleep apnea (OSA) can vary by age. For example,
OSA has been increasingly recognized as also occurring in infants, especially those with a his-
tory of prematurity. For these children, symptoms may include noisy breathing, nocturnal
sweating, disturbed or restless sleep, poor suck, and poor growth. OSA presenting during ado-
lescence tends to more closely resemble adult OSA in terms of risk factors (e.g., obesity) as
well as clinical presentation (e.g., snoring, apnea, hypersomnolence).
Common symptoms of pediatric OSA include the following.
n octurnal Symptoms
n Loud, continuous nightly snoring, although volume does not necessarily correlate with the
degree of obstruction.
n Apneic pauses, although these occur less frequently in children compared to adults. Parents
commonly describe their child as working hard to breathe. Other symptoms include episodic
choking, gasping, and snorting during the night. One of the best predictors of OSA severity is
parental anxiety about sleep respirations. However, it should be noted that, because symptoms
of OSA may be worse during REM sleep, which is concentrated in the last third of the night,
parents may not be awake to observe the most severe symptoms. Parents of older children and
adolescents may also be less likely to observe and note snoring and disturbed sleep.
n Paradoxical movement, of chest wall and abdomen during breathing.
n Restless sleep, thrashing, and increased body movement.
n Sweating during sleep, related to increased work of breathing.
n Abnormal sleeping position, such as propped on pillows or sleeping with the neck hyper-
extended.
n Mouth breathing, while asleep.
Daytime Symptoms (Physical)

n Mouth breathing and dry mouth.
n Chronic nasal congestion and rhinorrhea.
n Hyponasal speech.
n Morning headaches that may be related to carbon dioxide retention.
n Frequent infections (especially otitis media and sinusitis).
n Diff culty swallowing related to tonsillar hypertrophy.
n Poor appetite related (possibly) to dysphagia and chronic nasal obstruction.
Obstructive Sleep Apnea and Daytime Functioning

One of the most important but frequently overlooked sequelae of obstructive sleep apnea
(OSA) in children is the effect on mood, behavior, learning, and academic functioning. Be-
cause treatment of OSA can substantially mitigate these effects, it is key to identify these
children early.
Daytime Symptoms (c ognitive and Behavioral)

n Excessive daytime sleepiness, which may manifest as more classic symptoms of hyper-
somnolence (e.g., diff culty waking in the morning, falling asleep in school or at inappropriate
times, or increased napping in younger children) or with more subtle neurobehavioral signs.
Evidence of frank hypersomnolence tends to be less common in children (estimated to occur
in 7% to 10%) compared to adults with OSA.
n Mood changes, such as irritability, mood instability and emotional dysregulation, low frustra-
tion tolerance, and depression and anxiety.
n Internalizing behaviors, including increased somatic complaints and social withdrawal.

n Externalizing behaviors, including aggression, impulsivity, hyperactivity, oppositional be-
havior, and conduct problems.
n Attention def cit hyperactivity disorder (ADHD)like symptoms, such as inattention, poor
concentration, and distractibility. There is a substantial overlap between the clinical impair-
ments associated with OSA and the diagnostic criteria for ADHD. There also appears to be a
selective impact of OSA specif cally on executive functions, which include cognitive f ex-
ibility, task initiation, self-monitoring, planning, organization, and self-regulation of affect and
arousal; executive function def cits are also a hallmark of ADHD.
n Learning problems, with specif c neuropsychological function def cits in children with OSA
most consistently occurring for tasks involving reaction time and vigilance and sustained and
selective attention. Other cognitive def cits such as language delays and impairments in visual
perception, motor functions, and memory, have not been as consistently found.
n Academic problems, as an association between low levels of academic achievement and SDB
likely represents the combined inf uence of a number of these learning and attention-based
impairments.
Playing Detective
Sleep-disordered breathing (SDB) in children may present primarily with parental complaints
of behavior problems, inattentiveness (ADHD), and academic failure. Parents may not volun-
teer information about sleep and symptoms of SDB (snoring) unless these are directly elicited
by the primary care provider.
n Underlying Mechanisms for Impact on Daytime Function

Although yet to be fully elucidated, one of the primary mechanisms by which OSA is believed
to exert negative inf uences on cognitive function appears to involve repeated episodic arous-
als from sleep leading to sleep fragmentation and resulting sleepiness. In addition, a number
of more recent studies have posited at least an equally important role for intermittent hypoxia
leading directly to systemic inf ammatory vascular changes in the brain. Animal models sug-
gest that oxidative stress and inf ammatory processes lead to structural and neurochemical
changes in the hippocampus and prefrontal cortex, areas of the brain that are specif cally in-
volved in attention and executive functions. In humans, sleep apnea in adults has been found to
preferentially affect the hippocampus and cerebellum, and even mild levels of chronic or inter-
mittent hypoxia from a variety of causes have clearly been shown to be associated in children
with cognitive and behavioral disruption. Furthermore, levels of inf ammatory markers, such
as CRP and cytokine IL-6, have been shown not only to be elevated in children with OSA, but
also to be associated with cognitive dysfunction in these children, and to decrease following
adenotonsillectomy. Abnormal vascular reactivity and endothelial dysfunction in the central
nervous system may also play a role in neurocognitive dysfunction. Finally, the relative con-
tributions of additional factors such as hypercarbia, changes in REM latency and percentage,
and alternations in other stages of sleep have yet to be fully explored.
Diagnostic criteria
See Table 14.2.
Associated Features
n Enuresis (especially secondary), due to alterations in antidiuretic hormone secretion related
to sleep fragmentation.
n Growth failure (in severe cases, failure to thrive), possibly related to some combination of
decreased appetite and decreased intake, increased metabolic needs from increased work of
breathing, and alterations in normal nocturnal growth hormone secretion patterns. It is com-
mon for children, even those who are overweight, to gain weight after treatment (i.e., adeno-
tonsillectomy) for OSA.
n Increase in partial arousal parasomnias (e.g., sleepwalking, sleep terrors), in susceptible
children, which is related to sleep fragmentation and compensatory increases in slow-wave
sleep.
n Increase in seizure frequency in predisposed children, which is possibly related to increased
arousals and intermittent hypoxia.
n Other comorbid sleep problems, such as bedtime resistance and nightwakings, restless legs
syndrome or periodic limb movement disorder (PLMD), and circadian rhythm disorders are
common in children with primary OSA. These sleep problems may be secondary to the OSA
(sleep fragmentation related to arousals resulting in more nightwakings) or exist indepen-
dently. These comorbid sleep problems are important to identify as they may add signif cantly
to the adverse consequences of OSA; alternatively, failure to address these sleep issues may
compromise treatment success.
eVAl uAt io n
Evaluation for OSA includes taking a history of signs and symptoms, physical examination, and
overnight polysomnography (PSG). It is important to note that no constellation of symptoms and
physical f ndings has been found that reliably distinguishes OSA from primary snoring. Although
a number of pediatric SDB screening questionnaires exist, these are largely used for clinical re-
search purposes and are less useful for diagnosis in individual clinical situations.
n Medical history: Both medical risk factors for and medical sequelae of OSA may be pres-
ent. The history is often positive for both upper airway (chronic sinusitis) and lower airway
(asthma) disease, allergies, and frequent upper respiratory infections. There may be a history
of frequent episodes of streptococcal pharyngitis or tonsillitis. Symptoms that are suggestive
of gastroesophageal ref ux (heartburn, vomiting) should also be elicited.
n Developmental and school history: Although the developmental and school history may be
normal, there is commonly a history of signif cant academic concerns as well as attentional
and learning problems. Certain syndromes with developmental delay as a prominent feature
(e.g., Down syndrome, Prader-Willi syndrome) are associated with increased risk for OSA.
n Family history: A history of chronic loud snoring as well as diagnosed OSA is often reported
in family members.
n Behavioral assessment: Evaluation of behavioral and mood concerns is key in assessing the
extent of daytime sleepinessrelated sequelae.
n Physical examination: In many cases, the physical examination of children with SDB is com-
pletely normal. However, the primary care clinician should assess for the following:
n Growth: (including being overweight and obesity) as well as failure to thrive (especially in
younger children).
n HEENT (head, eyes, ears, nose, throat):
Facial structure, including adenoidal facies midface hypoplasia; retrognathia and mi-
crognathia are best appreciated by inspection of the lateral facial prof le.
Signs of atopy, including allergic shiners, nasal crease (allergic salute), and eczema.
Nasal passage patency, including asymmetry of the nares and septal deviation, mucosal
thickening, edematous turbinates, and the presence of nasal polyps.
Hyponasality, which can be determined by asking the child to repeat Mickey Mouse,
99, or my name is money while occluding the nose; a child with signif cant nasal
obstruction will sound the same with occlusion as without.
Mouth breathing, which may indicate enlarged adenoids and/or chronic congestion.
Oropharyngeal examination, including tongue size, palatal integrity, presence of a
high-arched, narrow, elongated, or low dependent palate, uvular size, position, and shape
t ABl e 14.2. Diagnostic criteria: Pediatric obstructive sleep apnea (327.23)
A. The caregiver reports snoring, labored, or obstructed breathing or both snoring and labored or
obstructed breathing during the childs sleep.
B. The caregiver of the child reports observing at least one of the following:
1. Paradoxical inward rib-cage motion during inspiration
2. Movement arousals
3. Diaphoresis
4. Neck hypertension during sleep
5. Excessive daytime sleepiness, hyperactivity, or aggressive behavior
6. Morning headaches
7. Secondary enuresis
C. Polysomnographic recording demonstrates one or more scoreable respiratory events per hour (i.e.,
apnea or hypopnea of at least two respiratory cycles in duration).
Note: Very few normative data are available for hypopneas, and the data that are available have been
obtained using a variety of methodologies. These criteria may be modif ed in the future once more
comprehensive data become available.
D. Polysomnographic recording demonstrates either 1 or 2.
1. At least one of the following is observed:
a. Frequent arousals from sleep associated with increased respiratory effort
b. Arterial oxygen desaturation in association with the apneic episodes
c. Hypercapnia during sleep
d. Markedly negative esophageal pressure swings
2. Periods of hypercapnia, desaturation, or hypercapnia and desaturation during sleep associated
with snoring, paradoxical inward rib-cage motion during inspiration, and at least one of the fol-
lowing:
a. Frequent arousals from sleep
b. Markedly negative esophageal pressure swings
E. The disorder is not better explained by another current sleep disorder, medical or neurological
disorder, medication use, or substance use disorder.
(e.g., bifed which may be associated with submucosal cleft palate), tonsillar size, and
posterior pharyngeal space (Figure 14.1).
n Neck examination, including assessing for thyromegaly, as hypothyroidism appears to be
a risk factor for OSA, at least in adults. Neck circumference is one of the best predictors of
OSA in adults, although similar studies have not been conducted in prepubertal children.
n Cardiac examination, including systemic hypertension (although less common in children
than in adults with OSA), signs of pulmonary hypertension (e.g., loud second pulmonary
heart sound), and, in severe cases, cor pulmonale. Fortunately, these signs of severe OSA are
now rarely seen.
n Diagnostic Tests
For the most part, laboratory studies are unnecessary in OSA, although in severe cases evi-
dence of polycythemia on complete blood count and/or compensatory metabolic alkalosis
associated with chronic hypoventilation may be noted.
Radiologic Studies and Electrocardiography

n An upright lateral neck x-ray to evaluate for hypertrophy of the tonsils and adenoids and upper
airway patency is frequently quite helpful. Cephalometric radiographs, computerized tomog-
raphy, and magnetic resonance imaging may be helpful in assessing the upper airway structure
in children with craniofacial anomalies, but are generally not necessary in typically develop-
ing children.
n Endoscopy and laryngoscopy of the upper airway is generally reserved for children with com-
plicated craniofacial anatomy.
n In cases of severe OSA, there may be evidence of right ventricular hypertrophy on chest x-ray.
The electrocardiogram (ECG) may also show evidence of right ventricular enlargement.
Polysomnography: The Gold Standard

At the present time, given that the only way to make a def nitive diagnosis and assess the severity
of OSA is with overnight PSG, a sleep study should ideally be performed on every child with
signif cant nocturnal and diurnal symptoms and risk factors for OSA (see Chapter 4 for more
Why a Sleep Study?

Although history and physical examination are important in making the diagnosis of obstruc-
tive sleep apnea (OSA) in children, no combination of symptoms and physical f ndings has
been found that reliably distinguishes OSA from primary snoring. Overnight polysomnogra-
phy (PSG), performed in an accredited sleep laboratory by technicians skilled in working with
children and interpreted by a sleep medicine physician with pediatric experience, remains the
diagnostic gold standard. PSG is also important as a baseline measure for children with ad-
ditional risk factors in whom OSA is not likely to completely resolve with adenotonsillectomy
alone.
Fig 14.1. Grading tonsillar size.

information on overnight PSG). PSG is also important as a baseline measure for children with
additional risk factors in whom OSA is not likely to completely resolve with adenotonsillectomy
alone (e.g., obesity, craniofacial anomalies), and who therefore may need a follow-up postopera-
tive sleep study.
American Thoracic Societys Indications for Cardiopulmonary Sleep Studies

in Children
Differentiate benign snoring from snoring associated with sleep-disordered breathing.
Assess severity of obstructive sleep apnea (OSA).
Clarify diagnosis when symptoms and risk factors are discordant.
Screen children at high risk for OSA (e.g., Down syndrome, achondroplasia).
Delineate severity of OSA in children at risk for peri- and postoperative symptoms.
Titrate continuous positive airway pressure in children with diagnosed OSA.
Overnight PSG should be performed in an accredited sleep laboratory by technicians skilled in

working with children and interpreted by a sleep medicine physician with pediatric experience.
Required channels include those for sleep staging, arousal measurement, cardiovascular param-
eters, and body movements (electroencephalography [EEG], electrooculography [EOG], chin
and leg electromyography [EMG], electrocardiography [ECG], body position sensors, and video
recording), and a combination of breathing monitors (oronasal thermal sensor and nasal air pres-
sure transducer for airf ow, chest and abdominal monitors (e.g., inductance plethysmography) for
respiratory effort, pulse oximeter for O2 saturation, end-tidal or transcutaneous CO2 for hypercar-
bia, snore microphone). Home monitoring with modif ed versions of this montage is becoming
increasingly common in adults, but little data exist in regards to its feasibility and validity in
children. Other screening studies (home audiotaping or videotaping, overnight oximetry) thus
far appear to have limited usefulness in children, as do shortened PSG or nap studies, because
they are likely to underestimate the presence and severity of disease. These types of studies are
helpful if the results are positive (high positive predictive value) but warrant corroboration with a
standard overnight sleep study if the results are negative (low negative predictive value).
Transesophageal balloon manometry is performed in some sleep laboratories to detect upper
airway resistance syndrome, especially in the face of signif cant OSA symptoms with a normal
sleep study. However, esophageal pressure monitoring is expensive and often not well tolerated
by children; thus, it is not currently considered a standard part of the overnight sleep study evalu-
ation. Furthermore, newer techniques to detect arousals, such as pulse transit time and cyclic
alternating patterns on EEG, may be more sensitive indicators of sleep fragmentation in children
and better predictors of neurocognitive outcomes.
The PSG parameter most commonly used in evaluating for SDB is the apnea-hypopnea in-
dex (AHI), which indicates the number of apneic and hypopneic events per hour of sleep. Fig-
ure 14.2 depicts an apneic event with a consequent decrease in oxygen saturation. The total AHI
includes central events (which may normally occur during sleep at all ages, especially in REM
sleep, and at the transition from wake to sleep or from one sleep stage to another) as well as mixed
and obstructive events. The apnea index (AI) is the number of apneic-only events per hour. The
sleep stage distribution of events (often signif cantly increased during REM sleep) and relation-
ship to sleeping position (frequently increased in the supine position) should also be noted; for
example, if the child has a less than expected amount of REM sleep for age (typically 20% to
25%) on the night of the study and/or does not spend much time sleeping in the supine position,
the AHI may underestimate the severity of OSA.
The arousal index (total number of arousals per hour of sleep) and the respiratory arousal
index (arousals related to respiratory events) are also important as indicators of the degree of
sleep fragmentation, although children are less likely than adults to have arousals accompanying
respiratory events. Many laboratories also include measurement of respiratory eventrelated

arousals (RERAs) that do not meet full criteria for apneas or hypopneas with arousal but may
indicate evidence of signif cant sleep fragmentation. The AHI and RERAs may be reported to-
gether as the respiratory disturbance index.
It should be noted that currently there are no universally accepted PSG normal reference
values and parameters for diagnosing OSA in children, and it is still unclear which parameters
best predict morbidity. Therefore, the following def nitions are based on commonly used criteria:
n AHI >1.5 or AI >1: Unlike in adults, obstructive apneas in normal children are rare; therefore,
most pediatric sleep specialists consider an AI >1 to be abnormal. Because several studies
have now suggested that normal preschool-aged and early school-aged children have a total
AHI of less than 1.5, this is the most widely used cut-off value for OSA in children ages 12
years and below; in adolescents, the adult cut-off of an AHI 5 is generally used. In cases in
which the AHI is between 1 and 5 obstructive events per hour, clinical judgment regarding risk
factors for SDB, evidence of daytime sequelae, and the technical quality of the overnight sleep
study should determine further management. In some cases, it may be prudent to consider re-
peating the sleep study if the clinical index of suspicion remains high in the face of a negative
study.
n O2 desaturation nadir <91%.
n Change in nadir O2 from baseline >9%.
n Maximal end-tidal CO2 >54.
n Increased end-tidal CO2 >45 torr for >46% of total sleep time.
Fig . 14.2. Obstructive sleep apnea. , initiation apneic event; , oxygen resaturation.

n Upper airway obstruction without sleep-related ventilatory abnormalities may be related
to laryngomalacia, vascular rings, or gastroesophageal ref ux.
n Nocturnal respiratory disturbances accompanied by ventilatory abnormalities (e.g., hypox-
emia, hypercarbia) during sleep can be due to central hypoventilation syndromes or asthma.
n Sleep related movements mimicking OSA-related gasping and arousals may occur with noc-
turnal seizures; periodic limb movements during sleep may occur in association with apneas
or hypopneas.
n Excessive daytime sleepiness and neurocognitive def cits can result from many other sleep
disorders, including narcolepsy, idiopathic hypersomnolence, insuff cient sleep syndrome, and
PLMD. Daytime sleepiness can also be related to psychiatric disorders, such as depression,
medical conditions, and drug therapy.
MAn Ag eMen t
w hen to r efer
When there are straightforward OSA symptoms (e.g., snoring, apneic pauses) with clear-cut
risk factors (e.g., adenotonsillar hypertrophy) in an otherwise healthy child, the primary care
pediatrician may be comfortable referring for an overnight sleep study and reviewing the results.
However, in cases in which there are additional risk factors (e.g., obesity, congenital syndromes),
evidence of severe disease (e.g., growth failure, signif cant neurobehavioral sequelae), or other
complicating factors (e.g., underlying medical conditions), consultation with a sleep center that
has pediatric expertise is warranted. In addition, children who are candidates for continuous posi-
tive airway pressure (CPAP) treatment should be referred to a pediatric sleep center.
t reatment
There are presently no universally accepted guidelines regarding the indications for treatment
of pediatric SDB (including primary snoring, upper airway resistance syndrome, and OSA), and
current recommendations largely emphasize weighing what is known about the potential cardio-
vascular, metabolic, and neurocognitive sequelae of SDB in children in combination with the
individual healthcare professionals clinical judgment. The decision of whether and how to treat
OSA specif cally in children is contingent on a number of parameters, including severity (noc-
turnal symptoms, daytime sequelae, sleep study results), duration of disease, and individual
patient variables, such as age, comorbid conditions, and underlying etiologic factors.
In the case of moderate to severe disease (AHI >10), the decision to treat is usually straight-
forward, and most pediatric sleep experts recommend that any child with an AI >5 should be
treated.
There is less of a consensus regarding the need for intervention in children with an AHI
between 1 and 5. However, it should be emphasized that most studies have failed to f nd a dose-
response relationship between PSGderived parameters of OSA disease severity and cognitive
and behavioral problems. Furthermore, several recent studies have found neurobehavioral def -
cits associated with primary snoring in children that are similar to those found in children with
OSA. Thus, although absolute numbers as def ned above in terms of PSG parameters (e.g., AHI,
O2 desaturation) are very helpful in delineating disease severity, intervention with children who
have subclinical PSG values but who also have evidence of daytime sequelae, should also be
strongly considered. Ongoing studies focused on delineating additional characteristics of chil-
dren at relatively higher risk for developing neurocognitive and/or cardiovascular sequelae with
SDB will hopefully guide more specif c treatment guidelines in the future.
Treatment Options
n Adenotonsillectomy is the most common treatment for pediatric OSA. It is the f rst-line treat-
ment in any child with signif cant adenotonsillar hypertrophy, even in the presence of ad-
ditional risk factors such as obesity. Adenotonsillectomy in uncomplicated cases generally

(70% to 90% of children) results in complete resolution of symptoms, although studies have
indicated that about 50% of obese children have evidence of residual OSA post-adenotonsil-
lectomy. Removal of both the tonsils and adenoids has been shown to be more effective than
either alone and in most cases is recommended to avoid recurrence of symptoms, even if one
appears to be the primary abnormality. Regrowth of adenoidal tissue after surgical removal
also occurs in some cases (as much as 10%15%).
Peri- and postoperative complications, especially respiratory compromise, appear to be
more common in general in children with OSA. Other potential complications include hemor-
rhage, pain, and poor oral intake with dehydration. Groups considered high risk include young
children (younger than age 3 years) as well as those with severe OSA documented on PSG;
signif cant clinical sequelae of OSA (e.g., failure to thrive); or associated medical conditions,
such as craniofacial syndromes, morbid obesity, and hypotonia. Relative contraindications to
adenotonsillectomy include children with cleft palate and velopharyngeal insuff ciency, as
well as submucous cleft.
Both the surgeon and the anesthesiologist should be provided with information about the
childs OSA, as well as with the results of the sleep study. Careful postoperative monitoring
is recommended for children with OSA. Some centers have adopted a policy that all children
undergoing adenotonsillectomy for OSA should be monitored overnight, as the immediate
postoperative period may not have adequate REM sleep in which to observe worsening of any
ventilatory abnormalities. Children with severe disease or medical complications may require
overnight monitoring in an intensive care setting.
Due to postoperative edema, OSA symptoms may take 6 to 8 weeks to completely resolve.
All patients should be reevaluated postoperatively to determine whether additional evaluation
and/or treatment are required. If there are signif cant residual risk factors (e.g., obesity) or con-
tinued symptoms of OSA, a follow-up sleep study at least 6 weeks post-adenotonsillectomy
may be indicated.
n Radiofrequency treatment of enlarged turbinates in appropriate patients may be helpful
when performed in conjunction with adenotonsillectomy. Surgical treatment for nasal septal
deviation may also be effective in selected cases.
n Other surgical procedures are seldom performed in children but may be indicated in selected
cases. These include epiglottoplasty, uvulopharyngopalatoplasty, and maxillofacial surgery
(mandibular distraction osteogenesis and maxillomandibular advancement). Tracheotomy is
rarely indicated, except in the case of severe, life-threatening OSA.
n CPAP and bilevel positive airway pressure (BiPAP): These are the most common treatments
for OSA in adults. CPAP is a noninvasive method of providing distending pressure to maintain
a patent upper airway. CPAP can be used successfully with children and adolescents, even chil-
dren as young as 1 year old. It should be considered a palliative rather than a curative therapy,
and may be needed for a prolonged period of time. CPAP may be indicated in the following
clinical situations:
n When adenotonsillectomy is not indicated or contraindicated.
n When adenotonsillectomy fails to completely resolve symptoms, usually in children with
additional risk factors such as obesity, craniofacial anomalies, or Down syndrome.

n Prior to surgery in children with severe OSA.
CPAP involves the use of a nasal or full-face interface that is securely attached to the head.
A full-face mask is often used when the patient is a mouth breather to prevent air escape;
however, there may be an increased risk of aspiration in children with full-face masks. It is
important to ensure a tight seal without air leaks; a chin strap may be added to prevent air leaks
through the mouth. Optimal pressure settings (that abolish or signif cantly reduce obstructive
events without increasing arousals or central apneas) are determined in the sleep laboratory
during a full-night CPAP titration. Eff cacy studies at the current pressure and retitrations
should be conducted periodically with long-term use (every 6 months in young children and at
least yearly or with signif cant weight changes in older children and adolescents). Side effects
of CPAP use are generally minimal and include nasal congestion, dryness, and rhinorrhea;
eye irritation; and facial dermatitis. Patients may complain of feelings of claustrophobia and
diff culty exhaling. Adding warmed and humidif ed air and slowly increasing pressure over a
10-minute to 20-minute period (ramp time) may alleviate some of these side effects. Poten-
tial exacerbation of craniofacial abnormalities with long-term use in young children has been
raised as a concern. In situations in which these problems prevent successful usage, BiPAP
(which allows an expiratory pressure to be set at a lower level than inspiratory pressure) may
be better tolerated.
Compliance with CPAP is a key factor in determining success. Adolescents pose a particu-
lar challenge. But even children with signif cant developmental delays or Down syndrome
can be successful CPAP users. It may be helpful to set up a behavioral program utilizing such
techniques as positive reinforcement, training parents to manage resistant behavior, modeling,
desensitization, and shaping in coordination with a behavioral therapist. For many children,
the dramatic improvement in quality of life with CPAP use is an important motivating factor
for continued use.
n Weight management: Weight management, including nutritional, exercise, and behavioral
components should be strongly encouraged for all children with OSA who are overweight or
obese. Children with insuff cient sleep are at increased risk for obesity, so interventions tar-
geted towards assuring adequate sleep duration may be helpful in reducing weight-related risk
for OSA. Signif cantly compromised obese patients may benef t from an inpatient weight loss
program; bariatric surgery may be considered in morbidly obese adolescents with severe OSA.
n Medications: Nasal decongestants and nasal steroids may be appropriate in cases in which
nasal congestion and/or mild adenoidal hypertrophy are contributing factors. Several studies
have demonstrated that intranasal corticosteroids reduce nasal airway obstruction and improve
parameters of OSA (e.g., AHI) in children. Recent studies have also suggested that leukotriene
inhibitors, such as montelukast, may be a therapeutic option in children with mild or residual
OSA.
n Avoidance of sedating agents and environmental triggers: Sedating agents, medications
containing alcohol, and medications with respiratory depressant effects should be avoided as
they may exacerbate OSA (see also Chapter 20). Exposure to environmental tobacco smoke
and other pollutants should also be avoided.
n Oral appliances: Mandibular advancing devices and tongue retainers are typically considered
for adolescents in whom facial bone growth is largely complete. However, rapid maxillary
expansion, a procedure that uses active expansion of a f xed oral appliance to increase the
transversal diameter of the hard palate over a 6- to 12-month period, has been used success-
fully in children with OSA as young as 6 years old. Referral to an orthodontist specializing in
these devices is indicated in these situations.
n Positional therapy: This can be used as an adjunct measure in some patients with mild OSA
or primary snoring in whom obstructive events are worse in the supine position. A tennis ball
or other f rm ball may be sewn into the pocket of a pajama top or tee-shirt that is worn back-
wards, preventing the child from sleeping in the supine position.
n Snore aids: External nasal dilator strips and nasal sprays have not been shown to have con-
sistent benef t in adults with OSA and have not been studied in children.
n Supplemental oxygen therapy: This is seldom warranted in children with OSA, unless there
are special circumstances. In fact, oxygen therapy may worsen hypoventilation.
Pr o g n o SiS
Studies that have looked at changes in behavior and neuropsychological functioning in children
following treatment (usually adenotonsillectomy) for OSA have largely documented signif cant
improvement in outcomes, both in the short and long term; these include daytime sleepiness,
mood, behavior, academics, and quality of life. However, because many studies have failed to
f nd a dose-dependent relationship between OSA in children and specif c neurobehavioral and

neurocognitive def cits, this has led to speculation that other factors, including individual genetic
susceptibility; environmental inf uences such as passive smoking exposure; and co-morbid con-
ditions, such as obesity, shortened sleep duration, and the presence of other sleep disorders, may
also inf uence neurocognitive outcomes.
Little is known about the spontaneous remission in untreated or partially treated children with
OSA, although the small amount of data available suggest that children with abnormal f nd-
ings on PSG are likely to continue to have these abnormalities if untreated. Longitudinal studies
also suggest that a signif cant percentage (40% to 50%) of children with habitual snoring will
continue to snore at follow-up several years later, while a much smaller percent (4% to 5%) will
initiate snoring during that period. Furthermore, the long-term neurobehavioral consequences of
untreated SDB have not been well studied.
Finally, children with OSA initially treated successfully with adenotonsillectomy may rede-
velop symptoms as older children or adolescents. Risk factors for recurrence of OSA after ad-
enotonsillectomy include obesity, gain velocity in BMI, and African-American race, as well as
persistent obstructive factors such as enlarged turbinates and septal deviation. Children with
OSA may also be predisposed to redevelop the condition as adults, although no long-term pro-
spective studies have been done.

Explain what obstructive sleep apnea (OSA) syndrome is in simple terms, including the
interaction between a childs narrow airway and obstructive elements (e.g., adenotonsillar
hypertrophy) on the one hand and the upper airway muscles that work to keep the airway
open on the other. Also discuss the associated sleep disruption (a good analogy for frequent
arousals is like being poked in the arm every few seconds while you are asleep) and the
subsequent effects of sleep fragmentation on daytime functioning.
Reassure parents who worry that their child will stop breathing during the night. Inform
parents that the brains respiratory control centers will respond to breathing pauses by re-
starting the breathing process.
Explain risk factors for OSA, primarily enlarged tonsils and adenoids. Discuss the poten-
tial role of other risk factors such as chronic allergies and asthma. If the child is signif cantly
overweight, address the issue up front.
Review the daytime consequences of OSA because parents may not attribute hyperactivity,
inattention, moodiness, or poor school performance, for example, to a sleep problem.
Explain what to expect from the overnight sleep study because it is particularly important
to directly address any concerns the child may have (e.g., Can my mom stay with me?
Are there any needles?) and to answer any parental questions regarding the procedure.
Review the results of the overnight sleep study as it is important to ask parents if the
childs breathing was typical on the night of the study. Parents frequently report that their
child slept much better compared to at home, which may be due to the absence of allergic
triggers in the lab. Explain the signif cance of breathing pauses and dips in oxygen level,
and put the numbers in context (e.g., Adults must have at least 5 breathing pauses per hour
to be diagnosed with sleep apnea, but in children we use a lower threshold of 12 pauses per
hour).
Discuss the risks and benef ts of treatment options including adenotonsillectomy, weight
loss, and other treatment choices.
Encourage any parent who snores loudly and has daytime symptoms to be evaluated for
sleep apnea.
See Appendix D10 for a parent handout on OSA and Appendix D11 for a handout on Your
Childs Sleep study.
Restless Legs Syndrome
15 and Periodic Limb
movement Disorder
Restless legs syndrome (RLS) is a neurological, primarily sensory disorder, characterized by

uncomfortable sensations in the lower extremities that are accompanied by an almost irresistible
urge to move the legs. These subjective uncomfortable and unpleasant sensations (dysasthesias)
occur primarily in the legs, although sometimes in the arms. Other body parts (e.g., arms) can
also be involved. The sensations and the urge to move are usually at least partially relieved by
movement, including walking, rocking, shaking, stretching, and rubbing, but only as long as the
motion continues. Most episodes begin or are exacerbated by rest or inactivity, such as lying in
bed to fall asleep or riding in a car for prolonged periods. Both the likelihood of having symptoms
and the severity of symptoms tend to increase with the duration of inactivity. A unique feature
of RLS is that the timing of symptoms also appears to have a circadian component, in that they
often peak in the evening hours. Some patients with RLS, however, do not describe a signif cant
sensory component, but instead experience the urge to move the legs and f dgetiness during pe-
riods of rest as the primary presenting symptom. RLS is a clinical diagnosis that is based on the
presence of these key symptoms.
In RLS, the conditions under which the symptoms are most likely to occur are also the same
conditions that promote sleep initiation (at night, during periods of inactivity, and rest). Con-
versely, the behaviors that relieve symptoms (physical activity and motion) are those most likely
to interfere with sleep onset. In young children in particular, parents may interpret these behav-
iors as bedtime resistance and refusal.
Restless Legs Syndrome

Restless legs syndrome is a clinical diagnosis, characterized by uncomfortable sensations in
the lower extremities accompanied by an urge to move the legs. Symptoms typically occur
during periods of inactivity and are worse, or exclusively present, at night. The discomfort is
temporarily relieved by increased movement of the legs. A common presenting complaint by
parents of children with RLS is bedtime resistance and diff culty falling asleep.
Periodic limb movement disorder (PLMD) is characterized by periodic, repetitive, brief (0.5
10 seconds), and highly stereotyped limb jerks typically occurring at 20- to 40-second intervals.
These movements occur primarily during sleep, although some patients have PLMs during wake
periods as well. Although upper extremities may also be affected, these movements most com-
monly occur in the legs and commonly consist of rhythmic extension of the big toe and dorsi-
f exion at the ankle. In contrast to patients with RLS, individuals with PLMs are usually unaware
of these movements; however, these movements may result in arousals during sleep and conse-
quent signif cant sleep disruption. The diagnosis of periodic limb movements requires overnight
polysomnography (PSG) to document the characteristic limb movements with anterior tibialis
electromyography (EMG) leads. The diagnosis of PLM disorder requires a minimum number of
limb movements per hour (5 in children) in the presence of a clinically signif cant sleep distur-
bance or complaint of daytime fatigue (e.g., nonrestorative sleep). Finally, it should be noted that
occasional PLMs that occur primarily or exclusively in association with other conditions, such
as sleep apnea, narcolepsy, or antidepressant use in adults, are considered by some to be a non-
specif c EMG f nding of unclear clinical signif cance.
116
RESTLESS LEGS SyNDROmE AND PERIODIC LImB mOvEmENT DISORDER 117
Periodic Limb Movements and Periodic Limb Movement Disorder

Periodic limb movements (PLMs) are characterized by periodic episodes of brief, repetitive,
and stereotypic limb movements during sleep, detectable on overnight polysomnography, and
which may be associated with a partial arousal or an awakening. A diagnosis of periodic limb
movement disorder requires a minimum number of PLMs (5 per hour in children) accompa-
nied by clinically signif cant sleep disruption and/or daytime sequelae.
Because RLS and PLMD appear to share a common underlying pathophysiology in regards to
dopaminergic dysfunction in the central nervous system (CNS), they often occur concomitantly
and result in sleep disruption (sleep onset delay in RLS and sleep fragmentation in PLMD). Al-
though similar studies have not been conducted with children or adolescents, f ndings in adults
indicate that 70% to 90% of adults with RLS have PLMs. Recent genetic evidence suggests that
comorbid RLS with PLMs may be a distinct phenotype from RLS alone. Conversely, the pres-
ence of PLMs on overnight PSG is supportive of (although not necessary for) the diagnosis of
RLS in both adults and children. Thus, although they are clinically distinct entities, these two
related sleep disorders are typically discussed together.
Although there has been substantial progress in our understanding of the biological basis,
epidemiology, genetics, and clinical management of RLS and PLMD over the past decade, many
questions remain. Furthermore, it is important to note that these two disorders have only been
recently recognized in children and adolescents. For example, consensus criteria for the diag-
nosis of RLS in children and adolescents were f rst published in 2003 (see Tables 15.3 to 15.5),
and there are currently no approved medications for the treatment of pediatric RLS and PLMs.
Recent investigations indicate that both of these disorders are much more common in adults than
previously thought, and the same is likely true in children and adolescents. Therefore, pediatric
practitioners should consider RLS and PLMD in the differential diagnosis for any sleep problem
presentation that includes signif cant diff culties falling asleep as well as nighttime awakenings
with restless sleep or unexplained symptoms of daytime somnolence, including neurobehavioral
symptoms (e.g., inattentiveness, irritability).
ePiDeMio l o g y
r estless l egs Syndrome
n Adults: Both RLS and PLMD are common disorders in adults, although signif cantly under-
diagnosed. In adults, the prevalence of RLS is estimated to be 5% to 10%, with about 3% of
patients having frequent and/or moderate to severe symptoms. Furthermore, a history of child-
hood onset (before the age of 10 years) is present in approximately 18% of adults with RLS,
while 25% of adults recall the onset of symptoms in the second decade of life.
n Pediatrics: Previous studies have examined the prevalence of RLS symptoms in a number
of different pediatric populations, using a variety of RLS def nitions, with prevalence rates
ranging from 1% to 6%. A recent large telephone survey study (pediatric REST study) of
over 10,000 families in the United States and the United Kingdom, using the 2003 National
Institute of Health pediatric RLS consensus criteria, found a prevalence of def nite RLS in
about 2% in both 8- to 11-year-olds and 12- to 17-year-olds; this represents some 980,000
school-aged children in the United States. One-quarter to one-half of these patients had mod-
erate to severe symptoms. In contrast to a female preponderance (2:1) in adult RLS, there does
not appear to be a gender difference in pediatric RLS.
Periodic l imb Movement Disorder

n Adults: The prevalence of PLMs in adults appears to be positively correlated with age (4% to
11% of adults ages 30 to 50 years, and 25% to 58% in the elderly).
n Pediatrics: Because a def nitive diagnosis requires PSG, there are fewer data regarding the
prevalence of PLMs in childhood.
n Prevalence rates of PLMs greater than 5 per hour in clinical populations of children referred
for sleep studies range from 5% to 27%; in survey studies of PLM symptoms, rates are be-
tween 8% and 12%.
n Several studies in referral populations have found that PLMs occur in as much as one-fourth
of children diagnosed with attention def cit hyperactivity disorder (ADHD). Other recent
studies have found an association between symptoms of hyperactivity and the presence of
PLMs; however, the prevalence of PLMD in the general population of children with ADHD
is unknown.
n PLMs appear to be more prevalent in Caucasian children than in African-American chil-
dren.
n Genetic link: Overall, it is estimated that 50% to 60% of adult RLS patients have a positive
family history. Early-onset RLS (i.e., onset of symptoms before 35 to 40 years of age), often
termed primary RLS, appears to have a particularly strong genetic component. It is esti-
mated that 40% to 92% of these cases are familial, and the prevalence of RLS in f rst-degree
relatives of patients with early-onset RLS appears to be 6 to 7 times that of the general popula-
tion. In the population-based REST study, between 70% and 80% of children with def nite
RLS had at least one biological parent with RLS and 16% had both parents affected. The
mode of inheritance was previously postulated to involve predominantly autosomal-dominant
or pseudodominant autosomal recessive patterns, but a more complex genetic schema is likely.
Although a number of genetic loci, such as the BTBD9 locus on chromosome 6p, have been
identif ed in large population studies, no candidate gene has been discovered, and there may
be different genotypes for various phenotypic manifestations of RLS and/or PLMs. Environ-
mental factors such as iron def ciency (see below) may also play a role in familial RLS.
n Sleep deprivation: Whether from poor sleep hygiene, late bedtimes, or an underlying sleep
disrupter (e.g., sleep apnea), sleep deprivation can exacerbate RLS symptoms.
n Medical conditions: What has traditionally been referred to as secondary RLS can occur in
relation to a number of different medical conditions. In secondary cases, the symptoms gen-
erally remit when the underlying condition has resolved. These include (some of which have
only been reported in adults):
n Iron def ciency, as a number of studies have implicated low iron in both adults and children
as an important etiologic factor for the presence and severity of both RLS symptoms and
PLMs. For example, magnetic resonance imaging (MRI) studies in adults with RLS have
demonstrated decreased iron stores in a number of regions in the CNS, including the basal
ganglia, putamen, and substantia nigra, irrespective of body iron stores. The postulated un-
derlying mechanism is related to the role of iron as a co-factor of tyrosine hydroxylase in a
rate-limiting step of the synthesis of dopamine; in turn, dopaminergic dysfunction has been
implicated as playing a key role, particularly in the genesis of the sensory component of
RLS. In addition, there are multiple other possible mechanisms for the effect of low iron on
dopamine. Recent studies have also explored potential roles for abnormalities in a number
of proteins and pathways involved in iron metabolism and storage, including transferrin re-
ceptor expression, ferritin subunits, hepcidin, and ferroportin. It should be noted, however,
that low iron is not universally present in patients with RLS; conversely, many children with
iron def ciency do not have RLS symptoms.
As a marker of decreased iron stores, serum ferritin levels in both children and adults
with RLS are commonly low. Several pediatric case series have suggested that lower-than-
normal ferritin levels (def ned as <50 ng/ml) are found in some 70% to 75% of children
with RLS. Other recent studies have suggested that children with RLS symptoms and
ADHD may be at particularly high risk for very low serum ferritin levels (<12 ng/ml). A
number of studies have suggested that a ferritin level below 50 ng/ml increases the risk of
RLS and is typically the threshold used to determine treatment with iron supplementation.
The threshold at which low iron stores appear to have a signif cant impact seems to be
different for peripheral versus central nervous system effects, for example, a reduction in
hemoglobin synthesis typically occurs only when ferritin levels drop below 12 ng/ml. Thus,
low iron can exacerbate RLS symptoms in the face of normal hemoglobin and hematocrit
levels. In addition, because ferritin is an acute phase reactant, elevated serum levels may
occur with systemic inf ammatory and metabolic processes, such as diabetes, and with con-
current illness. Therefore, a ferritin level within or above the normal range in the face of an
upper respiratory infection in a child, for example, does not necessarily indicate normal iron
stores, and the level should be repeated once the infection has resolved.
Serum Ferritin Levels

Although it may still be considered in the normal range, studies suggest that a ferritin level
below 50 ng/ml in a child or adolescent with restless legs syndrome or periodic limb move-
ment disorder warrants treatment with iron supplementation.
n Neurologic disorders, including polyneuropathy, lumbosacral radiculopathy, and myelopa-

thy.
n Medical disorders, such as diabetes mellitus, end-stage renal disease, cancer, peripheral
vascular disease, rheumatoid arthritis, and hypothyroidism. RLS appears to be more com-
mon in pediatric patients on dialysis. A few case reports have also suggested that RLS
symptoms may occur concurrently in children with a variety of infectious processes (i.e.,
mycoplasma, Group A streptococcus).
n Pregnancy, as RLS occurs in up to 15% of pregnant women, most commonly after the 20th
week in association with decreased iron levels. Some women (approximately 1 in 7) who
develop RLS in pregnancy continue to have symptoms postpartum.
n Medications, especially antihistamines such as diphenhydramine. Other medications
that may exacerbate RLS include antidepressants (selective serotonin reuptake inhibitors
[SSRIs], mirtazapine, and tricyclic antidepressants [TCAs]); neuroleptics; sedatives or nar-
cotics (withdrawal from); lithium; calcium channel blockers; H-2 blockers, such as cimeti-
dine; phenytoin; and dopamine receptor blockers (antiemetics such as prochlorperazine,
metoclopramide).
n Caffeine, as the additional stimulation can exacerbate underlying RLS.
n Drugs and chemicals, as even sedating substances, such as alcohol, may increase RLS
symptoms.
Periodic l imb Movement Disorder

n Altered iron metabolism and iron storage and central dopaminergic dysfunction: Studies
in adults utilizing MRI and autopsy data, as well as treatment studies with intravenous and oral
iron, suggest that both altered iron metabolism and storage and central dopaminergic dysfunc-
tion are also likely to be involved in the pathophysiology of PLMD.
n Secondary PLMD: Similar to RLS, secondary PLMD can occur in association with underly-
ing medical, developmental, and neurological conditions as well as with use of specif c drugs
and comorbid sleep disorders. These include:
n Iron def ciency anemia.
n Metabolic disorders, including uremia.
n Childhood leukemia.
n Spinal cord injury, multiple-system atrophy.

n Williams syndrome, as both symptoms and PSG documentation of PLMs have been re-
ported to be more common in children with this developmental disorder.
n Medications, most notably SSRIs, as well as tricyclic antidepressants and atypical antide-
pressants such as venlafaxine. Withdrawal from other medications, including anticonvul-
sants, benzodiazepines, and hypnotics, can exacerbate PLMs.
n Obstructive sleep apnea (OSA), and associated arousals may be associated with PLMs in
both adults and children. In one pediatric study, 50% of prepubertal children with PLMs
also had OSA documented by overnight PSG; treatment of the sleep apnea (adenotonsil-
lectomy) resulted in resolution of the PLMs in 52% of these cases.
n Narcolepsy, may also be accompanied by PLMs during sleep.
The cardinal features of RLS in children are listed below (a screening questionnaire for RLS
is provided in Appendix B4), but it should be kept in mind that the initial complaint in the pri-
mary care setting may be frequently delayed sleep onset and/or daytime behavior or attention
problems, rather than RLS symptoms per se. Similarly, patients with PLMs rarely present with
a chief complaint of kicking movements during the night but parents may report restless sleep
and increased body movements during sleep. Table 15.1 provides common symptoms for RLS
and PLMD.

Sensory Complaints
Even relatively young children are often able to articulate and describe the sensory symptoms of
RLS. In clinical interviews, children will often use colorful descriptors such as ants crawling on
Common childhood symptoms of restless legs syndrome and periodic limb

t ABl e 15.1. movement disorder
Sleep symptoms:
Bedtime resistance and behavior problems
Diff culty falling asleep
Restless sleep and nighttime awakenings
Motor symptoms:
Walking, pacing, or running about at bedtime
Increased leg movements and/or restlessness at bedtime, during sleep, and with long periods of inac-
tivity
Sensory symptoms:
Leg pain or discomfort in the evening or during the night with periods of prolonged inactivity
Growing pains
Daytime symptoms:
Excessive daytime sleepiness or fatigue, including diff culty waking in the morning, falling asleep in
school or at inappropriate times, and increased need for naps
Mood changes, such as irritability, low frustration tolerance, mood swings, and depression and anxi-
ety
Acting out behaviors, including aggression, hyperactivity, oppositional or def ant behavior, and
impulsivity
Attention def cit hyperactivity syndrome symptoms: inattention, poor concentration, distractibility,
academic problems
my legs, soda bubbling through my veins, goose-bumps on the inside, tiny nails poking my
legs, and people wrestling in my legs. They may use terms like squeezing, tingling, wiggling,
itching, popping, funny feelings, shaking, tiredness, aching, or pulling and tugging of the legs.
The symptoms are sometimes described as specif cally painful, and younger children may use
more nonspecif c descriptors like hurting. It should be noted that in the off ce setting children
may not volunteer these symptoms without some (non-directive) prompting from the clinician.
Parents may be able to offer descriptions that their child has used at home, although at times par-
ents are surprised by their childs responses following questioning in the off ce.
Does anything bother you at bedtime?

It is often diff cult to ascertain symptoms consistent with restless legs syndrome (RLS) from
children and even adolescents. One of the best ways to elicit symptoms is to ask if anything
bothers the child or adolescent at bedtime. Other ways to f nd out include asking the non-
directive question, When you are trying to fall asleep at bedtime, does anything hurt, like
your tummy, your head, your arms, your legs? Children and adolescents with RLS will usu-
ally positively respond to the legs aspect of the question.
n Growing pains: Growing pains may be described as recurrent limb discomfort or pain
often occurring at bedtime and/or resulting in nightwakings and are a common complaint of
children. Although this childhood symptom has been shown to be associated both with con-
current pediatric RLS and PLMD and with later development of RLS symptoms in adulthood,
it appears to be fairly nonspecif c. For example, in the pediatric REST study, a history of
growing pains was reported in 77% to 85% of children and adolescents meeting diagnostic
criteria for RLS, but it was also found in 61% to 64% of subjects without RLS.
n Increased sensory symptoms with inactivity: Although no specif c body position is associ-
ated with RLS symptoms, the conditions most likely to provoke symptoms are long periods
of motor inactivity combined with decreased mental activity, such as lying in bed or long car
rides. In milder cases, symptoms may only be precipitated by long periods of inactivity (e.g.,
plane f ights). Some children may experience RLS symptoms during prolonged periods of sit-
ting in school.
n Urge to move: Many children with RLS can describe a subjective need to move their legs
(stretching, kicking) or their whole body, which may be distinct from perceiving that the move-
ments relieves the sensory symptoms. This urge is typically experienced as both unpleasant
and under limited voluntary control, somewhat analogous to the drive children may describe
immediately preceding motor tics. Some children simply run around without indicating the
need to move their legs. In addition to movement, some children and parents report that symp-
toms may also be relieved by counter-stimulation, such as rubbing or application of hot or cold
stimuli.
n Bedtime struggles and diff culty falling asleep: Because RLS symptoms are usually worse
in the evening, this is one of the most common presenting complaints. In particular, children
with RLS may attempt to avoid going to bed because lying still exacerbates their symptoms,
and this may be interpreted as bedtime resistance.
n Problems maintaining sleep: RLS may also occur during nightwakings. Sleep disturbance
was reported in signif cantly more RLS subjects (66% to 70%) in the pediatric REST study
compared to 34% to 44% of those without RLS. PLMs may also result in arousals or even
awakenings during the night.
n Restlessness and increased motor movements during sleep: Parents of children with RLS
and PLMD may complain that their child is a restless sleeper, moves around or even falls out
of bed during the night, or that the childs bedcovers are always disheveled in the morning.
Kicking, jerking, or twitching leg movements may be observed during sleep.
See Tables 15.2 to 15.5 for RLS. For clinical purposes, in terms of diagnosis and treatment,
children should meet diagnostic criteria for def nite RLS. The criteria for probable and pos-
sible RLS that are also included below are largely for research purposes, although they may help
identify children who will go on to develop full-blown RLS symptoms. For adolescents ages 13
to 18 years, adult RLS diagnostic criteria should be used.
See Table 15.6 for PLMD.
Diagnosis
The diagnosis of restless legs syndrome (RLS) is based solely on clinical history, whereas
periodic limb movement disorder (PLMD) requires objective documentation by an overnight
sleep study (polysomnography, PSG). However, because a high percentage of RLS patients
also have PLMD, the f nding of periodic limb movements on PSG is also supportive of the
diagnosis of RLS.
Associated Features
n Daytime sleepiness and daytime behavior problems: Sleep onset and sleep maintenance
diff culties related to RLS and/or PLMs that lead to reduced sleep time may result in daytime
sleepiness. However, explicit symptoms of excessive daytime sleepiness (e.g., diff culty wak-
ing in the morning, drowsiness) are relatively uncommon. More commonly, neurobehavioral
symptoms indicative of daytime sleepiness (e.g., inattentiveness, poor focusing) are the pre-
dominant daytime symptom described in association with RLS and PLMD. Behavior prob-
lems, including mood problems and oppositional def ant behavior, may also result from the
frequent nighttime arousals.
n Neuropsychiatric conditions: In particular, there is now a considerable body of evidence
linking ADHD symptoms to RLS and PLMs in both clinical (pediatric neurology, sleep, psy-
chiatric settings) and community-based pediatric populations, although it should be noted
that a number of these studies were conducted before the diagnostic criteria for pediatric RLS
were established in 2003. In general, RLS symptoms and PSG-documented PLMs are signif -
cantly more common in children diagnosed with ADHD or with symptoms of hyperactivity
and impulsivity. For example, a recent literature review reported that up to 44% of children
t ABl e 15.2. Diagnostic criteria: Restless legs syndrome (333.94)
Diagnosis in adult patients (older than age 12 years)

1. The patient reports an urge to move the legs, usually accompanied or caused by uncomfortable and
unpleasant sensations in the legs.
2. The urge to move or the unpleasant sensations begin or worsen during periods of rest or inactivity,
such as lying or sitting.
3. The urge to move or the unpleasant sensations are partially or totally relieved by movement, such as
walking or stretching, at least as long as the activity continues.
4. The urge to move or the unpleasant sensations are worse, or only occur, in the evening or night.
The condition is not better explained by another current sleep disorder, medical or neurological
disorder, mental disorder, medication use, or substance use disorder.
National Institutes of Health Workshop: Diagnostic criteria for def nite RLS
t ABl e 15.3. in children and adolescents 212 years old (2003)
The child meets all four essential adult criteria for restless legs syndrome (RLS):
1. An urge to move the legs.
2. The urge to move begins or worsens when sitting or lying down.
3. The urge to move is partially or totally relieved by movement.
4. The urge to move is worse in the evening or night than during the day or only occurs in the evening
or during the night.
Plus A or B:
A. The child relates a description in his or her own words that is consistent with leg discomfort. (The
child may use terms such as oowies, tickle, spiders, boo-boos, want to run, and a lot of
energy in my legs to describe symptoms. Use of age-appropriate descriptors is encouraged.)
B. Two of three following supportive criteria are met.
i. Sleep disturbance for age.
ii. A biological parent or sibling has def nite RLS.
iii. The child has a polysomnographically documented periodic limb movement syndrome index of
5 or more per hour of sleep.
Allen R, Picchietti D, Hening W, et al. Restless legs syndrome: Diagnostic criteria, special considerations, and
epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop to the National Insti-
tutes of Health. Sleep Med 2003;4:10119.
National Institutes of Health Workshop: Research criteria for probable RLS

t ABl e 15.4. in children and adolescents 018 years old (2003)
The child has a biological parent or sibling with def nite restless legs syndrome (RLS), plus A or B:
A. The child meets all three of the following essential adult criteria for RLS.
1. An urge to move the legs.
2. The urge to move begins or worsens when sitting or lying down.
3. The urge to move is partially or totally relieved by movement.
B. The child is observed to have behavior manifestations of lower-extremity discomfort when sitting
or lying, accompanied by motor movement of the affected limbs; the discomfort has characteris-
tics of adult criteria 2, 3, and 4 (i.e., is worse during rest and inactivity, relieved by movement, and
worse during the evening and at night).*
*This last category is intended for young children or cognitively impaired children, who do not have
suff cient language to describe the sensory component of RLS.
epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop to the National Insti-
tutes of Health. Sleep Med 2003;4:10119.
National Institutes for Health Workshop: Research criteria for possible RLS
t ABl e 15.5. in children and adolescents 018 years old for research (2003)
The child has periodic limb movement disorder (for the childhood def nition, please see Table 15.6).
And
The child has a biological parent or sibling with def nite restless legs syndrome (RLS), but the child
does not meet def nite or probable childhood RLS def nitions (as outlined above).
epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop to the National
Institutes of Health. Sleep Med 2003;4:10119.
t ABl e 15.6. Diagnostic criteria: Periodic limb movement disorder (327.51)
A. Polysomnography demonstrates repetitive, highly stereotyped, limb movements that are:

1. 0.5 to 5 seconds in duration.
2. Of amplitude greater than or equal to 25% of toe dorsif exion during calibration.
3. In a sequence of four or more movements.
4. Separated by an interval of more than 5 seconds (from limb-movement onset) and less than 90
seconds (typically there is an interval of 20 to 40 seconds).
B. The periodic limb movements (PLMs) index exceeds 5 per hour in children and 15 per hour in most
adult cases.
Note: The PLMs index must be interpreted in the context of a patients sleep-related complaint. In
adults, normative values higher than the previously accepted value of 5 per hour have been found in
studies that did not exclude respiratory eventrelated arousals (using sensitive respiratory monitor-
ing) and other causes for PLMs. New data suggest a partial overlap of PLMs index values between
symptomatic and asymptomatic individuals, emphasizing the importance of clinical context over an
absolute cutoff value.
C. There is clinical sleep disturbance or a complaint of daytime fatigue.
Note: If PLMs are present without clinical sleep disturbance, the PLMs can be noted as a polysomno-
graphic f nding, but criteria are not met for a diagnosis of periodic limb movement disorder (PLMD).
D. The PLMs are not better explained by another current sleep disorder, medical or neurological dis-
order, mental disorder, medication use, or substance use disorder (e.g., PLMs at the termination of
cyclically occurring apneas should not be counted as true PLMs or PLMD).
with ADHD have RLS symptoms and up to 26% of patients with RLS have ADHD symp-
toms; RLS and ADHD may also coexist, and ADHD symptoms in this situation are typically
more severe than with ADHD alone. A recent meta-analysis of PSG studies in children with
ADHD concluded that the only signif cant polysomnographic difference between ADHD and
control children was an increase in PLMs. It has also been noted in several pediatric studies
that treatment of RLS, specif cally with dopaminergic agents, may reduce or eliminate ADHD
symptoms.
ADHD and RLS/PLMD

A number of studies have now indicated an association between restless legs syndrome (RLS)
and periodic limb movement disorder (PLMD) and symptoms of attention def cit hyperac-
tivity disorder (ADHD). Although the mechanism underlying this relationship is not fully
understood, several possibilities exist. First, inadequate and disrupted sleep resulting from
RLS or PLMD may cause ADHD-like symptoms. Second, daytime symptoms of RLS (e.g.,
f dgeting during periods of inactivity) may be interpreted as ADHD symptoms. Conversely,
ADHD-associated evening hyperactivity may be labeled as RLS (but there is typically not a
sensory component with ADHD). Finally, there may a common underlying metabolic (e.g.,
iron def ciency) or genetic predisposition for both disorders.
There are a number of possible mechanisms to explain this relationship: RLS or PLMD
mediated sleep disruption may result directly in ADHD-like symptoms, daytime or bedtime
RLS symptoms (e.g., increased movement) may be interpreted as hyperactivity associated
with ADHD, or, alternatively, ADHDmediated diurnal or nocturnal hyperactivity and rest-
lessness may be attributed to RLS symptoms. More recent data on the role of iron def ciency
in ADHD as well as the common etiologic feature of dopaminergic dysfunction in both disor-
ders, have led to speculation that there may be a shared underlying pathophysiology in ADHD
and RLS and PLMD; thus replenishing iron stores may have a positive effect on both. Finally,
the two disorders may coexist, perhaps with a common genetic component. In the latter situa-
tion, use of both daytime psychostimulants for ADHD and nighttime dopaminergic treatment
of RLS may be warranted.
Studies in adults have suggested that there is also an increased risk for depression and
anxiety symptoms in RLS. Anecdotal clinical and case reports suggest that this may be the
case in children with RLS as well, and that appropriate treatment of the RLS symptoms result
in improved mood. It should be emphasized that in situations in which depression and anxiety
appear to be comorbid with RLS, it is important to avoid the use of antidepressants known to
exacerbate RLS (i.e., SSRIs, TCAs). Noradrenergic medications, such as bupropion, may be a
better choice.
eVAl uAt io n
n Medical history: This may include a history of iron def ciency anemia. Children with the
medical conditions listed above are at increased risk for secondary RLS and PLMD. Concur-
rent medications (e.g., SSRIs, sedating antihistamines) should be reviewed as possible con-
tributory factors. Caffeine intake may also exacerbate symptoms of RLS.
n Developmental history: The history is generally noncontributory except for specif c neurode-
velopmental disorders that may have an increased risk of PLMs (e.g., William syndrome).
n Family history: In childhood-onset RLS, a positive family history (f rst-degree relative) is
very common. However, due to the under-recognition of this disorder, it should be kept in
mind that adult family members with RLS may not have been diagnosed, and instead there
may be a strong family history of insomnia, restless sleep, or growing pains. It is worth asking
parents about their own symptoms at bedtime.
n Behavioral assessment: This may reveal signif cant behavior problems, mood disturbances,
and ADHD.
n Physical examination: The examination is generally normal (including the neurologic exam)
in children with primary RLS or PLMD. However, the primary care clinician may note from
behavioral observation that many children with RLS are not able to sit still for long periods
and often jiggle their legs or move around while sitting for prolonged periods.
n Diagnostic tests:
n PSG:
RLS: RLS is a clinical diagnosis and, thus, PSG is not strictly required to make the
diagnosis. However, documentation of PLMs on an overnight sleep study is often help-
ful for the diagnosis because the presence of PLMs is part of the supportive diagnostic
criteria for RLS in children (see Table 15.1), particularly in situations in which the childs
description of RLS symptoms may be diff cult to elicit due to limited language skills. In
addition, the co-occurrence of RLS and PLMD may affect pharmacologic management
strategies, and reduction of PLMs on PSG may serve as a more objective marker of
treatment response.
PLMD: PSG is required for the diagnosis of PLMD. The anterior tibialis EMG used
to monitor PLMs is part of the standard PSG montage in all sleep laboratories for both
adults and children. PLMs are def ned as four or more consecutive leg movements of
minimal amplitude of 8 mV above baseline EMG, lasting 0.5 to 10 seconds, separated
by at least 5-second and no more than 90-second intervals. To assess sleep disturbance,
leg movements that are associated with an arousal (within 3 seconds of leg movement)
Fig 15.1. Periodic limb movements.
or awakening are scored, although in general children are less likely than adults to have
associated arousals. An overall index of periodic limb movements per hour is provided, as
is an index of periodic limb movements associated with arousals per hour. In adults, the
periodic limb movement index (PLMI) usually exceeds 15 per hour, while in children, a
PLMI 5 is generally considered signif cant (Fig. 15.1). Finally, it should be noted that
there may be considerable night-to-night variability in PLMs, and thus a single overnight
sleep study may under- or overestimate typical severity.
n Laboratory tests: Because of the association between RLS and PLMD and iron def ciency,
especially low ferritin, a complete blood count and serum ferritin level (hemoglobin and
hematocrit and indices may be normal) should be checked, particularly in children who may
be at high risk for iron def ciency (toddlers, adolescent girls). A serum ferritin <50 ng/ml is
associated with RLS symptoms.

n Nocturnal leg discomfort or pain is frequently associated with musculoskeletal and neuro-
muscular complaints in children, and may be confused with RLS or PLMD. Many of these
conditions have specif c signs and symptoms that distinguish them from RLS; these include
physical f ndings (e.g., tibial tuberosity tenderness with Osgood-Schlatter syndrome or ery-
thema, edema, and joint tenderness with juvenile rheumatoid arthritis [JRA]), exacerbation
(rather than relief) with movement and improvement with rest, lack of a temporal (evening)
association, and sporadic occurrence. These conditions include (listed from relatively more
common to less common):
n Exercise-related muscular pain.

n Transient nerve compression (pins and needles) following prolonged inactivity.
n Growing pains, nonspecif c limb discomfort that frequently wakes children from sleep;
may occur in association with RLS but are also common in children without RLS.
n Nocturnal leg cramps, which may be associated with electrolyte disturbance or neuromus-
cular disorders.
n Dermatitis and associated irritation or pruritus.
n Orthopedic conditions, such as Osgood-Schlatter syndrome and chondromalacia patella.
n Chronic rheumatologic conditions such as JRA.
n Peripheral neuropathy, radiculopathy, and myopathy.
n Sleep-related motor restlessness at bedtime or during the night may be due to:
n Hypnic jerks (sleep starts), which typically occur at wakesleep transition only.
n Myoclonic seizures, in which movements are more prominent in wakefulness.
n Sleep apnearelated movement arousals.
n Parasomnias.
n Movements associated with ADHD, as children with ADHD may manifest increased late-
day hyperactivity associated with inadequate control of ADHD in the evening or rebound
from psychostimulants. Children with ADHD have also been shown to have more motoric
activity during sleep.
n Akathisia (inner restlessness or urge to move), which is often associated with antipsychotics
and other medications.

n Prolonged sleep onset and nighttime awakenings may result from multiple other causes
including behavioral issues (see Chapters 6 and 7), delayed sleep phase (see Chapter 17), and
sleep-disordered breathing (see Chapter 14).
n Excessive daytime sleepiness and associated neurobehavioral impairments can result from
any other sleep disorder that impacts on sleep quality and quantity, including OSA and behav-
iorally induced insuff cient sleep.
MAn Ag eMen t
w hen to r efer
It is possible to diagnose and treat children presenting with symptoms of RLS and PLMD in the
primary care setting, although overnight PSG to detect PLMs requires referral to a sleep labora-
tory. In particular, assessment and replenishment of iron stores (when appropriate) as a f rst-line
treatment is a reasonable strategy before referral to a sleep specialist for additional management
is considered.
t reatment
The decision of whether and how to treat RLS and/or PLMD depends on (1) the level of severity
(intensity, frequency, and periodicity) of sensory symptoms; (2) the degree of interference with
sleep; and (3) the impact of daytime sequelae in a particular child or adolescent. For example, if
the symptoms of RLS result in prolonged sleep onset latency, severe complaints of leg discom-
fort, or attentional problems, treatment is generally warranted.
There is less of a consensus about the treatment threshold for PLMs in children. Sleep study
results can be helpful from the standpoint of quantifying the number of PLMs and associated
arousals and sleep fragmentation although, as noted above, PLMinduced EEG arousals in gen-
eral are seen with much less frequency in children compared with adults. For a PLM index less
than 5, usually no treatment is recommended; for an index of or over 5, the decision to specif -
cally treat PLMs should be based on the presence or absence of nocturnal symptoms (restless or
nonrestorative sleep) and clinical sequelae (e.g., excessive daytime sleepiness, neurobehavioral
complications). In addition, comorbid sleep disorders (e.g., OSA) may be associated with PLMs,
and thus treatment of the underlying sleep disorder may result in resolution of PLMs.
Treatment Strategies
n Sleep hygiene: It is recommended that children with RLS maintain consistent bedtimes and
waketimes on weekdays and weekends, have a bedtime routine, and obtain adequate nighttime
sleep, especially since fatigue may exacerbate the symptoms of RLS.
n Nonpharmacologic treatments: Moderate exercise up to a few hours before bedtime may
suppress symptoms. Walking, stretching, massaging the affected area, and applying hot or
cold packs may be helpful. Biofeedback and relaxation techniques may alleviate symptoms as
well as reduce stress. Keeping mentally occupied, especially during long periods of inactivity,
should also be encouraged, although this may be counterproductive at bedtime in terms of
sleep onset.
n Substances to avoid: Caffeine, alcohol, antihistamines, cold or sinus preparations, and anti-
emetics are known to exacerbate symptoms of RLS.
n Iron supplementation: Iron supplements are a reasonable choice as a f rst-line treatment for
RLS and PLMs in children if serum ferritin levels are low (<50 ng/ml). Although data are
limited, the recommended dose is typically in the range of 6 mg/kg/day for a duration of 3
to 6 months, in conjunction with increased dietary iron intake. However, there are a number
of caveats: (1) Oral iron is poorly absorbed in the GI tract; (2) compliance with 3 to 6 month
treatment periods is often poor; (3) tolerance may be problematic (i.e., constipation); and (4)
oral iron supplementation may only be effective at lower ferritin levels. Concomitant use of
ascorbic acid (vitamin C) appears to improve absorption, while iron absorption is reduced
when combined with calcium. Adult studies have found that intravenous iron in small multiple
daily doses is signif cantly more likely to be effective in raising ferritin levels and reducing
RLS symptoms, although this delivery system is seldom used in the pediatric population.
A very rare complication of iron supplementation is iron overload in individuals prone to
hemochromatosis.
n Medication: No empirical studies have been conducted on the eff cacy of specif c medica-
tions for RLS and PLMD in children. The following recommendations are based largely on
clinical experience. Similar to other drugs used for sleep, governing principles in the use of
medications for RLS in children include (1) using the lowest possible dose and (2) starting
at a minimal dose and titrating up according to eff cacy and tolerance. Medication should be
combined with nonpharmacologic interventions as outlined above.
The major medications used for RLS and PLMD in adults are listed below; dosages listed
are usual ranges for adults. Medications that increase dopamine levels in the CNS have overall
been found to be the most effective drugs in relieving RLS and PLMD symptoms. Currently,
ropinirole and pramipexole are the only medications approved by the Food and Drug Admin-
istration specif cally for the treatment of RLS and PLMD in adults. Overall, 70% to 80% of
adult patients experience some relief of symptoms with medication; effects seem to be most
robust in relieving RLS symptoms and improving sleep quality subjectively and in decreasing
PLMs. In choosing a medication to treat signif cant RLS or PLMD, consultation with a pedi-
atric sleep specialist or neurologist is recommended.
n Dopaminergic agents: Non-ergot dopamine D2/D3 agonists are considered f rst-line treat-
ment for both RLS and PLMs in adults.

n Levodopa and carbidopa (Sinemet): These are given regular or slow release in 100 to
125 mg or 200 to 250 mg dosages at bedtime. An additional dose of the regular preparation
may be needed during the night to avoid rebound PLMs. Problematic side effects, which
may include nausea, orthostatic hypotension, insomnia, daytime fatigue and somnolence,
augmentation in early evening (see below), and morning rebound, have tended to limit the
use of levodopa and carbidopa for RLS and PLMs in both adults and children.
n Dopamine agonists: Used to treat both RLS and PLMD, dopamine agonists are now gen-
erally considered the f rst-line medications in adults. They typically result in a predictable,
rapid, and nearly complete resolution of symptoms, although some recent data in adults
suggest that these medications may be relatively less effective in treating the sensory (pain)
component of RLS and more effective in treating PLMs. A number of published case re-
ports and small-case series have suggested that these medications may also be effective and
generally well tolerated in the pediatric population. Potential issues associated with the use
of dopamine agonists include augmentation (although less common than with levodopa
and carbidopa), development of tolerance, and rebound symptoms on discontinuation. Side
effects reported in association with dopamine agonists include nausea, headaches, constipa-
tion, and fatigue; orthostatic hypotension may occur. Rarely, behavioral changes, including
compulsive behaviors such as compulsive gambling, have been reported in adults.
n Pramipexole (Mirapex): This drug has been shown in a number of adult studies to be ef-
fective in reducing symptoms in moderate or severe RLS and in decreasing PLMs as well
as improving sleep quality. The dose is 0.125 to 0.75 mg at bedtime.
n Ropinirole (Requip): This drug has also been reported to be effective for treating RLS in
adults. The dose is 0.5 to 4 mg.

n Other medications for RLS and PLMD: Other classes of medications have been used in
adults, and to a much lesser extent in children, to treat RLS and PLMD; these include alpha
agonists, benzodiazepines, anticonvulsants, and opioids.
n Clonidine: This short-acting alpha agonist is largely used to treat RLS symptoms; side ef-
fects include hypotension. The dose is 0.05 to 0.2 mg at bedtime.

n Clonazepam (Klonopin): This is a benzodiazepine used to treat both RLS and PLMD;
side effects include daytime sedation. It may exacerbate OSA symptoms and tolerance may
develop. The dose is 0.5 to 2.0 mg at bedtime
n Codeine and other opiates (oxycodone, propoxyphene): Opiates are used to treat both
RLS and PLMD. They have been shown to demonstrate eff cacy in open-label trials in
adults, possibly related to effects on dopaminergic pathways. Side effects include constipa-
tion. Dependency and addiction issues do not seem to occur in adults treated with opioids
specif cally for RLS. The dose for codeine is 15 to 60 mg at bedtime; oxycodone (Perco-
dan), 5 mg at bedtime; propoxyphene (Darvon, Darvocet), 200 mg at bedtime.
n Gabapentin (Neurontin): This is an anticonvulsant that has been used for RLS and is re-
ported to improve both sensory and motor symptoms and improve sleep quality; side effects
include daytime somnolence. The dose is 100 to 400 mg at bedtime.
Many adult patients on medications, particularly those on dopaminergic agents, experience a
phenomenon called augmentation. Augmentation is def ned as an earlier temporal onset of RLS
symptoms (i.e., afternoon), more rapid onset of symptoms with inactivity, and/or spread of symp-
toms to other parts of the body, occurring as a direct result of a specif c therapeutic intervention.
Augmentation generally occurs within 6 weeks to 6 months after initiation of therapy or dosage
change and is often responsive to a change in pharmacologic agent. It appears to be more com-
mon in the face of low serum ferritin levels.
Pr o g n o SiS
No long-term studies have been conducted on the course of RLS or PLMD in children or ado-
lescents. It appears, however, that early onset RLS that begins in childhood or adolescence has a
more chronic and progressive course and is likely to be a lifelong disorder, although patients with
milder disease may have long periods of remission. Cases of secondary RLS and PLMD gener-
ally remit without recurrence when the underlying condition is resolved.

Explain what causes restless legs syndrome (RLS) and periodic limb movement disor-
der (PLMD) in simple terms, including the fact that these are biologically based disorders
that are often chronic and lifelong. In particular, parents may have heard or read media
claims that RLS is not a real disorder and may have questions about this statement.
Review the common sensory and motor symptoms of RLS and PLMD, as well as the
associated bedtime struggles or sleep onset delay and sleep disruption.
Explain common risk or exacerbating factors, such as iron def ciency anemia, caffeine
consumption, and medication use, including sedating over-the-counter antihistamines.
Discuss the familial component, and encourage any parent or family member with similar
symptoms to be evaluated.
Review the daytime consequences, as parents may not attribute moodiness or attention
def cit hyperactivity disorder symptoms to a sleep problem.
Explain what to expect from the overnight sleep study, and review the results of the over-
night sleep study (if appropriate).
Emphasize the importance of good sleep hygiene, especially ensuring adequate sleep.
Discuss the risks and benef ts of pharmacologic treatment options, including oral iron
supplementation and any medications, such as dopaminergic agonists, if these are being
considered.
Encourage parents to utilize reliable resources for further information, such as the RLS
Foundation (www.rls.org) and the National Sleep Foundation (www.sleepfoundation.org)
Web sites; the RLS Foundation has an excellent brochure on pediatric RLS and PLMD that
can be ordered from the Web site.
See Appendix D12 for a parent handout on RLS and Appendix D13 on PLMD.
Excessive Daytime
Sleepiness: Narcolepsy and
Other Hypersomnias
16
Excessive daytime sleepiness (EDS) is def ned as the inability to stay awake during the major
waking episodes of the day, resulting in unintended lapses into drowsiness or sleep. EDS may be
differentiated from fatigue by the presence of this sleep propensity, although the distinction is
not always readily apparent by history. Hypersomnia is a clinical term that is used to describe a
group of disorders characterized by recurrent episodes of EDS, reduced baseline alertness, and/
or prolonged nighttime sleep periods that interfere with normal daily functioning. It is important
to recognize that there are many potential causes of EDS, which may be broadly grouped as
extrinsic (e.g., secondary to insuff cient and/or fragmented sleep) or intrinsic (e.g., resulting
from an increased need for sleep). The most common causes of EDS in both adults and children
are primary sleep disorders that result in inadequate or disrupted sleep (i.e., obstructive sleep
apnea [OSA], insomnia, restless legs syndrome, and periodic limb movement disorder [PLMD])
and curtailment of sleep (e.g., behaviorally induced insuff cient sleep). The intrinsic disorders
of EDS discussed in this chapter, which are associated with hypersomnia of central nervous sys-
tem (CNS) origin, are less common, but nonetheless important causes of signif cant sleepiness-
related functional impairments in children and adolescents.
Narcolepsy
Narcolepsy is a chronic lifelong central nervous system disorder typically presenting in ado-
lescence and early adulthood that is characterized by profound daytime sleepiness and resul-
tant signif cant functional impairment. Other symptoms frequently associated with narcolepsy
include cataplexy, hypnagogic or hypnopompic hallucinations, sleep paralysis, automatic
behaviors, and disturbed nocturnal sleep. Narcolepsy may be further delineated as (1) pri-
mary narcolepsy with cataplexy; (2) primary narcolepsy without cataplexy; and (3) second-
ary narcolepsy due to medical conditions. The fundamental pathophysiology of narcolepsy
has been shown to involve dysfunction of the hypocretin/orexin neuropeptide system in the
hypothalamus.
Centrally mediated hypersomnias include both chronic and persistent (e.g., narcolepsy, idio-
pathic hypersomnia) and episodic and recurrent (e.g., Kleine-Levin syndrome) sleep disorders;
they may be further divided into primary versus secondary (i.e., due to neurologic or medical
conditions or substances such as medications and illicit drugs). The most clinically signif cant of
the central hypersomnias is narcolepsy, a chronic, lifelong sleep disorder that involves a funda-
mental disturbance in the regulation of REM sleep and wakefulness. The most prominent clinical
manifestation of narcolepsy is profound daytime sleepiness, characterized by both an increased
baseline level of daytime drowsiness and by the repeated occurrence of sudden and unpredict-
able sleep episodes. These sleep attacks are often described as irresistible in that the child or
adolescent is unable to stay awake despite considerable effort, and they occur even in the context
of normally stimulating activities (e.g., during meals, in the middle of a conversation). The sleep
episodes typically occur many times throughout the day, are of relatively short duration (10 to 20
minutes), and are often described as at least temporarily refreshing. Children and adolescents
with narcolepsy may also experience much briefer sleep episodes (microsleeps) of which they
are unaware, resulting in automatic behaviors and memory lapses.
131
Other symptoms commonly associated with narcolepsy, including cataplexy, hypnagogic and
hypnopompic hallucinations, and sleep paralysis, may be conceptualized as representing the in-
trusion of REM sleep features into the waking state. For example, cataplexy, def ned as a sudden
complete or partial loss of motor control with sparing of respiratory muscles, is related to the
muscle atonia characteristic of REM sleep occurrence during wakefulness. Similarly, the vivid
visual, auditory, and tactile sensory components of hypnagogic hallucinations are hypothesized to
result from REMrelated dream mentation experienced while awake. It should be noted that nar-
colepsy with cataplexy and narcolepsy without cataplexy appear to be relatively distinct entities,
both from the standpoint of etiology and risk factors, and in regards to therapeutic management.
The typical onset of symptoms of narcolepsy is in adolescence and early adulthood, although
symptoms may initially present in school-aged and even younger children. However, the early
manifestations of narcolepsy are often ignored, misinterpreted, or misdiagnosed as other medi-
cal, neurological, and psychiatric conditions, and the appropriate diagnosis is commonly delayed
for a number of years. It is estimated, for example, that as many as 200,000 people in the United
States have narcolepsy, but that fewer than one-quarter of those individuals have actually been
diagnosed. Because timely behavioral and pharmacologic intervention may have a profound ef-
fect on quality of life for these patients, it is important for the primary care physician to be able
to recognize and assess children and adolescents with narcolepsy and other central hypersomnias,
and to appropriately refer them for further diagnostic evaluation and treatment.
ePiDeMio l o g y
n Prevalence: The prevalence of daytime sleepiness in school-aged children and adolescents has
been estimated to be between 10% and 20%, but these f gures are highly dependent upon the
def nition of EDS used. In contrast, the prevalence of narcolepsy is reported to be between 3
and 16 per 10,000, with the prevalence of narcolepsy with cataplexy approximately 0.20.5 in
10,000. Narcolepsy without cataplexy is estimated to comprise half or less of all narcolepsy
cases (10% to 50%). Prevalence also appears to vary across various ethnic and racial groups,
with a six-fold increase in prevalence, for example, in Japan compared to Europe and North
America.
n Gender: There is equal preponderance in males and females.
n Age: Symptoms typically develop after puberty, with most individuals f rst reporting symp-
toms of narcolepsy between the ages of 15 and 30 years. While studies have indicated that as
many as one-third of adult patients report the onset of symptoms before age 15 years and about
15% before age 10 years, only about 4% of narcoleptics are diagnosed before the age of 15
years. The average time elapsed between onset of symptoms and diagnosis is 10 to 15 years.
n Family history: Overall, the prevalence of familial narcolepsy is low, and most cases are
sporadic. However, the risk of developing narcolepsy with cataplexy in a f rst-degree relative
of a narcoleptic patient is estimated at 1% to 2%; this represents an increase of 10- to 40-fold
compared to the general population, suggesting greater genetic loading in these families. The
prevalence of isolated narcolepsy symptoms in f rst-degree relatives of narcoleptic patients is
4% to 6%.
Both animal and human studies have now strongly implicated a specif c def cit in the hypotha-
lamic orexin/hypocretin neurotransmitter system in the genesis of narcolepsy with cataplexy.
The orexin/hypocretin system affects monoaminergic and cholinergic activity and is known to be
involved not only with maintenance of alertness, but also with feeding behavior, energy metabo-
lism, and locomotion. The underlying pathogenesis of narcolepsy is believed to involve selective
loss of cells that secrete hypocretin/orexin in the lateral hypothalamus; cerebrospinal f uid (CSF)
ExCESSIvE DAyTImE SLEEPINESS 133
hypocretin/orexin is reduced or undetectable in most (although not all) patients with narcolepsy
associated with cataplexy, especially in those patients who are human leukocyte antigen positive
(see below). It has been postulated that autoimmune mechanisms, possibly triggered by viral
infections, in combination with a genetic predisposition and environmental factors, may be in-
volved. It is believed that familial narcolepsy is related to mutations in the genes synthesizing
peptides in the hypocretin system or their receptors.
Human leukocyte antigen (HLA) testing also shows a strong association with narcolepsy;
more than 90% of European and Caucasian narcoleptics with cataplexy test positive for HLA
DQ antigens DQA1*0102 and DQB1-0602. In children, it appears that about 60% to 70% of
individuals with narcolepsy are HLA-positive. This compares to the general population, of which
it is estimated about one-quarter (12%38%) are positive for the DQB1-0602 antigen. Therefore,
the vast majority of individuals with this antigen do not have narcolepsy. In addition, some 60%
of patients with narcolepsy without cataplexy are DR2-negative, and less than 30% of monozy-
gotic twins have been found to be concordant for HLA subtype. Thus, the presence of this antigen
alone is not likely to be suff cient for the development of narcolepsy, and environmental factors
are probably involved.
Hypersomnias of central origin in general may also result from a variety of different processes
involving injury to the CNS, including medical disorders (infection, metabolic disorders), neuro-
logic disorders (head trauma and other causes of increased intracranial pressure), and any number
of medications and illicit substances that result in signif cant daytime sleepiness and reduced
alertness. Although the majority of cases of narcolepsy are considered idiopathic, secondary
narcolepsy with cataplexy may also result from CNS insults. These include inherited metabolic
and genetic disorders involving abnormalities of the CNS, such as Niemann-Pick disease type
C, and autosomal dominant cerebellar ataxia with deafness. Secondary narcolepsy may also be
associated with other disorders, such as Prader-Willi syndrome and myotonic dystrophy type 1;
CNS trauma (e.g., following closed head injury); brain tumors, such as astrocytomas and cranio-
pharyngiomas (particularly in the third ventricle, posterior thalamic, and brainstem regions); and
various vascular and infectious insults to the hypothalamus. The age of onset in these second-
ary (or symptomatic) narcolepsy cases is often lower (i.e., school age), and clinical evidence
of signs and symptoms of the primary medical or neurological condition are typically readily
apparent.
The tetrad of symptoms for narcolepsy includes excessive daytime sleepiness, cataplexy, hypna-
gogic and hypnopompic hallucinations, and sleep paralysis. It is estimated that about half of all
adult patients with narcolepsy have all four of the primary symptoms of narcolepsy. However,
pediatric case series suggest that the relative prevalence of symptoms other than EDS may be
lower at the time of diagnosis in children compared to adults, especially in younger children who
may not be able to describe these symptoms accurately.
n Excessive daytime sleepiness: A necessary component for the diagnosis of narcolepsy, ex-
cessive daytime sleepiness is most often the initial presenting complaint. The overwhelming
urge to fall asleep is more pronounced under conditions of decreased activity and low-level
environmental stimulation, such as watching a movie or listening to a boring lecture, but also
occurs in other situations, such as during a meal or while talking on the phone. The daytime
sleepiness in a pre-pubertal child may present as the reappearance of regular naps following
discontinuation of regular napping. This excessive sleepiness occurs despite adequate night-
time sleep duration, and periods of sleep only temporarily alleviate the sleepiness. Very brief
(several seconds) sleep attacks may also occur. The individual with narcolepsy is usually
unaware of these microsleeps and may stare off, appear unresponsive, or continue to en-
gage in an ongoing activity (automatic behavior); this may be interpreted by observers as day-
dreaming and inattentiveness related to attention def cit hyperactivity disorder (ADHD), or a
manifestation of absence (petit mal) seizures. Younger children in particular may manifest
an outward behavioral response to an internal sensation of drowsiness that is characterized by
increased motoric activity and disinhibition; this too may be interpreted as hyperactivity or
impulsivity associated with ADHD.
n Cataplexy: The second most common symptom of narcolepsy, occurring in 60% to 100% of
adult patients, and in at least one study, in as many as 80% of pediatric cases. Cataplexy is
considered pathognomonic for narcolepsy. Cataplexy is rarely the f rst symptom of narcolepsy,
but it often develops within the f rst year of the onset of excessive daytime sleepiness. It is
described as an abrupt, bilateral, partial or complete loss of muscle tone, classically triggered
by an intense positive emotion (e.g., laughter, surprise). The cataplectic attacks are typically
brief (seconds to minutes), and fully reversible, with complete recovery of normal tone when
the episode ends. The loss of muscle tone spares the diaphragm and ocular muscles, and can
range from subtle, localized sagging of the face, eyelids, or jaw or slurred speech, to head nod-
ding or knee buckling, to complete whole body collapse; the most common muscles affected
in partial attacks are knees, face, and neck. More subtle cataplectic episodes may involve a
subjective sense of weakness or unsteadiness without obvious external behavioral manifesta-
tions. During the episode, the individual maintains complete consciousness and awareness of
his/her surroundings; memory for the event is not impaired. Although laughter is the most
common precipitant, other emotions such as anger, sadness, or even the anticipation or recol-
lection of an emotion, as well as vigorous physical exercise can also trigger cataplexy. In some
children, there is no identif able trigger for the attacks. The frequency of episodes can range
from occurring multiple times per day to a few times per year. Cataplectic episodes may be in-
terpreted as clumsiness, seizures (drop attacks), or even psychosomatic phenomena (e.g.,
pseudoseizures, conversion reaction).
n Hypnagogic and hypnopompic hallucinations: These hallucinations involve vivid visual,
auditory, and sometimes tactile sensory experiences, which may be described by children as
scary dreams. These occur during transitions between sleep and wakefulness, primarily at
sleep onset (hypnagogic) and sleep offset (hypnopompic). They are reported by approximately
40% to 80% of adult patients with narcolepsy. Common hallucinations include faces and ani-
mals, and they are frequently described as frightening or threatening. These hallucinations
may be accompanied by sleep paralysis or occur independently, and may also occur during
daytime naps. It should be noted, however, that hypnagogic and hypnopompic hallucinations
are also experienced by normal individuals without narcolepsy (in up to 10% of the popula-
tion), especially in relation to sleep deprivation; thus they are not considered pathognomonic
for the disorder.
n Sleep paralysis: The inability to move or speak for a few seconds or minutes at sleep onset or
offset. The episodes may be accompanied by eye-f uttering, moaning, autonomic symptoms
(e.g., sweating), or a subjective sensation of struggling to move or breathe; stress or sleep de-
privation may exacerbate the episodes. The paralysis ends spontaneously or after mild sensory
stimulation (e.g., being touched or called). Sleep paralysis occurs in 40% to 80% of adults
with narcolepsy and may also accompany hypnagogic hallucinations. This combination of
frightening sensory phenomenon coupled with the inability to move or speak is understand-
ably experienced as very unpleasant. As with hypnagogic hallucinations, sleep paralysis oc-
curs in nonnarcoleptic individuals and, therefore, does not necessarily indicate the presence of
narcolepsy.
n Additional symptoms of narcolepsy:
n Nocturnal sleep disturbances: Sleep disruption and fragmentation are very common in
narcolepsy and occur in up to 90% of adult patients. Sleep disturbances may also include
abnormal REM sleep (i.e., preservation of muscle tone and increased muscle twitching in
REM). In particular, the presence of muscle movement in REM sleep may result in the in-
dividual acting out dreams, a clinical entity known as REM behavior disorder, which may
result in severe injury to the sleeper or bed partner.

n Automatic behaviors: These involve a semi-purposeful activity for which the individual
has no memory, and are more frequent with increasing levels of sleepiness. These activities
may last up to 30 minutes, and usually involve a repetitive or monotonous behavior, such as
uttering words out of context or writing a page of nonsense in the midst of doing homework.
These episodes may be misdiagnosed as complex partial seizures.
Common Symptoms of Narcolepsy

Nocturnal symptoms
Disrupted or fragmented sleep
Hypnagogic and hypnopompic (sleep onset and offset) hallucinations
Sleep paralysis
Excessive daytime sleepiness
Increased baseline sleepiness
Sudden, unpredictable, irresistible sleep episodes or attacks
Falling asleep in school or during active pursuits (e.g., in the midst of a conversation)
Other daytime symptoms
Cataplexy (sudden partial or complete loss of muscle tone with preservation of
consciousness)
Inattentiveness, poor concentration, distractibility
Academic problems
Mood dysregulation
Automatic behaviors
See Tables 16.1 and 16.2.
Associated Features
n Comorbid sleep disorders: OSA and periodic limb movements (PLMs) appear to be very
common in children with narcolepsy. In one referral population clinical series, 85% of chil-
dren had evidence of sleep-disordered breathing and 25% had PLMs on polysomnography
(PSG).
n Migraine headaches: The prevalence of migraines is reportedly increased in individuals with
narcolepsy.
n Overweight and obesity: A number of studies, as well as clinical observation, suggest that
children with narcolepsy are more likely to be overweight or obese; they are also more likely
to engage in abnormal eating behaviors such as bingeing. Associated hypothalamic dysfunc-
tion and the hypocretin/orexin systems effect on hunger and satiety, as well as a decrease in
physical activity related to sleepiness, may all play a role in increasing weight gain. Being
overweight and obesity also increases the risk of OSA in these children, potentially further
compromising daytime functioning.
n Impaired academic performance: Due to the propensity for falling asleep in school and the
attentional diff culties associated with narcolepsy, many children and adolescents with this
disorder experience signif cant problems with academic performance. In addition, children
and adolescents with narcolepsy are often labeled as lazy, inattentive, and diff cult.
n Psychological concerns: Many children and adolescents with narcolepsy experience signif -
cant psychological distress associated with functional impairments related to EDS, which may
be exacerbated by the delay in diagnosis. Compared to healthy controls, they are more likely
to have behavioral disturbances, depression, problematic peer relationships, and decreased
overall quality of life.
t ABl e 16.1. Diagnostic criteria: Narcolepsy with cataplexy (347.0)
A. The patient has a complaint of excessive daytime sleepiness occurring almost daily for at least 3
months.
B. A def nite history of cataplexy, def ned as sudden and transient episodes of loss of muscle tone trig-
gered by emotion, is present.
Note: To be labeled as cataplexy, these episodes must be triggered by strong emotionsmost reliably
laughing or jokingand must be generally bilateral and brief (less than 2 minutes). Consciousness is
preserved, at least at the beginning of the episode. Observed cataplexy with transient reversible loss
of deep tendon ref exes is a very strong, but rare, diagnostic f nding.
C. The diagnosis of narcolepsy with cataplexy should, whenever possible, be conf rmed by nocturnal
polysomnography followed by a multiple sleep latency test (MSLT); the mean sleep latency on
MSLT is less than or equal to 8 minutes, and two or more SOREMPs are observed following suf-
f cient nocturnal sleep (minimum 6 hours) during the night prior to the test. Alternatively, hypo-
cretin-1 levels in the cerebrospinal f uid (CSF) are less than or equal to 110 pg/mL or one-third of
mean normal control values.
Note: The presence of two or more SOREMPs during the MSLT is a very specif c f nding, whereas
a mean sleep latency of less than 8 minutes can be found in up to 30% of the normal population.
Low CSF Hypocretin-1 levels (less than or equal to 110 pg/mL or one-third of mean normal control
values) are found in more than 90% of patients with narcolepsy with cataplexy and almost never in
controls or in other patients with other pathologies.
D. The hypersomnia is not better explained by another sleep disorder, medical or neurological disorder,
mental disorder, medication use, or substance use disorder.
The Great Masquerader

The symptoms of narcolepsy (e.g., excessive daytime sleepiness, cataplexy) are frequently
misdiagnosed as psychiatric or behavioral disorders, including attention def cit hyperactivity
disorder, depression, conversion reactions, and even psychosis. In addition, patients with cen-
tral hypersomnia and narcolepsy are at increased risk for emotional, attentional, and academic
problems as a result of their EDS, particularly if the diagnosis is signif cantly delayed.
eVAl uAt io n
n Medical history: A thorough medical history should include evaluation for other possible
causes of EDS, including sleep disorders such as OSA, RLS, and PLMD; neurologic con-
ditions; psychiatric disorders, such as depression and substance use; and prescription and
nonprescription sedating medications. Because narcolepsy may be secondary to underlying
medical conditions (e.g., head injury, CNS tumors, demyelinating disorders), a thorough his-
tory should include screening for these disorders. It should be noted, however, that the most
common cause of EDS in the general population, particularly in adolescents, is chronic sleep
restriction related to environmental and lifestyle factors.
n Developmental and school history: The history is generally normal, although children with
secondary narcolepsy associated with underlying neurologic disorders such as Niemann-Pick
disease type C will have obvious developmental delays. There may be a history suggestive of
attentional problems or a diagnosis of ADHD; older children and adolescents with narco-
lepsy commonly have a history of signif cant academic concerns.
t ABl e 16.2. Diagnostic criteria: Narcolepsy without cataplexy (347.0)
months.
B. Typical cataplexy is not present, although doubtful or atypical cataplexy-like episodes may be
reported.
C. The diagnosis of narcolepsy without cataplexy must be conf rmed by nocturnal polysomnography
followed by a multiple sleep latency test (MSLT). In narcolepsy without cataplexy the mean sleep
latency on MSLT is less than or equal to 8 minutes, and two or more SOREMPs are observed fol-
lowing suff cient nocturnal sleep (minimum 6 hours) during the night prior to the test.
Note: The presence of two or more SOREMPs during the MSLT is a specif c f nding, whereas a mean
sleep latency of less than 8 minutes can be found in up to 30% of the normal population.
D. The hypersomnia is not better explained by another sleep disorder, medical or neurological disorder,
n Family history: Although still a rare occurrence, there is an increased risk of developing nar-
colepsy with cataplexy in f rst-degree relative of narcoleptic patients, compared to the general
population, the prevalence is estimated at 1% to 2%. It is estimated that up to 40% of individu-
als may have a family member with a history of excessive daytime sleepiness.
n Behavioral assessment: An assessment may indicate attention problems, mood issues, and
behavioral concerns, such as hyperactivity and poor impulse control. Because of the functional
impairment associated with EDS, older children and adolescents with undiagnosed narcolepsy
may have signif cant social problems as well.
n Physical examination: Assessment of anthropometric parameters may reveal increased body
mass index (BMI). In the majority of cases, the physical examination is completely normal,
although EDS in the off ce setting (i.e., falling asleep during the clinical interview) may be
noted. However, an abnormal neurologic examination suggests the possibility of secondary
narcolepsy, and necessitates appropriate additional diagnostic evaluation (e.g., neuroimaging).
n Diagnostic tests:
n A sleep diary, which may be helpful for documenting EDS and napping despite adequate
duration of nocturnal sleep, is recommended.

n Sleepiness scales, such as the Pediatric Daytime Sleepiness Scale in children and adoles-
cents and the Epworth Sleepiness Scale in older adolescents may assist in delineating the
severity of EDS.
n Overnight sleep study (PSG) and multiple sleep latency test (MSLT), are strongly rec-
ommended components of the evaluation of a patient with profound unexplained daytime

sleepiness or suspected narcolepsy. The purpose of the overnight PSG is to evaluate for
primary sleep disorders, such as OSA, that may cause EDS. In addition, the presence of
both a shortened sleep latency and shortened REM latency as well as fragmented nocturnal
sleep helps to support the diagnosis of narcolepsy. PLMs are also commonly seen on PSG
in patients with narcolepsy.
The MSLT provides an essential and objective quantif cation of daytime sleepiness and
assesses the presence of sleep onset REM periods, which is a cardinal feature of narcolepsy.
It comprises a series of f ve scheduled naps of 20 minutes duration on the day following
an overnight PSG. Prior to PSG, the patient should be withdrawn, if possible, from any
medications that may affect the CNS, with adequate time to prevent rebound changes in
sleep architecture (typically at least 2 weeks). The patient should also be instructed to obtain
adequate sleep for at least 2 weeks before the MSLT.
PSG diagnostic criteria (adult):
Sleep latency <10 minutes
REM sleep latency <20 minutes
Minimum 6 hours nocturnal sleep prior to MSLT
MSLT diagnostic criteria (adult):
Mean sleep latency (MSL) <8 minutes
Two or more sleep onset REM periods (SOREMPs) during the MSLT.
Sleep latency is def ned as the time elapsed between lights out and the onset of stage 1 sleep;
sleep latency is averaged over the f ve naps to yield the MSL. In adults, an MSL of less than
5 minutes and between 5 and 10 minutes is considered consistent with severe and moder-
ate hypersomnia, respectively. Although an MSL of less than 8 minutes is highly suggestive of
narcolepsy, it is estimated that up to 30% of the normal adult population would also meet this
criteria, and thus this f nding is nonspecif c. The prior night PSG is also essential in interpreting
the MSLT results, as a patient with OSA or PLMs may also have signif cant daytime sleepiness.
SOREMPs are def ned as REM sleep occurring within 15 minutes of lights out. More than two
SOREMPs are generally considered highly specif c for the diagnosis of narcolepsy, although
more recent data suggest that up to15% of the general population may have this f nding. The
combination of MSL of less than 5 minutes and more than 2 SOREMPs is estimated in adults to
have a 70% sensitivity and 96% specif city for narcolepsy.
In children and adolescents, conducting and interpreting the results of the MSLT may be par-
ticularly challenging for several reasons. Younger children may not cooperate with the lengthy
daytime procedure required, especially immediately following an overnight PSG. Children will
also often exhibit a last nap effect in which the anticipation of going home increases arousal
and results in spuriously prolonged sleep onset. Because children have an increased sleep need
compared to adults, the requirement for at least 6 hours of sleep before the MSLT may be inad-
equate. Finally, it has been suggested that MSL value thresholds signif cantly higher than those
used as the criteria for diagnosis in adults may still be pathologic in children; normative data in
prepubertal children suggest that a sleep onset latency of 15 minutes or less may be indicative of
signif cant daytime sleepiness. However, clinical data from pediatric sleep centers suggest that
the MSL in children with narcolepsy is similar to that in adults, i.e., less than 8 minutes. It should
be noted that the MSLT itself has not been validated in children less than 8 years old. Interpreta-
tion of MSLT results in children should take these factors into consideration, and it should be
noted that it might take several polysomnographic studies over a period of 6 months to several
years to make a def nitive diagnosis.
n Neuroimaging (magnetic resonance imaging) is not routinely indicated but should be
strongly considered if the EDS has a sudden onset, occurs in the presence of neurological
symptoms and/or an abnormal neurologic examination, or if there is a history of recent head
injury.
n HLA testing is not mandatory for the diagnosis of narcolepsy, but may be helpful in some
cases. Although most patients with narcolepsy and cataplexy are HLA-positive (75% to
90%), it should be kept in mind that some 25% of normal individuals are also positive for
the DQ antigens. Children with both DR15 and DQB1*0602 alleles present are more likely
to have severe EDS and cataplexy.
n CSF hypocretin/orexin levels are generally very low or non-detectable in patients with
narcolepsy with cataplexy. Interestingly, these low levels may occur after the appearance
of EDS but before the onset of cataplexy. Although not required for the diagnosis, and at
the current time not widely available, CSF levels may be helpful in select cases in which
a conf rmatory MSLT is diff cult to conduct or interpret. This testing may become a more
standard part of the evaluation in the future.

n Inadequate sleep is the primary cause of EDS in children and adolescents. Short sleep laten-
cies and SOREMPs on the MSLT can be manifestations of chronic sleep restriction and/or
delayed sleep phase syndrome (see Chapter 17).
n Idiopathic hypersomnia (IH) is a chronic disorder characterized by signif cant daytime
sleepiness that shares many common features with narcolepsy. All symptoms may occur in
both disorders, with the important exceptions of cataplexy and signif cant nocturnal sleep dis-
ruption being unique to narcolepsy. Patients with IH also frequently experience sleep drunk-
enness (extreme and prolonged confusion after awakening), and naps are typically described
as unrefreshing. Although the MSL in IH mean sleep latency (MSL) is typically less than 8
minutes, fewer than 2 SOREMPs are present. Idiopathic hypersomnia may be further classif ed
as polysymptomatic (or primary) or monosymptomatic IH. Principal differentiating factors
include prolonged nocturnal sleep (>10 hours) and diff culty in morning waking in primary
IH. Diagnostic criteria for both types of idiopathic hypersomnia are found in Tables 16.3 and
16.4. The prevalence of idiopathic hypersomnia is estimated to be 10% to 15% of sleep center
patients evaluated for hypersomnia, and is rarely seen prior to adolescence; occasional familial
clustering is observed. In select cases, IH may follow a viral illness, such as Guillain-Barr,
hepatitis, and Epstein Barr. Head injury can also result in IH. Treatment for the associated
EDS is similar to that for EDS in narcolepsy (e.g., modaf nil, psychostimulants), although the
daytime sleepiness associated with IH compared to narcolepsy is often even more refractory
to treatment in IH.
n Kleine-Levin syndrome is a rare sleep disorder characterized by episodic, recurrent, pro-
longed bouts of hypersomnia in which the individual sleeps for as many as 16 to 18 out of 24
hours for several days up to 3 to 4 weeks at a time. The syndrome also involves cognitive and
behavioral disturbances, which suggest an underlying hypothalamic dysfunction, including
t ABl e 16.3. Diagnostic criteria: Idiopathic hypersomnia with long sleep time (327.11)
months.
B. The patient has prolonged nocturnal sleep time (more than 10 hours) documented by interview,
actigraphy, or sleep logs. Waking up in the morning or at the end of naps is almost always laborious.
C. Nocturnal polysomnography (PSG) has excluded other causes of daytime sleepiness.
D. The PSG demonstrates a short sleep latency and a major sleep period that is prolonged to more than
10 hours in duration.
E. If a multiple sleep latency test (MSLT) is performed following overnight PSG, a mean sleep latency
of less than 8 minutes is found, and fewer than two SOREMPs are recorded. Mean sleep latency in
idiopathic hypersomnia with long sleep time has been shown be to 6.23.0 minutes.
Note: A mean sleep latency of less than 8 minutes can be found in up to 30% of the general population.
Both the mean sleep latency on the MSLT and the clinicians interpretation of the patients symptoms,
most notably a clinically signif cant complaint of sleepiness, should be taken into account in reaching
the diagnosis of idiopathic hypersomnia with long sleep time.
F. Hypersomnia is not better explained by another sleep disorder, medical or neurological disorder,
Note: Of particular importance, head trauma should be considered to be the cause of sleepiness.
t ABl e 16.4. Diagnostic criteria: Idiopathic hypersomnia without long sleep time (327.12)
months.
B. The patient has normal nocturnal sleep (greater than 6 hours but less than 10 hours), documented
by interview, actigraphy, or sleep logs.
C. Nocturnal polysomnography (PSG) has excluded other causes of daytime sleepiness.
D. PSG demonstrates a major sleep period that is normal in duration (greater than 6 hours but less than
10 hours).
E. A multiple sleep latency test (MSLT) following overnight PSG demonstrates a mean sleep latency
of less than 8 minutes and fewer than two SOREMPs. Mean sleep latency in idiopathic hypersom-
nia has been shown be to 6.23.0 minutes.
Note: A mean sleep latency of less than 8 minutes can be found in up to 30% of the general population.
Both the mean sleep latency on the MSLT and the clinicians interpretation of the patients symptoms,
most notably a clinically signif cant complaint of sleepiness, should be taken into account in reaching
the diagnosis of idiopathic hypersomnia without long sleep time.
F. The hypersomnia is not better explained by another sleep disorder, medical or neurological disorder,
hyperphagia with binge eating and hypersexuality. Between periods of hypersomnolence, the
patient is normal and has normal sleep patterns. Kleine-Levin is more common in males (4:1
ratio), and the usual onset is during adolescence. The syndrome may be associated with struc-
tural brain lesions or CNS viral illness, but is most often idiopathic in nature; HLAtyping is
negative. The usual course generally involves gradual attenuation of frequency and duration of
hypersomnia episodes with eventual complete resolution of symptoms over time.
n Menstrual-related periodic hypersomnia is another rare cause of episodic hypersomnia;
bouts of EDS are clearly cyclical and are generally manifested shortly after menarche.
n Psychiatric disorders and depression should be considered in children and adolescents who
present with signif cant sleepiness and associated neurobehavioral symptoms. Conversion re-
actions may mimic cataplectic attacks. However, it should be noted that the same pharmaco-
logic agents that are used for particular psychiatric conditions (e.g., stimulants for ADHD,
tricyclic antidepressants for depression) also improve symptoms of narcolepsy (e.g., EDS and
cataplexy). Therefore, treatment response to these agents should not be used to differentiate
psychiatric disorders from narcolepsy.
n Other neurologic causes of sleepiness can result in daytime sleepiness, such as posttraumatic
hypersomnia, medications, and alcohol or drug use.
MAn Ag eMen t
w hen to r efer
Children or adolescents with suspected narcolepsy should be referred to a sleep specialist or pe-
diatric neurologist for diagnosis and management. Any pharmacologic treatment should be done
in consultation with one of these specialists.
t reatment
Currently, there is no cure for narcolepsy but symptoms can usually be controlled so that a child
or adolescent with narcolepsy can lead a normal life. An individualized treatment plan usually
involves education, behavioral changes, and medication.
n Patient and family education: Narcolepsy can be a devastating disorder without appropriate
education. Daytime sleepiness may be mistaken for laziness, boredom, or lack of ability. The
experiences of cataplexy and dreaming during wakefulness may be wrongly interpreted as a
psychiatric problem. Education should not only include all family members, but also teachers,
coaches, and friends. In particular, school off cials should be notif ed that accommodations
at school may be necessary (e.g., scheduled naps, modif ed homework assignments to ensure
adequate sleep duration); children with narcolepsy are eligible for 504 accommodation plans.
n Sleep hygiene: Positive sleep habits are essential for children and adolescents with narcolepsy
(see Appendices C1 and C8), as is obtaining adequate nighttime sleep.
n Napping: Regularly scheduled short (15-minute) naps once or twice a day can help control the
daytime sleepiness, although they are seldom suff cient as a primary therapy.
n Behavioral changes: Lifestyle changes can provide substantial improvement of symptoms.
n A strict sleepwake schedule that ensures adequate sleep is essential.
n Increased physical activity can be helpful.
n Close supervision of activities that can be dangerous, such as driving, swimming, or cook-
ing, is essential. All adolescents with narcolepsy must be well controlled prior to receiving
permission to drive.
n Weight management: In particular, targeting abnormal eating behaviors and encouraging
physical activity are important in children with elevated BMI.
n Treatment of comorbid sleep disorders: Appropriate interventions, especially for OSA (e.g.,
adenotonsillectomy) and PLMs (e.g., iron supplementation), may be helpful in reducing (al-
Pharmacological Treatment of Narcolepsy in Children and Adolescents Sug-

t ABl e 16.5. gested Pediatric Doses for Selected Agents*
Children (<12 years) Adolescents/Adults (>12 years)
Medication for Excessive Daytime Sleepiness (EDS)

Methylphenidate 5 mg BID-TID OROS-methylphenidate1872 mg
OROS-methylphenidate 1854 mg
Dextroamphetamine 2.55 mg QDBID Extended release mixed amphetamine salts 530 mg
Modaf nil 50200 mg in morning Modaf nil 100400 mg; in morning
Medication for Cataplexy
Clomipramine 3 mg/kg/day at bedtime; Clomipramine 50 mg at bedtime
Imipramine 1.5 mg/kg/day (max 100 mg) Imipramine
Fluoxetine 520 mg daily Fluoxetine 1040 mg daily
Venlafaxine 75150 mg Venlafaxine 75150 mg
Medication for EDS, Cataplexy
Sodium oxybate 37 g Sodium oxybate 69 g
*There are no medications approved to treat either EDS or other associated symptoms (i.e., cataplexy) of narcolepsy
in patients less than 16 years old; thus, the use of these medications are off-label for the indication of narcolepsy,
and all suggested doses listed above are based on clinical experience.
Stimulants listed are those most commonly used to treat EDS in children with narcolepsy, although it should be
noted that any of the psychostimulants currently labeled for use in children with attention def cit hyperactivity dis-
order (ADHD) could also be used to treat EDS. Stimulant doses for narcolepsy are typically in the same dose ranges
as are used to treat ADHD; in general, longer-acting preparations are preferred in older children and adolescents.
Modaf nil may be started as a morning dose of 50 mg in younger children with increases of 2550 mg every 57
days as needed; older children may start with 100 mg in the morning and increase by 100 mg doses on a weekly
basis if needed, up to 400 mg. A second dose may be added in the afternoon if duration of effect is inadequate with
a single morning dose.
though obviously not eliminating) sleepiness and improving daytime function in patients with
narcolepsy.
n Medications: Medications are often prescribed to control the EDS (see Table 16.5). The goal
should be to allow the fullest possible return of normal functioning in school, at home, and
in social situations. Medication may also be used to control the REMassociated phenomena,
such as cataplexy, hypnagogic hallucinations, and sleep paralysis, when these are clinically
signif cant and affect the patients quality of life. Pharmacologic agents are often used in com-
bination to treat the individuals symptom constellation. As there is currently relatively little
long-term experience with any of these medications specif cally for the treatment of narco-
lepsy in children and adolescents, most of the recommendations below are based on adult
studies.
n Medications for EDS:
Psychostimulants are sympathomimetic amines also used for the treatment of EDS in
narcolepsy. Medication choices include methylphenidate (e.g., Ritalin, Metadate, Con-
certa, Daytrana) and dextroamphetamine (e.g., Dexedrine, Adderall XR, Vyvanse). Al-
though no longer considered the f rst-choice pharmacologic treatment for narcolepsy in
adults (see below), the extensive clinical experience with the use of psychostimulants in
ADHD in children may make them a relatively more acceptable choice for both providers
and families for treating EDS in pediatric narcolepsy. Although, in theory, any of the psy-
chostimulants currently labeled for use in children with ADHD could also be used to treat
EDS, most clinical experience thus far has been with the more established preparations,
such as short-acting methylphenidate and dextroamphetamine. More recently, the use
of longer-acting preparations, such as OROS-methylphenidate and mixed amphetamine
salts, has reduced the need for multiple daily dosing regimens. Dosage titration typically
follows a similar protocol to that used clinically for ADHD, with the goal of maximiz-
ing alertness while avoiding untoward side effects, including appetite suppression and
weight loss, mood changes, increases in heart rate and blood pressure, and sleep disrup-
tion. These medications should be used with caution in children with a pre-existing heart
condition or a family history suggestive of dysrhythmias. Combinations of long-acting
and short-acting forms of stimulants may be necessary to achieve adequate coverage, and
concomitant treatment with more than one class of medication may also be needed to
control debilitating symptoms of EDS in narcolepsy.
Modaf nil (Provigil) is a wakefulness-promoting drug, which is unrelated to the CNS
stimulants and is now considered the f rst-line pharmacologic treatment for the exces-
sive sleepiness of narcolepsy in adults. Although the exact mechanism of action is not
known, the alertness-enhancing properties of modaf nil may be related to effects on the
dopaminergic or histaminergic systems. Modaf nil appears to be generally well tolerated
in adults, with the most common side effects being disturbed nocturnal sleep, gastroin-
testinal discomfort (nausea, diarrhea), decreased appetite, headaches, dry mouth, anxiety,
and depression. The incidence of cardiovascular and psychiatric side effects appears to be
less than with stimulants, and abuse and dependence potential is low. It should be noted,
however, that modaf nil, similar to the psychostimulants, has acquired street value in
some settings in regard to use as a countermeasure for sleepiness and/or a study aid;
thus an increased risk of diversion exists. Failure to respond to psychostimulants (or
modaf nil) prescribed at an adequate dosage range should prompt a reevaluation for other
possible causes of or contributory factors for excessive daytime sleepiness.
n Medications for cataplexy, hypnagogic hallucinations, and sleep paralysis (typically
REM suppressants):
Tricyclic antidepressants (TCAs), such as imipramine (Tofranil) and clomipramine
(Anafranil), selective serotonin reuptake inhibitors (SSRIs), such as f uoxetine (Pro-
zac), and other antidepressants such as venlafaxine (Effexor) block the presynaptic
reuptake of catecholamines, including serotonin. There is more evidence for their eff -
cacy in treating cataplexy than for the other related symptoms of narcolepsy. Dosing typi-
cally starts at lower than the usual antidepressant dose and is titrated up; abrupt discon-
tinuation may cause rebound cataplexy, sleep paralysis, and hypnagogic hallucinations.
Side effects of TCAs include dry mouth, urinary retention, and nausea. Common side
effects of SSRIs include nausea, vomiting, and agitation; more activating SSRIs, such as
f uoxetine, may exacerbate sleep disruption. SSRIs have also been linked to an increase
in suicidal ideation in children and adolescents. It should be noted that both TCAs and
SSRIs might exacerbate PLMs during sleep. Because of signif cant potential toxicity of
TCAs in overdose, these medications should be used with extreme caution in situations
in which accidental or deliberate ingestion may occur and their use is not recommended
in pre-pubertal children.
n Other medications for narcolepsy: Sodium oxybate, a gamma-aminobutyric acid (GABA)
B receptor agonist has been approved by the Food and Drug Administration as the only
medication for the treatment of both EDS and cataplexy narcoleptic patients (adults over the
age of 16 years). Sodium oxybate is believed to modulate serotonin, dopamine, and opioid
activity as well as to increase slow-wave sleep. It appears to be effective for symptoms of
EDS, cataplexy, and disrupted nocturnal sleep, and may be effective for the treatment of
hypnagogic hallucinations and sleep paralysis. The typical adult dose is 6 to 9 gm and the
comparable pediatric dose appears to be about 60 mg/kg; due to the short elimination half-
life (4060 minutes), one half of the therapeutic dose is administered at bedtime, and the
second half 2.5 to 4 hours later. Side effects may include nausea and vomiting, tremor, con-
stipation, headache, and suicidal ideation, It should also be noted that sodium oxybate has a
signif cant potential for abuse and its availability is rigorously controlled; both patients and
physicians must register with the pharmaceutical company that supplies the drug.
Pr o g n o SiS
Narcolepsy is a chronic, lifelong disorder that will always require management; patients with
narcolepsy typically have a normal lifespan. The goal of treatment is adaptation and improved
quality of life.

Explain what narcolepsy is in basic terms: a chronic neurological disorder in which there
is an imbalance in the control of sleep and wakefulness.
Explain what is currently understood regarding the genetic and neurological basis of
narcolepsy.
Emphasize the patients relative lack of control over excessive daytime sleepiness, espe-
cially sleep attacks, and discuss possible related safety issues (e.g., driving).
Review the daytime consequences of narcolepsy because parents may not attribute day-
time sleepiness, academic problems, and apparent inattention, for example, to a sleep
problem.
Discuss the manifestations of the other common symptoms of narcolepsy (i.e., cataplexy,
hypnagogic hallucinations, sleep paralysis), and the relative possibility that the patient may
develop these feature in the future.
Emphasize that narcolepsy is currently viewed as a lifelong disorder but one that may
be controlled with behavioral and medication treatments.
Discuss the risks and benef ts of treatment options including lifestyle changes and medi-
cation choices.
Encourage any parent or other family member who experiences EDS to be evaluated for
narcolepsy.
See Appendix D14 for a parent handout on narcolepsy.
Delayed Sleep Phase Disorder
17
Delayed sleep phase disorder (DSPD), a circadian rhythm disorder, involves a signif cant, per-
sistent, and intractable phase shift in sleepwake schedule (later sleep onset and waketime) that
conf icts with the individuals normal school, work, and/or lifestyle demands. It is the timing
rather than the quality of sleep per se that is problematic, as individuals with DSPD typically
do not have sleep complaints if they are allowed to sleep on their preferred (later) schedule. The
most common clinical presentation is sleep initiation insomnia when the individual attempts to
fall asleep at a socially acceptable desired bedtime, accompanied by extreme diff culty getting up
in the morning, even for desired activities, and daytime sleepiness.
DSPD may occur at any age, but is most common in adolescents and young adults. Individu-
als with DSPD often start out as night owls; that is, they have an underlying predisposition or
circadian preference for staying up late at night and sleeping late in the morning, especially on
weekends, holidays, and summer vacations. The typical sleepwake pattern in DSPD is a consis-
tently preferred bedtime or sleep onset time after midnight (typically 2:006:00 a.m.) and wake-
time after 10:00 a.m. In order to cope, many adolescents with DSPD take lengthy afternoon naps
or catch up by extending sleep on weekends and days off. With DSPD, even highly motivated
adolescents are unable to shift their sleep back to an earlier time without assistance.
Delayed Sleep Phase Disorder

Delayed sleep phase disorder, a circadian rhythm disorder, involves a signif cant and persistent
shift in an individuals sleepwake schedules that interferes with environmental demands, usu-
ally resulting in signif cant daytime sleepiness and academic and behavior problems.
ePiDeMio l o g y
n Prevalence: Studies indicate that DSPD affects approximately 7% to 16% of adolescents.
n Age of onset: Onset is typically during adolescence, when an underlying circadian preference
for late bedtime and waketime (eveningness) may become exaggerated during the normal
pubertal shift to later sleep onset and waketimes. Younger children with a marked phase delay
may also develop DSPD.
In order to fully understand the sleep initiation insomnia and profound diff culties in morning
waking in patients with DSPD, it is important to recall some basic principles of circadian biology.
First, in the several hours prior to the habitual preferred bedtime, there is a marked circadian-
mediated increase in wake promotion, the so-called forbidden zone. Thus, an individual with
DSPD who gets into bed at a normal bedtime is typically attempting to fall asleep during this
period of maximum alertness. Similarly, the period 1.5 to 2 hours before the preferred wake time
represents the nadir of wakefulness promotion by the circadian system, resulting in extreme dif-
f culty in becoming alert at the desirable waketime in patients with DSPD. This morning sleepi-
ness is further compounded by an increased homeostatic sleep drive that results from chronically
144
DELAyED SLEEP PHASE DISORDER 145
insuff cient sleep in these individuals as schedule demands change (e.g., earlier school start times
in high school).
The etiology of DSPD is still unknown, with many theories postulated. Some theorize that
DSPD involves an intrinsic abnormality in the circadian oscillators that govern the timing of
the sleep period. That is, there may be a problem in the synchronization or entrainment of the
circadian clock to environmental cues or an intrinsic circadian period that is longer than average.
Evidence supporting a primarily neurobiological substrate for this disorder also includes persis-
tence of the disorder in the face of signif cant academic and social consequences, high rates of
relapse following successful intervention, and some evidence supporting a genetic component.
Others postulate that DSPS involves abnormalities in the circadian phase response curve to light;
not only are these patients less likely to be exposed to morning light because they sleep later and
more likely to be exposed to evening light as a result of delayed bedtimes, but they may have an
underlying increased sensitivity to even low levels of evening light.
In addition, those children or adolescents experiencing diff culties in school or school refusal
may present with a preferred or motivated phase delayrisk factors that favor persistence of
symptoms and make the disorder more diff cult to treat. The relationship between psychiatric
disorders and DSPD is a complex one; DSPD may result in symptoms of depression, and the
insomnia associated with primary depression may mimic DSPD.
n Sleep onset at a consistently late time, usually after midnight in adolescents.
n Minimal diff culty with sleep maintenance, with infrequent nighttime awakenings.
n Signif cant diff culty waking at the required time (e.g., waking for school) and decreased
alertness in the morning.
n Persistent diff culty going to sleep at an earlier time, rather than the preferred bedtime.
Although, with effort, the individual with DSPD may temporarily achieve sleep onset at an
earlier time, there is a natural tendency to drift to the later preferred bedtime.
n Complaints of insomnia, if the adolescent attempts to go to sleep at an earlier time; how-
ever, no sleep onset insomnia is experienced if bedtime coincides with the preferred sleep
onset time (e.g., on weekends, school vacations).
n Daytime sleepiness (e.g., napping, dozing off, mood changes, inattentiveness), in addition
to diff culty waking in the morning, may be experienced throughout the day due to chronic
insuff cient sleep.
See Table 17.1.
Associated Features
n Bedtime resistance and delayed sleep onset in younger children. Children with an evening
preference may have diff culty falling asleep at an age-appropriate bedtime, leading to pro-
tests, excuses, and oppositional behavior.
n Evening or night preference with optimal functioning (second wind) during the late after-
noon, evening, and night hours.
n Weekend oversleep until late morning or early afternoon in an attempt to make up for
weekday insuff cient sleep. Extended sleep periods are often seen during vacations as well,
especially in the f rst few days of the vacation.
n Poor school performance, as adolescents with DSPD are often chronically sleep deprived and
thus, even when highly motivated, may perform poorly in school.
n School tardiness and frequent absenteeism is often present. The sleep problem may lead
to a downward spiral of missed school due to the frequent tardiness and absences, resulting
Diagnostic criteria: Circadian rhythm sleep disorder, delayed sleep phase

t ABl e 17.1. type (delayed sleep phase disorder [327.31])
General Criteria for Circadian Rhythm Sleep Disorder
A. There is a persistent or recurrent pattern of sleep disturbance due primarily to one of the following:
1. Alterations of the circadian timekeeping system.
2. Misalignment between the endogenous circadian rhythm and exogenous factors that affect the
timing or duration of sleep.
B. The circadian related disruption leads to insomnia, excessive daytime sleepiness, or both.
C. The sleep disturbance is associated with impairment of social, occupational, or other areas of func-
tioning.
Specif c Criteria for Delayed Sleep Phase Type (Delayed Sleep Phase Disorder)
A. There is a delay in the phase of the major sleep period in relation to the desired sleep time and
waketime, as evidenced by a chronic or recurrent complaint of inability to fall asleep at a desired
conventional clock time together with the inability to awaken at a desired and socially acceptable
time.
B. When allowed to choose their preferred schedule, patients will exhibit normal sleep quality and
duration for age and maintain a delayed, but stable, phase of entrainment to the 24-hour sleepwake
pattern.
C. Sleep log or actigraphy monitoring (including sleep diary) for at least 7 days demonstrates a stable
delay in the timing of the habitual sleep period. (Note: In addition, a delay in the timing of other
circadian rhythms, such as the nadir of the core body temperature rhythm or DLMO, is useful for
conf rmation of the delayed phase.
D. The disturbance is not better explained by another sleep disorder, medical or neurological disorder,
in academic failure and, subsequently, in more school avoidance. In severe cases, the child or
adolescent may give up going to school altogether.
eVAl uAt io n
n Developmental and school history: Parents often note that these children are often lifelong
night owls. Questions regarding morningnesseveningness (owllark) preferences may
reveal a pattern of alertness and sleepiness during the day that is delayed relative to normal cir-
cadian peaks and troughs. Questions about feel best times for going to bed, morning waking,
and performing various tasks (e.g., taking tests, playing a sport) may be helpful in conf rming a
pattern of delayed circadian rhythms. Furthermore, academic problems are common and usu-
ally a result of the sleep disorder. When academic concerns predate the sleep problem, there
may be an element of school avoidance compounding the situation.
n Family history: The history may reveal other family members with a marked evening circa-
dian preference. Approximately 40% of individuals with DSPD have a positive family history.
n Behavioral assessment: It is extremely important to assess for possible substance use and
psychiatric issues, including depression, anxiety disorders, school refusal, and school phobia.
n Physical examination: The examination is generally benign.
n Diagnostic tests:
n Sleep diaries: Recording of sleepwake patterns is a very important component of the
evaluation for DSPD and will often graphically demonstrate the sleep phase delay and con-
sistent fall-asleep time.
MorningnessEveningness Preference
Sample questions to assess morningness or eveningness circadian preference:
1. If you were entirely free to plan your evening and had no commitments the next day, at what
time would you choose to go to bed?
1. 8:009:00 p.m.
2. 9:0010:15 p.m.
3. 10:15 p.m.12:30 a.m.
4. 12:301:45 a.m.
5. 1:453:00 a.m.
2. For some reason you have gone to bed several hours later than normal, but there is no need
to get up at a particular time the next morning. Which of the following is most likely to
occur?
1. Will wake up at the usual time and not fall asleep again.
2. Will wake up at the usual time and doze thereafter.
3. Will wake up at the usual time but will fall asleep again.
4. Will not wake up until later than usual.
3. You have to take a 2-hour test. If you were entirely free to choose, in which of the following
periods would you prefer to take the test?
1. 8:0010:00 a.m.
2. 11:00 am1:30 p.m.
3. 3:005:00 p.m.
4. 7:009:00 p.m.
4. If you had no commitments the next day and were entirely free to plan your own day, what
time would you get up?
1. 5:006:30 a.m.
2. 6:307:45 a.m.
3. 7:459:45 a.m.
4. 9:4511:00 a.m.
5. 11:00 a.m.12:00 p.m.
Adapted from Horne JA, Ostberg O. A self-assessment questionnaire to determine morning-
nesseveningness in human circadian rhythms. Int J Chronobiol 1976;4:97110.
n Actigraphy: Although currently still largely a research tool, the use of an actigraph (a
wristwatch-like device that measures and stores data regarding body movements over time;
this is transformed with a computerized algorithm into sleepwake patterns; see Chapter 3)
in conjunction with a sleep diary may be a very useful adjunct to more objectively docu-
ment sleepwake patterns over a period of several weeks.
n Polysomnography: In general, overnight sleep studies are not indicated unless there is a
concern regarding possible underlying sleep-disrupting factors.

n Insomnia: Diff culties falling asleep at night may be the result of psychophysiologic or
learned insomnia (see Chapter 18). One clear differentiating factor between the two is that
children and adolescents with DSPD have few or no diff culties falling asleep if they go to bed
at their preferred sleep onset time. In contrast, individuals with insomnia experience diff cul-
ties falling asleep no matter what time they go to bed and often do not exhibit a consistent
fall-asleep time. However it should be noted that, in clinical practice, patients with DSPD
frequently develop a secondary conditioned insomnia due to spending prolonged periods of
time in bed attempting to fall asleep; thus implementation of behavioral interventions targeted
at reversing this situation (e.g., stimulus control, sleep restriction) may be necessary.
n Restless legs syndrome (RLS): Symptoms of RLS (e.g., an urge to move the extremities ac-
companied by uncomfortable sensations in the legs that is worse with inactivity and relieved
by movement; see Chapter 15) may present as delayed sleep onset.
n Poor sleep hygiene: Maintenance of an erratic sleep schedule and use of caffeine or other sub-
stances may result in complaints of diff culty falling asleep. However, individuals with DSPD
will still have delayed sleep onset even after the establishment of an appropriate sleep schedule
and the institution of appropriate sleep habits (see Chapter 4).
n Circadian preference: Although a tendency towards eveningness (night owl) is a risk fac-
tor for DSPD, typically this preference does not have the same intractable quality and persis-
tence, and does not result in signif cantly compromised functioning.
n Lifestyle issues and voluntary curtailment of sleep: For example, socializing and late-night
television viewing can result in insuff cient sleep and diff culty awakening in the morning, but
patients do not complain of insomnia.
n School avoidance or refusal: Adolescents with primary school avoidance, such as that result-
ing from an anxiety disorder or related to a learning disability and academic failure, may have
a late bedtime and appear diff cult to awaken in the morning. In this situation, the sleep sched-
ule is not intractable, and a more appropriate sleep schedule may be maintained on weekends
and holidays. However, school avoidance frequently coexists with and exacerbates DSPD.
n Psychiatric disorders: Depression, bipolar disorder, and anxiety disorders, are associated
with diff culty falling asleep, but the set sleepwake schedule pattern that is characteristic of
DSPD is not usually present in these situations, and the sleep disturbance will co-vary with the
psychiatric symptoms.
MAn Ag eMen t
w hen to r efer
Children or adolescents with DSPD who also demonstrate symptoms of other underlying sleep
disrupters (e.g., obstructive sleep apnea) may require referral to a sleep specialist. When there are
concerns regarding school refusal, depression, or other psychological issues, referral to a mental
health specialist is warranted. Treatment programs involving chronotherapy, light therapy, and
melatonin are often best accomplished by or in consultation with a sleep specialist.
t reatment
The goal in the treatment of DSPD is basically twofold: f rst, shifting the sleepwake schedule
to an earlier time, and second, maintaining the new schedule. The choice of a target bedtime and
waketime should be discussed with the patient and family in the context of balancing the primary
goal of adequate sleep with lifestyle considerations. The initial treatment phase is generally more
intense and requires strict adherence to the treatment protocol; the maintenance phase is neces-
Motivation: Key to Successful Treatment

A highly motivated adolescent is required, as achieving success in realigning an adolescents
sleep schedule and maintaining the change can be diff cult. Thus, issues such as the motivation
of the child or adolescent, the resources of the family, and the existence of any psychiatric or
substance abuse problems must f rst be addressed before success can be expected. Suff cient
motivation for (and barriers to) instituting change must be explored. Similar to many other
behavioral interventions, a well-developed plan is essential to achieve success. Behavioral
contracts are often necessary, and psychological and family issues may need to be addressed
if resistance to change is encountered, as is frequently the case.
sary because of the natural tendency of these individuals to gradually shift to a later bedtime and
waketime.
Successful treatment requires a motivated patient and family, and a coordinated approach
that includes changes in sleep habits. Often, a combination of sleep scheduling, melatonin, and/
or bright-light therapy is used. However, it should be noted, that there is overall little consensus,
particularly in adolescents, regarding the relative contribution of these various treatment modali-
ties to treatment success or even the optimal procedures to implement them. Ideally, timing of
treatment should be based upon direct measurements of the phase response curve (e.g., core
body temperature, salivary melatonin levels); however, this is clearly not yet practical in most
clinical settings. Therefore, the following recommendations are based on guess-timates of cir-
cadian timing that are applicable to clinical practice, but consultation with a sleep specialist may
be warranted.
Shifting the Circadian Rhythm: Phase Advancement and Phase Delay (Chronotherapy)
Treatment for DSPD involves shifting the circadian sleepwake rhythm so that sleep onset and
morning waking occurs at the desired times. There have been positive case reports documenting
the eff cacy of phase shifting, although no controlled trials in adolescents have been conducted.
There are two primary strategies to accomplish this shift:
n Phase advancement: Phase advancement is used when the difference between the current
later sleep onset time and the target earlier sleep onset time is less than 3 hours. Bedtimes
and waketimes are shifted earlier by approximately 15 to 30 minutes per day, beginning with
the time that the adolescent is able to consistently fall asleep without diff culty. Thus, if the
patient is not typically falling asleep until 1:30 a.m., then the f rst night bedtime is set for 1:15
a.m., then 1:00 a.m., and so on. The shift is done gradually to increase the likelihood that the
patient will be able to fall asleep relatively quickly at the successively earlier bedtimes, which
avoids prolonged periods of lying awake in bed. The pace (shifting the bedtime earlier every
day versus every 2 or 3 days) and the time increment of the shift (advancing by 5 minutes
versus 15 or 30 minutes) is somewhat dependent on the chronicity of the delayed sleep phase
problem (the longer the duration, the more gradual the process needed), the patients ongoing
response to treatment, and how quickly the shift to the target bedtime and waketime must be
accomplished.
An additional sleep scheduling strategy that is a key component to successful phase ad-
vance is to simultaneously advance the morning wake time. This process involves setting the
morning waketime at the target earlier waketime right at the beginning of treatment while
more gradually advancing the bedtime over several weeks, resulting in relative sleep restric-
tion. Sleep restriction assists in accomplishing the phase shift by increasing the homeostatic
sleep drive during the initial period of treatment, thus increasing the likelihood that the patient
will be ready to fall asleep at the earlier bedtime.
Sample Phase Advancement Schedule

Bedtime Waketime
Baseline night 1:30 a.m. 10:00 a.m.
Treatment night 1 1:15 9:45
Continue to advance bedtime and waketime by 15 minutes nightly.
Goal night 10:30 p.m. 6:30 a.m.
n Phase delay (chronotherapy): Phase delay is used for more severely delayed sleep phase
cases (e.g., shift is greater than 3 hours) and involves delaying bedtime and waketime by 2 to
3 hours daily to every other day. Thus, if an adolescent usually goes to bed at 4:00 a.m., on the
f rst day of intervention bedtime is scheduled for 6:00 a.m. (or 7:00 a.m.), the second day 9:00
a.m., and so on, until the desired bedtime is achieved. Adolescents are often compliant during
the f rst phase of this treatment because of the perception that they are being allowed to stay
up later each day. Since the patient is usually sleepy by the successively later scheduled sleep
times, delayed sleep onset is not a problem; however, the patient may have diff culty remaining
awake for an additional 2 to 3 hours each day and may need family support and supervision
to accomplish this. Chronotherapy requires considerable motivation and commitment on the
adolescents part as the treatment phase is quite disruptive, and will necessitate missing school
during the period in which sleep is scheduled to occur in daytime hours. If possible, chrono-
therapy should be timed to coincide with a school vacation to avoid missing school during the
period of daytime sleep.
Sample Phase Delay Schedule

Bedtime Waketime
Baseline 4:30 a.m. 12:30 p.m.
Continue to advance bedtime and wake time by 3 hours nightly.
Goal night 10:30 p.m. 6:30 a.m.
n Sleep hygiene: The patients sleep habits should be reviewed and reorganized if necessary,
with an emphasis on the development of positive sleep routines and avoidance of caffeine.
Caffeine and other stimulant use can also contribute to a delayed sleep onset, especially late
afternoon and evening consumption. Secondary poor sleep habits, such as lying in bed awake
for long periods, also need to be addressed (see Appendices C7 and C8).
n Avoid napping and maintain sleep schedule: Napping must be avoided to help consolidate
sleep. In addition, the patient must maintain a consistent sleep schedule both on weekdays and
weekends, even after the initial treatment phase is completed.
n Bright light: Although there are no established guidelines regarding intensity, duration, and
timing of light exposure, scheduled exposure to bright light may be benef cial to help set the
sleepwake rhythm to an earlier time. However, light exposure at the wrong circadian time
(i.e., before the nadir in core body temperature) may actually exacerbate the phase delay; a
reasonable estimate of circadian nadir is 2 hours before the habitual (preferred) waketime. In
uncomplicated or mild cases, light exposure can consist of eating breakfast in a sunny area of
the home and spending time outdoors f rst thing in the morning. In more diff cult cases, morn-
ing exposure to 20 to 30 minutes of bright light (2,500 to 10,000 lux) provided by a specially
designed light box unit in the early morning (e.g., 68 a.m.) can be benef cial. Patients should
also avoid light exposure in the evening, and dark glasses may be worn during exposure to
sunlight late in the day. Commercially produced light boxes or visors are portable units, which
combine high-output (2,500 to 10,000 lux) f uorescent tubes with ref ectors, can be obtained
online at such sites as www.litebook.com, www.apollolight.com, and www.lighttherapyprod-
ucts.com. Some studies have suggested that short wavelength (blue) light may be relatively
more effective in phase shifting. Light exposure therapy should be continued for at least 2 to 4
weeks.
Tips for Bright Light Exposure Therapy

As each manufacturer has different specif cations, it is important to read instructions care-
fully for the individual light box or lamp unit.
The UV f lter (if needed) should be in place before use.
The patient should not look directly at the light but make sure the light shines on the eyes;
no sunglasses should be worn. Patients may read, watch television, or eat during the period
of light exposure.
Distance from the light box unit and head position determines the light intensity delivered.
If engaging in other activities (reading, eating) while using the light box, the light should be
positioned about 16 to 20 inches from the patient, at head or chest level.
Some patients experience eye or skin irritation (especially patients with fair skin, light eye
color), queasiness, and headaches with use of a light box. If this occurs, increasing the dis-
tance of the light box and decreasing the exposure time before gradually increasing it may
help.
Some antibiotics and acne or retinoic acid creams may increase light sensitivity.
n Pharmacotherapy:
n Melatonin: There have been several studies indicating the eff cacy of melatonin to promote
a corrective phase advance, although with variable results and relapse following discontinu-
ation. These studies have found that physiologic doses of oral melatonin (0.3 to 0.5 mg)
administered in the afternoon or early evening (i.e., 57 hours before the habitual sleep on-
set time) seem to be most effective in advancing the sleep phase. In general, the earlier the
melatonin is administered, the larger the phase advance; however, similar to phototherapy,
inappropriately timed melatonin administration may worsen the phase delay. It should be
noted that melatonin also has hypnotic (sedating) effects when given in larger doses just
before bedtime. Unfortunately, there is no consensus on the best time to take melatonin to
achieve a phase advance. Also note that there are some potential risks with the use of mela-
tonin (see Chapter 20).
n Hypnotics: Hypnotic use has been suggested as a means to induce sleepiness at the desired
bedtime. To date, there is insuff cient evidence as to the safety and eff cacy of such use in
the treatment of DSPS.
n Additional issues:
n Maintenance phase: Treatment for DSPD usually involves an intense treatment phase,
during which there can be no deviation from the prescribed schedule. Following this phase,
there will be a protracted maintenance phase, which is also quite diff cult. Many f nd this
phase to be the more diff cult aspect of treatment, as there will continue to be an evening
preference. All it takes is one weekend or vacation in which old habits are resumed to undo
all achievements. Once the new schedule is f rmly entrenched an occasional late night is
permitted, but the adolescent should not be allowed to sleep more than 1 or 2 hours later
than his or her usual weekday waketime. In addition, patients should continue to avoid
bright light in the evenings, whereas light exposure in the morning should be as bright as
possible. Daytime napping should continue to be avoided, as sleeping during the day will
decrease sleepiness at bedtime resulting in a delay of sleep onset.
n Other issues: Other issues must be addressed if warranted, such as school refusal and other
psychiatric problems (e.g., depression, substance use).
Pr o g n o SiS
DSPD is often a chronic disorder but with high motivation can be changed. However, a high rate
of relapse following initial treatment success is common.

Describe delayed sleep phase disorder (DSPD) and emphasize the persistent nature of the
circadian clock with this disorder.
Discuss treatment options including phase advancement or phase delay, light exposure,
and melatonin use.
Encourage parents to have the child or adolescent take responsibility for the sleep
schedule.
Explain the role of sleep hygiene in treatment success.
Discuss issues of sleep schedule maintenance following the shift in the circadian rhythm.
See Appendix D14 for a parent handout on DSPD.
Insomnia 18
Insomnia is broadly def ned as subjective diff culty initiating and/or maintaining sleep, early
morning awakening, and non-restorative sleep (although the latter two complaints are uncom-
mon in childhood). These sleep complaints must also result in some degree of impairment in
daytime functioning, which may range from fatigue, irritability, lack of energy, and mild cogni-
tive impairment to more signif cant effects on mood and school performance. Insomnia com-
plaints may be of a short-term and transient nature (usually related to an acute stressful event),
or may be characterized as long term and chronic. It is important to conceptualize insomnia as 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; an analogy would be a
presenting complaint of pain, which is clearly a symptom, for which a specif c etiology has to be
identif ed before appropriate treatment can be initiated.
Because the criteria for signif cant diff culties initiating and maintaining sleep is obviously
often quite subjective and dependent upon a number of factors (e.g., parental awareness, child
temperament, environmental conditions), a consensus def nition of pediatric insomnia has been
developed. This def nition states that pediatric insomnia involves repeated diff culty with sleep
initiation, duration, consolidation, or quality that occurs despite age-appropriate time and oppor-
tunity for sleep and results in daytime functional impairment for the child and/or family.
Although insomnia is one of the most common sleep complaints in adults, parents (as well as
children and adolescents themselves) are much more likely to present with bedtime problems
or nightwakings rather than insomnia as the chief concern. The etiology and management
of the most common causes of bedtime resistance (e.g., inadequate limit setting) and nightwak-
ings (e.g., inappropriate sleep onset associations) are discussed in Chapters 6 and 7 (behavioral
insomnia of childhood). The focus of this chapter is on what is termed psychophysiological or
primary insomnia as the cause of diff culties in initiating or maintaining sleep in children and
adolescents.
Symptoms of insomnia can be associated with a variety of underlying sleep problems or medi-
cal issues. When the insomnia is not secondary to another sleep disturbance, or to a psychiatric
or medical problem, it is referred to as psychophysiological insomnia (according to the Inter-
national Classif cation of Sleep Disorders II) or primary insomnia (according to the Diagnostic
and Statistical Manual, 4th ed.); also sometimes called learned insomnia or behavioral insom-
nia. Primary or psychophysiologic 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 intensif ed by this anxiety about sleep-
Insomnia
Insomnia involves diff culty falling asleep and/or maintaining sleep, including early morning
awakenings. In many cases, insomnia is a symptom secondary to another sleep or medical dis-
order. In contrast, primary insomnia is accompanied by learned sleep-preventing associations
and physiological arousal, resulting in a complaint of sleeplessness and decreased daytime
functioning.
153
lessness. Thus, in contrast to behavioral insomnia of childhood, which is most often a result of
parent behavior, primary insomnia represents a combination of an inherent predisposition and
maladaptive behaviors adopted by the individual with insomnia in an attempt to address the sleep
problems. For simplif cation purposes, the term insomnia will be used throughout this chapter to
refer to the diagnosis of psychophysiological or primary insomnia.
ePiDeMio l o g y
n Prevalence: Recent studies on insomnia in adolescents found that 9% to 13% experience
chronic insomnia, with up to 35% experiencing insomnia at least several times a month. In
contrast, primary insomnia appears to be quite uncommon in prepubertal children.
n Gender: Studies indicate that insomnia has an increased prevalence in girls post-puberty,
consistent with adults.
n Lower socioeconomic status: Low socioeconomic status associated with increased insomnia.
Studies indicate minimal differences in the prevalence of insomnia across ethnic groups.
There are a number of theories as to the mechanism of insomnia. Factors that have been studied
include physiologic arousal, emotional arousal, cognitive arousal, and faulty conditioning; how-
ever, empirical evidence is inconclusive. The two factors that are the most substantiated are:
n Sleep behaviors (maladaptive sleep habits), including excessive time in bed, irregular sleep
wake schedules, and daytime napping.
n Sleep cognitions (beliefs and attitudes about sleep and the possible consequences), such
as Ill never be able to fall asleep tonight, and If I cant fall asleep, I wont be able to get up
in the morning, Ill miss taking the test in my f rst class, and Ill fail the course).
Insomnia most likely results from a combination of predisposing factors (such as genetic vul-
nerability and underlying medical or psychiatric conditions) with precipitating factors (acute
stress) and perpetuating factors (poor sleep habits, caffeine use, maladaptive cognitions about
sleep).
In adults, a number of predisposing risk factors for insomnia have been identif ed:
n Personality traits:
n Hyperarousal (e.g., racing thoughts, increased vigilance)
n Obsessional thinking style (I can never fall asleep easily.)
n Repression of emotions (I wont let that bother me.)
n Medical and psychological problems: These include congestive heart failure, chronic ob-
structive pulmonary disease, anxiety disorders, and depression.
n Gender: Women are more at risk for developing insomnia.
n Family history: It is more likely that the insomnia is based on learned maladaptive sleep hab-
its, but there may be a genetic contribution in some cases.
n Sleep complaints: The insomnia may present as diff culty falling asleep, diff culty maintain-
ing sleep, or, less commonly, early morning awakenings. Thus, overall sleep eff ciency (time
asleep divided by time in bed) is reduced. Nonrestorative sleep may be expressed as subjec-
tive sleepiness and fatigue as a result of poor sleep quality despite adequate sleep duration and
in the absence of identif able sleep disrupters.
n Learned sleep-preventing associations: Insomnia, by def nition, involves learned sleep-pre-
venting associations. These may present as:
n Excessive daytime worrying about being unable to fall asleep or stay asleep.
INSOmNIA 155
n Trying too hard to fall asleep at bedtime, although sleep comes easily at other times (e.g.,
while watching television).
n Conditioned association of being in bed awake instead of asleep. Interestingly, indi-
viduals with insomnia may fall sleep more easily in other environments that do not have the
same conditioned associations of anxiety and wakefulness with the bed and bedroom.
n Increased somatic tension related to sleep, including agitation or muscle tension.
n Decreased daytime functioning: Insomniacs often complain of subjective cognitive impair-

ment and poor functioning.
See Tables 18.1, 18.2, and 18.3.
Associated Features
n Depression, changes in mood, and decreased sense of well-being. Studies also indicate that
insomnia is a signif cant risk factor for future depression, and that persistent insomnia may
predict depression relapse. Suicidal ideation and suicide attempts are also associated with
insomnia. It should be noted that in adults with primary insomnia, a concomitant psychiatric
disorder is found in 25% to 30% of cases.
n Daytime fatigue, including reduced energy, although rarely excessive daytime sleepiness.
n Poor school performance, related to decreased mood and fatigue.
n Excessive caffeine use, to maintain wakefulness and combat daytime fatigue.
n Alcohol, marijuana, and other drug use are associated with insomnia.
n Hypnotic use, including prescription or over-the-counter hypnotics (e.g., antihistamine prepa-
ration), is common in adults with insomnia and may be present in adolescent and college-aged
patients.
Insomnia during adolescence is a signif cant risk factor for future development of de-
pression and other mental health problems.
t ABl e 18.1. Diagnostic criteria (ICSD): General criteria for insomnia
A. A complaint of diff culty initiating sleep, diff culty maintaining sleep, or waking up too early or
sleep that is chronically nonrestorative or poor in quality. In children, the sleep diff culty is often
reported by the caretaker and may consist of observed bedtime resistance or inability to sleep inde-
pendently.
B. The above sleep diff culty occurs despite adequate opportunity and circumstances for sleep.
C. At least one of the following forms of daytime impairment related to the nighttime sleep diff culty
is reported by the patient:
1. Fatigue or malaise
2. Attention, concentration, or memory impairment
3. Social or vocational dysfunction or poor school performance
4. Mood disturbance or irritability
5. Daytime sleepiness
6. Motivation, energy, or initiative reduction
7. Proneness for errors or accidents at work or while driving
8. Tension, headaches, or gastrointestinal symptoms in response to sleep loss
9. Concerns or worries about sleep.
t ABl e 18.2. Diagnostic criteria (ICSD): Psychophysiological insomnia (307.42)
A. The patients symptoms meet the criteria for insomnia.

B. The insomnia is present for at least 1 month.
C. The patient has evidence of conditioned sleep diff culty and/or heightened arousal in bed as indi-
cated by one or more of the following:
1. Excessive focus on and heightened anxiety about sleep
2. Diff culty falling asleep in bed at the desired bedtime or during planned naps, but no diff culty
falling asleep during other monotonous activities when not intending to sleep
3. Ability to sleep better away from home than at home
4. Mental arousal in bed characterized either by intrusive thoughts or a perceived inability to voli-
tionally cease sleep-preventing mental activity
5. Heightened somatic tension in bed ref ected by a perceived inability to relax the body suff cient-
ly to allow the onset of sleep.
D. The sleep disturbance is not better explained by another sleep disorder, medical or neurological
disorder, mental disorder, medication use, or substance use disorder.
t ABl e 18.3. Diagnostic criteria (DSM-IV): Primary insomnia
A. The predominant complaint is diff culty initiating or maintaining sleep, or nonrestorative sleep, for
at least 1 month.
B. The sleep disturbance (or associated daytime fatigue) causes clinically signif cant distress or im-
pairment in social, occupational, or other important areas of functioning.
C. The sleep disturbance does not occur exclusively during the course of narcolepsy, breathing-related
sleep disorder, circadian rhythm sleep disorder, or a parasomnia.
D. The disturbance does not occur exclusively during the course of another mental disorder (e.g.,
major depressive disorder, generalized anxiety disorder, delirium).
E. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a
medication) or a general medical condition.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, fourth edition (DSM-IV).
Washington, DC: American Psychiatric Press, 1994:557.
eVAl uAt io n
n Medical history: A thorough medical history should include evaluation of other possible
causes of sleep onset and maintenance diff culties, including sleep disorders (e.g., obstructive
sleep apnea, restless legs syndrome), acute and chronic medical disorders (especially pain
conditions), psychiatric disorders, and alcohol and drug use. Concurrent medications should
be reviewed as possible contributory factors, especially psychostimulants (see Chapter 20).
Caffeine use and cigarette smoking may also play a role.
n Developmental and school history: The history is generally normal. Adolescents with pri-
mary insomnia may be anxious or depressed. Many are academic overachievers. This situa-
tion may lead to a cycle of heightened anxiety about the effects of the insomnia on academic
performance and even more diff culty falling asleep.
n Family history: Symptoms are often present in f rst-degree relatives, which may be an indica-
tion of genetic vulnerability and/or environmental modeling.
n Behavioral assessment: An assessment may reveal mood disturbances and anxiety disorders.
n Physical examination: The examination is usually unremarkable.
INSOmNIA 157
n Diagnostic tests:
n Sleep diaries will reveal prolonged sleep onset and/or nighttime awakenings and/or early
morning awakenings. Sleep diaries often yield important additional information on mal-
adaptive bedtime activities and behaviors when insomnia is suspected. Sometimes, sleep
diaries may indicate that the patients subjective perception of sleep diff culty is actually
signif cantly worse than the sleep log evidence would suggest (termed sleep state misper-
ception).
n Polysomnography is rarely indicated in the evaluation of insomnia unless an additional
underlying sleep disorder is suspected.

n Actigraphy can provide documentation of prolong periods of wakefulness. Alternatively,
some individuals with insomnia have sleep state misperception; i.e., they tend to perceive
and report getting less sleep than they actually do, and having more and longer awakenings
than can be objectively documented. In the latter situation, actigraphy can conf rm that the
patient is actually sleeping better than assumed, which may help to alleviate anxiety. Actig-
raphy is also benef cial when parents are unclear as to the severity of sleeplessness, either
overestimating or underestimating sleep.

Insomnia, as discussed above, is a symptom that can be the result of a number of sleep disorders.
Thus, differential diagnosis is critical in the diagnosis of insomnia.
n Transient insomnia: Transient, or short-term, insomnia typically occurs in individuals with
previously normal sleep. Transient insomnia can be the result of sleeping in an unfamiliar or
non-conducive (e.g., too noisy, too hot) sleep environment, stressful life event, disruption of
sleep schedule (e.g., trip, jet lag), or an illness.
n Delayed sleep phase disorder (DSPD): DSPD is characterized by few or no diff culties fall-
ing asleep at the individuals preferred (later) bedtime, in contrast to a patient with insomnia
who typically complains of delayed sleep onset no matter what time he or she goes to bed.
In addition, when allowed to choose their own schedule, patients with DSPD, fall asleep and
wake at consistent times (see Chapter 17).
n Inadequate sleep hygiene: Poor sleep habits (see Chapter 14), including maintaining an er-
ratic sleep schedule or the use of caffeine or other substances, and inadequate sleep can co-
exist with insomnia, although patients with psychophysiological insomnia often continue to
experience sleep disturbances even after maintaining adequate sleep hygiene. In those with
psychophysiological insomnia, there is conditional arousal to the sleep setting.
n Lifestyle issues: Practices such as staying up late to socialize or engage in other activities
(e.g., television viewing) are voluntary behaviors that may result in an individuals habitually
going to bed late.
n RLS and periodic limb movement disorder (PLMD): Individuals with RLS (see Chapter
15) often present with diff culty falling asleep at bedtime, whereas middle-of-the-night wak-
ings can be associated with PLMD. The key differentiation between insomnia and these disor-
ders is the reporting of uncomfortable sensations in the legs when trying to fall asleep and the
urge to move (RLS) and restlessness or leg movements (PLMD).
n OSA: Sleep-disordered breathing may result in diff culties falling asleep and maintaining
sleep given the frequent arousals that result from the apneic pauses. Children and adolescents
with sleep-disordered breathing will likely have additional symptoms, such as snoring, noisy
breathing, breathing pauses, and restlessness (see Chapter 14).
n Psychiatric disorders (e.g., depression, anxiety): In these cases, the sleep disturbance is
likely to coexist with the symptoms of the psychiatric disorder. Other related psychiatric
symptoms, such as vegetative signs (e.g., loss of appetite), are also present. In generalized
anxiety disorder, anxiety symptoms are reported both at bedtime and throughout the day, and
daytime functioning is impaired. In addition, the anxiety in insomnia is specif cally related to
the inability to sleep, whereas that associated with generalized anxiety disorder is more global
and diffuse.
n Medical factors: Diff culty falling asleep may be attributed to a primary medical disorder, in-
cluding asthma, allergies, and headaches (see Chapter 21 for a review of sleep and medical dis-
orders) as well as to associated conditions, such as pain, physical discomfort, or medications.
MAn Ag eMen t
w hen to r efer
Children or adolescents with insomnia who also present with symptoms of other underlying sleep
disrupters (e.g., OSA) should be referred to a sleep specialist. Children or adolescents whose
insomnia fails to respond to simple behavioral interventions may also benef t from referral to a
sleep clinic or behavioral medicine specialist with expertise in treating sleep problems, particu-
larly cognitive behavioral therapy. If there are concerns regarding psychiatric or psychological
issues, a referral to a mental health specialist is warranted.
t reatment
A thorough evaluation for possible causes of and contributing factors to the insomnia is critical
prior to the development of a treatment plan. The following treatment strategies can be effective
with primary insomnia. These strategies can also be benef cial in cases of secondary insomnia.
n Sleep hygiene: Maintenance of appropriate sleep hygiene (see Chapter 4 and patient handouts
in Appendices C7 and C8) is critical with insomnia, including:
n Developmentally appropriate bedtime, as a bedtime that is too early can lead to delayed
sleep onset.
n Consistent sleep schedule, on weekdays, weekends, and school vacations.
n Avoidance of naps, as daytime sleep can contribute to diff culties falling asleep at bedtime.
n Avoidance of caffeine, especially in the afternoon and evening.
n Sleep-conducive environment, including cool, dark, and quiet.
n Removal of electronics from the bedroom, as television viewing, computer use, and other
electronic use can be stimulating, both due to the activity itself and increased light to the
eyes.
n Bedtime routine, that is consistent night-to-night and relaxing
n Consistent morning waketime, regardless of the prior nights sleep, to regulate the internal
clock and synchronize the sleepwake cycle.

n Behavioral treatment: The goal of behavioral interventions is to disrupt the negative learned
associations that are often a prominent feature of primary insomnia. These include:
n Stimulus control: Stimulus control involves discontinuing any activities in bed that are
not conducive to sleep (including watching television, using a computer, and worrying), as
these activities often serve as cues for wakefulness rather than sleepiness. Rather, the bed
and bedroom should be associated with sleep only and a consistent sleepwake schedule
should be established. The patient should only go to bed when sleepy, so bedtime should
be delayed until he or she is sleepy (e.g., yawning, eyes drooping). Once in bed, the patient
should get out of bed if not asleep within 15 to 20 minutes, and engage in a quiet non-
stimulating activity (e.g., reading). When again drowsy, the patient should return to bed. It
may be necessary to repeat this cycle several times. It is critical for the patient to leave the
bed (and possibly bedroom) if unable to fall asleep or else the cycle will continue, with the
bedroom and bed associated with sleeplessness. In addition, the patient should only use the
bed and bedroom for sleep, should get up at the same time every day, and should avoid all
napping.
n Sleep restriction: Restriction of the time in bed to a minimum of hours, usually 6 to 7, will
increase sleep eff ciency, consolidate sleep, and disrupt the learned association of sleepless-
INSOmNIA 159
ness and being in bed. Consistent and accurate recording of sleep patterns in a sleep diary
is an essential component of sleep restriction therapy. To begin, the amount of time in bed
should be set to the estimated amount of nighttime sleep at baseline. Once the sleep eff -
ciency (total sleep time and time in bed) is greater than 85%, a schedule of increasing time
in bed (which is gradual enough to maintain the sleep eff ciency above 85%) is instituted
over a period of days to weeks. However, given the potential for daytime impairment, sleep
should never be restricted to less than 6 hours in children and adolescents.
n Cognitive restructuring: This cognitive-behavioral technique involves teaching the patient
to counter inappropriate thoughts, using a three-step process: (1) identifying the inappropri-
ate sleep cognition, (2) challenging the validity of each sleep cognition, and (3) replacing
the thought with a more productive one.
n Relaxation: Relaxation strategies, primarily progressive muscle relaxation as well as deep
breathing, visual imagery, and meditation, can be benef cial.
Seven Rules for Beating Insomnia

1. Choose a set wake-up time. Wake up at the same time every day, no matter how much
sleep you got the night before.
2. Choose a bedtime. Choose the earliest possible bedtime that is late enough that you are
sleepy but is not too early so it doesnt let you be in bed too long. You only want to spend
the amount of time in bed that you actually need for sleep.
3. Go to bed when you are sleepy, but not before your chosen bedtime. Dont go to bed
until you are sleepy. So, if you are still wide awake at your chosen bedtime, wait a while
longer until you are sleepy enough to fall asleep quickly.
4. Get out of bed when you cant sleep. If you are lying in bed and cant sleep, get out of
bed and do something relaxing out of the bedroom such as reading a book. Go back to bed
when you feel sleepy enough to fall asleep quickly. Again, if you do not fall asleep quickly,
get up. Keep repeating this cycle until you fall asleep. You need to get out of bed when you
cant sleep both at bedtime and in the middle of the night.
5. Dont worry or plan in bed. When lying in bed at night, dont spend the time worrying
or planning for the next day. Set aside another time of the day to do these things. If you
automatically start thinking and worrying when you get in bed, get up and dont head back
to bed until your thoughts wont interfere with falling asleep. Thinking in bed is a habit, and
one that you can break.
6. Only use your bed for sleep. Dont do anything but sleep in your bed. That is, dont do
other activities, such as watch television or do homework.
7. Avoid naps. Naps will interfere with your ability to fall asleep at bedtime, so no naps.
Adapted from Owens, J. A., & Mindell, J. A. (2005) Take Charge of Your Childs Sleep. New
York: Marlowe.
n Medication: Given that no medications are Food and Drug Administrationapproved for in-
somnia in children or adolescents, hypnotics are typically not recommended as a f rst-line in-
tervention in this age group for the treatment of insomnia. In specif c circumstances, hypnotics
may be necessary, but should always be used in combination with sleep hygiene and behavioral
interventions. A complete discussion of hypnotic use in the pediatric population is provided in
Chapter 19.
Pr o g n o SiS
Research has not been conducted on the long-term outcome of insomnia in children or adoles-
cents. However, given the persistence of some underlying predisposing factors for insomnia,
such as certain personality traits, some individuals are clearly at risk for recurrent problems. In
addition, the learned nature of the disorder makes it likely that insomnia will persist if untreated.
Tips for Talking to Parents (and Adolescents)

Distinguish between insomnia as a symptom and insomnia as a diagnosis.
Discuss the 3Ps of insomnia: predisposing, precipitating, and perpetuating factors.
Explain the learned nature of insomnia and the sleep-related behaviors that are often initi-
ated to relieve insomnia (e.g., napping, excessive time in bed) but may actually exacerbate
the problem.
Explain the conditioned association between bed and wakefulness and anxiety in indi-
viduals with insomnia.
Develop appropriate sleep hygiene.
Discuss treatment options including behavioral interventions, cognitive therapy, and, in
select cases, hypnotic use.
See Appendix D16 for a parent handout on insomnia.
Sleep and medications 19
MeDic At io n S Fo r Sl eeP
Most sleep disturbances in children and adolescents are appropriately managed with behavioral
therapy alone; however, there may be clinical situations in which pharmacologic intervention
or a combination of behavioral and pharmacologic intervention is considered by the pediatric
practitioner for a child or adolescent with signif cant diff culties in initiating and/or maintaining
sleep (medication use for specif c sleep disorders such as restless legs syndrome and narcolepsy
are covered in their respective chapters). There are a variety of over-the-counter (OTC) and pre-
scription medications in the category of sedatives and hypnotics that are used in clinical prac-
tice by healthcare practitioners, as well as by parents, to treat pediatric insomnia. However, it is
important to note that very little empirical data regarding the eff cacy, safety, and tolerability of
pharmacologic interventions for insomnia exist in the pediatric population. There are currently
no medications approved for use as hypnotics in children by the Food and Drug Administration
(FDA).
It should be emphasized in the context of the following discussion of medication use that
insomnia is a descriptive rather than a diagnostic term and does not specify etiology. There are
many possible causes for the same constellation of symptoms typically presenting as childhood
insomnia (e.g., bedtime resistance or diff culty initiating sleep and nightwakings), including
medical (e.g., drug-related or pain-induced or from primary sleep disorders such as obstructive
sleep apnea) and behavioral (e.g., associated with poor sleep hygiene or negative sleep onset as-
sociations) issues, or a combination of these factors. Therefore, it is imperative that the choice of
therapy, medication or otherwise, be diagnostically driven.
A host of variables impact the appropriateness of medication use in a given clinical situation.
These include:
n Patient variables, such as age, presence of comorbid psychiatric and developmental condi-
tions (e.g., attention def cit hyperactivity disorder, autism or pervasive developmental dis-
order, blindness or severe visual impairment), presence of chronic medical conditions (e.g.,
chronic pain) or acute medical conditions, and hospitalization.
n Provider and practice setting variables, including provider familiarity with behavioral treat-
ment strategies, time, and reimbursement issues.
n Cultural and societal variables, such as acceptance of psychotropic use in children in gen-
eral, and acceptance of alternative therapies.
Alternatively, there are a number of reasons why practitioners might be reluctant to prescribe or
recommend medications for sleep problems in children:
n Concerns about eff cacy, particularly given the lack of empirical data regarding effectiveness
of these drugs in children.
n Concerns about tolerance, including short- and long-term side effects, as well as rebound
insomnia once the medication is discontinued.
n Concerns about safety, including dependency issues, effects on sleep architecture, and risk of
accidental overdose.
n Ethical considerations, such as medicating a parent problem and giving the wrong mes-
sage to families about management of sleep issues.
161
162 SECTION III SLEEP AND mEDICATIONS
Unfortunately, concerns regarding safety and eff cacy are somewhat justif ed, as sleep distur-
bances remain one of the most poorly researched areas in pediatric psychopharmacology. Most
of the information available regarding use of these medications is taken from adult data. There
have been only a handful of studies that have examined the effectiveness of hypnotic and seda-
tive use in children and adolescents using the gold standard of randomized placebo-controlled
clinical trials. The empirical evidence that does exist primarily comes from case reports or small
case series. Despite this, a number of studies both in the United States and Europe suggest that
prescribing or recommending sedatives and hypnotics for sleep complaints is relatively com-
mon practice among pediatricians and general practitioners as well as child psychiatrists. These
studies also suggest that even in infants and preschoolers, sleep complaints often dominate the
presenting symptoms for which psychotropic medications in general are prescribed.
Sleeping Pills for Sleepless Nights?

Selection of specif c intervention strategies for children and adolescents with insomnia, in-
cluding behavioral treatment and pharmacologic management, must f rst and foremost be
diagnostically driven. Specif c pharmacokinetic and pharmacodynamic properties of avail-
able sedative and hypnotics should be considered in the context of the given clinical situa-
tion. Treatment goals should be clearly outlined and the emergence of side effects carefully
monitored.
Faced with what is admittedly inadequate empirical support for the use of sleep medications in
children and adolescents coexisting with what is sometimes a pressing clinical need, how does the
pediatric practitioner help families make rational choices regarding medication use? In addition
to considering the factors listed above, some additional considerations should be kept in mind:
n Careful evaluation of the causes of and contributing factors to a sleep disturbance in
the individual child or adolescent is key. First and foremost, selection of specif c interven-
tion strategies, including behavioral treatment as well as pharmacologic management, must
address the underlying etiologies. Diagnostic classif cation systems, such as the International
Classif cation of Sleep Disorders (ICSD-II), allow sleep disorders in children to be reliably
described and diagnosed, which provides a rationale for the use of specif c treatment strategies,
including pharmacologic ones, in the clinical setting.
n Thorough evaluation of the impact of the sleep disturbance on the childs health and
daily functioning must be combined with diagnostic assessment. In particular, possible neu-
robehavioral signs of daytime sleepiness (e.g., mood changes, attention problems, impulsivity,
poor school performance) must be carefully assessed.
n Thorough evaluation of the impact of the sleep disturbance on the family must also be
combined with diagnostic assessment. Parent and family variables that are important to con-
sider include educational level, parenting skills, household composition, parental stress level
and caregiver exhaustion, and previous experience with and acceptability of pharmacologic
treatment. There are situations, albeit relatively rare, in which families are so exhausted and
overwhelmed by a childs sleep problems that concerns about both safety and parental mental
health are warranted. This situation is particularly likely to occur in the setting of other devel-
opmental and medical issues.
When to Consider Medications for Sleep

There may be clinical situations in which a combination of frequency, severity, chronicity, and
functional impact on both child and family of the sleep problem; family variables including
stress and parental exhaustion; and characteristics of the child (including comorbid medical,
psychiatric, and neurodevelopmental issues) may make it appropriate to consider the use of
sedative or hypnotic medication in combination with behavioral therapy and good sleep hy-
giene for insomnia in children.
SLEEP AND mEDICATIONS 163
n Characteristics of the individual clinical situation must be reviewed. These include type
and severity of the sleep problem, duration, frequency, and previous failed attempts at conven-
tional behavioral therapy.
Once the decision to include pharmacologic management has been made, additional specif c is-
sues to consider include the following:
n In almost all cases, medication is not the f rst treatment choice nor the sole treatment
strategy for children with insomnia, and should be viewed only within the context of a more
comprehensive treatment plan. Empirically supported behavioral interventions (e.g., gradu-
ated extinction, positive routines, parent education) are the mainstay and f rst choice for the
treatment of pediatric insomnia. Thus, medication should be used in combination with non-
pharmacologic strategies. While pharmacologic interventions are likely to have a more rapid
and potent effect, non-pharmacologic treatments have been shown to have more long-lasting
effects (i.e., persistent after medication has been discontinued).
n Dosing should be initiated at the lowest level likely to be effective and titrated up as neces-
sary. Furthermore, whenever possible, medications should also be used for the shortest pos-
sible duration (<1 month). The duration of therapy should be discussed and clarif ed with the
family before initiating medication.
n The institution of appropriate sleep hygiene measures that revolve around the basic envi-
ronmental (e.g., room temperature), sleepwake scheduling, sleep practice (e.g., bedtime rou-
tine), and physiologic (e.g., caffeine use) factors promoting optimal sleep are also a necessary
component of the treatment approach to pediatric insomnia (see Chapter 18).
n Rational treatment selection should be based on the clinicians judgment of the best pos-
sible match between the clinical circumstances (e.g., type of sleep problem, patient char-
acteristics) and the individual properties of currently available drugs (e.g., onset of action,
safety, tolerability). Thus, clinicians should have some degree of familiarity with the pharma-
cologic prof le of the sedatives and hypnotics currently available for use in the pediatric
population (Tables 19.1 and 19.2). Medication selection, particularly in terms of duration of
action, should be appropriate for the presenting complainti.e., for children with sleep
onset problems, a shorter acting medication is generally desirable, whereas for sleep mainte-
nance problems, longer acting medications may be considered. Timing and type of medication
should minimize morning hangover or persistent grogginess. In general, this means choos-
ing an agent with the shortest possible half-life. Another consideration involves the timing of
drug administration relative both to the targeted time of sleep onset (e.g., within 30 minutes
of lights out) and to the second wind phenomenon, in which circadian-mediated alertness
in both adults and children typically increases in the evening hours just before sleep onset,
making it more diff cult to fall asleep during this 1-hour to 2-hour window. Most hypnotic
medications have their onset of action within 30 minutes of administration and peak within
12 hours. Thus, giving the medication too early (e.g., 2 hours before sleep onset) is not only
less likely to be effective than dosing closer to bedtime, but may in fact induce dissociative
phenomenon (i.e., hallucinations) when administered during the circadian alertness window.
Finally, the little pediatric pharmacokinetic and pharmacodynamic data that exist for hypnotic
drugs suggests that some medications (e.g., zolpidem) are metabolized differently in younger
children, who may require higher dosing than do adults. Thus, a dose that is not adequate to
actually induce sleep could still potentially result in a paradoxical reaction in which the child
becomes groggy, and subsequently agitated and disinhibited.
n All medications prescribed for sleep problems should be closely monitored for the emer-
gence of side effects. Side effects should be reviewed with the family as well as with the child
or adolescent as appropriate. Furthermore, discontinuation of these agents may also result in
increased sleep problems; for example, increased nightmares as a result of REM rebound may
occur if a REM-suppressant medication is withdrawn abruptly.
164
t ABl e 19.1. Pharmacology of Selected Medications Used for Pediatric Insomnia
Time to
Maximum
Plasma DrugDrug Interactions Sleep
Mechanism of Elimination Half-Life Metabolic Concentration (pharmacokinetic and Architecture
Drug Class Action (h) Pathways (min) dynamic) Effects
Diphenhydramine Antihista- H1 subtype re- 46 Hepatic Rapid absorp- ETOH/CNS depressants Decrease
(Benadryl) mines ceptor agonists; tion and (barbiturates, opiates) SOL; may
1st generation onset of impair
Brompheniramine 46
drugs cross action; sleep qual-
Chlorpheniramine bloodbrain 46 Peak levels ity
Hydroxyzine barrier 624 24 h
(Atarax)
Melatonin7 Hormone Main effect su- 3050 min. Hepatic 3060 Largely unknown; Decreases
analogue prachiasmatic Returns to baseline NSAIDs ETOH, SOL; main
nucleus; weak levels in 48 h; (sustained caffeine, BZDs may effect on
hypnotic (may biphasic elimination; release peak interfere with normal circadian
have GABA-re- 3 min and 45 min level 4 h) melatonin production rhythms
ceptor effects) 90% excreted in 4 h
Flurazepam BZD Bind to central 2100 CYP450 3A 30 min13 h CYP450 3A inhibitors Suppress
(Dalmane)* receptor GABA (gama- oxidation (f uoxetine/grapefruit SWS;
agonists aminobutyric juice) increases levels reduce fre-
Quazepam 48100 CYP450 3A 60180
(BzDRA): acid) receptors ETOH/barbiturates quency of
(Doral)* oxidation/
BZDs6 increase CNS depression nocturnal
glucuroni-
Temazepam 3.518 6090 arousals
dation
(Restoril)*
Estazolam 828 CYP450 3A 120
(ProSom)* oxidation
Triazolam 26 CYP450 3A 60120
(Halcion)* oxidation
Zolpidem BZD BZD-like 2.53 CYP450 90 ETOH, CNS depressants Decrease
(Ambien/ receptor oxidation/ may potentiate effects SOL,
Ambien CR)* agonists aldehyde little effects
(BzDRA): oxidation sleep archi-
Zaleplon 1 60
Non-BZDs tecture
(Sonata)*
Eszopiclone 56 60
(Lunesta)*
Ramelteon Synthetic Selective aff nity 12.6 CYP1A2 45 Avoid use with P1A2 in- Decreases
(Rozerem)* melatonin MT-1, MT-2 (CYP3A4/ hibitors (f uvoxamine) SOL; no
receptor receptors CYP2A9) effect NW
agonist
Clonidine Alpha ago- Alpha adren- 624 50%80% Rapid absorp- Decreases
(Catapres) nists ergic recep- of dose tion; bioavail- SOL; re-
tor agonists; excreted ability 100%; duce REM,
(guanfacine 17 unchanged onset action SWS
more selective) in urine within 1 h;
decrease NE peak effects
release 24 h
Trazodone Atypical 5-HT, serotonin Biphasic; f rst T1/2 36 CYP450/ 30120 Potentiates effects ETOH, Decreases
(Desyrel) antide- agonist h; second T1/2 59 h CYP2D6 CNS depressants, SOL,
pressant 1036 h post-ingestion digoxin, phenytoin, improves
antihypertensives sleep
continuity,
decreases
REM,
increases
SWS
SWS = Slow-wave sleep (Stage N4); SOL = Sleep onset latency; BZD = Benzodiazepine; NSAID = Non-steroidal anti-inf ammatory drug; ETOH = Alcohol
*FDAapproved as hypnotic in adults; CNS = central nervous system; NW = night wakings; REM = rapid eye movement.
165
166
t ABl e 19.2. Clinical Properties of Selected Medications Used for Pediatric Insomnia
Development
Adult Dosing Range Tolerance/ Safety Prof le/
Drug (mg/d) Formulation Side Effects Withdrawal Effects Overdose Comments
Diphenhydramine 25100 (should not Tablet, cap- Daytime drowsiness, OD: hallu- Weak soporif cs; high
exceed daily dose sule, syrup, GI (appetite loss, nausea/ cinations, level parental/practitio-
300 mg)/12.550 injectable vomiting, constipation, seizures, ner acceptance
dry mouth), paradoxical excessive
Brompheniramine 4
excitation stimulation
Chlorpheniramine 4
Hydroxyzine 25100;
0.6 mg/kg (children)
Melatonin 2.55 Sublingual, Largely unknown; reported Tolerance does not Unknown Used in children with
(range 0.325) liquid, cap- hypotension, bradycar- appear to develop developmental disabili-
0.110 (children) sule, tablet; dia, nausea, headache; ties, autism, neurologic
various possible exacerbation of impairment, blindness;
strengths comorbid arthritis, asthma ADHD; jet lag
Flurazepam* 1530 Capsules, Residual daytime sedation, Yes, especially with Marked abuse Also used to reduce
tablets rebound insomnia on dis- shorter acting potential partial arousal para-
Quazepam* 7.515
continuation, psychomo- BZD; withdrawal somnias (sleep terrors,
Temazepam* 1530 tor/cognitive impairment, effects include sleepwalking); use short
Estazolam* 12 anterograde amnesia seizures half-life BZD for sleep
(dose-dependent); impair- onset; longer half-life
Triazolam* 0.1250.25 ment respiratory function for sleep maintenance
Zolpidem/zolpi- 510/6.2512.5; pedi- Capsules Headache, May develop toler- Well tolerated Little clinical experience
dem CR* atric study suggests retrograde amnesia; few ance/adaptation in adults/OD: in children
0.25 mg/kg up to residual next-day effects with extended use; CNS depres-
20 mg in 218 y may develop re- sion; hypoten-
bound insomnia on sion
Zaleplon* 520
discontinuation
Eszopiclone* 13
Ramelteon 8 Tablets No signif cant side effects No evidence re- No signif cant
noted bound/withdrawal safety issues
identif ed; no
abuse liability
Clonidine 0.0250.3 (up to 0.8) Tablet, trans- Dry mouth, bradycardia, Narrow thera- Also used in daytime
Increase by 0.05 dermal hypotension, rebound peutic index; treatment of ADHD
increments patch hypertension on discon- OD: bradycar- Contraindicated if his-
0.0250.4 (children) tinuation dia, decreased tory of cardiovascular
consciousness disease, depression
hypotension
Trazodone 2550 (up to 150) Tablets Dizziness, CNS over- OD: hypoten- May be used with comor-
stimulation. Cardiac sion, cardiac bid depression
arrhythmias, hypotension, effects
priapism
ADHD = attention def cit hyperactivity disorder; BZD = benzodiazepine; CNS = central nervous sytem; GI = gastrointestinal; OD = overdose.
167
n Insomnia in children commonly co-occurs with other primary sleep disorders (e.g., OSA,
RLS), leading to increased daytime sequelae. Thus, the presence of both medically based
and behaviorally based sleep disorders must be assessed and appropriately addressed. In
addition, pharmacologic treatment of insomnia could potentially exacerbate co-existing sleep
problems. For example, sedatives and hypnotics with respiratory depressant properties and
medications that may cause signif cant weight gain should be avoided if the insomnia occurs
in the presence of OSA. In addition, selective serotonin reuptake inhibitors (SSRIs) should be
used with caution in treating insomnia, as they may increase symptoms of comorbid RLS.
n Medication should also be used with caution in situations in which there may be poten-
tial pharmacodynamic drugdrug interactions with concurrent medications (e.g., seda-
tives and hypnotics and opiates) or pharmacokinetic drugdrug interactions (e.g., f uoxetine,
a CYP2D6 and 2C19 inhibitor, and diphenhydramine). In particular, adolescents should be
screened for alcohol and drug use, as well as pregnancy, prior to initiation of therapy, as many
recreational substances may have synergistic clinical effects when combined with sedatives
and hypnotics. In addition, hypnotics with high toxicity levels in overdose should be used with
extreme caution in situations in which there is any risk of accidental or intentional overdose.
n Caregivers and patients should be questioned regarding concurrent use of parent- or
self-initiated non-prescription sleep medications (e.g., Tylenol PM, melatonin, herbal
preparations) as well as other OTC medications. It should be noted that, in many cases,
the use of medication for sleep problems in children is initiated by parents (or by adolescent
patients themselves) without the physicians recommendation or knowledge. Parents may as-
sume that OTC medications commonly utilized to induce sleepiness, such as diphenhydr-
amine, are harmless. In addition, while generally viewed by parents as safe, the potential
drugdrug interactions between most herbal preparations and sedatives and hypnotics, as well
as other medications, is largely unknown, and thus should be approached with caution. Lack
of knowledge about possible side effects or about interactions of these OTC medications with
other drugs may pose a safety threat. For example, parents may not be aware that the active
ingredient in Tylenol PM (diphenhydramine) is the same as that in Benadryl. In some cases,
OTC sleep medications may interact with other prescription or OTC drugs, and, in others, with
an underlying medical condition. Because parents may be embarrassed about the home use
of sedative medications, they may be reluctant to share this information with their healthcare
provider. In addition, adolescent patients may fail to consider use of OTC sleep-aids as taking
any medication when queried. Thus, maintaining an open and nonjudgmental approach is key
to optimal communication and allows for the development of more effective and appropriate
treatment strategies in cooperation with the family.
n Treatment goals should be clearly outlined and measurable (e.g., sleep onset consistently
less than 30 minutes, improvement in mood and attentiveness, decrease in subjective distress
about the insomnia in caregiver and/or patient). The immediate goal of treatment should be to
alleviate or improve rather than eliminate sleep problems. Monitoring of both eff cacy and side
effects should take place frequently and systematically.
There are currently no sedative or hypnotic medications approved for use in children by
the Food and Drug Administration.
SPec iFic MeDic At io n S c o MMo n l y uSeD Fo r PeDiAt r ic in So Mn iA

A summary of pharmacologic and clinical properties of medications that are currently most com-
monly used in the treatment of pediatric insomnia is presented below. Because the currently
available empirical evidence regarding safety and eff cacy of pharmacologic insomnia treatment
in children is inadequate to rank recommendations for the use of these medications, the focus
is on a description of the drug properties and any specif c precautions regarding their use in the
pediatric population.
A summary of individual medication properties can be found in Tables 19.1 and 19.2. High-
lighted below are mechanism of action, effects on sleep architecture, relevant pharmacodynamic
and kinetic properties, relevant eff cacy data, side effects likely to impact on pediatric popula-
tions, and other clinical considerations. Unless specif cally indicated, all clinical trial data is from
adult populations; pediatric-specif c information regarding safety and eff cacy is included when
available. Most manufacturers do not list pediatric soporif c doses for these drugs, so that dos-
ing in clinical practice is often based on a relative percentage of the adult dose. OTC drugs are
discussed; then, as is standard in the adult insomnia literature, prescription medications that are
currently FDAapproved for use in insomnia (in adults) are listed f rst (benzodiazepine receptor
agonists, melatonin receptor agonists). Finally, prescription medications commonly used off-la-
bel for insomnia are listed in alphabetical order, in order to avoid any implied preference in rank.
o ver- the- c ounter Medications

Antihistamines
Both prescription (e.g., hydroxyzine) and OTC (e.g., diphenhydramine) antihistamines are the
most commonly prescribed and recommended sedatives in pediatric practice. First-generation
drugs (diphenhydramine, hydroxyzine, chlorpheniramine) cross the bloodbrain barrier and
bind to H1 receptors in the central nervous system; second and third generation antihistamines,
such as terfenadine and loratadine, are signif cantly less sedating. They are generally rapidly ab-
sorbed and effects on sleep architecture are minimal. OTC sleep aids contain diphenhydramine
or doxylamine, both of which have demonstrated modest eff cacy in reducing sleep onset latency
in a few clinical trials, including in adults with psychiatric disorders. A double-blind placebo-
controlled pediatric study of diphenhydramine HCL (1 mg/kg) showed signif cant subjective
improvement in sleep latency and nightwakings, although a more recent study in 6- to 15-month-
olds found that diphenhydramine was no better than a placebo in reducing nightwakings. Po-
tential side effects include daytime drowsiness, anticholinergic effects (e.g., dry mouth, blurred
vision, urinary retention), and paradoxical excitation; fatal overdoses with diphenhydramine have
been reported in infants. It should also be noted that tolerance to antihistamines tends to develop,
necessitating increasing doses. Parental and provider familiarity tend to make antihistamines
a more acceptable choice for many families, and widespread clinical experience indicates that
these medications are largely well tolerated in children.
Melatonin
Melatonin is a hormone secreted by the pineal gland in response to decreased light, mediated
through the suprachiasmatic nucleus. The mechanism of action of commercially available mela-
tonin is to supplement the endogenous pineal hormone. The plasma level of exogenous mela-
tonin peaks within 1 hour of administration. Thus it may be helpful in reducing sleep onset
latency when taken close to bedtime; sustained release preparations may assist in maintaining
sleep. Clinical uses for melatonin include chronic or acute circadian rhythm disturbances (e.g.,
delayed sleep phase syndrome, jet lag) in normal children and in children with special needs or
neurodevelopmental disorders (e.g., blindness, Rett syndrome, autism). The pediatric literature
on the safety and eff cacy of melatonin use is fairly robust, particularly compared with other
hypnotic drugs frequently used in clinical practice. For example, a number of studies have now
demonstrated that melatonin is effective in reducing sleep onset latency specif cally in children
with ADHD; the rationale is based on the premise that at least some of these children have a
circadian-mediated phase delay (i.e., delayed sleep onset and offset compared to developmental
norms). In addition to effects on circadian regulation of sleepwake cycles, melatonin has mild
hypnotic properties.
Although generally regarded as safe, potential side effects of melatonin include suppression of
the hypothalamicgonadal axis (triggering precocious puberty on discontinuation), and increased
reactivity of the immune system in children with immune disorders or on immunosuppressants
(i.e., corticosteroids).
Melatonin is not regulated by the FDA; therefore, the commercially available formulations
tend to vary in strength and purity. Pharmaceutical grade melatonin, which is, in theory, >99%
pure, is available on a number of Internet sites. Reported doses for melatonin include: 1 mg in
infants, 2.5 to 3 mg in older children, and 5 mg in adolescents; use of melatonin in children with
special needs have reported doses ranging from 0.5 mg to 10 mg, irrespective of age. It should
be noted that studies of melatonin use in adults for advancing sleep phase in delayed sleep phase
disorder have reported that smaller doses (e.g., 0.5 mg) 5 to 7 hours before sleep onset may be
more effective in treating sleep onset delay in the context of a circadian rhythm disorder.
Herbal Preparations
Most herbal preparations are considered generally safe. However, this is based on only a handful
of studies that have suggested that some herbal preparations may be useful for sleep in the pedi-
atric population, and these products in general remain largely untested in children. Valerian root,
St. Johns wort, and Humulus lupulus (hops) have been shown to have some evidence of eff cacy
in adult and/or pediatric studies; lemon balm, chamomile, and passionf ower have limited to no
evidence, and kava-kava and tryptophan have been associated with signif cant safety concerns
(e.g., hepatotoxicity and eosinophilic myalgia syndrome, respectively). Valerian root, which has
benzodiazepine-like properties, has been shown in several studies in adults to have sleep-promot-
ing effects without the hangover effects seen with the benzodiazepines, although effects may
not be seen for several weeks. Chamomile is reported anecdotally to have mild sedating effects.
It should be noted that herbal preparations, including herbal teas and weight loss and laxative
preparations, contain a signif cant percentage of caffeine and thus may disrupt sleep. Lavender
appears to have a CNS depressive effect and as such may potentiate the effects of other CNS
depressants such as alcohol; aromatherapy with the volatilized lavender oil has been reported to
improve sleep quality.
FDAApproved insomnia Drugs

Benzodiazepine Receptor Agonists (BzRAs): Benzodiazepines
The hypnotic effect of the benzodiazepines (BZD) is mediated by their action at the gamma-
aminobutyric acid-type A receptors (GABAA): GABA is the major inhibitory neurotransmitter
in the brain. These medications shorten sleep onset latency and increase total sleep time (TST),
and improve non-REM sleep maintenance. Most disrupt slow-wave sleep (SWS). They also have
muscle relaxant, anxiolytic, and anticonvulsant properties. The shorter onset of action of some
benzodiazepines has led to their use in treating sleep onset insomnia, while agents with a longer
half-life and duration of action have been more commonly used to address sleep maintenance.
In general, this class of medication should only be used for short-term or transient insomnia, or
in clinical situations in which their other properties (e.g., anxiolytic) are advantageous. Of note,
BZDs are occasionally used to treat intractable partial arousal parasomnias (e.g., sleep terrors)
in children because of their SWS-suppressant effects. However, use of longer-acting BZDs may
lead to morning hangover, daytime sleepiness, and compromised daytime functioning. Antero-
grade amnesia and disinhibition may also occur. There is a risk of habituation or addiction with
these medications as well as withdrawal phenomena, all of which makes them of very limited use
in children and adolescents.
Nonbenzodiazepine Receptor Agonists

Nonbenzodiazepine BzRAs have a more selective prof le, binding preferentially to GABAA re-
ceptor complexes containing alpha1 subunits. Effects on sleep architecture appear minimal, al-
though they may increase SWS.
n Zaleplon (Sonata). Zaleplon has a very short half-life, making it potentially useful for mid-
dle-of-the-night administration (if at least 5 hours remain before the desired waketime) as well
as for sleep onset insomnia. Side effects include dizziness, anterograde amnesia, confusion,
and hallucinations. The most common adverse event reported in adults is headaches.
n Zolpidem (Ambien). Zolpidem also acts by binding selective GABAA receptors; half-life
is 2 to 3 hours. Zolpidem-CR has a longer half-life, which may make it more useful in sleep
maintenance. A single case study reported that zolpidem was effective in reducing sleep onset
latency in a 7-year-old with autism and insomnia. Longer duration trials in adults suggest
continued hypnotic benef t at 6 months, without the development of tolerance. Disinhibition
with any of the BzRAs may occur in the period immediately after taking the medication, and
hallucinations have been reported. Recent reports of sleep-related events (sleep-eating, sleep-
driving) in adults taking zolpidem have raised additional concerns about its use in children.
Although rebound insomnia may occur with either of these compounds, studies in adults sug-
gest that as needed administration is well tolerated.
n Ezopiclone (Lunesta). Ezopiclone is a newer GABA-ergic sleep medication that, because
of its longer half-life, has been used in adults for both sleep initiation and sleep maintenance.
Peak drug concentration occurs at 60 minutes; half-life and clinical effect are approximately
6 hours. Fatty foods tend to delay the absorption. Side effects include unpleasant taste and
headache. Abrupt withdrawal with prolonged use (>2 weeks) may be associated with rebound
insomnia. Studies in adults have shown no development of tolerance at 6 months; this medica-
tion has been approved for longer-term use.
Melatonin Receptor Agonists

Ramelteon (Rozerem) is a synthetic melatonin receptor agonist, acting selectively at the MT1
and MT2 receptors. Its sleep-promoting effect may be related to reduction of the alerting output
of the suprachiasmatic nucleus. Ramelteon is approved for use in sleep initiation insomnia, and
shows moderate eff cacy in reducing sleep onset latency (in adults). In clinical trials, subjective
improvements are typically less consistently reported than are objective (i.e., polysomnography)
improvements in sleep onset latency. It is the only non-scheduled approved hypnotic.
o ff- l abel insomnia Drugs

Alpha Agonists
Clonidine, a central alpha2 agonist that decreases adrenergic tone, is one of the most widely used
medications for insomnia in pediatric and child psychiatry practice, particularly in children with
sleep onset delay and ADHD. Despite its widespread use, data regarding safety and eff cacy in
children with ADHD and sleep problems is limited, although several descriptive studies have
reported adequate clinical response and a relatively low side effect prof le. The drug is rapidly
absorbed, with an onset of action within 1 hour, and peak effects at 2 to 4 hours. Tolerance often
develops, necessitating increases in dose. Mid-sleep awakening may also occur as blood levels
drop during the night. Effects on sleep architecture are fairly minimal but may include decreased
REM and SWS; thus, discontinuation can lead to rebound increase in these stages. Clonidine has
a narrow therapeutic index and there has been a recent dramatic increase in reports of overdose
with this medication. Potentially signif cant side effects include hypotension and bradycardia,
anticholinergic effects, irritability, and dysphoria. Rebound hypertension may occur on abrupt
discontinuation. Clonidine should be avoided in patients with diabetes and Raynauds syndrome.
Antidepressants
In general, antidepressants are believed to mediate sleep promotion by inf uencing activity of
non-GABA neurotransmitters (e.g., histamine, acetylcholine, serotonin) involved in the regula-
tion of sleep and wakefulness. Most antidepressants, especially those with anticholinergic effects,
suppress REM and increase latency to REM sleep; abrupt withdrawal may lead to increased
nightmares (REM rebound). Although frequently used in clinical practice, there is overall a lack
of methodologically rigorous research supporting the use of antidepressants for insomnia in

adults or children. Thus, the use of antidepressants for insomnia should take into consideration
the presence of concurrent mood issues, and whether hypersomnia is part of the clinical picture,
as the use of an antidepressant may increase daytime sleepiness. Treating the underlying mood
disorder will often result in improved sleep, and successful sleep interventions often result in
improvements in mood. The antidepressant dose for insomnia is typically less than the dose used
to treat mood disorders.
Atypical Antidepressants
n Mirtazapine (Remeron) is an 2-adrenergic 5-HT antagonist with a high degree of sedation.
It has been shown to decrease sleep onset latency, increase sleep duration, and reduce wake
after sleep onset in both healthy adults and those with major depression, with relatively little
effect on REM sleep. It may, however, result in daytime somnolence.
n Nefazodone (Serzone) is a 5-HT antagonist and norepinephrine reuptake inhibitor, which is
associated with signif cant sedation.
n Trazodone, a 5-HT antagonist commonly used in child psychiatry clinical practice, is one
of the most sedating antidepressants because it both inhibits binding of serotonin and blocks
histamine receptors. Despite patient reports of improved sleep quality, the empirical evidence
supporting the eff cacy of trazodone is modest at best, and limited to two clinical trials (in
adults). Trazodone has suppressant effects on REM and may increase SWS. Morning hang-
over is a common side effect. It has been associated with reports of priapism in adults in the
50150 mg dose range.
Serotonin Antagonists and Selective Serotonin Reuptake Inhibitors

These agents are felt to promote sleep primarily by inhibiting uptake of serotonin. They vary
widely in their propensity to cause sedation (e.g., f uvoxamine, paroxetine, citalopram) vs. activa-
tion with sleep onset delay and sleep disruption (e.g., f uoxetine, sertraline). The more activating
SSRIs are often associated with reports of sleep disruption in adults. Newer generation SSRI
medications such as citalopram (Celexa) appear to have fewer sleep-disrupting effects and may
be useful in the management of insomnia associated with depression. SSRIs suppress REM sleep
and often prolong REM onset, while increasing the number of rapid eye movements; a charac-
teristic polysomnographic f nding in patients on SSRIs is so-called Prozac eyes due to this
increased REM density. SSRIs also tend to suppress SWS. Most increase sleep onset latency and
sleep eff ciency (time asleep/time in bed). SSRIs frequently are associated with motor restless-
ness, and may exacerbate pre-existing RLS and periodic limb movements.
Tricyclic Antidepressants
Most tricyclic antidepressants (TCAs) are sedating, although the degree of sedation is variable.
Amitriptyline, doxepin, and trimipramine, the most sedating. TCAs are those most frequently
used for insomnia (in adults). TCAs can be used to treat insomnia associated with depression,
as they decrease sleep onset latency and decrease arousals during sleep stage transitions. Ami-
triptyline has not been studied in primary (non-comorbid) insomnia, whereas doxepin appears
to improve sleep onset latency during acute administration. Most TCAs are potent REM sup-
pressants, thus rapid withdrawal may lead to REM rebound and nightmares. TCAs also tend to
suppress SWS, which may be particularly problematic in young children, and withdrawal may
lead to SWS rebound and an increase in partial arousal parasomnias (sleepwalking, sleep terrors).
TCAs have been used clinically to treat severe partial arousal parasomnias because of these direct
effects on SWS.
The most commonly reported side effects of TCAs are anxiety and agitation as well as anti-
cholinergic effects (blurred vision, dry mouth, urinary retention, orthostatic hypotension). There
is a risk of cardiotoxicity, especially with desipramine in prepubertal children, and TCAs should
be used with extreme caution in clinical situations in which there is a risk of accidental or inten-
tional overdose. TCAs may also exacerbate RLS symptoms.
Additional Medications
Other classes of medications that reportedly have been used in clinical practice for pediatric
insomnia include mood stabilizers and anticonvulsants (carbamazepine, valproic acid, topi-
ramate, gabapentin), atypical antipsychotics (risperidone, olanzapine, quetiapine), and chloral
hydrate. In most instances, these medications are prescribed for other indications (e.g., bipolar
disorder, aggression) but may simultaneously be used for their sedating (i.e., sleep-promoting)
properties. It should be emphasized that all of these medications should be used with extreme
caution, if at all, for insomnia in children, as there are no or limited data on safety and tolerability
for this indication in either adults or children. Furthermore, the sedating effects may interfere
with daytime functioning and learning, and tolerance to the effect of decreasing sleep onset la-
tency frequently develops, necessitating dosage adjustments. In addition, there may be effects on
other sleep parameters; for example, many of the newer atypical antipsychotics have weight gain
as a signif cant side effect, and thus can worsen OSA. They also tend to suppress REM sleep and
increase motor restlessness during sleep. Chloral hydrate and barbiturates are not indicated for
use in children because of signif cant side effects; in 1993 the American Association of Pediatri-
cians recommended that chloral hydrate be used in children for short-term sedation only, because
of the risk of hepatotoxicity.
MeDic At io n eFFec t S o n Sl eeP

Many OTC and prescription drugs have profound effects on sleep in adults. Although these effects
are much less well studied in children and adolescents, certain basic pharmacologic principles
may be applied to both adults and children. Drugs may exert their effects on sleep in several ways:
n Direct pharmacologic effect on sleep architecture, sleep fragmentation.
n Disturbance in sleep patterns (e.g., nightmares).
n Exacerbation of a primary sleep disorder (e.g., OSA, RLS).
n Drug withdrawal effects.
n Daytime sleepiness.
Understanding a medications effects on sleep architecture (either direct or as a result of medica-
tion withdrawal) can help predict the likely clinical effect on sleep.
n Decreased SWS may lead to subjective feelings of non-restorative sleep or the sense of not
being well rested.
n Increased SWS may increase partial arousal parasomnias in susceptible individuals.
n Decreased REM sleep may result in impairment of memory consolidation.
n Increased REM sleep may result in increased nightmares and may potentially worsen sleep
apnea (as obstructive events are typically increased in REM).
Drug effects on various neurotransmitters of sleep and wakefulness may also be responsible for
their clinical effects. For example, GABA agonists like BZDs promote sleep (increase non-REM
sleep), whereas adenosine receptor blockers like caffeine promote wakefulness (inhibit non-REM
sleep).
Sleepw ake effects of Selected Drugs used in Pediatrics

Anticonvulsants
Anticonvulsants typically cause dose-dependent sedation, although tolerance may develop.
n Carbamazepine (Tegretol) is associated with increased daytime somnolence and may de-
crease sleep onset latency.
n Phenobarbital tends to be very sedating in a dose-dependent fashion, with some development

of tolerance over time. It also decreases sleep onset latency.
n Phenytoin (Dilantin) may cause relatively less daytime sleepiness than other anticonvulsants.
n Valproic Acid (Depakote) is associated with increased daytime somnolence. There are no
reported major direct effects on sleep.
n Newer anticonvulsants have varying degrees of daytime sedation. For example, sedation rates
with topiramate (Topamax) are 15% to 25%, and with gabapentin (Neurontin) are 5% to 15%;
sedation tends to improve over time. Direct effects on sleep are largely unknown. It should be
noted that gabapentin, which has effects on dopamine, serotonin, and norepinephrine, appears
to increase SWS and has been shown to decrease RLS symptoms. Both carbamazepine and
valproic acid may also be used to treat symptoms of RLS.
Allergy and Asthma Medications

n Beta agonists may reduce nocturnal arousals.
n Corticosteroid use has been associated with insomnia in asthma and cancer patients as well
as subjective increases in wakefulness. Objective documentation of sleep-disrupting effects is
less consistent. Corticosteroids decrease REM sleep, although inhaled steroids do not appear
to have signif cant sleep effects.
n Decongestants (such as pseudoephedrine and phenylpropanolamine) may cause insomnia as
well as increase plasma caffeine levels, potentiating the stimulant effect of caffeine.
n Theophylline use is associated with increased sleep complaints (diff culty falling asleep, dis-
rupted sleep) in patients with asthma in comparison with other medications. However, allevia-
tion of nocturnal asthma symptoms may improve sleep quality.
Analgesics
Nonsteroidal anti-inf ammatory agents have a suppressant effect on nocturnal melatonin se-
cretion and have been shown to decrease sleep eff ciency and increase nightwaking. However,
improved sleep quality resulting from pain reduction may offset these sleep disrupting effects.
Opioids often result in daytime sedation, which may be persistent. They also disrupt sleep con-
tinuity and suppress REM sleep and SWS. Because opioids are respiratory depressants, they
may worsen OSA. Abrupt discontinuation may lead to insomnia and nightmares. Suppression of
muscle activity, however, may result in improvement in RLS symptoms.
Cardiovascular Drugs
Antihypertensive agents that are beta antagonists, such as propranolol, may be associated with
insomnia and increased nightmares. Other antihypertensives appear to have negligible effects on
sleep. Anti-arrhythmic drugs may cause daytime fatigue. For example, digoxin has been associ-
ated with both fatigue and insomnia.
Psychotropics
n Antidepressants
n Bupropion (Wellbutrin) is a norepinephrine and dopamine reuptake inhibitor that increas-
es REM sleep and reduces REM onset latency. Insomnia has been reported in 5% to 19%
of adults with the use of bupropion; thus bupropion should be avoided in patients with pre-
existing insomnia.
n Venlafaxine (Effexor) is a serotonin and norepinephrine reuptake inhibitor that has been
associated at medium level doses with diff culty initiating and maintaining sleep and at high
doses with severe insomnia in adults, as well as increased daytime somnolence.
n Antipsychotics in general interfere with neurotransmitters regulating sleep and wakefulness,
including dopamine, norepinephrine, serotonin, acetylcholine, and histamine. Traditional
antipsychotics (e.g., thioridazine [Mellaril] and to a lesser extent haloperidol [Haldol]) are
often associated with signif cant daytime somnolence. Newer atypical agents overall tend to
be less sedating, but there is some variability among individual agents (clozapine [Clozaril] >
olanzapine [Zyprexa] = quetiapine [Seroquel] > risperidone [Risperdal]). Most antipsychot-
ics decrease sleep onset latency, increase sleep continuity, and suppress REM sleep (in higher
doses). They also may promote sleep by attenuating psychiatric symptoms that interfere with
sleep.
n Lithium may improve nocturnal sleep, but also increase daytime sleepiness. It tends to in-
crease SWS, with variable suppression of REM sleep.
Psychostimulants
Both amphetamine and methylphenidate may have a direct dose-dependent medication effect that
interferes with sleep. Studies have demonstrated an increase in subjective parental perception of
severe sleep diff culties, including sleep onset delay and nightwakings in children on psycho-
stimulants for ADHD. Results of studies assessing objective measures of direct psychostimulant
effects on sleep, although less consistent, have found increased sleep onset latency, decreased to-
tal sleep time, REM sleep suppression, and variable decreases in SWS. A rebound effect late in
the day also may result in an increase in evening ADHD symptoms above baseline and increased
sleep onset latency. Discontinuation of stimulants after prolonged therapy may cause rebound
increases in REM sleep, SWS, and subjective sleepiness. The wake-promoting properties of the
psychostimulants make them useful agents in the treatment of primary disorders of excessive
daytime sleepiness such as narcolepsy. Atomoxetine (Strattera), the only non-stimulant medi-
cation indicated for ADHD, typically has less effect on sleep initiation than do the stimulants,
although an increase in sleep maintenance insomnia has been noted in adults; evening coverage
of ADHD symptoms with atomoxetine may reduce bedtime resistance.
Other Substances
n Alcohol is frequently used by adults with sleep initiation insomnia to hasten sleep onset. How-
ever, despite the fact that alcohol decreases sleep onset latency, it may also signif cantly impair
sleep continuity and cause sleep disruption. Alcohol has a biphasic effect on sleep architec-
ture, in that it increases SWS and suppresses REM sleep in the f rst part of the night but, as
alcohol levels decline, it results in REM rebound, decreased SWS, and sleep fragmentation.
The increase in SWS may exacerbate partial arousal parasomnias. REM rebound can increase
nightmares, as well as OSA symptoms. Acute withdrawal is associated with increased wake-
fulness, increased REM sleep, and decreased SWS.
n Caffeine increases alertness by blocking the sedative effects of the neurotransmitter adenos-
ine and increasing excitatory neurotransmitter release. Increased consumption is associated
with decreased daytime sleepiness and increased alertness. The degree of impact on sleep
onset latency, sleep disruption, and nonrestorative sleep is both time and dose dependent, al-
though sensitivity to these effects may vary across individuals. Caffeine may exacerbate RLS
symptoms. Many products contain caffeine (see Table 4.1), including a number of OTC cold
remedies, pain relievers, and weight loss preparations. There are a number of herbal stimulants
(see above) that also contain caffeine as the active ingredient.
n Nicotine (cigarette smoking) is associated with increased sleep onset latency and disrupted
and nonrestorative sleep. Nicotine also may increase symptoms of RLS and sleep-disordered
breathing. Nicotine withdrawal may result in disrupted sleep and daytime somnolence. In
terms of treatment for nicotine dependence, nicotine gum reduces SWS, and the patch reduces
sleep eff ciency (time asleep and time in bed) and prolongs sleep onset latency.
20 Sleep and Neurodevelopmental
Disorders
Sleep disturbances in children with neurodevelopmental disabilities, such as autism and a variety
of congenital and inherited conditions, are extremely common and often a source of consider-
able stress for the families of these children. The types of sleep disorders that occur in children
with neurodevelopmental disabilities are varied and generally not unique to these populations.
However, the prevalence of sleep issues is considerably higher, and the sleep problems tend to be
more severe, chronic, and resistant to treatment compared to those in typically developing chil-
dren. Multiple sleep disorders also are likely to occur concurrently. Furthermore, the impact of
disrupted and/or inadequate sleep on cognitive, emotional, and social development and behavior
in these already at-risk children is potentially profound.
This chapter will focus on the etiology, clinical evaluation, and management of sleep problems
in children across a spectrum of neurodevelopmental disorders. Sleep problems in children with
primarily mental health conditions, such as attention def cit hyperactivity disorder (ADHD) and
depression, are addressed in Chapter 22.
Sleep Screening in Children with Neurodevelopmental Disorders

The high prevalence of sleep disturbances in developmentally delayed children underscores
the role of ongoing screening for sleep problems in these populations. In addition, practitio-
ners need to consider multiple factors in evaluating an individual child with a sleep distur-
bance. The heterogeneity of possible etiologies for and contributing factors to sleep disorders
in this population is considerable, and successful treatment is contingent on identifying and
addressing these multiple issues.
Much of the sleep research in children with neurodevelopmental disabilities has been conducted
on heterogeneous diagnostic groups, rather than on homogeneous groups of children with spe-
cif c diagnoses. Overall, nonspecif c sleep problems, such as shortened sleep duration, irregular
sleeping patterns, delayed sleep onset, frequent nightwakings, and early morning waking, are
common across the spectrum of neurodevelopmental disorders. Some sleep disorders are more
commonly associated with specif c neurodevelopmental disorders or syndromes, such as ob-
structive sleep apnea (OSA) in Down syndrome and circadian rhythm disturbances in blindness.
Although there is obviously considerable heterogeneity among the various disorders that may be
included under the umbrella of neurodevelopmental disorders, many children with developmen-
tal delays and other special needs share common risk factors that may predispose them to sleep
disorders. These include:
n Medical issues:
n Central nervous system malformations or injuries that affect structures involved in con-
trol of sleepwake rhythms (thalamus, basal forebrain) or respiration (brainstem) increase

the likelihood of sleep disturbances and sleep-disordered breathing.
176
SLEEP AND NEURODEvELOPmENTAL DISORDERS 177
n Craniofacial abnormalities that result in obstruction at various levels of the upper airway,
such as choanal stenosis, midface hypoplasia, maxillary and mandibular hypoplasia, or hy-
pertrophy of soft tissue structures, are frequently found in a number of syndromes (e.g.,
Pierre Robin, achondroplasia, Treacher-Collins, Goldenhar, Crouzon, and Apert syndromes
and mucopolysaccharidoses). These craniofacial anomalies may predispose a child to sleep-
disordered breathing (see Chapter 21).
n Neuromuscular disease with associated weakness of respiratory muscles, such as con-
genital myopathies, muscular dystrophies, and other forms of hypotonia, often result in
hypoventilation. The ability to maintain a patent airway during sleep, especially in the pres-
ence of upper airway obstruction, is also decreased in these children (sleep issues related to
neuromuscular disease are discussed in more detail in Chapter 21).
n Medication use (including a variety of psychotropics), may result in altered sleep patterns
and sleep disturbance.

n Obesity associated with Prader-Willi and other congenital syndromes signif cantly increas-
es the risk of OSA.

n Seizure disorders (especially of the frontal and temporal lobes) may disrupt nocturnal
sleep and result in daytime sleepiness and fatigue. For example, Landau-Kleffner syndrome
is associated with continuous epileptiform activity during sleep, and children with Lennox-
Gastaut syndrome frequently have tonic seizures during sleep. Sleep deprivation, in turn, in-
creases seizure propensity; comorbid sleep-disordered breathing may also increase seizure
frequency in susceptible children. In addition, although suppression of nocturnal seizures
by anticonvulsants generally improves sleep quality and continuity, medications used to
treat seizures may also contribute to insomnia and daytime somnolence (sleep and seizures
are presented in more detail in Chapter 21).
n Sensory def cits: Sensory def cits can signif cantly impact sleep. For example, visual im-
pairment involving complete lack of light perception is associated with profound sleep dis-
turbances, often resulting in disruption of the circadian sleepwake pattern (e.g., delayed or
advanced sleep phase, non-24-hour or free-running sleepwake rhythms), with associated
diff culty falling asleep, early morning waking, and daytime sleepiness. This is presumably
due to alterations in the normal suppression of melatonin by ambient light.
Lack of a normal response to social and environmental cues in children with autism and
other forms of pervasive developmental disorder may contribute to irregular sleepwake pat-
terns. Alternatively, heightened or altered sensitivity to tactile, auditory, or other environmen-
tal sensory stimuli (e.g., sounds, ambient light, tags and seams on pajamas, texture and weight
of bedclothes) may lead to diff culties in settling and problematic nightwakings.
n Daytime behavioral problems: Daytime behavior problems, such as aggression and noncom-
pliance, may result in similar behaviors during sleep times, such as bedtime resistance and
prolonged nightwakings. In addition, self-injurious behavior has been reported both to result
from and to be exacerbated by sleep problems. Children with repetitive, stereotypic, or ritual-
istic behaviors may increase these behaviors in the evening, prolonging bedtime routines and
interfering with settling at bedtime and sleep onset.
n Cognitive impairment: In general, higher degrees of cognitive impairment tend to be associ-
ated with more frequent and severe sleep problems; prevalence of sleep problems in children
with severe mental retardation have been estimated to be on the order of 30% to 80%, com-
pared to 50% in children with less severe cognitive impairment. Children who have diff culty
communicating their needs or understanding and responding to environmental demands are
more likely to have problematic sleep. In addition, children with social interaction impair-
ments may be more prone to behavioral sleep disorders
n Comorbid psychiatric disorders: Psychiatric disorders, such as depression and anxiety, are
common in children and adolescents with developmental delays and autistic spectrum dis-
orders, and may contribute to sleep problems. Severe hyperactivity and ADHD and/or mood
178 SECTION Iv SLEEP IN SPECIAL POPULATIONS
instability is common to many chromosomal and genetic disorders, including velocardiofacial

syndrome, Angelman syndrome, Williams syndrome, Fragile X syndrome, and Klinefelter
syndrome, and may contribute to the genesis of sleep onset and maintenance diff culties in
these children (see Chapter 22 for more detailed information).
n Parenting-related variables: Parenting issues, such as diff culty with limit setting and high
levels of family stress, may contribute to and be exacerbated by sleep diff culties in the devel-
opmentally delayed child. Parents of developmentally delayed children may have inappropri-
ate expectations regarding sleep patterns and behaviors that are based on the childs chrono-
logic rather than on the developmental age. Alternatively, caregivers may see sleep problems as
inevitable and, therefore, make only brief or limited attempts at managing them; for similar
reasons, parents may be less likely to seek professional advice for treating sleep problems.
SPec iFic n eur o DeVel o PMen t Al DiSo r Der S

The association between autism spectrum disorders (ASD) and sleep problems is one that poses
signif cant clinical challenges, and thus is presented in some detail below. Other specif c neuro-
developmental syndromes that have also been reported in association with sleep disturbances are
also discussed below, in alphabetical order (meningomyelocele and neuromuscular disorders are
discussed in Chapter 21).
n Autism and autism spectrum disorders: Studies examining sleep problems in children with
autism and pervasive developmental disorder (PDD), including Asperger Syndrome (AS),
suggest that these children are prone to a variety of sleep problems, even when compared
with non-autistic children with similarly low levels of intellectual functioning. The prevalence
of caregiver-reported sleep problems across the spectrum in these studies ranges from 34%
to 89%. In autism and PDD, the prevalence of past or concurrent sleep problems, depending
upon the def nitions used, has been estimated from 44% to 89%. Rates of sleep problems ap-
pear to be largely independent of IQ, although there appears to be some positive correlation
between sleep disturbances and the severity of daytime behavior problems and communication
impairments.
The types of subjective sleep problems most commonly described include highly irregular
sleepwake cycles; diff culty settling and delayed sleep onset; frequent, prolonged, and disrup-
tive nightwakings; short sleep duration; and early morning waketimes. Sleep routines may be
both unusual and problematic in these children because of stereotypic and repetitive behaviors,
and there are frequently diff culties in adapting to any alterations in routines. Some studies
have reported an increase in parasomnias, such as sleepwalking and bruxism; also reported is
a relative increase in REM behavior disorder, an otherwise extremely rare condition in child-
hood, which is characterized by absence of the normal muscle atonia associated with REM
sleep and results in acting out of dream content. In general, sleep problems in these children
are distinguished less by their unique characteristics than by their severity, chronicity, and high
relapse rate. In contrast to subjective sleep complaints, there have been few reliable and con-
sistent clinically signif cant objective differences in sleep architecture demonstrated in autistic
children, with the possible exception of some alterations in REM sleep variables (e.g., REM
percent, muscle tone in REM) and increased sleep fragmentation. However, the prevalence
of primary sleep disorders (e.g., obstructive sleep apnea syndrome, periodic limb movement
disorder [PLMD], bruxism) is signif cantly increased in ASD patients with parent-reported
sleep disruption, emphasizing the importance of recognizing the possible contribution of these
disorders to sleep complaints in children with ASD and of screening for them accordingly.
There are a number of biological hypotheses that have been put forth to explain the high
prevalence of sleep disturbances in ASD, although it should be pointed out that these are
largely speculative at this time. First, because of the irregular sleepwake patterns commonly
displayed by autistic children, circadian rhythm abnormalities have been postulated to account
for a signif cant percentage of sleep issues. An underlying disturbance in melatonin produc-
tion in autism has been proposed; in particular, there appear to be altered levels of mela-
tonin precursors (e.g., tryptophan, serotonin) in these children. Furthermore, children with
ASD demonstrate abnormal patterns of melatonin secretion, including decreased amplitude,
and paradoxical daytime elevations accompanied by nocturnal decreases in melatonin. Other
hypotheses regarding circadian dysregulation include possible anomalies in circadian clock
genes, which in turn impact both motor planning and sleep; greater sensitivity to changes
in photoperiod resulting in the frequently observed seasonal variations in sleep problems in
these children; and a decreased awareness of and sensitivity to social and environmental fac-
tors, resulting in lower levels of entrainment or synchronization of the circadian system by
environmental cues. Other proposed biologic mechanisms includes abnormalities in secretin,
an endogenous gastrointestinal polypeptide which has been hypothesized to have a role in
language development, behavior, and regulation, of sleep; increased activation of the inf am-
matory response system in autism, resulting in higher levels of inf ammatory markers (e.g.,
cytokines) with effects on sleep regulation; a primary arousal dysfunction characterized by
altered sleep homeostasis (sleep drive), and an underlying dysfunction in monoaminergic
pathways (dopamine, serotonin).
In addition, a number of psychosocial and environmental factors are likely to contribute
to the increase in severe sleep problems in these children. These include learned maladap-
tive sleep patterns, inadequate parent limit setting, and increased parental awareness of sleep
issues.
Children and adolescents with AS are particularly prone to anxiety, thus sleep problems
related to nighttime fears, separation anxiety, and obsessive-compulsive behaviors are com-
monly observed. Finally, it is important to recognize that many patients will have a multi-
factorial etiology for their sleep problems.
Sleep in Autism and Pervasive Developmental Disorder

Sleep problems in children with autism and autism spectrum disorders are extremely com-
mon. Parents of these children may view the sleep disturbance as intrinsic or inevitable to
the disorder and, thus, may not spontaneously seek medical advice until the problem becomes
severe. Sleep problems in these children are often chronic but can be successfully treated with
a combination of behavioral and pharmacologic strategies.
n Angelman syndrome: The prevalence of subjective caregiver reports of sleep problems in

children with Angelman syndrome ranges from 20% to 80%; increased rates are found in
younger patients (toddlers and preschoolers), and may improve in adolescence. Decreased
sleep duration, frequent nightwakings, and irregular sleepwake cycles are reported. Poly-
somnography (PSG) studies have demonstrated an increase in sleep onset latency and night-
waking, decreased REM and increased slow-wave sleep (SWS) percent, and increased sleep
fragmentation, especially associated with seizures. Some studies have reported an increase in
PLMs in these children, although not all studies have concurred with this f nding.
n Down syndrome: Children with Down syndrome are clearly at increased risk for sleep-disor-
dered breathing (estimated OSA prevalence range across studies 30% to 80%) for a number of
reasons, including generalized hypotonia, obesity with central distribution of adipose tissue,
midfacial hypoplasia and glossoptosis (large, posteriorly placed tongue), hypothyroidism, and
adenotonsillar hypertrophy. OSA prevalence does not appear to be related to age or the pres-
ence of congenital heart disease. Central sleep apnea and Cheyne-Stokes respiratory pattern
has also been reported to be more common in Down syndrome. PSG studies have demon-
strated increased arousals and sleep fragmentation not solely attributable to OSA and an in-
crease in movement arousals and PLMs. In addition, subjective sleep complaints, particularly
diff culties with sleep onset, occur in up to 70% of these children.
n Prader-Willi syndrome (PWS): Reported rates of sleep-disordered breathing are highly vari-
able (0% to 100%) in children with PWS, but most studies have supported a signif cant in-
crease in OSA related to the associated obesity. The severity of the OSA appears to correlate
with body mass index, and may improve signif cantly with weight loss. These children have
high rates of post-adenotonsillectomy complications. In addition, several studies have sug-
gested that there is an increased risk for sudden death in children with PWS associated with
the initiation of growth hormone replacement therapy for short stature. The risk appears to be
greatest during the initial treatment period, and may be increased both by the presence of co-
morbid OSA and concurrent acute upper respiratory illnesses. Additional associated ventila-
tory abnormalities include chronic hypoventilation and central sleep apnea, especially in REM
sleep, and intermittent oxygen desaturation.
REM sleep abnormalities, including decreased REM onset latency and an increased preva-
lence of REM intrusion phenomena, such as sleep attacks, cataplexy, and sleep paralysis, have
also been identif ed in children with PWS. The percentage and depth of SWS also appears
to be increased in these patients. Finally, both subjective complaints and objective evidence
(mean sleep onset latency less than 5 minutes and sleep onset REM periods on multiple sleep
latency tests) of signif cant daytime sleepiness are common in PWS, especially in adolescence
and adulthood. Although the hypersomnolence may be associated with OSA and may improve
with treatments such as continuous positive airway pressure, it may also occur independently
of obesity and sleep-disordered breathing, and signif cantly compromise daytime functioning.
It has been hypothesized that these patients may have a primary hypersomnia that is secondary
to hypothalamic dysfunction; alternative explanations have included non-REMREM (ultra-
dian) cycling dysregulation, abnormalities in melatonin secretion patterns, and dysfunction of
the hypocretin/orexin system.
n Rett syndrome: Although ventilatory (hyperventilation and apnea) abnormalities are com-
mon during the day, sleep apnea and other sleep-related respiratory disturbances, such as pe-
riodic breathing, appear to be uncommon in children with Rett syndrome. However, these
children are more prone to diff culties falling asleep; fragmented sleep; nightwakings; noc-
turnal events, such as night laughing and inconsolable screaming; early morning awakening;
and shortened sleep duration. Dysregulation of melatonin secretion responsive to exogenous
melatonin administration has been demonstrated in some girls with Rett syndrome. They may
also have increased sleep fragmentation related to nocturnal seizure activity.
n Smith-Magenis syndrome: The prevalence of subjective signif cant sleep diff culties is high
(60% to 100%) in children with Smith-Magenis syndrome. Caregivers frequently report dif-
f culty falling asleep, short sleep duration, frequent and prolonged nightwakings, daytime
sleepiness, and nocturnal enuresis. PSG studies indicate decreased total sleep time and REM
percent, with a tendency for early sleep onset and offset. Inversion of the normal circadian
rhythm of melatonin secretion has also been reported in those with Smith-Magenis syndrome.
n Williams syndrome: Subjective sleep complaints, including diff culties initiating and main-
taining sleep and restless sleep, are common in children with Williams syndrome. There is
mixed evidence that Williams syndrome is associated with an increase in PLMs and associated
arousals and sleep fragmentation.
Sleep and Breathing in Neurodevelopmental Disorders

Sleep-disordered breathing is particularly common in many populations of children with
neurodevelopmental disabilities, especially in children who have conditions characterized by
craniofacial abnormalities, such as midface hypoplasia and micrognathia, hypotonia, and/or
obesity. The resulting sleep fragmentation may contribute signif cantly to learning and behav-
ior problems already present as part of their underlying disorder. Many of these children, once
identif ed, can be successfully treated with continuous positive airway pressure, if appropriate
behavioral support is available.
eVAl uAt io n
Evaluation of sleep problems in children with neurodevelopmental disabilities is similar to the
screening and assessment of sleep problems in other pediatric populations, although given the
high prevalence, a high index of suspicion should be maintained and regular screening is key. A
functional assessment of sleep problems, in which parents are asked to track the antecedent and
consequence of each disruptive nighttime behavior, can also be performed. Nighttime behaviors
of children with developmental disabilities are often perpetuated by social consequences, such as
parent attention in the form of comfort, play, or even verbal warnings.
t r eAt Men t
Sleep Practices
n Sleep hygiene principles, including environmental (e.g., temperature, noise level, ambient
light), scheduling (e.g., regular sleepwake patterns), sleep practice (e.g., bedtime routine),
and physiologic (e.g., exercise, timing of meals, caffeine use) factors, are frequently over-
looked in preventing and treating sleep problems in developmentally delayed children. Sleep
hygiene practices have a positive impact, especially in this population, because they help to
entrain intrinsic circadian rhythms to the external environment and 24-hour-day/night cycle.
In addition, behavioral conditioning results in the association of certain activities and environ-
ments with sleep.
n Sleep environment that is conducive to sleep can be challenging to implement and often need
to be modif ed and individually tailored. Achieving an appropriate level of comfort and safety
in the sleeping environment, particularly for children with sensory and motor disabilities, is
important. Positioning in bed of children with limited mobility and choosing an appropriate
sleep surface (e.g., waterbeds, adjustable mattresses) that is tailored for physical comfort may
need to be considered. Some children may require a fortif ed crib or bed that is surrounded
by a mesh material to conf ne the child to bed while allowing visibility both from within and
without.
Sensory Issues
Specif c occupational therapy techniques and devices that have been used to address sensory
integration issues (e.g., brushing, weighted vests and blankets for children with tactile sen-
sory issues, white noise generators that produce a mixture of all frequencies and can mask
environmental sounds, body pillows) may be useful in alleviating sleep problems in children
with sensory issues. Evaluation and consultation with a pediatric occupational therapist may
be helpful.
n Alarm systems that alert caregivers when a child has left the bedroom may be necessary, as
some children may wander around the house during the night. A two-way monitor or Webcam
in the bedroom may reassure parents and reduce the need for parental intervention during the
night.
n Bedroom lighting may need to be adapted. Although a dark sleeping environment is prefer-
able, some anxious children might benef t from a dim night-light. However, children with
cortical blindness may stare into a light source for self-stimulation (light gazing), keeping
them in an alert state.
n Bedtime routines are especially important and should include specif c and predictable steps.
Children with neurodevelopmental disorders may be easily overstimulated, so bedtime activi-
ties must be carefully planned and calming, such as the use of gentle, rhythmic, repetitive, low-
frequency movements, quiet sounds, light massaging, brushing, vibrating pillows and beds,and
soft music. However, parental presence at time of falling asleep should be curtailed if possible
to avoid the development of problematic sleep onset associations, Expectations around night-
time behavior must be clearly communicated and consistently enforced. Encouraging the use
of appropriate transitional objects may be particularly important in these children.
n Caregivers need to be considered in the development of the treatment plan. That is, sleep hy-
giene is most effective when it provides for the sleep needs of both the child and the parents,
and it is important for healthcare providers to directly address and support caregivers need
for adequate sleep. Thus, assisting parents to make operational changes, such as arranging for
respite or night nursing care, can have a signif cant positive impact.
n Additional sleep practices include ensuring that the development of conditioned associations
between the childs bed and bedroom and behaviors incompatible with sleep (e.g., watching
television) is avoided. In particular, any activities that require parental participation should be
curtailed if possible before actual sleep onset to avoid the development of problematic sleep
onset associations; expectations around nighttime behavior must also be clearly communi-
cated and consistently enforced. It is also particularly important to maintain a regular daytime
routine for mealtime, playtime, and other activities with these children to help synchronize
sleepwake rhythms. Unless developmentally appropriate, daytime sleep periods and naps
should be restricted to avoid compromising consolidation of nighttime sleep.
Behavioral Management of Sleep Problems

Sleep disturbances in children with developmental delays are frequently amenable to manage-
ment with a variety of behavioral strategies. These should be tailored to the developmental
level of the child and the resources of the family. Choosing reasonable, attainable, and mutu-
ally acceptable target goals in terms of bedtime behaviors, nightwakings, and sleep duration is
particularly important in assisting families.
Behavioral Management
Children with neurodevelopmental disorders have many of the same sleep problems as typically
developing children, such as sleep onset association and limit-setting subtypes of behavioral in-
somnia of childhood (see Chapters 6 and 7), which warrant similar intervention strategies, sleep
scheduling, graduated extinction procedures, and fading of adult intervention at bedtime and
during nightwakings. These strategies can be as effective with children with neurodevelopment
disorders; however, positive changes may simply take longer. Of course, all of these strategies
involve commitment and consistency from parents; as with many behavioral treatments, the tar-
geted problem often becomes worse before it gets better. Families with disabled children often
face numerous challenges on a daily basis, and caregivers may be hesitant to disrupt established
patterns of home behavior for the sake of intervening with their childrens sleep problems. Edu-
cating parents about the link between decreased daytime functioning and disrupted sleep and
providing ongoing support, are necessary for caregivers to successfully approach what is likely
to be a diff cult and possibly lengthy process.
Some special considerations should be given to the application of behavioral management
strategies in these special populations. Ensuring the safety of these children, especially if night-
waking is a problem or if there is a history of self-injurious behavior, needs to be a key consider-
ation. In general, parents tend to be more comfortable with more gradual treatment approaches.
Furthermore, the severity and chronicity of sleep problems in many of these children often neces-
sitate long-term treatment and utilization of a variety of treatment strategies. Finally, collabora-
tion with a behavioral therapist in designing and implementing treatment plans may be prudent
if there are complex, chronic, or multiple sleep problems or if initial behavioral strategies have
failed.
Pharmacologic t reatment
The use of pharmacologic intervention may be required in some children with severe sleep prob-
lems that are not or only partially responsive to behavioral techniques, particularly if daytime
functioning is compromised and/or caregiver mental or physical health is adversely affected. A
wide variety of medications have been used in children with neurodevelopmental disorders. Gen-
eral principles of drug selection and medication management are detailed in Chapter 19.
As in all children, pharmacologic treatment should be combined with behavioral interven-
tions. Short-term use of a hypnotic medication can rapidly decrease sleep onset delay, eliminate
prolonged bedtime struggles, and reduce problematic nightwakings, enabling parents to be more
successful in implementing bedtime behavioral strategies, which ultimately are likely to have a
more enduring impact. However, there are situations in which the severity and chronicity of the
sleep problem necessitate long-term use of sedating medication; in these cases, the importance
of choosing an agent with minimal long-term side effects is paramount.
Practitioners should be aware of the potential pitfalls in using hypnotic medications, espe-
cially unpredictable side effects in this population. In general, using medications with combined
effects when appropriate (e.g., sedating anticonvulsants for children with seizures, sedating atyp-
ical antipsychotics in patients with aggression), thus potentially reducing drug exposure and
minimizing adverse effects, is desirable. Finally, specif c medications have been demonstrated to
be helpful in select conditions; for example, the PLMs associated with Williams syndrome often
respond to clonazepam, and sleep disruption in children with ASD has been shown to improve
with clonazepam as well.
Melatonin
Melatonin is the best-studied pharmacologic intervention for developmentally delayed chil-
dren with sleep problems, particularly in children with persistent alterations in circadian
rhythm or sleepwake schedule. Studies indicate that melatonin can result in signif cant im-
provements in sleep onset delay, nightwakings, early morning waking, and total hours of sleep
in up to 80% of children with a variety of neurodevelopmental disorders (cortical blindness,
Rett syndrome, autism, tuberous sclerosis, Asperger syndrome).
Studies have typically used doses in the range of 2 to 5 mg of melatonin, administered 30
to 60 minutes before bedtime (see Chapter 19 for more detailed information). Some studies
have used doses up to the 10-mg range for refractory cases without reported adverse effects,
although the rationale for such supra-physiologic doses remains unproven. It should be em-
phasized that melatonins positive effect on sleep may be due either to its chronobiotic
(circadian sleepwake pattern re-setting) or hypnotic (sedating) effects; studies in adults
with delayed sleep phase have suggested that a small (i.e., 0.10.5 mg) physiologic dose of
melatonin 5 to 7 hours before the habitual late bedtime may actually be more effective in ad-
vancing sleep onset time in the case of a true circadian-based sleep onset delay, while larger
doses just before bedtime have primarily a hypnotic effect. Melatonin is available in liquid and
sublingual as well as tablet formulations, and as a slow-release preparation.
Although generally considered safe, there are some caveats regarding the use of melato-
nin in children with neurodevelopmental delays. Due to its suppressive effects on the hypo-
thalamicgonadal axis, there is a theoretical possibility of initiation of precocious puberty
if melatonin is withdrawn abruptly after chronic administration. In addition, little is known
about long-term side effects with chronic use. Given the over-the-counter availability of mela-
tonin, the purity of preparation and inconsistent dosing are also concerns. Overall, melatonin,
as with all pharmacologic interventions, is likely to work best in combination with behavioral
interventions.
l ight t herapy and Sleepw ake Scheduling

Primary circadian rhythm disturbances may also be treated with bright light therapy and sleep
wake scheduling or chronotherapy. Morning phototherapy with a light box delivering 2,000 to
8,000 lux has been used to successfully treat refractory sleep phase delay in severely brain-
damaged children. Duration and timing of light exposure are typically 1 hour right after morning
wake time, and are often combined with a gradual advance to an earlier sleep onset and offset
time over a period of days to weeks. However, inappropriate timing of the phototherapy may
actually worsen the circadian disturbance, so this treatment is best done under the supervision
of a sleep professional. Chronotherapy, or the successive delay of the sleepwake cycle over a
period of days until the desired bedtime is reached, has also been used effectively to treat severe
sleep onset delay in autistic and blind children. It should also be noted that children who are
prone to circadian rhythm disturbances may be relatively sensitive to and disrupted by circadian
desynchronization (e.g., jet lag, daylight savings shift). Therefore, parents may need to carefully
anticipate these situations.
Sleep and medical Disorders 21
Children with both acute and chronic medical conditions may suffer from sleep disturbances,
including both primary sleep disorders and sleep problems that are secondary to the underlying
disease processes. Sleep disturbances, including diff culty initiating sleep, bedtime resistance,
and nightwakings, are common in children with both acute and chronic medical conditions. It
is likely that a host of factors contribute to the development and exacerbation of sleep problems
in medically compromised children, including physical issues, such as pain control and medica-
tions; psychological factors, such as comorbid mood and anxiety disorders and family stress;
and environmental variables such as hospitalization. In turn, the effects of sleep fragmentation
and sleep deprivation in these children are also likely to be particularly signif cant, given what
is known about the psychological and emotional impact of inadequate sleep and the physiologic
effects of sleep deprivation on the immune system and the bodys ability to respond to stress.
Sleepiness versus Fatigue

A distinction between sleepiness and fatigue may be relevant in assessing the role of sleep in
some medical conditions, although this is sometimes more of a semantic difference that may
be diff cult to elicit in young children. By def nition, sleepiness is the persistent propensity
to doze off or fall asleep. Although sleepiness may be affected by a host of intervening vari-
ables, including time of day, motivation, physiologic states such as hunger, and level of stimu-
lation, true daytime sleepiness generally implies the presence of inadequate and/or disrupted
sleep. Fatigue, on the other hand, is more likely to refer to a subjective state of low energy and
low motivation, which may or may not primarily be a result of poor sleep.
Pain
Both acute and chronic pain have major physical and psychological effects on sleep, and these
are often bidirectional in nature. Pain may cause sleep onset delay, nightwakings, fragmented and
restless sleep, and frequent arousals as well as daytime fatigue. Even adaptive behaviors, such
as protection of the injured area by positioning and increased attention to movements during
sleep, may further impact on sleep quality. One study reported that approximately half of a group
of children with newly diagnosed cancer suffered pain-related sleep disturbances. Alternatively,
the sleepiness and fatigue associated with sleep problems may exacerbate pain. The interaction
between pain and sleep is also impacted by a number of psychological variables. Coping skills
needed to deal with pain may be compromised by the mood changes, irritability, low frustration
tolerance, and poor regulation of emotions caused by sleep deprivation. Learned associations
with both sleep and pain tend to be very powerful, and children may become conditioned to
associate bedtime and sleep with negative and painful experiences. Finally, implementation of
behavioral management strategies may be impacted by decreased motivation and goal-directed
behavior and by decrements in attention and behavioral and impulse control in the sleep-deprived
child.
185
Additional factors that are involved in the complex relationship between sleep and pain in-
clude stress, hyperarousal, and anxiety. These may be particularly problematic at sleep onset,
as it requires the relaxation of vigilance and attention to the surrounding environment. Sleep
may also represent a temporary psychological escape from pain; thus, the inability to initiate or
maintain sleep may further heighten anxiety and decrease pain tolerance. Some children with
chronic medical conditions associated with pain may have comorbid psychiatric disorders, such
as anxiety and depression, which may lead to further deterioration of sleep patterns and quality
(see Chapter 22). Children with pain conditions related to trauma may also have posttraumatic
stress disorder (PTSD) symptoms that may signif cantly disrupt sleep.
Finally, medications used for pain management may directly disrupt sleep by affecting sleep
patterns and architecture. For example, opiates decrease REM sleep and slow-wave sleep (SWS)
and increase sleep fragmentation. Side effects of analgesics, such as gastrointestinal discom-
fort, and withdrawal effects of pain medications may result in sleep disturbances. For example,
withdrawal of medications with REM suppressant effects, such as benzodiazepines, may result
in REM sleep rebound and increased nightmares. Finally, inadequate pharmacologic control of
nocturnal pain may lead to more disrupted sleep, increased daytime fatigue, and a further dete-
rioration in pain management.
Family issues
Families of children who have had life-threatening illnesses or who have chronic medical condi-
tions may develop a vulnerable child syndrome, in which parents are unwilling or unable to set
limits because of concerns about compromising the childs physical condition or upsetting the
child. Bedtime resistance and reactive co-sleeping with parents may result. In addition, parents
of children with medical problems may be unwilling to enforce good sleep hygiene rules such
as regular sleepwake schedules and avoidance of inappropriate daytime napping, further com-
pounding poor sleep.
h ospitalization
Hospitalization is a stressful event for children and their families, and behavioral regression to
a previous developmental level (e.g., dependence on parental presence in order to fall asleep)
is a common response, particularly in younger children. This may result in an acute adjustment
sleep disorder with diff culties initiating and maintaining sleep or exacerbate preexisting sleep
problems or both. Although there are relatively few studies of sleep disturbances in hospitalized
children, prolonged sleep latencies, signif cantly later bedtimes, shortened sleep duration, and
reduced napping have been described. For example, in a recent study, hospitalized school-aged
children reported later bedtimes, later wake times, more nightwakings, and shorter total sleep
time, while adolescents reported later wake times, more nightwakings, and longer total sleep time
during hospitalization. Children with more prolonged and/or life-threatening illnesses requiring
frequent hospitalizations, such as cancer, may be even more at risk for chronic sleep disturbances.
In addition to issues related to the underlying medical condition and stress and anxiety about
hospitalization, factors in the hospital environment may contribute signif cantly to the develop-
ment of sleep problems in children in the inpatient setting. These factors include noise (including
sudden and unexpected noises as well as a high level of background noise), frequent nocturnal in-
terruptions for medication and vital sign checks, and bright and/or inappropriately timed lighting,
which may affect the normal circadian release of melatonin and thus further compromise regular
sleep patterns. It has been shown that relative sleep loss and sleep fragmentation are particularly
common in intensive care units (ICU). One pediatric ICU study documented an average total
sleep time of 4.7 hours, reduced 50% from baseline home sleep amounts, as well as decreased
amounts of SWS. These sleep disturbances may also persist after discharge from the hospital,
often as a result of learned associations and inadvertent parental reinforcement of maladaptive
sleep patterns.
SLEEP AND mEDICAL DISORDERS 187
A number of potentially modif able factors related to the hospital environment and hospital
procedures may have a signif cant detrimental impact on the quality and quantity of sleep in hos-
pitalized patients. Accordingly, relatively minor adjustments in the patients surroundings could
potentially have major positive consequences. These include:
n Increasing daytime activity levels and limiting daytime naps to promote nocturnal sleep.
n Maintaining home patterns of bedtimes and waketimes.
n Encouraging daytime and limiting nighttime light exposure as well as providing a regular
schedule of daily activities to assist in maintaining normal circadian rhythms.
n Decreasing late evening stimulation (noise level, social interactions).
n Limiting nursing and medical assessments and procedures during the night.
n Encouraging parents to provide familiar bedtime comfort objects from home and to maintain
home bedtime routines as much as possible in the hospital.
n Making the hospital room a safe haven by conducting potentially painful and anxiety-
provoking procedures as much as possible in alternative locations.
n Implementing proactive sleep-promoting measures, including the use of relaxation exercises
and tapes, massage, and dream-catchers, which can also facilitate restorative sleep and pre-
vent the development of sleep problems.
While studies have suggested that between 50% and 75% of adult hospitalized patients are pre-
scribed a sedative or hypnotic to improve sleep, hypnotic use in pediatric inpatients appears to be
much less common. A recent large multi-site study of sleep medication use in almost 10,000 pe-
diatric inpatients reported that approximately 3% to 6% of hospitalized children had been treated
pharmacologically with a variety of sleep medications; children with a psychiatric diagnosis
were almost 3 times more likely to receive a sleep medication. Given that there may be situa-
tions in which behavioral interventions alone are not practical for hospitalized children because
of the length of time and staff resources needed to implement these treatments, use of hypnotic
medications may be indicated (see Chapter 19). Finally, excessive daytime sleepiness and fatigue,
particularly in cancer patients, may be responsive to psychostimulant medication, such as meth-
ylphenidate or modaf nil, as well as bright light therapy.
Medications
Many of the medications used to treat children with a variety of medical problems are known to
have potential adverse effects on sleep and/or to be associated with daytime sedation (see Chap-
ter 19 for a more detailed discussion of pharmacologic effects on sleep). These include analgesics
for pain management, antihistamines and antipruritics for allergies, bronchodilators and cortico-
steroids for asthma, various chemotherapeutic agents, and anticonvulsants for seizures.
o besity
Congenital or acquired conditions and syndromes characterized by or commonly accompanied
by obesity (e.g., Prader-Willi syndrome) have an increased risk of sleep problems, particularly
sleep-disordered breathing (SDB) and daytime sleepiness. Alternatively, shortened sleep duration
in children is both concurrently associated with and predictive of the development of being over-
weight and obesity. A separate section below provides an overview of the complex relationship
between sleep and obesity.
Sleep and Quality of Life

Virtually any medical condition, acute or chronic, may have adverse effects on a childs sleep
quality and quantity. Multiple possible contributing factors should be considered, including
concomitant medications, psychosocial factors, and pain. Because of the potential impact of
sleep disturbances on both the underlying disease process and the childs and familys quality
of life, the practitioner should make every effort to assess for and address sleep problems in
the setting of medical illness.
SPec iFic MeDic Al c o n Dit io n S

Specif c medical conditions that have been reported in association with poor quality and/or inad-
equate sleep are discussed below. However, it should be noted that virtually every medical condi-
tion in children and adolescents, because of related issues such as stress, pain, and medication
use, might be accompanied and exacerbated by disrupted sleep. For example, a primary cardiac
or respiratory disease may result in sleep disturbances, and the underlying disease may be exac-
erbated by sleep disruption.
(Note: Medical conditions are presented in alphabetical order, with obesity, seizures, and central
hypoventilation syndrome covered as separate sections at the end of the chapter.)
Allergies
Chronic allergy-mediated rhinitis with nasal congestion, post-nasal drip, and cough, as well as
chronic or frequent sinusitis, are associated with diff culties initiating sleep and particularly with
frequent arousals and disrupted sleep. Environmental allergies also contribute to upper airway
resistance and are considered to be risk factors for obstructive sleep apnea (see Chapter 14). Use
of sedating antihistamines to control allergic symptoms during the day may also disrupt regular
sleepwake patterns, and decongestants such as pseudoephedrine have been associated with in-
somnia. Adequate nocturnal, as well as diurnal, control of symptoms such as wheezing, cough,
and pruritus, should be a primary goal in the management of atopic disease. This often requires
measures to control allergens in the sleeping environment (e.g., protective mattress and pillow
covers made of soft, tightly woven fabric with a pore size less than 10 microns, frequent launder-
ing of bedclothes in hot water, wooden instead of carpeted f oors, humidity levels in the bedroom
less than 50%, HEPA f lters) as well as pharmacologic intervention (e.g., immunotherapy, nasal
steroids, oral antihistamines). Stuffed animals, a frequent source of dust mites, can be laundered
at high temperatures (130 F) or stored in the freezer overnight and then washed.
Asthma
Asthma in children is associated with poorer subjective sleep quality, decreased sleep duration,
increased nocturnal wakings with decreased sleep eff ciency, reduced SWS, and greater daytime
sleepiness and increased napping. The underlying asthma symptoms may worsen at night as a re-
sult of circadian variations in respiratory function and peak f ows (e.g., lung function is at its low-
est at about 4 a.m.), resulting in an up to 50% reduction in lung function during sleep compared
to daytime. Other factors such as increased allergen exposure in the bedroom (e.g., dust mites,
animal dander) and use of short-acting bronchodilators, which wear off during sleep, may also
play important roles in nocturnal asthma exacerbations. In a number of studies, sleep symptoms
have been correlated with subjective (symptoms) and objective (such as pulmonary function
tests) measures of disease severity.
Although asthma-related sleep disturbances have been reported in approximately 80% of adult
patients with asthma, pediatric studies have been more limited. Available research indicates that
one-third of asthmatic children report at least one awakening per night, and the overall preva-
lence of sleep problems in children with asthma has been reported to be 60%. Nocturnal asthma
symptoms have been associated with impaired daytime cognitive functioning and attention, poor
school performance and decreased attendance, and fatigue. Furthermore, asthmatic children rate
themselves as signif cantly more tired in the morning than normal controls. Cognitive function
appears to improve with medication adjustment and optimal symptom control; however, some
studies suggest that even children with well-controlled asthma may have more disrupted sleep
than normal controls.
A number of nocturnal physiological changes could contribute to the exacerbation of asthma
during sleep, including a decrease in lung volume, increase in intrapulmonary blood volume,
reduced mucociliary clearance, and nocturnal gastroesophageal ref ux. Asthma also seems to be
an independent risk factor for OSA, further disrupting sleep and exacerbating daytime impair-
ment. Asthma medications themselves may also have adverse effects on sleep. For example, oral
corticosteroids may cause signif cant sleep disruption, and theophylline is known to have a stimu-
latory effect on the central nervous system (CNS) with resultant increased wakefulness. Insomnia
has been reported as an occasional side effect of leukotriene inhibitors; most of the newer asthma
medications have more selective beta-adrenergic and fewer CNS effects. In considering treatment
options, it is important to weigh the benef ts of good pharmacologic control against the possible
negative effects of bronchodilators and other medications on sleep.
Atopic Dermatitis and eczema

Atopic dermatitis may cause diff culty falling asleep, sleep disruption and fragmentation, night
awakenings, decreased sleep duration, and resulting daytime sleepiness as a result of frequent
scratching and discomfort. Parents of children with chronic allergies and/or atopic dermatitis
may also be more aware of and pay more attention to nightwakings, further perpetuating the cycle
of disrupted sleep. Aggressive treatment and prevention measures for the underlying skin condi-
tion may include use of topical steroid and non-steroid creams and ointments and oral sedating
antihistamines at bedtime, physical barriers (e.g., socks on hands to prevent scratching during
sleep), bedroom environmental allergen control (e.g., cotton pajamas), and dietary changes if
appropriate.
Burns
Children who are severely burned are at particularly high risk for sleep problems, which, in
turn, may have signif cant adverse effects on their recovery. Diff culty falling asleep, increased
arousals, nightmares, and increased daytime sleepiness are common in the acute phase and may
persist for up to 1 year after the event. Changes in sleep architecture have been reported, includ-
ing decreased SWS, which may contribute to the growth hormone insuff ciency seen in burned
children. It has been postulated that increases in particular types of peripheral cytokines in re-
sponse to thermal injury (interleukin-1 and tumor necrosis factor) may contribute to sleep disrup-
tion through their specif c role in sleep regulation. Burned children obviously also have multiple
sources of pain, as well as severe pruritus, which may disrupt sleep. Additional factors are those
common to all medically compromised and traumatized children, such as depression, anxiety
and stress, PTSD, and hospitalization or ICU-related factors. Narcotic analgesics, sedatives, and
other medications used to treat anxiety (benzodiazepines) and depression in burned children may
also alter sleep architecture.
c ancer
Because of the relative scarcity of studies examining sleep disturbances in children with various
forms of cancer, little is known regarding overall prevalence rates. Sleep problems, including
diff culty initiating and maintaining sleep, have been reported to be common in children with
leukemia and brain tumors, which account for about 50% of childhood cancers. There are a
myriad factors that are likely to increase the risk for sleep problems in these children, including
stress and anxiety related to the diagnosis, pain, nausea and other effects of chemotherapy, medi-
cation effects (i.e., insomnia and sedation), frequent hospitalization, caregiver exhaustion and
reluctance to enforce appropriate limits, and disruption of normal developmental processes with
increased dependence on and decreased tolerance of separation from parents. Chemotherapeutic
agents may be primarily sleep-disrupting (e.g., corticosteroids,) or sedating (e.g., l-asparaginase,
beta interferon) or both (e.g., vincristine, cytarabine). Children with CNS malignancies, particu-
larly involving the brainstem and hypothalamus, or who receive cranial radiation treatment are at
high risk for disruption of normal sleepwake regulation and circadian rhythm processes as well
as nocturnal seizures; injury to central respiratory control centers (e.g., medulla) may result in
central sleep apnea. Long-term survivors of childhood cancer may continue to experience sleep
problems in up to 50% of cases; sleep problems associated with PTSD may also occur in these
patients.
In particular, cancer-related fatigue (CRF), which has been reported in 70% of cancer patients
overall, can have a devastating effect on quality of life for these children. Fatigue may be related
to physical factors such as anemia, poor nutrition, and underlying disease processes as well as
to depression and other emotional issues. Complaints of fatigue may persist for months to years,
even after treatment has been concluded, and continue to impact signif cantly on these patients
ability to resume a normal life. Alterations in daytime activity levels and sleepwake schedules
in response to fatigue and excessive daytime sleepiness (EDS) may further disrupt nocturnal
sleep regulation and circadian rhythms. Fatigue-related symptoms may be diff cult to distinguish
from EDS (e.g., diff culty getting up in the morning, increased sleep duration, frequent napping,
dozing off during activities), and both are commonly present, especially in children with CNS
neoplasms; these children are also at increased risk for secondary narcolepsy. Initial studies in
adults with breast cancer indicate that bright light exposure in the morning can ameliorate some
of the daytime fatigue, and thus the use of a light box for 30 to 60 minutes in the morning may
be worth considering. Hypersomnia associated with cranial radiation therapy occurs in some
60% of children, and consists of a constellation of symptoms including nausea, headaches, and
low-grade fever that occurs 3 to 12 weeks post-radiation and lasts for up to 2 weeks. Radiation-
related sleepiness appears to be dose-dependent, and evidence of increased sleep needs have been
demonstrated as long as 15 years after treatment.
c hronic Fatigue Syndrome

Chronic fatigue syndrome in adults and children has been reported to be associated with chronic
sleep disturbances, including sleep onset and maintenance problems, impaired sleepwake
rhythms, and daytime sleepiness despite what is often an increase in total sleep time. These may
further exacerbate symptoms of daytime fatigue.
c ystic Fibrosis
Prolonged sleep onset, increased arousals and awakenings, and decreased sleep eff ciency have
been reported to occur in about 40% of children and adolescents with cystic f brosis, complaints
of EDS and fatigue occur in 75%. Nocturnal awakenings are frequently correlated with disease
severity; reduced sleep eff ciency as well as reduced amounts of REM sleep also appear to be
related to severity. Furthermore, nocturnal hypoxemia and oxygen desaturations during sleep
are more common with progressive disease. There also appears to be an increased prevalence of
sleep disordered breathing in cystic f brosis, especially within the presence of nasal polyps and
chronic sinusitis.
Diabetes
Although children and adolescents with type 1 diabetes have been reported to have more frequent
nightwakings, these are not necessarily correlated with nocturnal hypoglycemia. Patients with
type 2 diabetes are more likely to be overweight and obese, increasing the risk of SDB.
Fibromyalgia
Poor sleep is also part of the diagnostic criteria for juvenile f bromyalgia and may include pro-
longed sleep onset, frequent arousals, and decreased sleep eff ciency as well as PLMs disrupting
sleep. These sleep disturbances can potentially contribute to the daytime sleepiness or fatigue,
depressed mood, and cognitive diff culties frequently associated with this painful musculoskel-
etal condition.
g astrointestinal Disorders
Gastrointestinal disorders, especially those of a more chronic nature such as irritable bowel
syndrome, have been associated with poor sleep quality in adults; an underlying dysregulation
mechanism resulting in both altered gastrointestinal function and sleepwake regulation has been
postulated. Chronic steroid use in inf ammatory bowel disease may result in increased agitation
at bedtime with sleep onset delay and increased hunger, leading to nocturnal eating. Children
with functional abdominal pain are more likely to have symptoms of behavioral sleep disorders,
increased nightmares, and daytime fatigue.
g astroesophageal r ef ux Disease
Chronic acid ref ux is often associated with frequent arousals during sleep. In addition, gastro-
esophageal ref ux disease (GERD) is associated with increased risk of aspiration, particularly in
children with neurodevelopmental problems such as cerebral palsy. GERD may disrupt sleep be-
cause of secondary chronic cough and other respiratory symptoms as well as heartburn. GERD is
also considered to be a risk factor for OSA because of the associated mucosal edema. Anti-ref ux
medications that have serotonergic effects, such as cisapride, may also result in sleep disruption.
h eadaches
Migraine headaches have been associated with sleep onset and maintenance problems as well as
with an increased incidence of sleepwalking. On PSG, adults with migraines show an increase
in both SWS and REM sleep, while children with chronic migraine have shorter sleep duration,
longer sleep onset, and more arousals compared to patients with other types of headaches; these
changes in sleep architecture appear to be correlated with both headache severity and chronic-
ity. Some studies have reported an increased prevalence of SDB in pediatric patients with mi-
graine (>50%). Furthermore, sleep deprivation may trigger migraines as well as other types of
headaches in susceptible individuals, and migraines may awaken the child from sleep or early in
the morning. The underlying pathophysiology of this relationship between migraines and sleep
disruption has been postulated to involve hypothalamic-mediated decreases in serotonin and/or
alternations in melatonin secretion; melatonin has been used clinically to treat migraines in both
adults and children.
More sleep problems, including insomnia and EDS, have been reported to occur with other
types of headaches in children. With tension headaches, this may be related to increased stress
and anxiety. Patients with tension headaches also appear to have reduced total sleep time and
frequent awakenings on PSG; in addition, the risk of bruxism is increased two-fold. Rebound
headache pain related to frequent use of analgesic medications and secondary depression and
anxiety may be contributing factors in some children. Finally, children with OSA may complain
of morning headaches on waking, presumably related to either hypoxia or elevated CO2 levels.
Juvenile r heumatoid Arthritis

As noted above, any chronic medical condition that is characterized by recurrent pain may be
associated with sleep disruption. Children with juvenile rheumatoid arthritis have been shown
to have more frequent nightwakings and sleep fragmentation, which may be associated with
daytime sleepiness, and can be correlated with both pain and disease activity. For example, over
50% of pediatric rheumatology patients with complaints of limb pain have signif cant insomnia,
which in turn greatly impacts their quality of life. This suggests that there may be potential sleep
and daytime benef ts with aggressive nocturnal pain management.
Meningomyelocele and c hiari Malformations

Meningomyelocele (especially thoracic and thoracolumbar) and Chiari malformation type II can
be associated with blunted ventilatory and arousal responses, central hypoventilation syndrome,
and increased central and obstructive apneas. It is estimated that about one-third of the children
with meningomyelocele have moderate to severe ventilatory abnormalities; patients with thoracic
or lumbar lesions, restrictive lung disease, and wheelchair-dependent patients with scoliosis are
at particularly high risk for sleep-disordered breathing. Most individuals with type I Chiari mal-
formation are asymptomatic, but SDB (obstructive and central apnea) can be a rare complication.
Surgical decompression of the posterior fossa in Chiari malformation or tethered cord release in
children with meningomyelocele may be necessary. Adenotonsillectomy can also improve ob-
structive disease, but positive pressure mechanical ventilation with continuous positive airway
pressure or bi-level positive airway pressure is often needed, especially in children whose respira-
tory function is further compromised by kyphoscoliosis or obesity.
n euromuscular Disorders
Sleep-disordered breathing (SDB) and upper airway obstruction are more common in children
with a variety of neuromuscular conditions, including Duchenne muscular dystrophy, Charcot-
Marie-Tooth disease, myotonic dystrophy, and congenital myopathies characterized by hypoto-
nia. In some of these conditions, the SDB is a result of respiratory muscle weakness and in
others it is related to reduced central ventilatory drive. The risk of respiratory desaturations or
hypoxemia is greatest during REM sleep. Many of these children also have reduced vital capac-
ity associated with scoliosis, which may further compromise respiratory function and exacerbate
SDB. Many of these patients do not report OSAassociated symptoms (e.g., snoring, daytime
sleepiness, morning headaches) unless specif cally asked, so that frequent screening for SDB
symptoms is mandatory.
Increased risk for respiratory failure also is associated with generalized or proximal muscle
weakness in these children, particularly those with diaphragmatic involvement and those who
have had an earlier age of onset of symptoms. Signif cant SDB can occur in the setting of even
mild respiratory muscle weakness. The hypoxemia and chronic respiratory failure in these pa-
tients is usually preceded by periods of increased end-tidal CO2 during sleep. Daytime blood
gases may be normal. Pulmonary function tests are often noncontributory but may show restric-
tive lung disease, and there may be minimal symptoms of sleep-disordered breathing. Further-
more, pulmonary function testing to assess maximal inspiratory and expiratory pressures can be
helpful to assess the severity of muscle weakness.
Sleep and Neurologic Disorders

The primary care practitioner should maintain a high level of suspicion for sleep-disordered
breathing, particularly in children with neuromuscular disorders and spina bif da, as this may
be overlooked in the context of multiple other medical needs. Close collaboration with a mul-
tidisciplinary neuro-rehabilitation team for follow-up is strongly recommended.
Phenylketonuria
Phenylketonuria may be associated with diff culties in sleep onset and maintenance as well as
nightmares related to an increase in REM sleep. These sleep disturbances may be a result of al-
terations in the phenylalanine/tyrosine/tryptophan ratio. A balanced phenylalanine-restricted diet
may be helpful in reducing sleep disruption.
r enal Failure
Sleep disruption in children with chronic renal failure may be related to a number of factors,
including medications, dialysis, or decreased urine output. There is an increased prevalence of
restless legs syndrome and periodic limb movement disorder (see Chapter 15) in chronic renal
failure, which may lead to delayed sleep onset, fragmented sleep, and EDS. Increased daytime
somnolence may also be a result of increasing renal failure.
Sickle c ell Disease

Painful nocturnal crises and direct and indirect effects of analgesics, including opiates, may im-
pact sleep in children with sickle cell disease. It is estimated that 40% have nocturnal oxygen
desaturations. These children may also be prone to SDB as a result of adenotonsillar hypertro-
phy related to compensatory lymphoid hyperplasia with functional asplenia, repeated infections,
and airway narrowing related to the anatomic effects of bone marrow hyperplasia. Hypoxemia
related to OSA may lead to increased nocturnal sickling and pain crises, with resultant exacer-
bation of the disease. Hypoxemia may signif cantly improve with adenotonsillectomy, although
clearly these children are at higher surgical risk for perioperative complications as a result of
their disease.
t raumatic Brain injury

Changes occurring in sleep architecture during the acute phase following head injury electro-
encephalography include increased SWS. A postconcussive syndrome and/or PTSD symptoms
with resultant diff culties in sleep initiation and maintenance, early morning waking, decreased
sleep quality, and daytime sleepiness have been reported with even relatively minor head injuries.
These sleep abnormalities may persist for several years. Furthermore, signif cant hypersomno-
lence, and in some cases narcolepsy, have been reported following head injury.
Sl eeP An D o BeSit y
Some 37% of children in the United States between the ages of 6 and 11 years are currently de-
f ned by Centers for Disease Control standards as overweight or obese; this represents an increase
of 20% from 1998 to 2004 alone. A number of both cross-sectional and longitudinal studies
published in the past 5 years have demonstrated a strong association between short sleep duration
and increased weight in both adults and children; this relationship appears to be more robust in
children versus adults and to persist despite controlling for a number of potential confounding
factors such as diet, exercise, parental obesity, and television viewing. Virtually all pediatric
cross-sectional studies have conf rmed this dose-dependent relationship between decreased sleep
amounts and increased weight. A meta-analysis of recent studies in children reported a pooled
odds ratio of almost two (i.e., short sleepers have twice the risk of being overweight or obese).
Furthermore, the converse is true. One study in adolescents estimated that for each additional
hour of sleep, the odds of being obese decreased by 80%. Prospective cohort studies in a number
of pediatric populations around the world have shown that short sleep duration at Time A, par-
ticularly before the age of 3 years, predicts weight status at Time B (e.g., in middle childhood),
independent of weight status at Time A. Furthermore, the demographic groups at increased risk
for obesity are also the same populations (blacks and Hispanics and those with low socioeco-
nomic status) at increased risk for late bedtimes and inadequate sleep duration.
The mechanisms underlying this association are likely to be multifactorial and appear to in-
volve neurohormonal and metabolic alterations, including increased leptin and decreased ghre-
lin, the combination of which is known to increase hunger and increase caloric intake. In addi-
tion, sleep loss appears to increase insulin resistance by increasing circulating cortisol, activating
the sympathetic nervous system and upregulating proinf ammatory markers such as C-reactive
protein. In addition, fatigue associated with inadequate sleep may lead to a decrease in physical
activity and calorie expenditure. Behavioral, mood-related, and cognitive mechanisms linked to
inadequate sleep may also play a role, especially in children. For example, parents may use food
to pacify an irritable, sleep-deprived child and children themselves may use food to self-soothe;
alternatively, caregivers may have diff culty setting limits on both eating and sleep behavior. In
older children and adolescents, sleepiness-related impairments in impulse control, judgment, and
motivation may contribute to overeating and the development of obesity.
It should also be emphasized that the relationship between short sleep and obesity is further
complicated by the presence of sleep-disordered breathing, the risk for which is increased not
only by obesity, but by which is more relevant in the same populations at risk for inadequate
sleep (e.g., minority and poor children). Comorbid SDB may further intensify the metabolic
consequences and long-term cardiovascular morbidity associated with both obesity and inad-
equate sleep (e.g., insulin resistance and glycemic control, systemic inf ammation), and insuf-
f cient sleep may add to the neurocognitive sequelae of SDB (e.g., impairments in attention and
memory, academic failure) in a kind of perfect storm scenario.
Sleep and Obesity

There is a clear bi-directional relationship between sleep and obesity. For example, a multitude
of studies have convincingly supported a robust association between short sleep duration and
an increased risk of being overweight and obesity in the pediatric population. The underlying
mechanisms are likely to involve alterations in neurohormonal and metabolic pathways as
well as behavioral components. Alternatively, obesity increases the risk for sleep-disordered
breathing (SDB) and other sleep disturbances. Thus, systematic screening for both inadequate
sleep duration and symptoms of SDB in overweight and obese children, especially in high-risk
groups, is an important role for primary care practitioners.
Sl eeP An D Seiz ur e DiSo r Der S

Although a detailed description of the complex interaction between epilepsy and sleep is be-
yond the scope of this book, a number of important points relevant to the primary care physi-
cian must be mentioned. It is estimated that 20% to 40% of seizures in childhood occur during
sleep, and sleep-related epilepsy accounts for about 30% of seizure disorders in children. Fur-
thermore, some types of seizures, such as benign rolandic epilepsy and frontal lobe seizures,
occur primarily or exclusively during sleep. Childhood seizures are especially prominent in sleep
stages 1 and 2, although a signif cant percentage also occur at the sleepwake transition (e.g.,
infantile spasms, some tonic-clonic seizures). In general, seizures are uncommon during other
sleep stages, such as SWS, although partial complex seizures may occur solely in REM sleep.
In one study, about half of f rst-time unprovoked seizures occurred during sleep. Furthermore,
the likelihood of recurrence was signif cantly increased (42% versus 18%) in those children who
presented with nocturnal seizures.
Seizures and Sleep

In contrast to prevalence in adults, nocturnal seizures are quite common in children, and some
types of seizures (e.g., benign rolandic epilepsy) occur predominantly during sleep. Nocturnal
seizures may cause signif cant sleep disruption and daytime sleepiness. Conversely, sleep de-
privation is a well-established trigger factor for seizures.
Seizures (including rolandic epilepsy, tonic-clonic) may cause sleep disruption, and there is a
higher incidence of sleep disturbances in patients with epilepsy in general. Seizure activity does
not need to be overt to disrupt sleep but rather may consist of brief stereotypic arousals and
microarousals that result in signif cant daytime sleepiness. Successful anticonvulsant therapy
may alleviate daytime somnolence even in the absence of frank seizure activity, although anti-
convulsants may clearly cause sedation as well. Neurodevelopmental disorders (e.g., severe de-
velopmental delay, blindness) that are commonly associated with seizures as part of their clinical
presentation may also predispose the patient to sleep disorders. Sleep disorders and sleep depri-
vation may also exacerbate seizures in patients with known epilepsy. For example, hypoxia and
sleep fragmentation associated with OSA may trigger seizures in a predisposed child.
Sleep Studies and Seizures

Because not all sleep laboratories perform a full electroencephalographic (EEG) seizure mon-
tage as part of routine polysomnography, an overnight sleep study alone may not be suff cient
to rule out nocturnal seizures. Additional diagnostic procedures, such as 24-hour ambulatory
EEG monitoring, may be necessary in cases in which there is a high index of suspicion.
Nocturnal seizures may be diff cult to distinguish from other episodic nocturnal phenomena,
including partial arousal (e.g., sleep terrors, sleepwalking) and REM parasomnias (e.g., night-
mares; see Chapter 10 for complete coverage of differentiating seizures from parasomnias). Im-
portant potential differentiating factors include timing of the events and arousal threshold (in-
dicative of sleep stage); level of autonomic arousal; presence of stereotypic or unusual behaviors
such as drooling, incontinence, tongue biting; recall for the event, and daytime sleepiness. The
differential diagnosis also includes other primary sleep disorders: bruxism, rhythmic movement
disorders, nocturnal myoclonus and sleep starts, periodic limb movements, OSA, REM behav-
ior disorder (extremely rare in childhood and only reported in the setting of CNS pathology),
enuresis, hypnagogic hallucinations and sleep paralysis associated with narcolepsy, nocturnal
physiologic arousals related to medical conditions (e.g., GERD, asthma), psychiatric disorders
(nocturnal panic attacks, PSTD), and psychogenic seizures.
Specif c sleep-related epilepsies include:
n Benign rolandic epilepsy is a common, autosomal dominant form of epilepsy, usually pre-
senting in middle childhood. These children have normal sleep organization with a central or
midtemporal focus that is increased by sleepiness. Seizures are usually limited to sleep, are
focal in nature, generally involve the face or upper extremities with associated speech arrest,
drooling, and are frequently described as tingling, twitching, and/or numbness by the patient
who is awake and aware of the sensations. Seizures may occasionally spread to generalized
tonic-clonic activity.
n Electrical status epilepticus of sleep is associated with subclinical continuous spike-and-
wave discharges occurring during at least 85% of non-REM (NREM) sleep.
n Infantile spasms commonly have their onset in the f rst 4 to 7 months of life and are character-
ized by abrupt spasms, extension of the arms and legs, and f exion at the waist, occurring in
clusters at the sleepwake transition or shortly after awakening.
n Juvenile myoclonic epilepsy is an autosomal dominant lifelong disorder that presents in ado-
lescence (ages 1218 years) and is characterized by myoclonic activity (jerking of the arms
and commonly the legs) and generalized tonic-clonic seizures typically occurring upon wak-
ing in the morning. Alcohol, stress, sleep deprivation, and f ickering lights may exacerbate
seizure activity.
n Landau-Kleffner syndrome is associated with continuous and prolonged epileptiform activ-
ity during both REM and NREM sleep.
n Nocturnal frontal lobe epilepsy often presents with nocturnal repetitive events of short dura-
tion (2030 seconds) with unusual minor (e.g., scratching or rubbing the nose, pelvic thrust-
ing) and major (e.g., elevation of head and trunk with complex behaviors) motor manifesta-
tions. EEG f ndings are commonly negative.
n Nocturnal paroxysmal dystonias are characterized by sustained dystonic posturing of the
trunk and extremities in NREM sleep with immediate return to sleep after seconds to several
minutes. Nocturnal paroxysmal dystonia may be diff cult to distinguish from nocturnal frontal
lobe epilepsy.
n Syndrome of continuous spikes and wave during sleep is characterized by atypical spike
and wave discharges in 85% to 100% of NREM sleep as well as by atypical absence seizures.
Finally, although effective treatment of nocturnal seizures may substantially improve sleep qual-
ity, anticonvulsants may also compromise sleep by causing daytime sedation and impacting sleep
architecture. Phenobarbital acts as a REM sleep suppressant, while phenytoin and carbamazepine
increase SWS; lamotrigine increases REM percentage. Withdrawal from anticonvulsants follow-
ing discontinuation can also result in sleep diff culties. For example, anticonvulsants associated
with decreased REM sleep may lead to REM rebound symptoms (e.g., increased nightmares) on
withdrawal, and discontinuation of GABA-ergic medications like benzodiazepines may result in
increased SWS. Oftentimes, however, appropriate treatment with anticonvulsants to eliminate
or reduce nocturnal seizure activity actually improves sleep by decreasing sleep onset time and
nighttime arousals.
c en t r Al h yPo Ven t il At io n Syn Dr o MeS

Defective autonomic control of breathing may occur in association with medical conditions such
as Hirschsprung disease, inborn errors of metabolism and neuroblastoma, or in a congenital
form (idiopathic congenital central hypoventilation syndrome [CCHS]). CCHS is a rare disorder,
likely affecting fewer than 300 living children worldwide. It typically presents in the newborn pe-
riod with symptoms including duskiness or cyanosis upon falling asleep, and decreasing oxygen
saturation with hypercarbia and hypoventilation during sleep. Because of the lack or reduction of
ventilatory sensitivity to hypoxemia and hypercarbia, children with CCHS do not have an arousal
response or behavioral awareness of asphyxia. Prompt referral and evaluation is warranted for
children with persistent hypoxemia or hypercarbia or abnormal gas exchange even in the absence
of respiratory or neurocognitive symptoms.
t r eAt Men t
Management of sleep problems in children with acute and chronic medical conditions f rst re-
quires recognition on the part of the practitioner of the existence of possible risk factors for sleep
disturbances and the high likelihood of their occurrence, particularly in some disease states and
in certain settings, as outlined above. Symptoms such as fatigue, mood changes, and, particularly,
daytime sleepiness in chronically ill children should not be automatically attributed to the un-
derlying disease process, and every effort should be made to screen for and address primary and
secondary sleep problems when they occur. Medication choices should take into consideration
any possible negative effects on sleep. In addition, those pain medications likely to disrupt sleep
or signif cantly alter sleep architecture, such as opiates and benzodiazepines, should be avoided
or used for short time intervals. In contrast, nonsteroidal antiinf ammatory and non-opiate anal-
gesics, especially when used in the short term, appear to have little overall effect on sleep.
Approaches to pain management in children that may have particularly benef cial effects on
sleep as well include:
n Use of relaxation techniques, including hypnosis and biofeedback.
n Use of other non-pharmacologic pain measures such as warm baths, massage, and application
of warm or cold compresses.
n Incorporation of cognitive behavioral therapy aimed at management of chronic pain and devel-
opment of age-appropriate and adaptive coping skills.
n Support of parent education and modeling of good sleep habits.
n Maintenance of regular daytime and particularly bedtime routines.
Consultation for Sleep Issues

Children with chronic medical conditions and sleep issues, and hospitalized children in par-
ticular, often benef t from consultation with a child life specialist and/or behavioral therapist
regarding specif c management strategies. Additional input from a consultation-liaison child
psychiatry team may be benef cial if pharmacologic intervention is being considered
Any child with a medical condition that may pose an increased risk for SDB (e.g., neuromuscular
disorders, chronic allergies) should be monitored regularly for the development of possible signs
and symptoms, such as snoring, restless sleep, and daytime sleepiness. A high index of suspicion
and a low threshold for obtaining an overnight sleep study evaluation is particularly important
in these children. Ongoing consultation with a pediatric sleep specialist and/or pulmonologist is
recommended.
Sleep and Psychiatric Disorders 22
The relationship between disturbed sleep and psychiatric disorders in children and adolescents
is one that is complex, but highly clinically relevant for both mental health professionals and
primary care practitioners. Studies indicate that sleep disturbances are very common in chil-
dren with mental health concerns. These sleep problems often have a signif cant impact upon
both the clinical presentation and symptom severity of psychiatric disorders and pose signif cant
management challenges in clinical practice. Virtually all psychiatric disorders in children and
adolescents may be associated with sleep disruption. The spectrum of sleep disturbances ranges
from diff culties with initiating and maintaining sleep and complaints of poor quality or non-
restorative sleep, to daytime fatigue and sleepiness and increased sleep need (hypersomnia), to
circadian rhythm dysregulation. Treatment of psychiatric disorders with psychotropic medica-
tions that potentially have signif cant negative effects on sleep often adds an additional layer of
complexity. In addition, growing evidence suggests that insomnia is a risk factor for the later de-
velopment of psychiatric conditions, particularly depression and anxiety disorders. Finally, there
is considerable overlap between symptoms of mental health disorders, such as mood lability,
inattention, and disruptive behaviors, and those associated with a wide range of sleep disorders,
including obstructive sleep apnea (see Chapter 14) and restless legs syndrome and periodic limb
movement disorder (PLMD; see Chapter 15).
Given the prevalence of sleep problems associated with psychiatric conditions, it is important
that healthcare practitioners are comfortable screening, diagnosing, and treating sleep distur-
bances in all children presenting with psychiatric, behavioral, and academic concerns. Although
details of the management of sleep concerns in specif c psychiatric disorders is beyond the scope
of this chapter, and many of these patients will require referral for more intensive behavioral and
pharmacologic management, a general approach to understanding and evaluating sleep problems
in the most common psychiatric disorders in childhood is highlighted below.
Sleep and Neurobehavioral Symptoms: A Bidirectional Relationship

There is clearly a bi-directional relationship among sleep, mood, and behavior in childhood.
Inadequate sleep often results in neurobehavioral symptoms, including mood disturbances,
cognitive impairment, inattentiveness, and behavior problems. Conversely, children with
mood and behavior disorders often experience sleep disturbances.
At t en t io n DeFic it h yPer Ac t iVit y DiSo r Der

g eneral Description
Sleep problems, particularly diff culty initiating and maintaining sleep, are commonly reported
in children and adolescents with ADHD (hyperactive or impulsive, inattentive, and combined
subtypes). Parents of children with ADHD frequently complain of bedtime struggles and de-
layed sleep onset as well as increased nightwakings, restless sleep, and shortened sleep duration.
However, the relationship between sleep problems and ADHD is not straightforward, as there is
considerable overlap between many of the most common behavioral consequences of inadequate
197
or disrupted sleep in children and the symptoms of ADHD (i.e., problems with attention and fo-
cusing, hyperactivity, irritability and disturbed mood, and increased aggression and poor impulse
control). In fact, a number of studies have now suggested that a percentage of children labeled as
ADHD actually have a primary sleep disorder that accounts for their symptoms. Although the
number of children misdiagnosed in this way is not known, one study reported that up to 25%
of children with ADHD symptoms had evidence of sleep-disordered breathing, and in another
study, more than half of children evaluated for ADHD had evidence of RLS and/or PLMD. Fur-
thermore, sleep disorders add to the severity of ADHD symptoms when they coexist.
Sleep Disorders and Attention Def cit Hyperactivity Disorder

The relationship between sleep disturbances and attention def cit hyperactivity disorder
(ADHD) is a complex and multifactorial one. Sleep problems in these children may be re-
lated to a variety of issues including coexisting primary sleep disorders, comorbid psychiatric
conditions, or concomitant psychotropic medications; in some children, a more intrinsic
ADHDrelated diff culty with settling may be present. A thorough and systematic search for
possible etiologic factors is necessary in order to make an accurate diagnostic formulation and
develop the most appropriate treatment plan.
epidemiology
Parent-reported sleep problems, particularly diff culties in initiating and maintaining sleep, are
reported in an estimated 25% to 50% of children and adolescents with ADHD in clinical practice.
These prevalence rates are generally 2 to 3 times that of children without ADHD. Differences in
the rates of sleep problems are also found within ADHD samples as a function of ADHD subtype,
psychiatric comorbidities, and medication use.
etiology
From a theoretical perspective, there is substantial empirical evidence supporting an overlap in
those central nervous system (CNS) centers as well as neurotransmitter pathways that regulate
sleep and those that regulate attention and arousal, suggesting disruptions in one system might
well have parallel effects on the other. The framework for the common underlying CNS pathology
linking sleep disruption or deprivation and ADHD primarily involves the prefrontal cortex and
associated integrative functions, such as working memory and the ability to organize information
and prioritize tasks.
In regards to other CNS mechanisms potentially linking sleep and ADHD, a role for a primary
circadian disruption in ADHD has also been proposed, which may involve alterations in the cir-
cadian clocks timing or responsiveness to environmental cues such as light. For example, a num-
ber of studies have documented the presence of a circadian-based phase delay in children with
ADHD, as evidenced by a delayed onset of nocturnal melatonin secretion compared to controls.
Finally, a few studies that have examined the issue of arousal level and daytime sleepiness in chil-
dren with ADHD have reported that children with ADHD demonstrate an increase in objectively
measured sleep propensity compared to control children, suggesting that hyperactivity, at least in
some children, may actually be an adaptive behavior that counteracts the effects of hypoarousal
and underlying daytime sleepiness.
Despite this, studies do not in general demonstrate reliable objective differences in either
sleep architecture and/or sleep patterns in children with ADHD compared to typically develop-
ing controls, with the possible exception of increased activity levels and movement during sleep
and more night-to-night variability in sleep patterns. However, in direct contrast to studies which
have utilized more objective measures, parental report surveys have almost universally reported
a higher frequency of signif cant sleep problems in children with ADHD compared with various
control groups, which is ref ected in the clinical experience of most healthcare practitioners who
SLEEP AND PSyCHIATRIC DISORDERS 199
work with these children. It has been suggested that this discrepancy between objective measures
and subjective reports may be related to the fact that parents of behaviorally disordered children
may be more likely to perceive and report high levels of both daytime and sleep-related disruptive
behaviors; in addition, both caregivers and clinicians may be relatively more vigilant about ob-
serving and eliciting evidence of sleep problems in these children. Caregivers may be more likely
to remember and report extremes in sleep behaviors, such as a 2-hour sleep onset latency, even if
these occur only occasionally. Finally, what parents attribute to sleep problems may actually be
more accurately described as problematic evening behaviors (e.g., increased activity level, dif-
f culty settling, oppositionality) that are a ref ection of a resurgence in ADHD symptoms after
medication has worn off at the end of the day.
Because the etiology of sleep problems in children with ADHD is so varied and often multi-
factorial, a systematic approach is necessary to tease out the relevant contributory factors. The
discussion below and Figure 22.1 outline the major issues that should be considered; it should be
noted that many of these etiologic factors may also play an important role in sleep problems in
children with other psychiatric disorders, such as depression and anxiety, and thus the evaluation
algorithm outlined in Figure 22.1 serves as a useful template for examining sleep problems in
other mental health conditions as well.
n A primary sleep disorder may result in ADHD-like symptoms: A patient with any sleep
disorder that results in inadequate sleep duration or fragmented or disrupted sleep may pres-
ent primarily with daytime sleepiness and neurobehavioral symptoms, many of which overlap
with the cardinal symptoms of ADHD. For example, a large number of pediatric studies have
now been published that provide compelling evidence of a wide range of neurobehavioral
and neurocognitive def cits in children with both clinical symptoms of and polysomnographi-
cally conf rmed obstructive sleep apnea (OSA), including inattention, impaired memory, and
executive functions, mood disturbance, externalizing and internalizing behavior problems,
and academic diff culties. Furthermore, studies that have looked at changes in behavior and
neuropsychological functioning in children following treatment for OSA (e.g., adenotonsil-
As s e s s :
S le e p ha bits Anxie ty/mood s ymptoms Eve ning ADHD Timing s le e p ons e t in re la tion to De gre e be dtime
s ymptoms be dtime re s is ta nce
(HA/IMP , re s tle s s ne s s )
In a d e q u a te
S le e p Hyg ie n e
Cons is te nt S e ve re ,
P rima rily be dtime -re la te d Da ytime a nd be dtime Fa lls a s le e p
prolonge d s le e p pe rs is ta nt
e a s ily a t la te r
be dtime ons e t
MDD, GAD, S AD
Occurs Occurs on S e ns ory
on me ds a nd off s ymptoms Conflicts pa re nt-child
me ds inte ra ctions ,
Anxie ty re : fa lling Difficulty proble ma tic child
or s ta ying a s le e p fa lling a s le e p Urge to S e n s o ry
>Ba s e line =Ba s e line be ha vior
P rim a ry a lone move , le g in te g ra -
in s o m n ia In trin s ic s e ns a tions , tio n
ADHD- wors e a t d e fic its
re la te d night/re s t
Dire c t m e d In a d e q u a te p m
s e ttlin g Re s tle s s P rima rily Da ytime
e ffe c t; ADHD
p ro b le m Le g be dtime - a nd
re b o u n d c o ve ra g e
S yn d ro m e re la te d be dtime
Younge r a ge olde r a g e P a re nta l pre s e nce

ne e de d to s le e p; a nd Be dtime
during nightwa kings re fus a l,
BIC: S le e p On s e t de la ying ta ctics ; ODD/CD
De ve lo p m e n ta lly Circ a d ia n De la ye d As s o c ia tio n no or fe w
In a p p ro p ria te p re fe re n c e S le e p P h a s e
nightwa kings
b e d tim e S yn d ro m e
BIC: Lim it-
S e ttin g
Fig 22.1. Sleep and ADHD: Bedtime resistance and prolonged sleep onset.
lectomy) have also largely documented signif cant improvement in daytime sleepiness, neu-
ropsychological measures of impairment, behavior, and academic performance. Signif cant
neurobehavioral consequences may also occur related to RLS and PLMD, and may present as
symptoms of ADHD. Delayed sleep phase disorder and narcolepsy are other sleep disorders
that have been reported to result in ADHD-like symptoms.
n Coexisting sleep disturbances may exacerbate the symptoms of ADHD: Sleep disorders
such as OSA may also occur in conjunction with ADHD, and the cognitive, mood, and be-
havioral disturbances associated with ADHD may be worsened by their presence. Inadequate
sleep related to environmental or lifestyle factors (e.g., erratic schedules), particularly if
chronic, also may exacerbate ADHD symptoms. Some children with ADHD, especially older
children, may have a delayed sleep phase, which may contribute to diff culties settling at bed-
time, prolonged sleep onset, and diff culty waking in the morning for school. Treatment of co-
morbid sleep disorders and interventions targeted at ensuring adequate sleep may substantially
improve daytime ADHD symptoms.
n Coexisting psychiatric disorders may be the underlying cause of sleep disturbance in a
child with ADHD: The majority of children with ADHD (about 70%) have comorbid psychi-
atric disorders in addition to ADHD that may contribute to sleep problems. For example, limit-
setting problems associated with oppositional def ant disorder (ODD; 40% to 60% of children
with ADHD) may result in bedtime resistance. An estimated 30% of children with ADHD have
a comorbid anxiety disorder and 10% to 30% a comorbid mood disorder; sleep onset prob-
lems, particularly relating to bedtime fears and need for parental presence at bedtime, are com-
mon presenting complaints in children with anxiety disorders, and sleep initiation complaints
are common in depression. Problems with sensory integration and associated diff culties in
self-soothing may also predispose children with ADHD to settling and sleep onset problems.
n Pharmacologic agents used to treat ADHD and/or comorbid psychiatric conditions may
cause or exacerbate sleep problems: In particular, psychostimulant medication may be as-
sociated with sleep onset and maintenance problems as well as restless sleep. Sleep problems
may be a direct effect of the medication itself. In other cases, stimulant medication may wear
off just before bedtime, resulting in rebound hyperactivity and, indirectly, sleep onset diff -
culties. Finally, other psychiatric medications used in children with ADHD, including different
classes of antidepressants (see Chapter 19), may also potentially either alleviate or exacerbate
sleep problems.
n CNS dysregulation of arousal and activity associated with ADHD may result in sleep
disturbances: Although, as discussed above, the presence of an intrinsic dysfunction link-
ing sleep disturbances and ADHD is still largely speculative at this point, diff culties in set-
tling or turning off at bedtime are commonly reported in children with ADHD. Signif cant
problems with delayed sleep onset appear to occur in some children in the absence of other
identif able causes, such as use of medication or comorbid psychiatric disorders. It has been
postulated that dysregulation of the homeostatic sleep drive and resulting alterations in the
normal build-up of sleep propensity with continuous wakefulness may be involved. Alterna-
tively, some of these children may have a primary circadian disruption (e.g., delayed sleep
phase).
evaluation
n Screening for sleep disorders should be part of the evaluation for every child with sus-
pected ADHD: Screening questions regarding sleep onset, nightwakings, restless sleep, snor-
ing, sleep regularity and duration, and daytime sleepiness should be part of every ADHD
evaluation (see Chapter 3). Sleep diaries can be very helpful. Clinical suspicion of a sleep
disorder warrants appropriate diagnostic evaluation, including assessment of the severity (e.g.,
time to fall asleep), frequency (e.g., nights per week), and duration (e.g., number of months or
years symptom has been present) of the presenting complaint.
Sleep Diagnostic Tests in Attention Def cit Hyperactivity Disorder

Polysomnography is considered the gold standard in children for the diagnosis of obstruc-
tive sleep apnea syndrome and periodic limb movement disorder, and should be strongly con-
sidered if there is clinical suspicion of symptoms (e.g., snoring, restless sleep) and/or risk
factors (e.g., adenotonsillar hypertrophy, positive family history) of either. A multiple sleep
latency test should be reserved for situations in which there is documented pathologic sleepi-
ness (i.e., narcolepsy).
Because of the clinical association between ADHD and RLS and PLMD, and recent studies
which suggest that iron def ciency is a risk factor for both RLS/PLMD and ADHD, a serum
ferritin level should be considered, particularly in populations at increased risk for iron def -
ciency (e.g., adolescent girls).
n Periodic screening for sleep disorders should be part of the ongoing management of every
child with diagnosed ADHD: Comorbid psychiatric conditions and associated sleep problems
may evolve in children with ADHD. Changes in medication type, dose, and dosing schedule
over the course of treatment may result in sleep disturbances. Comorbid sleep problems, such
as OSA, may also develop over time, especially in high-risk groups such as children who are
also obese. Thus the importance of regular clinical assessment for emergent sleep problems is
paramount.
n Overall evaluation strategy: Figure 22.1 illustrates an evaluation strategy for the child who
presents with the most common sleep complaint reported in ADHD: bedtime refusal or resis-
tance and/or delayed sleep onset (i.e., time to fall asleep once in bed). In younger children,
these two symptoms are often indistinguishable; that is, children who have diff culty falling
asleep for a variety of reasons often exhibit protest behavior (crying, getting out of bed, calling
out to parents) at bedtime. In contrast, older children and adolescents may lie in bed quietly
after lights out and parents may not even be aware of the sleep onset diff culties. Thus, it is
important to question the child directly as well as the caretaker about symptoms. The follow-
ing specif c issues are important to assess:
n Sleep hygiene: Many families of children with ADHD have either never developed or have
abandoned basic good sleep habits. These include environmental (e.g., low noise and ambi-
ent light levels, cool temperature,), scheduling (e.g., regular bedtime, sleepwake sched-
ule), sleep practice (e.g., bedtime routine), and physiologic (e.g., exercise, timing of meals,
caffeine use) factors which promote optimal sleep.
n ADHD symptoms in the evening and at bedtime: Children on time-limited ADHD medi-
cations may experience a return to baseline levels of ADHD symptoms as the medication ef-
fects diminish, or have a temporary increase in symptoms above baseline (i.e., rebound).
The associated hyperactivity and f dgetiness or restlessness may result in problematic eve-
ning behaviors and diff culty settling at bedtime. Psychostimulants may also have a direct
effect on sleep, resulting in prolonged sleep onset. Conversely, nighttime ADHD symptoms
(motor restlessness) as well as symptoms associated with sensory integration def cits, may
actually be a primary sleep disorder (e.g., RLS). Finally, for some children, diff culty in
settling occurs independent of medication status, suggesting an intrinsic ADHDrelated
mechanism.
n Timing of sleep onset relative to bedtime: Some parents will attempt to put a child to bed
earlier as a strategy to reduce sleep onset delay; thus, it is f rst important to establish that the
current bedtime is developmentally appropriate. Older children (particularly adolescents),
who fall asleep easily at a later bedtime (and adopt this later bedtime as well as a later wa-
ketime, on weekends and during school vacations) may have a circadian-based phase delay
(see above).
n Degree and persistence of bedtime resistance: In families in which limit setting is par-
ticularly problematic, bedtime resistance may be a corollary of the caregivers inability

or resistance to setting limits in general. In this situation, parents may need assistance in
developing and implementing appropriate bedtime schedules, rules, and routines. Children
with ADHD and disruptive behavior disorders (ODD and obsessive-compulsive disorder)
may be particularly prone to develop bedtime conf icts.
t reatment
n Diagnostically driven intervention: It is paramount that treatment for sleep disturbances
in ADHD be diagnostically driven and should correspond to the underlying etiology in each
individual case. Thus, if a primary sleep disorder, such as OSA or PLMD, is felt to play an
etiologic or exacerbating role regarding ADHD symptoms, a prudent approach would then be
to treat any documented sleep disorder (e.g., adenotonsillectomy for OSA) before conf rming
(or rejecting) the diagnosis of ADHD and initiating treatment. The treatment of sleep problems
related to comorbid psychiatric conditions should focus on the specif c symptoms; for ex-
ample, treatment of anxiety might involve progressive muscle relaxation, anti-anxiety agents,
and/or psychotherapy.
n Behavioral interventions and sleep hygiene: Standard behavioral techniques used to treat
sleep problems in typically developing children (see Chapters 6 and 7), such as graduated
extinction and bedtime fading, are also effective in children with ADHD. Problems with limit
setting, for example, generally respond to some combination of decreased parental attention
for bedtime delaying behavior, establishment of a consistent bedtime routine that does not in-
clude stimulating activities such as television viewing, and positive reinforcement (e.g., sticker
charts) for appropriate behavior at bedtime. Studies have suggested that adoption of good
sleep hygiene alone may be adequate to successfully treat sleep initiation problems in some
children with ADHD; thus, it should be a component of every treatment package.
n ADHD medication adjustments: Adjustments in the types (e.g., methylphenidate versus
dextroamphetamine, short-acting versus longer duration of action), dose, and dosing sched-
ules of ADHD medications may be warranted if these are suspected of contributing to the
sleep problems. In some children, delayed sleep onset may be responsive to a decrease in drug
dosage, as sleep-related effects of stimulants are often dose dependent. If inadequate evening
ADHD coverage appears to be a contributing issue or there appears to be a more intrinsic
settling problem, one approach in this case would be to treat with an ADHD medication with
24-hour coverage; an alternative strategy frequently employed in clinical practice is the use of
medication to reduce adrenergic tone (i.e., alpha agonists). Rebound ADHD symptoms may
respond to late-day supplementation with a short-acting psychostimulant. Finally, in patients
with comorbid Tourettes syndrome, pharmacologic treatment of the tics (e.g., clonidine, clon-
azepam) may improve sleep quality in these patients.
n Pharmacologic interventions for sleep: As an adjunct to behavioral intervention and institu-
tion of appropriate sleep hygiene, in cases of severe insomnia, or in that subgroup of ADHD
children for whom sleep problems appear to be intrinsic and not apparently attributable to
other modif able factors, medication may be an appropriate intervention. The focus in mak-
ing medication decisions should be on choosing the most appropriate drug for the underlying
condition (e.g., melatonin for delayed sleep phase; iron supplementation or dopamine agonists
for RLS; sedating antidepressants for children with comorbid mood disorders; and antihista-
mines, benzodiazepine receptor agonists, or melatonin receptor agonists for primary insom-
nia), safety prof le, duration of action (short-acting medications for sleep onset problems; lon-
ger-acting medications for sleep maintenance), possible interaction with current psychotropic
medications, and potential exacerbation of sleep disorders by psychotropic medication (e.g.,
selective serotonin reuptake inhibitors [SSRIs] and tricyclic antidepressants may exacerbate
RLS and PLMD).
Although there are currently no medications approved for use in children for ADHDrelated
sleep problems, a variety of medications are prescribed in clinical practice (for detailed informa-
tion regarding sedatives and hypnotics, see Chapter 19). These include the alpha agonist cloni-
dine, originally developed as an antihypertensive medication, and sometimes used to treat day-
time symptoms of hyperactivity and impulsivity in ADHD, as well as melatonin.
Mo o D An D An x iet y DiSo r Der S

g eneral Description
As with ADHD, the interaction between sleep disturbances and symptoms of mood dysregula-
tion, including anxiety and depression, may pose a diagnostic dilemma because of the overlap in
symptoms. Studies of mixed clinical psychiatric populations suggest that 40% to 50% of these
children have parent-reported nightwakings, nightmares, and diff culty waking in the morning.
In addition, there may be therapeutic challenges in setting treatment priorities regarding inter-
ventions for mood disorders. For example, some pharmacological agents for mood disorders
may cause sleep disruption and result in worsening of the mood problems. At the very least, the
consequences of poor sleep can exacerbate mood disorders, which may lead to additional sleep
disturbances in a negative spiral.
Specif c Disorders
Depression
Major depressive disorder is estimated to affect 2% of prepubertal children and 6% to 8% of
adolescents. A number of studies indicate that signif cant diff culty in initiating and maintaining
sleep is commonly associated with childhood depression (including major depressive disorder
and dysthymia). Subjective poor sleep quality, sleepwake cycle irregularities, and disturbing
dreams are also common. Up to half of prepubertal children with depression are reported to have
terminal insomnia (early morning awakening). Hypersomnia, or excessive sleep, is also associ-
ated with childhood depression, occurring in as many as 25% of depressed adolescents. Many
antidepressants, most notably the SSRIs, also have sleep disruptive effects or may cause daytime
sedation (see Chapter 19).
It is estimated that, at least in young adults, a history of insomnia increases the risk of de-
veloping future major depression four-fold. Similar results have been found in pre-adolescents
and adolescents. Conversely, some three-quarters of depressed prepubertal children and 90% of
depressed adolescents report signif cant sleep disturbance. Not only do sleep disturbances persist
once the mood symptoms are resolved in approximately 10% of children, the persistence of sleep
problems following successful treatment of mood symptoms may in fact predict later recurrence
of depression. For example, reduced sleep eff ciency and prolonged sleep onset latency appear
to be uniquely powerful predictors of short-term (i.e., within 12 months) depression relapse in
adolescents. Depressed children with insomnia also appear to have more severe and chronic
mood symptoms, and are more likely to have comorbid anxiety. Insomnia also appears to confer
an increased risk, at least in depressed adults, for suicidal behavior. Adolescents with comorbid
depression and sleep problems are also more likely to abuse substances, such as caffeine, nico-
tine, and alcohol, potentially further contributing to sleep disturbances.
There is increasing evidence for a biologic basis for the relationship between mood disorders
and sleep disturbance; in particular, monoaminergic neurotransmitter systems (e.g., norepineph-
rine, dopamine, serotonin) play a role in the regulation of both sleep and mood. Electroenceph-
alographic sleep changes consistently found in adults with depression, particularly decreased
latency to REM sleep onset and an increased percentage of REM sleep, are considered to be a re-
f ection of this underlying imbalance in monoaminergic and cholinergic activity. Similarly, most
antidepressant medications, which primarily affect the norepinephrine and serotonin systems,
have powerful REM sleep suppressant effects. Depressed adults also demonstrate decreased
slow-wave sleep (SWS) and increased sleep discontinuity on polysomnography (PSG). These
sleep architecture abnormalities have not been consistently found in depressed children. Similar
to what has been observed in ADHD, the lack of objective documentation of prolonged sleep
onset latencies and increased sleep fragmentation in depressed children contrasts with a high
frequency of subjective sleep complaints.
Bipolar Disorder
Bipolar disorder (BPD) has been increasingly recognized in the past decade in childhood and
adolescence. Although childhood prevalence rates are not reliably known, adult prevalence rates
are between 3% and 4%, with 20% of adults with BPD reporting the onset of symptoms before
or during adolescence. Particularly in its earliest stages, the symptoms of extreme mood swings
that are non-episodic and frequently characterized by an ultra-rapid or ultradian cycling pat-
tern, psychomotor agitation, extreme irritability, explosive outbursts, and marked def ance may
be labeled as severe ADHD or ODD.
Children with BPD very commonly (in up to 95% of young children with early onset BPD)
have signif cant parent-reported sleep problems, including highly erratic sleep patterns, restless
sleep, and intense nightmares. An apparent decreased need for sleep without accompanying day-
time fatigue or sleepiness, especially during hypomanic periods, appears to be one of the most
important characteristics distinguishing BPD from other psychiatric disorders. This dramatically
decreased sleep requirement has been reported to occur in 40% in children with BPD during
manic episodes, compared to 6% of children with ADHD. Furthermore, a period of increasingly
shorter sleep intervals may herald the onset of a manic episode, with insomnia more common
during the depressive phase. One small pediatric bipolar study utilizing PSG found decreased
sleep eff ciency, increased number of awakenings, increased SWS, and decreased REM sleep
percentage compared to controls. In contrast to studies of children with ADHD and depression,
in this study parent-reported sleep disturbance correlated with PSG f ndings. Finally, medica-
tions used to treat BPD may result in sleep disruption or daytime sedation (e.g., valproic acid,
risperidone).
Seasonal Affective Disorder

Seasonal affective disorder (SAD) is characterized by periods of depression that occur only in the
autumn and winter months; the pediatric prevalence has been estimated to be between 3% and
4%. In contrast to adults, children and adolescents with SAD do not appear to sleep more during
the winter months, although low energy levels, fatigue, and decreased daytime activity levels
have been described. It is postulated that there is an attenuation of the normal circadian rhythm
amplitude in children with SAD. Bright light phototherapy in the morning and early evening has
been reported to be benef cial.
Anxiety Disorders
Anxiety disorders are common in childhood, affecting 12% to 20% of children and adolescents
overall and about 30% of children with ADHD. Symptoms typically include physiologic hyper-
arousal (e.g., tachycardia, somatic complaints), cognitive hyper-vigilance, and behavioral symp-
toms, such as avoidance of anxiety-inducing situations and increased need for caregiver proxim-
ity. Given these characteristic features, it is not surprising that anxious children are particularly
prone to developing sleep disturbances; in fact, criteria for the diagnosis of generalized anxiety
disorder, separation anxiety disorder, and post-traumatic stress disorder (PTSD) specif cally in-
clude sleep disturbances, such as frequent nightmares and bedtime fears. Not only are anxiety
disorders associated with a signif cantly increased risk of subsequently developing insomnia, per-
sistent early sleep problems have been shown to be a reliable predictor of the later development
of anxiety disorders; diff culties initiating and/or maintaining sleep are often the initial presenting
complaint in anxious children.
The biologic basis for this relationship between anxiety and sleep is postulated to involve an
overlap between the systems regulating sleep and affect and arousal. In particular, dysregulation
of the hypothalamicpituitary axis and alterations in cortisol secretion patterns (e.g., increased
cortisol levels prior to sleep onset and decreased levels in the early morning) have been impli-
cated in increasing the risk for both anxiety disorders and sleep disturbances in children.
n Nighttime fears: Nighttime fears, which are a ref ection of normal developmental processes,
are extremely common, especially in young children, and may lead to signif cant bedtime re-
sistance and problematic nightwakings (see Chapter 8). It is important to distinguish between
developmentally appropriate nighttime anxietyrelated behaviors, and sleep-disrupting fears
that are accompanied by daytime anxiety symptoms. The former is usually circumscribed and
self-limited, and seldom requires intervention, whereas the latter may be indicative of a more
global anxiety disorder. If an anxiety disorder is present, the cognitive-behavioral techniques
often used successfully to treat isolated nighttime fears may be ineffective, and more intensive
intervention strategies (psychotherapy, anxiolytics) may be warranted.
n Adjustment disorders: Sleep problems are commonly associated with adjustment issues,
which involve temporary but maladaptive emotional and behavioral responses to both major
and minor stressful life events, such as brief separation from a parent, birth of a sibling, or
school transitions. These sleep problems, which commonly include bedtime resistance and
nightwakings, may immediately follow the stressful event or may have a more gradual onset.
Delayed sleep onset is often characterized by clinginess and refusal to be separated from the
caregiver in younger children, and rumination and free-f oating anxiety in the older child.
Although adjustment reactions are self-limited by def nition, parents may inadvertently pro-
long sleep problems by providing ongoing reinforcement (attention) for bedtime resistance,
even after the original anxiety symptoms have been alleviated, and by failing to provide chil-
dren with developmentally appropriate coping strategies.
n Separation anxiety and generalized anxiety disorder (GAD): Children with separation
anxiety and GAD frequently experience an exacerbation of symptoms at night. The degree,
duration, and pervasiveness of the anxiety symptoms as well as a family history of anxiety and
mood disorders may help to differentiate the child with more transient and situational night-
time anxiety from one with more chronic symptoms. Experiencing anxiety during the day
typically indicates a more global anxiety issue rather than a more specif c sleep problem.
n Post-traumatic stress disorder (PTSD): Reports of sleep complaints, especially bedtime
resistance, refusal to sleep alone, increased nighttime fears, and recurrent nightmares, are
common in children with PTSD who have experienced severely traumatic events (including
physical and sexual abuse). Children may also experience nocturnal panic attacks character-
ized by extreme hyperarousal and increased autonomic activity, which may be misinterpreted
as behaviorally based nightwakings, sleep terrors, or even nocturnal seizures.
Sleep and Anxiety

Diff culties in initiating and maintaining sleep commonly occur in children with acute and/or
chronic anxiety. Similar to mood disorders, this relationship is a bi-directional one in which
the presence of disturbed sleep also increases anxiety symptoms. In older children and ado-
lescents in particular, it is important to differentiate between more transient, situational, and
circumscribed nighttime anxiety, and sleep symptoms associated with more global daytime
anxiety. The approach to treatment and the need for additional counseling and psychopharma-
cology in these two situations may be quite different.
epidemiology
Sleep disturbances, especially insomnia (usually def ned as diff culty initiating and/or maintain-
ing sleep), are reported in up to 90% of children and adolescents with depression and anxiety
disorders. For example, it has been reported that up to 75% studies of children with major depres-
sive disorder meet the diagnostic criteria for insomnia, and 30% for severe insomnia, although as
noted above, objective data (e.g., PSG) do not always support these subjective complaints. It is re-
ported that up to 85% of children with an anxiety disorder also have signif cant sleep complaints.
evaluation
It is often diff cult from a clinical standpoint to clearly distinguish between primary and comorbid
sleep disorders in children with depression and anxiety. However, it is incumbent on healthcare
providers to evaluate and appropriately treat both, because improvement in one is likely to have
a positive impact on the other. As discussed above, screening for sleep disorders should be part
of the psychiatric evaluation for every child. Furthermore, periodic screening for sleep disorders
should be part of the ongoing management of every child with diagnosed psychiatric disorders,
especially depression and anxiety.
t reatment
Integrated Treatment Approaches
Because of the frequent coexistence and bi-directional effects of sleep disturbances and mood
and anxiety disorders, the most effective treatment approach generally involves addressing
both concerns simultaneously. At the very least, care should be taken to avoid treatment strate-
gies that may exacerbate comorbid sleep problems (e.g., antidepressants that have disruptive
effects on sleep).
Although a substantial number of treatment studies have demonstrated the eff cacy of cognitive-
behavioral (e.g., controlled exposure, relaxation-mental imagery), psychosocial, and pharma-
cologic (e.g., SSRIs) interventions for relieving mood and anxiety symptoms in children, there
is a marked paucity of studies evaluating treatment interventions of sleep problems in pediatric
depression and anxiety disorders. However, clinical experience indicates that treatment should
include the following:
n Development of strategies to optimize regular and adequate sleep that include basic prin-
ciples of sleep hygiene, such as a consistent bedtime and bedtime routine (see Chapter 19).
n Specif c behavioral strategies to reduce nighttime anxiety may be helpful (see also Chap-
ter 8). Note that bedtime strategies may be negotiated initially with the child, but once es-
tablished, should be consistently and f rmly enforced to avoid inadvertent reinforcement of
stalling behaviors. However, in cases of severe anxiety, the primary goal initially is to avoid
exacerbating the anxiety symptoms at bedtime, and any of these approaches may need to mod-
if ed. An excellent self-help workbook resource for school-aged children with sleep-related
anxiety is What to Do When You Dread Your Bed.
n Bedtime fading: Setting a temporary later bedtime that coincides more closely with the
actual sleep onset time may relieve some of the anxiety associated with trying to fall asleep.
n Reducing reliance on parental presence: A variety of developmentally appropriate gradu-
ated extinction procedures targeted at reducing the childs reliance on parental presence at
bedtime are available (see Chapter 6). Two-way baby monitors, which allow the child to
have verbal contact with a parent without having to leave the bed or bedroom, may be a use-
ful interim step for younger children.
n Positive reinforcement: The use of reward systems (e.g., sticker or star charts) can increase
appropriate bedtime behaviors.

n Bedtime pass: The bedtime pass, a technique in which the child is given a single nightly
opportunity (e.g., pass) to get up out of bed after lights out is particularly well-suited to
anxious children, who may feel reassured simply by having this option available.
n Institution of environmental changes such as the use of night-lights, installation of a f sh
tank, or allowing a pet to sleep in the childs bedroom may help relieve anxiety symptoms that
occur at bedtime and throughout the night.
n Teaching of relaxation techniques such as deep breathing, progressive muscle relaxation, and
guided visual imagery may help children to develop a sense of control over anxiety symptoms.
n Identif cation and elimination of additional factors (e.g., alcohol or nicotine use) that may
be impacting on both the psychiatric disorder and the sleep disturbance.
n Treatment of the primary psychiatric disorder with psychotherapy and pharmacologic
agents that do not exacerbate sleep disturbances. Because of the sleep-disrupting effects of
some antidepressant medications (including some SSRIs, venlafaxine, and bupropion), treat-
ment of the underlying depression may actually exacerbate the sleep disturbance.
n Pharmacologic treatment of insomnia may be appropriate when combined with behavioral
interventions (e.g., stimulus control, cognitive-behavioral therapy) and sleep hygiene mea-
sures. In general, although sedatives and hypnotics may provide a more rapid therapeutic re-
sponse, behavioral interventions are more effective long-term solutions. Use of single-agent
medications that combine mood and anxiety effects with sedating properties may be a reason-
able choice that limits exposure to multiple drugs and thus minimizes side effects.
n Referral for mental health counseling in cases of severe anxiety or if mood symptoms are
persistent and affect daytime functioning is recommended.
Appendix
A Resources for Families
r eSo ur c eS o t h er o r g An iz At io n S
American Academy of Sleep Medicine (AASM) National Institute of Mental Health (NIMH)
One Westbrook Corporate Center, Suite 920 (866) 615-6464
Westchester, IL 60154 www.nimh.nih.gov
(708) 492-0930
www.aasmnet.org National Institute of Health (NIH)
(301) 496-4000
Sleep Research Society (SRS) www.nih.gov
One Westbrook Corporate Center, Suite 920
Westchester, IL 60154 US Consumer Product Safety Commission
(708) 492-0930 (301) 504-7923
www.sleepresearchsociety.org Toll-free consumer hotline: (800) 638-8270
www.cpsc.gov
National Sleep Foundation (NSF)
1522 K Street, NW, Suite 500 American Academy of Pediatrics
Washington, DC 20005 (847) 434-4000
(202) 341-3471 www.aap.org
www.sleepfoundation.org
American Psychological Association
Narcolepsy Network (800) 374-2721
79A Main Street www.apa.org
North Kingstown, RI 02852
(888) 292-6522 American Academy of Child and Adolescent
www.narcolepsynetwork.org Psychiatry
(202) 966-7300
RLS (Restless Legs Syndrome) Foundation www.aacap.org
1610 14th Street NW, Suite 300
Rochester, MN 55901 National SIDS (Sudden Infant Death
(507) 287-6465 Syndrome) Resource Center
www.rls.org (866) 866-7437
www.sidscenter.org
American Sleep Apnea Association
A.W.A.K.E. Network First Candle/SIDS (Sudden Infant Death
6856 Eastern Avenue NW, Suite 203 Syndrome) Alliance
Washington, DC 20012 (800) 221-7437
(202) 293-3650 www.sidsalliance.org
www.sleepapnea.org
National Center on Sleep Disorders Research

PAr en t in g Bo o kS
(NCSDR) Childrens Sleep
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APPENDIx A: RESOURCES FOR FAmILIES 209
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General References
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2007;2(3):321329.
Sadeh A, Gruber R, & Raviv A. Sleep, neurobehavioral functioning, and behavior problems in school-age
children. Child Development 2007;73:405417.
Sadeh A, Gruber R, & Raviv A. The effects of sleep restriction and extension on school-age children:
What a difference an hour makes. Child Development 2003;74:444455.
Saper CB, Scammell TE & Lu J. Hypothalamic regulation of sleep and circadian rhythms. Nature
2005;437(7063):12571263.
Chapter 2: Sleep in Infancy, Childhood, and Adolescence

Carskadon MA, ed. Adolescent sleep patterns: biological, social, and psychological inf uences. Cam-
bridge: Cambridge University Press, 2002.
Horsley T, Clifford T, Barrowman N, et al. Benef ts and harms associated with the practice of bed sharing:
a systematic review. Arch Pediatr Adolesc Med 2007;161(3):237245.
Iglowstein I, Jenni OG, Molinari L, & Largo RH. Sleep duration from infancy to adolescence: Reference
values and generational trends. Pediatrics 2003;111:302307.
Jenni OG, Molinari L, Caf isch JA, & Largo RH. Sleep duration from ages 1 to 10 years: variability and
stability in comparison with growth. Pediatrics 2007;120(4):e769776.
Milan S, Snow S, & Belay S. The context of preschool childrens sleep: racial/ethnic differences in sleep
locations, routines, and concerns. J Fam Psychol 2007;21(1):2028.
Mindell JA, Meltzer LJ, Carskadon MA, & Chervin R. Developmental aspects of sleep hygiene: Findings
from the 2004 National Sleep Foundation Sleep in America Poll. Sleep Medicine in press.
Owens J. Socio-cultural considerations and sleep practices in the pediatric population. Sleep and Disorders
of Sleep In Women, Driver H (editor); Sleep Clinics of North America 2008; March, 3(1):97107.
Sadeh A, Mindell JA, Luedtke K, & Weigand B. Sleep and sleep ecology in the f rst 3 years: a web-based
study. J Sleep Res 2009;8(1):6073.
Stremler R, et al. A behavioral-educational intervention to promote maternal and infant sleep: a pilot
randomized, controlled trial. Sleep 2006;29:16091615.
Chapter 3: Evaluation of Pediatric Sleep Disorders

Grigg-Damberger M, Gozal D, & Marcus CL, et al. The visual scoring of sleep and arousal in infants and
children. J Clin Sleep Med 2007;3(2):201240.
Iber C, Ancoli-Israel S, Chesson A, & Quan SF for the American Academy of Sleep Medicine. The AASM
Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specif ca-
tions, 1st ed.: Westchester, Illinois: American Academy of Sleep Medicine, 2007.
211
212 SUGGESTED READINGS
Kushida CA, Littner MR, & Morgenthaler T, et al. Practice parameters for the indications for polysomnog-
raphy and related procedures: An Update for 2005. Sleep 2005;28(4):499521.
Morgenthaler T, Alessi C, & Friedman L, et al. Standards of Practice Committee; American Academy of
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Chapter 4: Sleep Hygiene

Dworak M, Schierl T, Bruns T, & Struder HK. Impact of singular excessive computer game and tele-
vision exposure on sleep patterns and memory performance of school-aged children. Pediatrics
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Chapter 6: Bedtime Problems

Chapter 7: Nightwakings
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wakings in infants and young children. Sleep 2006;29:12631276.
Morgenthaler TI, Owens J, & Alessi C et al. Practice parameters for behavioral treatment of bedtime
problems and night wakings in infants and young children: An American Academy of Sleep Medicine
report. Sleep 2006;29:12771281.
Chapter 8: Nighttime Fears

Chapter 9: Nightmares
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Chapter 10: Partial Arousal Parasomnias: Sleepwalking Sleep Terrors, and Confusional
Arousals
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2008;122:e11641167.
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2007;119:e10161025.
Chapter 11: Sleep-Related Rhythmic Movements: Head Banging, Body Rocking, and
Head Rolling
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2007;16:110116.
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hood and adulthood. Sleep 2005;28:851857.
Walters AS. Clinical identif cation of the simple sleep-related movement disorders. Chest
2007;131:12601266.
Chapter 12: Bruxism

Barbosa TDS, Miyakoda LS, & Pocztaruk RDL, et al. Temporomandibular disorders and bruxism in child-
hood and adolescence: Review of the literature. Int J Ped Otorhinolaryngology 2008;72:299314.
Nissani M. A bibliographical survey of bruxism with special emphasis on non-traditional treatment mo-
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Chapter 13: Sleep Enuresis

Butler RJ, & Heron J. The prevalence of infrequent bedwetting and nocturnal enuresis in childhood. A
large British cohort. Scand J Urol Nephrol 2008;42(3):257264.
Friman PC. Evidence-based therapies for enuresis and encopresis. In Steele R, Elkin TD, Roberts MC.
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Ramakrishnan K. Evaluation and treatment of enuresis. Am Fam Physician 2008;78:489496.
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Chapter 14: Sleep-Disordered Breathing and Obstructive Sleep Apnea Syndrome

American Thoracic Society. Cardiorespiratory sleep studies in children: establishment of normative data
and polysomnographic predictors of morbidity. American Thoracic Society workshop summary. Am J
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Baldassari CM, Mitchell RB, Schubert C, & Rudnick EF. Pediatric obstructive sleep apnea and quality of
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Fauroux B. Whats new in paediatric sleep? Paediatr Respir Rev 2007;8(1):8589.
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Chapter 15: Restless Legs Syndrome and Periodic Limb Movements Disorder
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Chapter 16: Excessive Daytime Sleepiness: Narcolepsy and Other Hypersomnias

Morgenthaler TI, Kapur VK, & Brown T, et al. Standards of Practice Committee of the American Acad-
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central origin. Sleep 2007;30:17051711.
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Kothare S, & Kaleyias J. The clinical and laboratory assessment of the sleepy child. Seminars in Pediatric
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Chapter 17: Delayed Sleep Phase Disorder

Bjorvatn B, & Pallesen S. A practical approach to circadian rhythm sleep disorders. Sleep Med Rev.
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Mundey K, Benloucif S, & Harsanyi K, et al. Phase-dependent treatment of delayed sleep phase syndrome
with melatonin. Sleep 2005;28:12711278.
Morgenthaler TI, Lee-Chiong T, & Alessi C, et al. Standards of Practice Committee of the American
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Sack RL, Auckley D, & Auger RR, et al. American Academy of Sleep Medicine. Circadian rhythm
sleep disorders: part II, advanced sleep phase disorder, delayed sleep phase disorder, free-running
disorder, and irregular sleepwake rhythm. An American Academy of Sleep Medicine review. Sleep
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Wyatt JK. Delayed sleep phase syndrome: Pathophysiology and treatment options. Sleep
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Chapter 18: Insomnia

Johnson EO, Roth T, Schultz L, & Breslau N. Epidemiology of DSM-IV insomnia in adolescence: lifetime
prevalence, chronicity, and an emergent gender difference. Pediatrics 2006;117:e247e256.
Morgenthaler T, Kramer M, & Alessi C, et al. American Academy of Sleep Medicine. Practice parameters
for the psychological and behavioral treatment of insomnia: an update. An American Academy of
Sleep Medicine report. Sleep 2006;29:14151419.
Morin CM, et al., Psychological and behavioral treatment of insomnia:update of the recent evidence
(19982004). Sleep 2006;29:13981414.
Roane BM, & Taylor DJ. Adolescent insomnia as a risk factor for early adult depression and substance
abuse. Sleep 2008;31:13511356.
Roberts RE, Roberts CR, & Chan W. Persistence and change in symptoms of insomnia among adoles-
cents. Sleep 2008;31:177184.
Roberts RE, Roberts CR, & Duong HT. Chronic insomnia and its negative consequences for health and
functioning of adolescents: a 12-month prospective study. J Adolesc Health 2008;42:294302.
Chapter 19: Sleep and Medications

Owens JA, Rosen CL, & Mindell JA. Medication use in the treatment of pediatric insomnia: Results of a
survey of community-based pediatricians. Pediatrics 2003;111:e628e635.
Owens JA, Babcock D, & Blumer J, et al. The use of pharmacotherapy in the treatment of pediatric insom-
nia in primary care: Rational approaches. A consensus meeting summary. Journal of Clinical Sleep
Medicine 2005;1:4959.
Owens J. Pharmacotherapy of Pediatric Insomnia. J Am Acad Child Adolesc Psychiatry
2009;48(2):99107.
Stojanovski SD, Rasu RS, Balkrishnan R, & Nahata MC. Trends in medication prescribing for pediatric
sleep diff culties in US outpatient settings. Sleep 2007;30(8):10131017.
Chapter 20: Sleep and Neurodevelopmental Disorders

Andersen IM, Kaczmarska J, McGrew SG, & Malow BA. Melatonin for insomnia in children with autism
spectrum disorders. J Child Neurol 2008; prepublished January 1.
Jan J, Owens J, & Weiss M, et al. Sleep hygiene for children with neurodevelopmental disabilities. Pediat-
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Malow BA, Marzec ML, & McGrew SG, et al. Characterizing sleep in children with autism spectrum
disorders: a multidimensional approach. Sleep 2006;29(12):15631571.
Stores G, & Wiggs L. Sleep disturbance in children and adolescents with disorders of development: its
signif cance and management. New York, NY: Cambridge University Press, 2003.
Chapter 21: Sleep and Medical Disorders

Kohrman MH, & Carney PR. Sleep-related disorders in neurologic disease during childhood. Pediatr
Neurol 2000;23(2):107113.
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Meltzer LJ, & Moore M. Sleep disruptions in parents of children and adolescents with chronic illnesses:
prevalence, causes, and consequences. J Pediatr Psychol 2008;33(3):279291.
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Chapter 22: Sleep and Psychiatric Disorders

Cortese S, Konofal E, & Yateman N, et al. Sleep and alertness in children with attention-def cit/hyperactiv-
ity disorder: a systematic review of the literature. Sleep 2006;29(4):504511.
Forbes EE, Bertocci MA, & Gregory AM, et al. Objective sleep in pediatric anxiety disorders and major
depressive disorder. J Am Acad Child Adolesc Psychiatry 2008; Feb; 47(2):14855.
Lofthouse N, Fristad M, Splaingard M, & Kelleher K. Parent and child reports of sleep problems associ-
ated with early-onset bipolar spectrum disorders. J Fam Psychol 2007;21(1):114123.
Ivanenko A (Editor). Sleep and Psychiatric Disorders in Children and Adolescents. Informa Healthcare,
New York, 2008.
Owens J. A clinical overview of sleep and attention def cit hyperactivity disorder in children and adoles-
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meta-analysis of polysomnographic studies. Sleep Med Rev 2006;10(6):381398.
Subject Index
Page numbers followed by f indicate f gures. sleep effects of, 175

Page numbers followed by t indicate tables. Allergies, 188
Note: Medications are listed by generic Allergy medications, 174
names Alpha agonists, 171. See also Clonidine
Ambien/Ambien CR. See Zolpidem
American Academy of Pediatrics
A bed-sharing statement by, 16, 66
obstructive sleep apnea syndrome practice
Academic problems
guidelines, 101
delayed sleep phase syndrome as cause of, 145
Analgesics, 174, 186
insuff cient sleep and, 2
Angelman syndrome, 179
narcolepsy and, 135
Anticholinergics, 99
obstructive sleep apnea and, 106
Anticonvulsants, 174, 194195
Acetylcholine, 7
Actigraphy Antidepressants. See also Selective serotonin
reuptake inhibitors; Tricyclic
description of, 4142
antidepressants
insomnia evaluations, 157
narcolepsy evaluations, 146147 insomnia managed with, 172
Active sleep, 4, 16 partial arousal parasomnias treated with, 83
Adderall XR. See Dextroamphetamine sleep effects of, 174175
Adenotonsillectomy, for obstructive sleep apnea, sleep related rhythmic movements treated with,
101, 112113, 115, 192, 257 89
ADHD. See Attention def cit hyperactivity Antihistamines, 169
disorder Antihypertensive agents, 174
Adjustment disorders, 205 Antipsychotics, 173, 175
Adolescents Anxiety
anticipatory guidance for, 15t management of, 244
bruxism in, 253 parental, 60, 67
caffeine consumption by, 29, 235, 238 sleep affected by, 204205
circadian factors that affect, 2627 Anxiety disorders
daytime sleepiness in, 27 in Asperger syndrome patients, 179
developmental issues in, 2627 attention def cit hyperactivity syndrome and,
fears commonly seen in, 68 200
insuff cient sleep in, 28 nightmares and, 73
napping by, 236, 238 nighttime fears and, 67, 69, 205206
restless legs syndrome screening questionnaire prevalence of, 204
for, 224225 restless legs syndrome and, 122
risk-taking behaviors by, 2728 symptoms of, 204
sleep in Apnea-hypopnea index, 110111. See also
architecture of, 6t Obstructive sleep apnea
deprivation of, 26, 28, 235236 Apneic pauses, 101, 105
normal patterns of, 26 Arousals
promotion strategies, 236, 238 by children, 58
sleepwake cycle in, 26 confusional. See Confusional arousals
African-Americans by infants, 58
co-sleeping, 22 nighttime, in infants, 18
napping, 22 practices that affect, 43
obstructive sleep apnea in, 101, 115 respiratory event related, 110
Alarm clock, 36 sleep related rhythmic movements secondary
Alcohol to, 86
bruxism risks, 91 threshold for, 4
217
218 SUBj ECT INDEx
Ascending arousal systems, 7f8f Bedtime pass, 57, 206, 240

Asperger syndrome, 178179 Bedtime problems
Asthma, 188189 algorithm for evaluating, 50
Asthma medications, 174 behavior management strategies for, 56
Atarax. See Hydroxyzine daytime behaviors secondary to, 53
Atopic dermatitis, 189 diagnostic criteria for, 53t
Attachment, 17, 60 differential diagnosis, 54
Attention def cit hyperactivity disorder epidemiology of, 52
anxiety disorder and, 200 etiology of, 52
bedtime resistance associated with, 199f, evaluative approach, 5354
201202 family tension caused by, 51, 53
behavioral interventions for, 202 features associated with, 53
central nervous system dysregulation limit-setting problems as cause of, 51, 56
associated with, 200 management of, 5457, 239240
clonidine for, 171 naps, 55
coexisting sleep disturbances with, 200 nightwakings and, 53
comorbid psychiatric disorders, 200 parental tips for, 57
description of, 197198 presentation of, 5253
epidemiology of, 198 prognosis for, 57
etiology of, 198199 referrals for, 54
evaluation of, 200202 risk factors for, 52
medications for, 202 sleep habits for, 5556
obstructive sleep apnea and, 106 stalling, 3334, 5157
periodic limb movement disorder and, 122, 201 standards of practice for, 63
psychostimulants for, 200 symptoms of, 5253
restless legs syndrome and, 122, 201 treatment of, 5457
sleep disturbances and, 197198 Bedtime resistance
treatment of, 202203 attention def cit hyperactivity syndrome and,
Augmentation, 129 199f, 201202
Autism, 178179 characteristics of, 5057, 6869
Awakenings delayed sleep phase syndrome as cause of, 145
morning, 3536 nightmares as cause of, 73
nighttime. See Nightwakings nighttime fears as cause of, 6869
restless legs syndrome as cause of, 121
B Bedtime routines
for adolescents, 26
Baby bottle caries, 18 consistency of, 5556
Basal forebrain, 6 for developmentally delayed children, 181182
Bed evaluation of, 33
crib transition to, 21 importance of, 4546, 55, 237, 239240
getting out of, 240 for infants, 19, 229
type of, 34 nightwakings managed with, 63, 242
Bedding, 34 positive reinforcement for, 56
Bedroom, 34, 237 for school-aged children, 233
Bedroom lighting, 181 strategies for enforcing, 56
Bed-sharing, 16, 20, 66. See also Co-sleeping for toddlers, 21, 230
Bedtime Bedwetting. See Sleep enuresis
complaints or protests about, 56, 240 Behavioral assessment, 37
crying at, 6364, 240 Behavioral insomnia of childhood
drowsy but awake at, 63 limit-setting type. See Bedtime problems
schedule for, 33 sleep onset association type. See Nightwakings
setting of, 55, 239 Behavioral therapist, 65
sleep onset and, 201 Benadryl. See Diphenhydramine
voiding before, 98 Benign rolandic epilepsy, 195
Bedtime fading, 55, 206, 239 Benzodiazepines
SUBj ECT INDEx 219
mechanism of action, 9 Circadian rhythms

partial arousal parasomnias treated with, 83 phase advancement, 149
pharmacokinetics of, 170 phase delay, 149150
Bilevel positive airway pressure production of, 9
obstructive sleep apnea treated with, 113114 shifting of, 149150
polysomnography for titration of, 39 Circadian timing, 52
Bipolar disorder, 204 Circadian troughs, 10
Bladder training, 98 Clomipramine, 141t, 142
Body rocking, 8589, 251252 Clonazepam, 89, 129, 183
Body rolling, 86 Clonidine, 129, 165t, 167t, 171
Bottle-feeding Codeine, 129
nighttime awakenings and, 18 Coffee, 44t
sleep duration and, 13 Cognition, 3, 154
Breast-feeding Colic, 5960
nightwakings and, 18, 59 Concerta. See Methylphenidate
sleep duration and, 13 Confusional arousals
Bright light exposure therapy, 150151, 184 characteristics of, 77
Brompheniramine, 164t, 166t def nition of, 249
Bruxism, 9093, 191, 253 diagnostic criteria for, 80t
Bupropion, 174 differential diagnosis, 82t
Burns, 189 epidemiology of, 78
evaluation of, 81
management of, 8283
c parental tips for, 84
Caffeine presentation of, 79
adolescent consumption of, 29, 235, 238 sleep inertia associated with, 77
arousals caused by, 43 Constipation, 255
avoidance before bedtime, 237238 Continuous positive airway pressure
periodic limb movement disorder exacerbated compliance with, 113114
by, 263 obstructive sleep apnea treated with, 113114,
school-aged children consumption of, 25, 234 257
sleep effects of, 175 polysomnography for titration of, 39
sources of, 43, 44t side effects of, 113
Cancer, 189190 Coping skills, 185, 243
Carbamazepine, 174 Corticosteroids, 174
Cataplexy Co-sleeping. See also Bed-sharing
def nition of, 132 assessment of, 3435
medications for, 141t, 142143 culture and, 22
narcolepsy with, 132, 134, 136t, 264 def nition of, 20
Catapres. See Clonidine nightwakings and, 59, 66
CD40 ligand, 104 in preschoolers, 23
Central hypoventilation syndromes, 196 reactive, 22, 66, 186
Centrally mediated hypersomnias, 131 CPAP. See Continuous positive airway pressure
Chemotherapeutic agents, 189 Craniofacial abnormalities, 177
Chiari malformations, 191192 Crib, 21, 252
Child abuse, 69 Crying, 6364, 240
Chloral hydrate, 173 Culture, 22
Chlorpheniramine, 164t, 166t Curtain calls, 5152, 68
Cholinergic neurons, 6 Cystic f brosis, 190
Chronic fatigue syndrome, 190
Chronic respiratory failure, 192 D
Chronotherapy, 149150, 184
Cigarette smoking, 43, 103, 175 Dalmane. See Flurazepam
Circadian clock, 910 Day/night reversal, 16
Circadian nadirs, 10, 52 Daytime behaviors
220 SUBj ECT INDEx
bedtime problems and, 53 Depakote. See Valproic acid

bruxism and, 91 Depression
evaluation of, 35 attention def cit hyperactivity syndrome and,
naps. See Naps 200
in neurodevelopmental disorder patients, 177 characteristics of, 203204
Daytime sleep habits, 55 delayed sleep phase disorder and, 145, 148
Daytime sleepiness in developmentally delayed children, 177
in adolescents, 27 excessive daytime sleepiness and, 140
algorithm for, 48f insomnia and, 155, 157, 172
delayed sleep phase syndrome as cause of, 145, maternal, 17, 19, 60
267 postpartum, 17, 60
evaluation of, 36, 48f rebound headache and, 191
excessive. See Excessive daytime sleepiness restless legs syndrome and, 122
periodic limb movement disorder as cause of, selective serotonin reuptake inhibitors for, 172
121122, 262 Desmopressin, 99
polysomnography evaluations, 39 Desyrel. See Trazodone
in Prader-Willi syndrome, 180 Detrol. See Anticholinergics
restless legs syndrome as cause of, 121122, Developmental history
261 in delayed sleep phase syndrome evaluation,
in school-aged children, 25 146
Daytrana. See Methylphenidate description of, 36
Delayed sleep onset in insomnia evaluations, 156
algorithm for evaluating, 50 in narcolepsy evaluations, 136137
nightwakings and, 60 Developmental issues
Delayed sleep phase disorder in adolescents, 2627
academic problems secondary to, 145 in infants, 17
age of onset, 144 in newborns, 16
bedtime problems secondary to, 54 in preschoolers, 2223
def nition of, 144, 267 in school-aged children, 2425
diagnosis of, 146t, 268 in toddlers, 2021
differential diagnosis, 147148 Developmentally delayed children
epidemiology of, 144 Angelman syndrome, 179
etiology of, 144145, 267 Asperger syndrome, 178179
evaluation of, 146147 autism, 178179
features associated with, 145 cognitive impairments, 177
hypnotics for, 151 craniofacial abnormalities, 177
insomnia vs., 147, 157 Down syndrome, 176, 179
light therapy for, 269 parenting variables that exacerbate, 178
management of, 148151 Prader-Willi syndrome, 180
melatonin for, 150151, 164t, 166t, 169170, psychiatric disorders presenting with, 177178
179, 269 Rett syndrome, 180
motivation to change, 148149 sensory issues in, 181
parental tips for, 151152 sleep disorders in
pharmacotherapy for, 150151 behavioral management of, 182
presentation of, 145 bright light therapy for, 184
prognosis for, 152 description of, 176178
referrals for, 148 evaluation of, 181
restless legs syndrome vs., 148 pharmacologic treatment of, 183
risk factors for, 144145 sleep-disordered breathing, 180
school avoidance or refusal and, 148 sleepwake scheduling for, 184
sleep hygiene for, 148, 150, 268 treatment of, 181184
sleepwake schedule changes for, 268269 sleep related rhythmic movements, 86
symptoms of, 267268 Smith-Magenis syndrome, 180
treatment of, 148151, 268269 Williams syndrome, 120, 180, 183
Delta sleep, 3 Dextroamphetamine, 141t, 142
Dental appliances, for bruxism, 93 Diabetes, 190
SUBj ECT INDEx 221
Dilantin. See Phenytoin Epilepsy, 194195

Diphenhydramine, 164t, 166t, 169 Episodic nocturnal phenomena, 3940, 74
Distraction, 69 Estazolam, 164t, 166t
Ditropan. See Anticholinergics Eszopiclone, 165t166t, 171
Divorce, 37 Ethnicity, 101
Doral. See Quazepam Excessive daytime sleepiness. See also Daytime
Down syndrome, 176, 179 sleepiness
Driving accidents, 29 in cancer patients, 190
Drowsy driving, 29, 236, 238 causes of, 131
Drugdrug interactions, 168 characteristics of, 2
DSPD. See Delayed sleep phase disorder in cystic f brosis patients, 190
Dual diagnoses, 30 def nition of, 131
differential diagnosis, 111, 127
fatigue vs., 131
e insuff cient sleep as cause of, 2
Early-morning awakenings, 61 medications for, 141t, 142
Eczema, 189 narcolepsy as cause of, 133134, 264
Electrocardiography, 108109 obstructive sleep apnea as cause of, 105, 111
Electroencephalography, 194 in school-aged children, 25
Endogenous circadian rhythm, 9 Exercise, 46, 237
Energy drinks, 44t Extinction
Enuresis, sleep def nition of, 63
bladder capacity and, 95 graduated, 64
bladder training to prevent, 98 nightwakings managed with, 6364
characteristics of, 94 Extinction burst, 57
costs of, 96
diagnostic criteria for, 96t F
differential diagnosis, 97
emotional effects of, 96 Falling asleep, 34
epidemiology of, 94, 254 Family. See also Parent(s)
etiology of, 9495 bedtime problems effect on, 51, 53
evaluation of, 97 functioning evaluations of, 37
features associated with, 9596 interactions in, 38
imipramine for, 98 of children with chronic medical conditions,
management of, 9798 186
obstructive sleep apnea and, 95, 106 of narcolepsy patient, 140141
parental tips for, 9899, 254255 resources for, 208
physical examination for, 97 sleep behaviors affected by, 22
presentation of, 9596 stress in, 60
primary, 9495, 254 Family bed, 66
referrals for, 97 Family history
risk factors for, 9495 in bruxism evaluations, 91
secondary, 9495, 254 in delayed sleep phase syndrome evaluation,
treatment of, 9798 146
vasopressin production and, 95 description of, 3637
voiding before bedtime to prevent, 98 in narcolepsy evaluations, 132, 137
Enuresis alarms, 98, 255 in obstructive sleep apnea syndrome
Enuresis diary, 97 evaluation, 103
Environment in restless legs syndrome evaluation, 124, 260
for adolescents, 27 in sleep enuresis evaluation, 95
for developmentally delayed children, 181 in sleepwalking evaluation, 78
effects of, 13, 16 Fatigue
evaluation of, 3435 cancer-related, 190
for newborns, 16 in cystic f brosis patients, 190
nightwakings caused by disruptions in, 62 evaluation of, 36
sleep-conducive, 46 excessive daytime sleepiness vs., 131
222 SUBj ECT INDEx
insuff cient sleep as cause of, 2 Hypnopompic hallucinations, 134

sleepiness vs., 185 Hypnotics
Fearful behaviors, 53, 68 delayed sleep phase syndrome treated with,
Fears 151
developmentally common types of, 68 in developmentally delayed children, 183
nighttime. See Nighttime fears during hospitalization, 187
Ferber method, 6 insomnia and, 155, 159
Ferritin, 118119, 126, 261, 263 Hypocretin, 7, 8f, 132, 138
Fibromyalgia, 190 Hyponasality, 107
Floppy airway, 102 Hypoxemia, 192193
Fluoxetine, 141t, 142
Flurazepam, 164t, 166t
Frontal lobe epilepsy, 195 i
Idiopathic hypersomnia, 139, 139t140t
g Imipramine
cataplexy treated with, 141t, 142
Gabapentin, 129 sleep enuresis treated with, 98
Gamma-aminobutyric acid, 7, 143 Infants
Gastroesophageal ref ux disease, 191 anticipatory guidance for, 14t15t
Gastrointestinal disorders, 190191 arousals by, 58
Gender bedtime routines for, 19, 229
insomnia and, 154 body rocking in, 85
narcolepsy and, 132 bruxism in, 253
obstructive sleep apnea syndrome risks, 101 developmental issues in, 17
sleep related rhythmic disorders and, 86 fears commonly seen in, 68
General appearance, 38 night feedings for, 1819
Generalized anxiety disorder, 205 normal sleep patterns for, 17
Good morning light, 65 obstructive sleep apnea syndrome in, 105
Graduated extinction, 64 REM sleep in, 4
Growing pains, 121 safe sleep practices for, 1617
sleep in, 6t, 12, 228229
h Inf ammatory bowel disease, 191
Insomnia
Halcion. See Triazolam def nition of, 153, 205, 270
Headaches, 191 delayed sleep phase syndrome vs., 147, 157
Head banging, 8589, 251252 depression and, 155, 203
Head rolling, 8589, 251252 diagnosis of
Herbal preparations, 170 criteria for, 155t156t
Histamine, 7 tests used in, 157, 270
Homeostatic process, 9 differential diagnosis, 157
Hospitalization, 186187 epidemiology of, 148
Human leukocyte antigen testing, 133, 138 etiology of, 154, 270
Hydroxyzine, 89, 164t, 166t, 169 evaluation of, 156157
Hypersomnia features associated with, 155
centrally mediated, 131 hypnotics and, 155, 159
central nervous system injuries as cause of, learned, 147, 154155
133 management of, 158159, 270271
cranial radiation therapy-related, 190 medications for, 170173, 207
def nition of, 131 parental tips for, 160
depression and, 203 periodic limb movement disorder vs., 157
idiopathic, 139, 139t140t personality traits associated with, 154
menstrual-related periodic, 140 presentation of, 154155
Hypnic jerks, 3 prevalence of, 148
Hypnogogic hallucinations, 3, 134, 264 primary, 147148, 156t
Hypnogram, 4, 5f prognosis for, 159160
SUBj ECT INDEx 223
psychiatric disorders and, 157158, 205206 Lunesta. See Eszopiclone

psychophysiological, 153, 156t
referrals for, 158
relaxation strategies for, 159
M
restless legs syndrome vs., 157 Major depressive disorder, 203205
risk factors for, 154 Mandibular advancing devices, 114
sleep-disordered breathing vs., 157 Maternalchild attachment, 60
sleep hygiene and, 157158, 271 Maternal depression, 60
sleep restriction for, 158159 Maximum sleepiness, 10
stimulus control for, 158 Medical conditions, 188193
symptoms of, 270 Medical history
tips for preventing, 159 description of, 36
transient, 54, 157 in insomnia evaluations, 156
treatment of, 158159, 168, 170173, 207, in narcolepsy evaluations, 136
270271 in obstructive sleep apnea evaluations, 107
Insuff cient sleep in partial arousal parasomnias evaluation, 81
in adolescents, 28 in periodic limb movement disorder evaluation,
causes of, 3, 30 123124
excessive daytime sleepiness caused by, 2 questionnaire for, 213215
manifestations of, 23 in restless legs syndrome evaluation, 123124
narcolepsy vs., 139 Medications. See also specif c medication
nightwakings vs., 62 asthma, 189
Intensive care units, 186 attention def cit hyperactivity disorder treated
Iron def ciency, 118119, 128, 261, 263 with, 202
Iron supplementation, 128 bedtime problems caused by, 54
behavioral interventions before use of, 163
cataplexy treated with, 141t, 142143
J considerations before prescribing, 161162
Jet lag, 5, 27 drugdrug interactions, 168
Juvenile myoclonic epilepsy, 195 excessive daytime sleepiness treated with,
Juvenile rheumatoid arthritis, 191 141t, 142
indications for, 162163
narcolepsy treated with, 141143, 265
k nightmares caused by, 73
obstructive sleep apnea treated with, 114
K complexes, 3
over-the-counter, 44t, 168170
Kleine-Levin syndrome, 139140
restless legs syndrome and, 119, 128129
Klonopin. See Clonazepam selection of, 163
side effects monitoring, 163
l sleep affected by, 173175, 186187
sleep enuresis treated with, 255
Landau-Kleffner syndrome, 177, 195 timing of administration, 163
Laterodorsal tegmental nucleus, 6 Melatonin
Learned behavior characteristics of, 164t, 166t, 169170, 179
night feedings as, 18 delayed sleep phase syndrome treated with,
sleep as, 1011, 13 150151, 269
Learned insomnia, 147, 154155 developmentally delayed children treated with,
Lennox-Gastaut syndrome, 177 183
Lethargy, 2 Meningomyelocele, 191192
Levodopa/carbidopa, 128129 Menstrual-related periodic hypersomnia, 140
Lightdark cycle, 10 Methylphenidate, 141t, 142
Light therapy, 150151, 184, 269 Middle childhood. See School-aged children
Limit-setting by parents, 51, 56, 201202, 239 Migraine headaches, 191
Lithium, 175 Mirapex. See Pramipexole
Locus coeruleus, 7 Mirtazapine, 172
224 SUBj ECT INDEx
Modaf nil, 141t, 142 features associated with, 135136

Mood, 2 human leukocyte antigen testing for, 133, 138
Mood disorders hypnagogic and hypnopompic hallucinations
anxiety. See Anxiety disorders associated with, 3, 134, 264
bipolar disorder, 204 idiopathic hypersomnia vs., 139, 139t140t
depression. See Depression Kleine-Levin syndrome vs., 139140
seasonal affective disorder, 204 lifestyle changes for, 264
Morning awakening, 3536 management of, 140143, 265266
Morning larks, 10, 26, 61 medical history evaluations, 136
Morning light, 10, 55 medications for, 141143, 265
Morningnesseveningness preference, 147 misdiagnosis of, 136
MSLT. See Multiple sleep latency test neuroimaging evaluations, 138
Multiple sleep latency test obesity and, 135
indications for, 41 obstructive sleep apnea associated with, 135
narcolepsy evaluations, 136t137t, 137138 parental tips for, 143
Muscle atonia, 7 periodic limb movement disorder and, 120
physical examination for, 137
polysomnography evaluations, 137138
n
prevalence of, 132
Naps prognosis for, 143
by adolescents, 236, 238 psychological distress caused by, 135
age-appropriate considerations, 45, 237 referrals for, 140
description of, 5 risk factors for, 132133
diff culties with, 55 secondary, 133
duration of, 17 sleep attacks associated with, 131
evaluation of, 35 sleep disturbances associated with, 134135,
by infants, 17 265
late-day, 45 sleep paralysis associated with, 134, 264
narcolepsy managed with, 141 symptoms of, 131136, 264265
nightwakings managed with, 63 treatment of, 140143, 265266
by parents, 19 Nasal obstruction, 102
by preschoolers, 22 Nefazodone, 172
routine setting for, 55 Neuroanatomy, 69
by toddlers, 21 Neurodevelopmental disorders
unplanned, 35 Angelman syndrome, 179
Narcolepsy Asperger syndrome, 178179
academic problems caused by, 135 autism, 178179
age of onset, 131 cognitive impairments, 177
with cataplexy, 132, 134, 136t, 264 craniofacial abnormalities, 177
characteristics of, 264 Down syndrome, 176, 179
comorbid sleep disorders with, 135, 141 parenting variables that exacerbate, 178
diagnosis of Prader-Willi syndrome, 180
criteria for, 136t137t psychiatric disorders presenting with, 177178
multiple sleep latency test for, 136t137t, Rett syndrome, 180
137138, 265 seizures and, 194
tests used in, 137138, 265 sensory issues in, 181
differential diagnosis, 139140 sleep disorders in
education about, 140141, 266 behavioral management of, 182
epidemiology of, 132 bright light therapy for, 184
etiology of, 132133, 265 description of, 176178
evaluation of, 136138 evaluation of, 181
excessive daytime sleepiness caused by, pharmacologic treatment of, 183
133134, 264 sleep-disordered breathing, 180
family education about, 140141, 266 sleepwake scheduling for, 184
family history of, 132, 137 treatment of, 181184
SUBj ECT INDEx 225
Smith-Magenis syndrome, 180 features associated with, 68

Williams syndrome, 120, 180, 183 gender and, 67
Neuromuscular diseases and disorders, 177, 192 management of, 6971, 243244
Neurontin. See Gabapentin nightmares as cause of, 69
Neurotransmitters, 7 parental interventions for, 6970
Newborns parental tips for, 70, 243244
anticipatory guidance for, 14t presentation of, 68
day/night reversal in, 16 prognosis for, 71
developmental issues in, 16 referrals for, 69
normal sleep patterns in, 13, 16 relaxation strategies for, 244
positioning of, 16 reward systems for changing, 70
safe sleep practices for, 16 risk factors for, 67
sleep in, 6t, 226227 symptoms of, 68
Nicotine, 43, 175 treatment of, 6971
Night feedings Nighttime feedings, 65
in infants, 1819 Nightwakings
in toddlers, 21 algorithm for, 49f
Night lights, 34, 244, 246 bedtime problems and, 53
Nightmare(s) bedtime routines for, 63, 242
bedtime resistance caused by, 73 breast-feeding and, 18, 59
content of, 72 cessation of adult interventions for, 65
def nition of, 72, 245 co-sleeping and, 59
diagnostic criteria for, 73t diagnosis of, 61t, 62
differential diagnosis, 74 differential diagnosis, 62, 127
epidemiology of, 72 epidemiology of, 59
etiology of, 7273, 245 etiology of, 5960
evaluation for, 35 evaluation of, 35, 49f, 6162
evaluation of, 73 features associated with, 6061
management of, 7475, 245246 history-taking, 62
nighttime fears secondary to, 69 inappropriate sleep associations and, 58
parental response to, 7475 management of, 6266, 241242
parental tips for, 75, 245246 parental tips for, 57, 239240
partial arousal parasomnias vs., 74 in preschoolers, 23
presentation of, 73 presentation of, 60
prevalence of, 72 prevalence of, 5859
prognosis for, 75 prognosis for, 66
referral for, 74 referrals for, 62
relaxation strategies for, 75 reinforcement strategies for, 65
REM behavior disorder vs., 74 restless legs syndrome as cause of, 121
risk factors for, 7273 risk factors for, 5960
symptoms of, 73 sleep associations and, 5859, 241
systematic desensitization for, 75 standards of practice for, 63
treatment of, 7475 in toddlers, 21
Nightmare seizure disorder, 81 treatment of, 6366
Night owls, 10, 23, 52, 144 Nocturnal behaviors, 35
Night terrors. See Sleep terrors Nocturnal leg pains, 126127
Nighttime arousals, 18 Nocturnal panic attacks, 81
Nighttime fears Nocturnal paroxysmal dystonias, 195
anxiety disorders and, 67, 69, 205206 Nonbenzodiazepine receptor agonists, 170
bedtime problems secondary to, 54 Non-REM sleep. See NREM sleep
characteristics of, 67 Nonsteroidal anti-inf ammatory drugs, 174
differential diagnosis, 6869 Norepinephrine, 7
epidemiology of, 67 NREM sleep
etiology of, 67 cholinergic neurons in, 6
evaluation of, 68 control of, 7, 8f
226 SUBj ECT INDEx
def nition of, 3 parental tips for, 115

stages of, 34 partial arousal parasomnias and, 106
pathophysiology of, 103104
periodic limb movement disorder associated
o with, 120
Obesity physical examination for, 107108
narcolepsy risks, 135 in Prader-Willi syndrome, 180
obstructive sleep apnea syndrome risks, 103, presentation of, 104107
114, 257 prognosis for, 114115
in Prader-Willi syndrome, 180, 187 radiologic studies for, 108109
prevalence of, 193 recurrence of, 115
sleep-disordered breathing and, 103, 193194 risk factors for, 102104
sleep disturbances secondary to, 187, 193194, screening questionnaire for, 221
233 sleep enuresis risks associated with, 95
weight management problems for, 114 snoring associated with, 100101, 104105,
Object permanence, 17 114115
Obstructive hypoventilation, 100 symptoms of, 104107, 256257
Obstructive sleep apnea. See also Sleep- treatment of, 112114, 257
disordered breathing upper airway obstruction as cause of, 102
adenotonsillectomy for, 101, 112113, 115, Opiates, 129, 186
192, 257 Oppositional behavior, 69
American Academy of Pediatrics practice Oppositional def ant disorder, 54, 200
guidelines, 101 Oral appliances, for obstructive sleep apnea, 114
apneic pauses associated with, 101, 105 Orexin, 7, 8f, 132, 138
attention def cit hyperactive disorder and, 106 Oropharyngeal examination, 107108
bilevel positive airway pressure for, 113114 Otolaryngologic examination, 38
characteristics of, 101 Overnight sleep study. See Polysomnography
comorbidities, 107 Oversleep, 35, 145, 236, 238
continuous positive airway pressure for, Over-the-counter medications, 44t, 168170
113114, 257 Overtired, 13
daytime effects of, 105106, 115 Oxycodone, 129
def nition of, 100, 256
diagnosis of P
criteria for, 108t
polysomnography for, 39, 109111, 111f, Pacif er, 1819
115, 201, 257 Pain, 185186, 196
tests used in, 108111 Panic attacks, 81
differential diagnosis, 111 Parasomnias. See Partial arousal parasomnias
in Down syndrome, 176, 179 Parent(s). See also Family
electrocardiography evaluations, 108109 bed-sharing with, 16
enuresis associated with, 106 bedtime problems caused by, 52
environmental factors, 103 bedtime supervision by, 33
epidemiology of, 101 discipline styles of, 52
etiology of, 102104, 256 divorce/separation of, 37
evaluation of, 107111 functioning evaluations, 37
excessive daytime sleepiness secondary to, graduated extinction training for, 64
105, 111 limit-setting by, 51, 56, 201202, 239
family history of, 103 napping by, 19
hypoxemia associated with, 193 of developmentally delayed children, 178
in infants, 105 responses by, to nightmares, 7475
management of, 112114, 257 sleep affected by, 13
medical conditions associated with, 103, 104t sleep terror management by, 83
medical history evaluations, 107 sleepwalking management by, 83
narcolepsy and, 135 tips for talking with. See Parental tips
obesity and, 103, 257 Parental anxiety
SUBj ECT INDEx 227
nightwakings and, 60 diagnosis of

partial arousal parasomnias and, 8081 criteria for, 116117, 125t
sleep related rhythmic movements and, 86 tests used in, 126, 262
Parental tips differential diagnosis, 126127, 157
for bedtime problems, 57 dopamine agonists for, 129
for body rocking, 8889, 251252 dopaminergic dysfunction and, 117118
for body rolling, 8889 epidemiology of, 117118
for bruxism, 9293, 253 etiology of, 119120, 262
for confusional arousals, 84 evaluation of, 35, 123126
for delayed sleep phase syndrome, 151152 features associated with, 121122
for head banging, 8889, 251252 insomnia vs., 157
for head rolling, 8889 iron metabolism alterations and, 119, 263
for insomnia, 160 laboratory tests for, 126
for narcolepsy, 143 management of, 127129, 263
for nightmares, 75, 245246 narcolepsy and, 120
for nighttime fears, 70, 243244 obstructive sleep apnea associated with, 120
for nightwakings, 57, 239240 parental tips for, 129
for obstructive sleep apnea, 115 pathophysiology of, 117
for periodic limb movement disorder, 129 polysomnography evaluations, 39, 116, 126,
for restless legs syndrome, 129 126f, 201
for sleep enuresis, 9899, 254255 presentation of, 120t, 120123
for sleep terrors, 84, 250 prevalence of, 117118
for sleepwalking, 84, 248 prognosis for, 129
Partial arousal parasomnias restless legs syndrome and, concomitant
benzodiazepines for, 83 presentation of, 117
characteristics of, 76 risk factors for, 119120
confusional arousals. See Confusional arousals secondary, 119
def nition of, 76 symptoms of, 120t, 120123, 262
diagnostic criteria for, 80t treatment of, 127129, 263
differential diagnosis, 74, 81, 82t Periodic limb movements, 117, 135, 183
epidemiology of, 7778 Pervasive developmental disorder, 178179
etiology of, 78 Phase advancement, 149
evaluation for, 35 Phase delay, 149150
evaluation of, 81 Phenobarbital, 174, 195
exacerbating factors, 78 Phenylketonuria, 192
management of, 8283 Phenytoin, 174
nightmare seizure disorder vs., 81 Phobias, 69
nightmares vs., 74 Phototherapy, 150151, 184
obstructive sleep apnea and, 106 Physical examination
parental response to, 83 description of, 3738
parental tips for, 84 narcolepsy evaluations, 137
presentation of, 79 obstructive sleep apnea evaluations, 107108
prognosis for, 8384 sleep enuresis evaluations, 97
referrals for, 82 Physiology, 69
risk factors for, 78 PLMD. See Periodic limb movement disorder
scheduled awakening for, 83 Polysomnography
sleep terrors. See Sleep terrors age of child for, 41
sleepwalking. See Sleepwalking apnea-hypopnea index, 110111
treatment of, 8283 def nition of, 38
Pedunculopontine nucleus, 6 description of, 258259
Periodic limb movement disorder indications for, 3839
attention def cit hyperactivity disorder and, 122 American Thoracic Society, 110
characteristics of, 116, 262 headaches, 191
daytime sleepiness secondary to, 121122, 262 insomnia, 157
def nition of, 262 narcolepsy, 137138
228 SUBj ECT INDEx
obstructive sleep apnea, 109111, 111f, 115, Referrals

201 bedtime problems, 54
periodic limb movement disorder, 39, 116, confusional arousals, 82
126, 126f, 201 delayed sleep phase syndrome, 148
restless legs syndrome, 125126 insomnia, 158
parameters measured with, 40 narcolepsy, 140
parental participation in, 41 nightmares, 74
sample, 40f, 111f nighttime fears, 69
scoring of, 41 nightwakings, 62
settings for, 4041, 110, 258 partial arousal parasomnias, 82
transesophageal balloon manometry, 110 sleep enuresis, 97
Positive reinforcement, 56, 244 sleep terrors, 82
Post-traumatic stress disorder, 204205 sleepwalking, 82
Prader-Willi syndrome, 180, 187 Refusal behaviors, 3334
Pramipexole, 128129 Reinforcement
Preschoolers nighttime fears managed through, 244
anticipatory guidance for, 15t nightwakings managed through, 65
developmental issues in, 2223 Relaxation strategies
fears commonly seen in, 68 anxiety disorders managed with, 207
sleep in, 6t, 22, 232 insomnia managed with, 159
Primary insomnia, 147148, 156t nightmares managed with, 75
Primary sleep enuresis, 9495, 254 nighttime fears managed with, 244
Primary snoring, 100101 REM behavior disorder, 74, 178
Propoxyphene, 129 Remeron. See Mirtazapine
ProSom. See Estazolam REM sleep
Provigil. See Modaf nil age-based increased in, 5
PSG. See Polysomnography characteristics of, 4
Psychiatric disorders cholinergic neurons in, 6
depression. See Depression control of, 7, 8f
description of, 197 description of, 1
in developmentally delayed children, 177178 medications that affect, 73
insomnia and, 157158, 205206 muscle atonia, 7
mood disorders. See Mood disorders opiates effect on, 186
Psychiatric history, 213215 in Prader-Willi syndrome patients, 180
Psychophysiological insomnia, 153, 156t rebound in, 175
Psychosocial factors, 10 Renal failure, 192
Psychosocial history, 37 Requip. See Ropinirole
Psychostimulants Resources, 208
attention def cit hyperactivity syndrome treated Respiratory event related arousals, 110
with, 200
Restless legs syndrome
excessive daytime sleepiness treated with,
attention def cit hyperactivity disorder and,
141t, 142
122, 201
mechanism of action, 9
bedtime problems secondary to, 54
sleep effects of, 175
characteristics of, 116
Puberty, 38
daytime sleepiness secondary to, 121122, 261
def nition of, 260
Q delayed sleep phase syndrome vs., 148
diagnosis of
Quality of life, 187 criteria for, 123, 123t125t
Quazepam, 164t, 166t tests used in, 125126
differential diagnosis, 126127, 157
r dopamine agonists for, 129
dopaminergic dysfunction and, 117118
Ramelteon, 165t, 167t, 171 early-onset, 118
Reactive co-sleeping, 22, 66, 186 epidemiology of, 117
Rebound headache, 191 etiology of, 118119, 260
SUBj ECT INDEx 229
evaluation of, 123126 Secondary sleep enuresis, 9495, 254

family history of, 124, 260 Second wind, 23, 26, 52
features associated with, 121122 Security objects, 18, 21, 241, 243, 246
genetic factors, 118, 124, 260 Seizure disorders
insomnia vs., 157 partial arousal parasomnias vs., 81
iron def ciency and, 118119, 128, 261 sleep affected by, 194195
laboratory tests for, 126 sleep enuresis vs., 97
management of, 127129, 261 Selective serotonin reuptake inhibitors. See also
medical conditions associated with, 119 Antidepressants
medications and, 119, 128129, 261 bruxism risks, 91
nightwakings secondary to, 121 cataplexy treated with, 142143
parental tips for, 129 insomnia treated with, 172
pathophysiology of, 117 side effects of, 142
periodic limb movement disorder and, Self-soothing, 1718, 58, 228
concomitant presentation of, 117 Separation anxiety, 12, 54, 205, 245
polysomnography evaluations, 125126 Serotonin agonists, 172
in pregnancy, 119 Serotonin reuptake inhibitors, 9
presentation of, 120t, 120123 Serum ferritin, 118119, 126, 261, 263
prevalence of, 117 Serzone. See Nefazodone
prognosis for, 129 Shift work, 5
resources for, 129 Sickle cell disease, 192193
risk factors for, 118119 SIDS. See Sudden infant death syndrome
screening questionnaire for, 222225 Signalers, 58
sensory complaints associated with, 120121 Sinemet. See Levodopa/carbidopa
symptoms of, 120t, 120123, 260261 Sleep
treatment of, 127129, 261 in adolescents. See Adolescents, sleep in
Restoril. See Temazepam amount of, 13, 45
Rett syndrome, 180 architecture of, 36, 12, 173
Reward systems, 70, 240 as biological process, 1011
Rhinitis, allergy-mediated, 188 cognition functions of, 3
Risk-taking behaviors cultural context of, 22
by adolescents, 2728 def nition of, 1
insuff cient sleep and, 2, 28 factors that affect, 1213
Ritalin. See Methylphenidate family context of, 22
RLS. See Restless legs syndrome functions of, 12
Ropinirole, 128129 in infants, 6t, 12, 228229
Rozerem. See Ramelteon as learned behavior, 1011
medication effects on, 173175, 186
S neuroanatomy of, 69
in newborns, 226227
Scheduled awakening, 83 NREM. See NREM sleep
School-aged children partial loss of, 2
anticipatory guidance for, 15t physiology of, 69
bedtime routines for, 233 in preschoolers, 6t, 22, 232
circadian preferences in, 26 psychosocial factors that affect, 10
developmental issues, 2425 REM. See REM sleep
fears commonly seen in, 68 restorative functions of, 1
sleep in, 24, 233234 in school-aged children, 24, 233234
well-child care for, 24 as social behavior, 17
School history, 36 stages of, 36, 9f
School start times, 3, 2728, 235 time spent in, 1
Screening questions tips for promoting, 237
description of, 31 in toddlers, 6t, 20, 230231
for obstructive sleep apnea, 221 Sleep apnea. See Obstructive sleep apnea
for restless legs syndrome, 222225 Sleep associations, 18, 33, 58, 241
Seasonal affective disorder, 204 Sleep consolidation, 12, 1718
230 SUBj ECT INDEx
Sleep cycles, 46 Sleep drunkenness. See Confusional arousals

Sleep debt Sleep enuresis
in adolescents, 26 alarms for, 98, 255
def nition of, 2 bladder capacity and, 95
Sleep deprivation, 26, 28 bladder training to prevent, 98
Sleep diaries characteristics of, 94
in delayed sleep phase syndrome evaluations, costs of, 96
146 diagnostic criteria for, 96t
description of, 38 differential diagnosis, 97
in insomnia evaluations, 157 emotional effects of, 96
in narcolepsy evaluations, 137 epidemiology of, 94, 254
in partial arousal parasomnias evaluations, 81 etiology of, 9495
sample, 217220 evaluation of, 97
Sleep-disordered breathing. See also Obstructive features associated with, 9596
sleep apnea imipramine for, 98
clinical patterns of, 100101 management of, 9798
craniofacial abnormalities and, 177 obstructive sleep apnea and, 95, 106
description of, 100 parental tips for, 9899, 254255
differential diagnosis, 111 physical examination for, 97
epidemiology of, 101 presentation of, 9596
etiology of, 102104 primary, 9495, 254
evaluation for, 35 referrals for, 97
insomnia vs., 157 risk factors for, 9495
migraine headaches and, 191 secondary, 9495, 254
neurodevelopmental disorders and, 180 treatment of, 9798
in neuromuscular disorder patients, 192 vasopressin production and, 95
obesity and, 103, 193194 voiding before bedtime to prevent, 98
polysomnography evaluations, 3839 Sleep evaluation
presentation of, 104107 bedtime behaviors, 33
risk factors for, 102104 behavioral assessment, 37
snoring, 100 daytime behaviors, 35
symptoms of, 104107 daytime sleep, 35
Sleep disorders. See also specif c disorder developmental history, 36
in adolescents, 28 family history, 3637
in infants, 19 medical history, 36
neurodevelopmental disorders and, 176178 morning awakening, 3536
in preschoolers, 23 nocturnal behaviors, 35
in school-aged children, 25 overview of, 3132
in toddlers, 22 physical examination, 3738
Sleep disturbances polysomnography. See Polysomnography
in adolescents, 2728 psychosocial history, 37
attention def cit hyperactivity disorder and, questionnaire for, 210216
197198 school history, 36
conceptual framework of, 30, 31f screening questions used in, 31
developmental context of, 12 sleep diaries. See Sleep diaries
during hospitalization, 186 sleep history, 3236
in infants, 19 Sleep fragmentation
in narcolepsy, 134135, 265 causes of, 30, 5960
in newborns, 17 in intensive care units, 186
in preschoolers, 23 Sleep habits
prevalence of, 12 bedtime problems managed with changes in,
in school-aged children, 25 5556
in toddlers, 21 daytime, 55
transient, nightwakings vs., 62 description of, 1213, 3233
Sleep drive, 10, 27 Sleep history, 3236, 210213
SUBj ECT INDEx 231
Sleep hygiene bedtime problems and, 54, 57

attention def cit hyperactivity disorder and, evaluation of, 3233
201202 importance of, 19, 23, 45, 57, 237
delayed sleep phase syndrome and, 148, 150, nightwakings managed with, 63
268 sleepwalking managed with, 248
in developmentally delayed children, 181 Sleep spindles, 3
insomnia and, 157158, 271 Sleep terrors
in narcolepsy management, 141 characteristics of, 77
in partial arousal parasomnia management, 83 def nition of, 249
promotion of, 4346, 163 diagnostic criteria for, 80t
in restless legs syndrome management, 128, differential diagnosis, 82t
261 epidemiology of, 78
Sleep inertia, 10, 77 etiology of, 249250
Sleepiness evaluation of, 81
daytime. See Daytime sleepiness management of, 8283
def nition of, 2, 36 parental response to, 83
evaluation of, 34 parental tips for, 84, 250
excessive daytime. See Excessive daytime presentation of, 79
sleepiness risk factors for, 249250
fatigue vs., 185 Sleep training, 64
maximum, 10 Sleepwake cycle
scales for evaluating, 137 in adolescents, 26
Sleeping through the night, 1718 bright light exposure therapy for setting of,
Sleep latency, 138 150151
Sleep onset delayed sleep phase disorder management and,
associations for, 18, 33, 58, 241 268269
bedtime and, 201 morning light exposure effects on, 10
location of, 34 in newborns, 16
Sleep paralysis, 134, 142143, 264 Sleepwalking
Sleep patterns characteristics of, 7677
adolescents, 26 def nition of, 247
evaluation of, 3233 diagnostic criteria for, 80t
infants, 17 differential diagnosis, 82t
newborns, 13, 16 epidemiology of, 7778
preschoolers, 22 etiology of, 247
school-aged children, 24 evaluation of, 81
toddlers, 20 injury risks associated with, 79
Sleep position management of, 8283, 248
for bruxism management, 92 parental response to, 83
for newborns, 16 parental tips for, 84, 248
Sleep regulation presentation of, 79
in infants, 12, 17 prevalence of, 7778
physiology of, 910 prognosis for, 8384
Sleep-related eating disorder, 79 Slow-wave sleep
Sleep related rhythmic movements in depressed patients, 203
body rolling, 8589, 251252 description of, 1, 3
bruxism, 9093, 253 factors that affect, 4
head banging, 8589, 251252 parasomnias during, 76
head rolling, 8589 percentage of, 4
Sleep restriction Smith-Magenis syndrome, 180
insomnia managed with, 158159 Smoking, 43, 103, 175
sleep related rhythmic movements managed Snacks, 46, 237238
with, 89 Snore aids, 114
Sleep schedule Snoring, 100101, 104105, 114115
for adolescents, 235, 238 Sodas, 44t
232 SUBj ECT INDEx
Sodium oxybate, 141t, 143 Triazolam, 164t, 166t

Somnogens, 9 Tricyclic antidepressants. See also
Sonata. See Zaleplon Antidepressants
Status epilepticus, 195 cataplexy treated with, 142143
Stimulants insomnia managed with, 172173
attention def cit hyperactivity syndrome treated mechanism of action, 9
with, 200 partial arousal parasomnias treated with, 83
bruxism risks, 91 side effects of, 142, 173
excessive daytime sleepiness treated with, sleep related rhythmic movements treated with,
141t, 142 89
mechanism of action, 9 Tuberomammillary nucleus, 7
sleep effects of, 175
use of, 23
Stress, 60, 90
u
Sudden infant death syndrome, 16, 19 Ultradian cycles, 4, 6
Supplemental oxygen therapy, 114 Unplanned napping, 35
Suprachiasmatic nucleus, 9 Upper airway obstruction, 102, 111, 192
SWS. See Slow-wave sleep Upper airway resistance syndrome, 101
Systematic desensitization, 75
V
t
Valproic acid, 174
Tea, 44t Vasopressin, 95
Tegretol. See Carbamazepine Venlafaxine, 141t, 142, 175
Television viewing, 3, 2425, 43, 45, 236238 Ventrolateral preoptic area, 7
Temazepam, 164t, 166t Vulnerable child syndrome, 186
Temperament, 60 Vyvanse. See Dextroamphetamine
Tension headaches, 191
Terrors. See Sleep terrors
Theophylline, 174 w
Tiredness, 36
Wait and see approach, for nightwakings, 63
Toddlers
Wakefulness
anticipatory guidance for, 15t
neurotransmitters involved in, 7
bedtime routines for, 21, 230
physiology of, 69
developmental issues in, 2021
regulation of, 910
fears commonly seen in, 68
Weekend oversleep, 35, 145, 236, 238
sleep in, 6t, 20, 230231
Wellbutrin. See Bupropion
Tofranil. See Imipramine
Williams syndrome, 120, 180, 183
Tonsils
adenotonsillectomy, 101, 112113, 115, 192,
257 z
grading of, 109f
hypertrophy of, 102 Zaleplon, 165t166t, 171
Topiramate (Topamax), 174 Zeitgebers, 10
Transesophageal balloon manometry, 110 Zolpidem, 165t166t, 171
Transient insomnia, 54, 157
Transitional objects, 18, 21, 241
Trazodone, 165t, 167t, 172
Sleep Evaluation Questionnaire
ID #
Sleep Evaluation Questionnaire

Directions
Please answer each of the following questions by writing in or choosing the best answer. This
will help us know more about your family and your child.
CHILDS INFORMATION
Childs name: Childs gender: Male Female
Childs birthdate: Childs age:
Childs White/Caucasian Black/African-American Asian American
racial/ethnic Native-American Hispanic-Latino Multi-racial
background: Other
What are your major concerns about your childs sleep?
What things have you tried to help your childs problem?
SLEEP HISTORY
Weekday Sleep Schedule
Write in the amount of time child sleeps during a
24-hour period on weekdays (add daytime and night-
time sleep): ________ hours ________ minutes
The childs usual bedtime on weekday nights: ________ : ________
The childs usual waketime on weekday mornings: ________ : ________
Mindell JA & Owens JA (2010). A Clinical Guide to Pediatric Sleep: Diagnosis and
1
Management of Sleep Problems, 2nd ed. Philadelphia: Lippincott Williams & Wilkins
2 Sl EEp Eva l u a t io n Qu ESt io n n a ir E
Weekend/Vacation Sleep Schedule

Write in the amount of time child sleeps during a
24-hour period during weekends and vacations (add
daytime and nighttime sleep): ________ hours ________ minutes
The childs usual bedtime on weekend/vacation
nights: ________ : ________
The childs usual waketime on weekend/vacation
mornings: ________ : ________
Nap Schedule
Number of days each week child 0 1 2 3 4 5 6 7
takes a nap:
If child naps, write in usual nap time(s):
Nap 1: ________ : ________ a.m. p.m. to ________ : ________ a.m. p.m.
Nap 2: ________ : ________ a.m. p.m. to ________ : ________ a.m. p.m.
General Sleep
Does the child have a regular bedtime routine? yes no
Does the child have his/her own bedroom? yes no
Does the child have his/her own bed? yes no
Is a parent present when your child falls asleep? yes no
Child usually falls Child sleeps most of Child usually wakes in
asleep in the night in the morning in
own room in own bed own room in own bed own room in own bed
(alone) (alone) (alone)
parents room in own bed parents room in own bed parents room in own bed
parents room in parents parents room in parents parents room in parents
bed bed bed
siblings room in own bed siblings room in own bed siblings room in own bed
siblings room in siblings siblings room in siblings siblings room in siblings
bed bed bed
Child is usually put to bed by: Mother Father Both Parents Self Others
Write in the amount of time the child spends
in his/her bedroom before going to sleep: ________ minutes
Child resists going to bed? yes no If yes, do you think this is a problem? yes no
Child has diff culty falling yes no If yes, do you think this is a problem? yes no
asleep?
Child awakens during the yes no If yes, do you think this is a problem? yes no
night?
After nighttime awakening, yes no If yes, do you think this is a problem? yes no
child has diff culty falling
back to sleep?
Child is diff cult to awaken yes no If yes, do you think this is a problem? yes no
in the morning?
Child is a poor sleeper? yes no If yes, do you think this is a problem? yes no
Sl EEp Eva l u a t io n Qu ESt io n n a ir E 3
Current Sleep Symptoms

(b) (c) (d) (e)
(a) not often sometimes often always
never (less than (1 to 2 (3 to 5 (6 to 7 (f)
(does not 1 night/day nights/days nights/days nights/days do not
happen) a week) a week) a week) a week) know
1. Diff culty
breathing when a b c d e f
asleep
2. Stops breathing
a b c d e f
during sleep
3. Snores a b c d e f
4. Restless sleep a b c d e f
5. Sweating when
a b c d e f
sleeping
6. Daytime
a b c d e f
sleepiness
7. Poor appetite a b c d e f
8. Nightmares a b c d e f
9. Sleepwalking a b c d e f
10. Sleeptalking a b c d e f
11. Screaming in
a b c d e f
his/her sleep
12. Kicks legs in
a b c d e f
sleep
13. Wakes up at
a b c d e f
night
14. Gets out of bed
a b c d e f
at night
15. Trouble staying
a b c d e f
in his/her bed
16. Resists going
to bed at a b c d e f
bedtime
17. Grinds his/her
a b c d e f
teeth
18. Uncomfortable
feeling in
his/her legs; a b c d e f
creepy-crawly
feeling
19. Wets bed a b c d e f
Current Daytime Symptoms

(b)
(a) not often (c) (d) (e)
never (less than sometimes often always (f)
(does not 1 days a (1 to 2 days (3 to 5 days (6 to 7 days do not
happen) week) a week) a week) a week) know
1. Trouble getting
a b c d e f
up in the morning
2. Falls asleep in
a b c d e f
school
3. Naps after school a b c d e f
4. Daytime
a b c d e f
sleepiness
5. Feels weak or
loses control of
his/her muscles a b c d e f
with strong
emotions
6. Reports unable
to move when
a b c d e f
falling asleep or
upon waking
7. Sees frightening
visual images
before falling a b c d e f
asleep or upon
waking
PREGNANCY/DELIVERY
Pregnancy Normal Diff cult
Delivery Term Pre-term Post-term
Childs
birthweight:
If no, circle
Only child? Yes No 1st 2nd 3rd 4th 5th 6th 7th
birth order:
MEDICAL AND PSYCHIATRIC HISTORY

PAST MEDICAL HISTORY
Frequent nasal congestion Yes Age of diagnosis:
Trouble breathing through his/her nose Yes Age of diagnosis:
Sinus problems Yes Age of diagnosis:
Chronic bronchitis or cough Yes Age of diagnosis:
Allergies Yes Age of diagnosis: Allergies to what:
Asthma Yes Age of diagnosis:
Frequent colds or f us Yes Age of diagnosis:

Frequent ear infections Yes Age of diagnosis:
Frequent strep throat infections Yes Age of diagnosis:
Diff culty swallowing Yes Age of diagnosis:
Acid ref ux (gastroesophageal ref ux? Yes Age of diagnosis:
Poor or delayed growth Yes Age of diagnosis:
Excessive weight Yes Age of diagnosis:
Hearing problems Yes Age of diagnosis:
Speech problems Yes Age of diagnosis:
Vision problems Yes Age of diagnosis:
Seizures/Epilepsy Yes Age of diagnosis:
Morning headaches Yes Age of diagnosis:
Cerebral palsy Yes Age of diagnosis:
Heart disease Yes Age of diagnosis:
High blood pressure Yes Age of diagnosis:
Sickle cell disease Yes Age of diagnosis:
Genetic disease Yes Age of diagnosis:
Chromosome problem (e.g., Downs) Yes Age of diagnosis:
Skeleton problem (e.g., dwarf sm) Yes Age of diagnosis:
Craniofacial disorder (e.g., Pierre-Robin) Yes Age of diagnosis:
Thyroid problems Yes Age of diagnosis:
Eczema (itchy skin) Yes Age of diagnosis:
Pain Yes Age of diagnosis:
PAST PSYCHIATRIC/PSYCHOLOGICAL HISTORY
Autism Yes Age of diagnosis:
Developmental delay Yes Age of diagnosis:
Hyperactivity/ADHD Yes Age of diagnosis:
Anxiety/Panic Attacks Yes Age of diagnosis:
Obsessive Compulsive Disorder Yes Age of diagnosis:
Depression Yes Age of diagnosis:
Suicide Yes Age of diagnosis:
Learning disability Yes Age of diagnosis:
Drug use/abuse Yes Age of diagnosis:
Behavioral disorder Yes Age of diagnosis:
Psychiatric Admission Yes Age of diagnosis:
Please list any additional psychological psychiatric, emotional, or behavioral problems diag-
nosed or suspected by a physician/psychologist
CURRENT MEDICAL HISTORY

Please list any medications your child currently takes:
Medicine Dose How often:
1.
2.
3.
4.
LONG-TERM MEDICAL PROBLEMS
If your child has long-term medical problems, please list the three you think are most
important.
1.
2.
3.
SURGERIES/HOSPITALIZATIONS
Has your child ever had his/her tonsils removed? Yes Age of surgery:
Has your child ever had his/her adenoids removed? Yes Age of surgery:
Has your child ever had ear tubes? Yes Age of surgery:
Please list any additional hospitalizations or surgeries:
HEALTH HABITS
Does your child drink caffeinated No Yes Amount per day:
beverages? (e.g., Coke, Pepsi,
Mountain Dew, iced tea)
SCHOOL PERFORMANCE
CURRENT SCHOOL PERFORMANCE (if school-aged)
Your childs grade:
Has your child ever repeated a grade? No Yes
Is your child enrolled in any special education class? No Yes
How many school days has your child missed so far this year?
How many school days did your child miss last year?
How many school days was your child late so far this year?
How many school days was your child late last year?
Childs grades this year: Excellent Good Average Poor Failing
Childs grades last year: Excellent Good Average Poor Failing
FAMILYS INFORMATION
MOTHER FATHER
Age Age
Marital Single Divorced Separated Marital Single Divorced Separated
Status: Married Widowed Remarried Status: Married Widowed Remarried
Education: Education:
Work: Unemployed Part-time Full-time Work: Unemployed Part-time Full-time
Occupation: Occupation:
PERSONS LIVING IN HOME
Name Relationship Age
FAMILY SLEEP HISTORY

Does anyone in the family have a sleep disorder? Yes No
If yes, mark the disorder(s):
Insomnia Mother Father Brother/sister Grandparent
Snoring Mother Father Brother/sister Grandparent
Sleep apnea Mother Father Brother/sister Grandparent
Restless legs syndrome Mother Father Brother/sister Grandparent
Periodic limb movement disorder Mother Father Brother/sister Grandparent
Sleepwalking/sleep terrors Mother Father Brother/sister Grandparent
Sleep talking Mother Father Brother/sister Grandparent
Narcolepsy Mother Father Brother/sister Grandparent
Other: Mother Father Brother/sister Grandparent
REFERRAL
Who asked that your child be seen by a sleep specialist?
Pediatrician/Family physician
Childs parent or guardian
Surgical specialist (e.g., ENT)
Pediatric specialist (e.g., allergist, neurologist, pulmonologist
Mental health specialist (e.g., psychiatrist, psychologist, social worker)
School teacher, nurse, counselor
Child himself/herself
Other:
Questionnaire Copyright 2000 by The Childrens Hospital of Philadelphia.
1
Sleep Diaries
2
PEDIATRIC SLEEP LOG
Your name: ___________________________________________________
Your birth date: _____ / _____ / _____
Example:
Date Day Shade in the periods when you were asleep. Mark your bedtime and any nap times with downward arrows.
1
2
Mark the time you get up in the morning
and after any naps with upward arrows.
Mid- Mid-
Date Day night 2 AM 4 AM 6 AM 8 AM 10 AM Noon 2 PM 4 PM 6 PM 8 PM 10 PM night
Sleep Diary
Every morning when you get up complete the sleep diary for the previous night.
For example, on Monday morning f ll in the information for Sunday night.
Last night This morning It took me ____ minutes Total amount

Day I went to bed at I woke up at: to fall asleep of sleep:
Example:
Sunday 12:15 9:20 25 910
3
4
DAY: _____________________________________________
Morning
Time child woke in AM: ________________________ Child was awakened by: Self
Parent
Time child got out of bed: _______________________ Sibling/other
Mood on waking: 1 2 3 4 5 (circle one) Alarm
Unhappy Happy
Naps and Daytime Sleepiness
Time(s) and lengths of plannede nap(s) during the day:
Did child fall asleep today (check all that apply): ______ riding in the car?
______ watching TV?
______ while eating?
______ while pllaying?
______ in school?
______ other? Please describe ________________________________________________________
Bedtime
Time went to bed in PM (lights out): _________________________
Describe any problems going to bed: ____________________________________________________________________________________
____________________________________________________________________________________
____________________________________________________________________________________
____________________________________________________________________________________
Time child actually fell asleep: _____________________________
Night Wakings
Time(s) and length(s) of night waking:
Time awoke: 1) Back to sleep: 1) Brief y describe what happened: 1)
2) 2) 2)
3) 3) 3)
4) 4) 4)
Screening Questionnaire for
o bstructive Sleep a pnea
Screening Questionnaire: Obstructive Sleep Apnea

Name: __________________________________
Person completing form: ____________________________________ Date: ____/____/____
Please answer the following questions as they pertain to your child in the past month.
1. While sleeping, does your child:
Snore more than half the time?. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Always snore? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Snore loudly? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Have heavy or loud breathing? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Have trouble breathing, or struggle to breathe? . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
2. Have you ever seen your child stop breathing during the night? . . . . . . . . . Y N DK
3. Does your child:
Tend to breathe through the mouth during the day? . . . . . . . . . . . . . . . . . . . . . . Y N DK
Have a dry mouth on waking up in the morning?. . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Occasionally wet the bed? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
4. Does your child:
Wake up feeling unrefreshed in the morning? . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Have a problem with sleepiness during the day? . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
5. Has a teacher or other supervisor commented that your child
appears sleepy during the day? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
6. Is it hard to wake your child up in the morning? . . . . . . . . . . . . . . . . . . . . . Y N DK
7. Does your child wake up with headaches in the morning? . . . . . . . . . . . . . . Y N DK
8. Did your child stop growing at a normal rate at any time since birth? . . . . Y N DK
9. Is your child overweight? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
10. This child often:
Does not seem to listen when spoken to directly. . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Has diff culty organizing tasks and activities. . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Is easily distracted by extraneous stimuli. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Fidgets with hands or feet or squirms in seat. . . . . . . . . . . . . . . . . . . . . . . . . . . Y N DK
Is on the go or often acts as if driven by a motor. . . . . . . . . . . . . . . . . . . . . Y N DK
Interrupts or intrudes on others (e.g., butts into conversations or games) . . . . . Y N DK
Scoring Yes = 1 No = 0
Average all scores to obtain a score between 0.00 and 1.00. Preliminary analyses suggest a cut-
off of >0.33 for abnormal.
(For more information see Chervin RD, Hedger K, Dillon JE, Pituch KJ (2000). Pediatric
Sleep Questionnaire (PSQ): validity and reliability of scales for sleep-disordered breathing, snor-
ing, sleepiness, and behavioral problems. Sleep Medicine 1:21-32.)
1
Screening Questionnaire for
RESTLESS SLEEP QUESTIONNAIRE

(PARENT)
Childs Name __________________________________________________
Person f lling out form (circle one): Mother Father Other (specify): ___________________
Dont
Yes No Know
1. Does your child complain of
uncomfortable or funny feelings
(creepy-crawly, tingling, burning,
squeezing, etc.) in his/her legs?
Occasionally Sometimes Frequently
If yes, do these funny feelings in (less than (12x/ (12x/wk Dont
his/her legs: Never 1x/month) month) to daily) Know
a. Seem worse when lying down
or sitting still?
b. Get better or go away with
movement (wiggling feet, toes,
or walking)?
c. Seem worse at night?
Dont
Yes No Know
2. Does your child feel like he or
she has an urge to (needs to or
has to) move his/her legs?
If yes, does this need to move (less than (12x/ (12x/wk Dont
his/her legs: Never 1x/month) month) to daily) know
or sitting still?
b. Get better or go away with
or walking)?
c. Seem worse at night?
1
2 Sc r EEn in g Qu ESt io n n a ir E f o r r ESt l ESS l Eg S Syn Dr o mE

(less than (12x/ (12x/wk Dont
Never 1x/month) month) to daily) Know
3. Does your child having growing
pains?
4. Does your child f dget or wiggle
his/her feet or toes when sitting
or lying down?
5. Does your child have repeated
jerking or kicking movements in
the toes or legs while sleeping?
6. Does your child appear restless
while sleeping (thrashing around,
banging feet against wall,
throwing off covers, or falling out
of bed)?
7. Does your child seem more
restless, f dgety or hyperactive
than most children his/her age?
9. a. Has anyone in the family (including parent, grandparents, siblings) been diagnosed with
restless legs? Yes No Dont know
If so, who: ______________________________________
b. Has anyone in the family (including parent, grandparents, siblings) been diagnosed with
periodic leg movements during sleep? Yes No Dont know
If so, who: ______________________________________
c. Does anyone in the family (including parent, grandparents, siblings) have severe problems
falling or staying asleep? Yes No Dont know
If so, who: ______________________________________
Has your child ever been diagnosed and/or treated for iron-def ciency anemia?
Yes No Dont know
If yes, when? ________________
Type of treatment: ________________________________________________
Sc r EEn in g Qu ESt io n n a ir E f o r r ESt l ESS l Eg S Syn Dr o mE 3
RESTLESS SLEEP QUESTIONNAIRE

(ADOLESCENT)
Your Name _________________________________________________________________

Dont
Yes No know
1. Do you ever have uncomfortable
or funny feelings (creepy-crawly,
tingling, burning, squeezing, etc)
in your legs?
If yes, do these funny feelings in (less than (12x/ (12x/wk Dont
your legs: Never 1x/month) month) to daily) Know
or sitting?
b. Have partial relief with
or walking)?
c. Feel worse at night?
d. Have a lot of f dgeting or
wiggling of the feet or toes
when sitting or lying down?
e. Have repeated jerking
movements in toes or legs
or the whole body while
sleeping?
Dont
Yes No know
2. Do you ever feel like you need
to or have to move your legs?
If yes, does this need: Never 1x/month) month) to daily) Know
or sitting?
or walking)?
c. Feel worse at night?
sleeping?
4 Sc r EEn in g Qu ESt io n n a ir E f o r r ESt l ESS l Eg S Syn Dr o mE

Never 1x/month) month) to daily) Know
3. Do you have growing pains?
4. Do you f dget or wiggle your
feet or toes when sitting or lying
down?
Dont
5. Do you ever: Yes No Know
a. Notice funny feelings in your
legs (or do they seem worse)
when lying down or sitting?
or walking)?
c. Complain that the feelings are
worse at night?
sleeping?
Sleep in n ewborns
(02 months)
WHAT TO EXPECT
Newborns sleep between 10 and 19 hours per day (average is 13 to 14.5 hours), with no regular
or def ned pattern. For the f rst few weeks, your baby will sleep for anywhere from a few minutes
to a few hours at a time, although babies who are breast-fed tend to sleep for shorter periods (13
hours of sleep) than do bottle-fed babies (25 hours). There will also be little difference between
nighttime and daytime sleep patterns in the f rst few weeks. However, you will start to see a more
regular sleep schedule develop between 2 and 4 months of age. Expect your baby to be quite ac-
tive while he sleeps. All babies smile, grimace, suck, snuff e, and move (twitch, jerk) while they
sleep. This is perfectly normal, and your baby is getting sound sleep.
WHERE AND HOW SHOULD YOUR BABY SLEEP?

n Sleeping arrangements: There are many choices as to where your newborn sleeps, whether in
a bassinet or a crib in the parents bedroom, a siblings bedroom, or the babys own room. For
a variety of reasons, some parents prefer to have their baby sleep in bed with them. However,
you should be aware that there is a small but real risk of accidental suffocation associated with
this practice in infants under age 1 year. If you choose to share a bed with your infant, please
discuss this with your babys doctor, to make sure you are doing so under the safest possible
conditions. For example, you should not share a bed with your baby if you are taking sedating
medications, have consumed alcohol, or if you smoke.
n Back to sleep: All babies should be put to sleep on their backs to reduce the risk of sudden
infant death syndrome.
Safe Sleep Practices for Newborns

Place your baby on his back to sleep at night and during naptimes.
Place your baby on a f rm mattress with a well-f tting sheet in a safety-approved crib with
slats no greater than 238 inches apart.
Make sure your babys face and head stay uncovered and clear of blankets and other cover-
ings during sleep. If a blanket is used, make sure your baby is placed feet-to-foot (feet at
the bottom of the crib, blanket no higher than chest-level, blanket tucked in around mattress)
in the crib. Remove all pillows and stuffed toys from the crib. Consider using a sleeper rather
than a blanket.
Create a smoke-freezone around your baby.
Avoid overheating your baby during sleep and maintain your babys bedroom at a tempera-
ture comfortable for an average adult.
Never have your baby sleep on a chair, couch, in a bureau drawer, or on any furniture that is
not designed specif cally for sleeping.
1
2 Sl EEp in n Ewbo r n S (02 mo n t h S)
HOW TO HELP YOUR NEWBORN BECOME A GOOD SLEEPER

n Learn your babys signs of being sleepy: Some babies fuss or cry when they are tired, whereas
others rub their eyes, stare off into space, or pull on their ears. Your baby will fall asleep more
easily and more quickly if you put him down to sleep when he lets you know that he is tired.
n Encourage nighttime sleep: Many newborns have their days and nights reversed, sleeping
much of the day and being awake much of the night. To help your baby sleep more at night,
keep lights dim during the night and keep play to a minimum. During the day, play with your
baby and be sure to wake him regularly for feedings and play time. Morning exposure to natu-
ral light can also help, so head out for a walk in the morning.
n Respond to your babys sleep needs: Newborns often need to be rocked or fed to sleep,
which is f ne for the f rst few weeks or months. However, once your baby is 2 to 3 months old,
begin to establish good sleep habits.
n Develop a bedtime routine: Even babies as young as a few weeks respond well to bedtime
routines. Your newborns bedtime routine should be soothing and can include any activities
you choose, such as bathing, rocking, and cuddling.
n Sleep when your baby sleeps: Parents need sleep also. Try to nap when your baby naps, and
be sure to ask others for help so that you can get some rest.
n Contact your doctor if you are concerned: Babies who are extremely fussy or frequently dif-
f cult to console may have a medical problem, such as colic or ref ux. Also, be sure to contact
your doctor if your baby ever seems to have problems breathing during the night.
Sleep in infants (212 months)
WHAT TO EXPECT
Infants, on average, sleep between 9 and 10 hours during the night and nap for between 3 and 4
hours during the day. Especially in the f rst year, though, there is great variability in how much
individual babies sleep. At 2 months, infants usually take between two and four naps each day,
and by 12 months, they take either one or two naps. Expect factors such as illness or a change in
routine to disrupt your babys sleep. Developmental milestones, including pulling to standing and
crawling, may also temporarily disrupt sleep.
By 6 months of age, most healthy full-term babies are physiologically capable of sleeping
through the night and no longer require middle-of-the-night feedings. However, 25% to 50% of
babies continue to awaken during the night. Short nightwakings are part of a normal sleep pat-
tern; in fact, all babies on average wake brief y between 2 and 6 times a night. Babies who are
able to soothe themselves back to sleep (self-soothers) awaken for a few minutes and go right
back to sleep on their own. In contrast, signalers are those babies who cry or fuss, awaken their
parents, and need their help to get back to sleep. Many of these signalers have not developed the
ability to fall asleep on their own and, thus, have diff culty self-soothing. This is often the result
of parents developing the habit of helping their baby to fall asleep at bedtime by rocking, feeding,
holding, or bringing their child into their own bed. Over time, babies may learn to rely on this
kind of help from their parents in order to fall asleep. Although this may not be a problem at bed-
time, it may lead to diff culties with your baby failing back to sleep on her own during the night.
Safe Sleep Practices for Infants

Place your baby on her back to sleep at night and during naptimes.
Place your baby on a f rm mattress with a well-f tting sheet in a safety-approved crib with
slats no greater than 238 inches apart.
Make sure your babys face and head stay uncovered and clear of blankets and other cover-
ings during sleep. If a blanket is used, make sure your baby is placed feet-to-foot (feet at
the bottom of the crib, blanket no higher than chest-level, blanket tucked in around mattress)
in the crib. Remove all pillows and stuffed toys from the crib. Consider using a sleeper rather
than a blanket.
Create a smoke-freezone around your baby.
Avoid overheating your baby during sleep and maintain your babys bedroom at a tempera-
ture comfortable for an average adult.
Remove all mobiles and hanging crib toys by about the age of 5 months, when your baby
begins to pull up in the crib.
If you choose to share a bed with your baby, please discuss this with your babys doctor to
make sure you are doing so under the safest possible conditions, as there is a small but real
risk of accidental suffocation associated with this practice in infants under age 1 year. For
example, you should not share a bed with your baby if you are taking sedating medications,
have consumed alcohol, or if you smoke.
Never have your baby sleep on a chair, couch, in a bureau drawer, or on any furniture that is
not designed specif cally for sleeping.
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HOW TO HELP YOUR INFANT SLEEP WELL

n Learn your babys signs of being sleepy: Some babies fuss or cry when they are tired, whereas
others rub their eyes, stare off into space, or pull on their ears. Your baby will fall asleep more
easily and more quickly if you put her down the minute she lets you know that she is sleepy.
n Decide where your baby is going to sleep: Try to decide by 3 months of age where your baby
is going to sleep over the long run, as changes in sleeping arrangements will be harder on your
baby as she gets older. For example, if your baby is sleeping in a bassinet, move her to a crib
by age 3 months. For a variety of reasons, including ease of breast feeding, some parents prefer
to have their baby sleep in bed with them. If your baby is sharing your bed, decide whether you
want to continue this arrangement and make sure you are doing so in the safest way possible.
n Develop a daily sleep schedule: Babies sleep best when they have consistent sleep times and
waketimes. Note that cutting back on naps to encourage nighttime sleep often results in over-
tiredness and a worse nights sleep.
n Encourage use of a security object: Once your baby is old enough (by age 12 months), in-
troduce a transitional or love object, such as a stuffed animal, a blanket, or a tee-shirt that was
worn by you (tie it in a knot). Include it as part of your bedtime routine, at naptime, and when-
ever you are cuddling or comforting your baby. Dont force your baby to accept the object, and
realize that some babies never develop an attachment to a single item.
n Develop a bedtime routine: Establish a consistent bedtime routine that includes calm and en-
joyable activities, such as a bath and bedtime stories, and that you can stick with as your baby
gets older. The activities occurring closest to lights out should occur in the room where your
baby sleeps. If an evening feeding is part of the bedtime routine, make the feeding the f rst step
in the routine and avoid letting your baby fall asleep while nursing or bottle-feeding.
n Set up a consistent bedroom environment: Make sure your childs bedroom environment is
the same at bedtime as it is throughout the night (e.g., lighting). Also, babies sleep best in a
room that is dark, cool, and quiet.
n Put your baby to bed drowsy but awake: Starting at about 3 months of age, put your baby to
bed drowsy but awake after your bedtime routine. This practice will encourage her to soothe
herself to sleep and fall asleep independently, without needing to be held or fed or rocked.
Babies who learn to fall asleep on their own at bedtime are able to fall back to sleep without
parents help when they naturally awaken during the night.
n Sleep when your baby sleeps; parents need sleep also: Try to nap when your baby naps, and
be sure to ask others for help so you can get some rest.
n Contact your doctor if you are concerned: Babies who are extremely fussy or frequently dif-
f cult to console may have a medical problem, such as colic or ref ux. Also, be sure to contact
your doctor if your baby ever seems to have problems breathing during the night.
Sleep in t oddlers (13 years)
WHAT TO EXPECT
Toddlers sleep, on average, between 11 and 13 hours across the day and night. By age 18 months,
most toddlers have given up their morning nap and are taking one long afternoon nap of 1.5 to 3
hours. Some toddlers, though, will continue taking 2 shorter naps a day until age 20 or 21 months.
The number of hours a toddler sleeps will be different for each child, but expect your toddler to
sleep about the same amount each day. Anticipate that sleep may be disrupted by illness, changes
in routine, and other stressful events. Separation anxiety may also cause problems at bedtime.
Most toddlers switch from a crib to a bed between 2 and 3 years of age, but it is better to wait until
closer to age 3 years. If the change happens too early, it can disrupt sleep. In this case, switch back
to the crib and try again when your child is older.
Many toddlers continue to awaken during the night, usually as a result of poor sleep habits.
All children wake brief y throughout the night. However, a toddler who has not learned how to
fall asleep on his own at bedtime, such as needing to be rocked or have a parent lie down with
him, will not be able to return to sleep without help when he naturally awakens during the night.
HOW TO HELP YOUR TODDLER SLEEP WELL

n Develop a daily sleep schedule: Have a regular bedtime, waketime, and nap times, bedtime
that ensures adequate nighttime sleep. In general, avoid late bedtimes (after 9:00 p.m.) for your
toddler. Although his morning schedule may allow him to sleep in, morning light and house-
hold activity may wake him up and prevent him from getting enough sleep. Having an early
bedtime will also help establish a routine that will be compatible with childcare and preschool
start times. In addition, napping too late in the afternoon can make it hard for your toddler to
fall asleep at bedtime, but avoid cutting back on naps as a way of encouraging nighttime sleep,
as this will result in overtiredness and a worse nights sleep.
n Encourage use of a security object: Helping your toddler become attached to a security
object that he can keep in bed with him can be benef cial. This often helps a child feel more
relaxed at bedtime and throughout the night.
n Develop a bedtime routine: Establish a consistent bedtime routine that includes calm and
enjoyable activities, such as a bath and bedtime stories. Avoid including television viewing as
part of the bedtime routine, as this interferes with falling asleep. The activities occurring clos-
est to lights out should occur in the room where your toddler sleeps.
n Set up a consistent bedroom environment: Make sure your childs bedroom environment is
the same at bedtime as it is throughout the night. Some older toddlers may f nd a night-light
reassuring. Also, toddlers sleep best in a room that is cool and quiet. Dont put a television or
computer or a gaming system in your childs bedroom.
n Put your toddler to bed drowsy but awake: Encourage your toddler to fall asleep indepen-
dently by putting him to bed drowsy but awake. This will enable him to fall back to sleep on
his own when he naturally awakens during the night.
n Set limits: If your toddler stalls at bedtime, be sure to set clear limits ahead of time, such as
how many books you will read.
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n Contact your childs doctor if:

n Your child appears to have any trouble breathing, snores, or is a noisy breather.
n Your child has unusual nighttime awakenings or signif cant nighttime fears that are concern-
ing.
n Your child has diff culty falling asleep, staying asleep, and/or if sleep problems are affecting
his behavior during the day.
Sleep in preschoolers
(35 years)
WHAT TO EXPECT
Preschoolers sleep, on average, between 9 and 10 hours (nighttime sleep plus naps). The number
of hours a preschooler sleeps will be different for each child, but expect your preschooler to sleep
for about the same amount of time each day. Most preschoolers stop taking naps between 3 and 5
years of age. Some preschoolers continue to awaken during the night, usually as a result of poor
sleep habits. All children normally wake brief y throughout the night. However, a preschooler
who has not learned how to fall asleep on her own at bedtime, such as needing a parent to lie
down with her, will not be able to return to sleep without help during the night.
Sleep problems are common during the preschool years, including nighttime fears and night-
mares. Typically, these nighttime fears and nightmares are a normal part of development during
this stage, and will lessen over time. Sleepwalking and sleep terrors often f rst appear during the
preschool years. In addition, snoring, although common, may be a sign of sleep apnea.
HOW TO HELP YOUR PRESCHOOLER SLEEP WELL

n Develop a regular sleep schedule: Your preschooler should go to bed and wake up about the
same time each day, on a schedule that allows her to get adequate sleep. Also, be sure that
your child is ready for sleep before putting her to bed. This may seem obvious, but you may
f nd, for example, that your preschooler has a second wind (being more alert and more ac-
tive) in the evening right around bedtime. Moving bedtime a bit later will often avoid bedtime
struggles. However, in general, late bedtimes (after 9:00 p.m.) should be avoided. Although
your preschoolers morning schedule may allow her to sleep in, morning light and household
activity may wake her up and prevent her from getting enough sleep. An early bedtime also
helps establish a routine that will be compatible with childcare and kindergarten start times.
n Maintain a consistent bedtime routine: Establish a bedtime routine that is the same every
night and includes calm and enjoyable activities, such as a bath and bedtime stories. Avoid in-
cluding television viewing as part of the bedtime routine, as this interferes with falling asleep.
The activities occurring closest to lights out should occur in the room where your pre-
schooler sleeps. Making a bedtime chart that shows all the steps of the bedtime routine can
help keep a preschooler on track and help provide predictability.
n Set up a soothing sleep environment: Make sure your childs bedroom is comfortable, dark,
cool, and quiet. A nightlight is f ne; a television, computer, or gaming system is not.
n Set limits: If your preschooler stalls at bedtime, be sure to set clear limits ahead of time, such
as how many books you will read.
n Avoid caffeine: Do not allow your child to have caffeinated beverages or products (soda, en-
ergy drinks), as these may result in disrupted nighttime sleep.
n Contact your childs doctor if:
n Your child appears to have any trouble breathing, snores, or is a noisy breather.
n Your child has unusual nighttime awakenings or signif cant nighttime fears that are concern-
ing.
n Your child has diff culty falling asleep, staying asleep, and/or if her sleep problems are af-
fecting her behavior during the day.
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Sleep in School-a ged
c hildren (612 years)
WHAT TO EXPECT
School-aged children typically need between 10 and 11 hours of sleep per night, but many aver-
age between 9 and 10 hours of sleep. Not getting enough sleep is becoming more common in this
age group, often as a result of increasing school obligations (e.g., homework), extracurricular
activities, increased evening use of electronics (television, computers, cell phones), and later bed-
times. Sleep problems are also common in the school-aged child. These include diff culty fall-
ing and staying asleep, sleepwalking, sleep terrors, teeth grinding, nighttime fears, nightmares,
bedwetting, snoring, and noisy breathing. However, as children get older, parents often become
less aware that their child is having sleep problems. Be sure and know the signs that indicate your
child may not be getting enough sleep, including the following.
n Moodiness: Inadequate sleep may cause your school-aged child to be moody, irritable, and
cranky, as well as to become frustrated or upset more easily.
n Behavior problems: School-aged children who do not get enough sleep are more likely to
have behavior problems, such as noncompliance, aggressiveness, poor impulse control, and
hyperactivity. Even just 30 to 60 minutes less sleep than he needs can affect your childs
behavior.
n Poor thinking skills: Inadequate sleep may result in problems with attention, memory, de-
cision-making, organization, and creativity, all of which are clearly important for success in
school.
n Dozing off: School-aged children are normally wide awake during the day. This means that if
they are falling asleep in class, in the car, or in front of the TV on a regular basis, something
is wrong! Assume, until proven otherwise, that if this is happening to your child, that he is not
getting enough sleep or the sleep he is getting is not good quality, or both.
n Weight problems: Many studies have now shown that there is a link between not getting
enough sleep and being overweight or obese in both children and adults. This association is
most likely related to the effects of sleep loss on chemical substances in the body that control
hunger and appetite. That is, children who sleep less are hungrier and tend to eat more. They
may also exercise less because they are tired. Being overweight is also an important risk factor
for sleep apnea in children.
HOW TO HELP YOUR SCHOOL- AGED CHILD SLEEP WELL

n Develop a regular sleep schedule: Your child should go to bed and wake up at about the same
time each day. Set (and stick to) a bedtime that ensures that your child gets enough sleep, pref-
erably before 9:00 p.m.
n Maintain a consistent bedtime routine: School-aged children continue to benef t from a
bedtime routine that is the same every night and includes calm and enjoyable activities, such
as reading. Including one-on-one time with a parent is helpful in maintaining communication
with your child and having a clear connection every day.
n Set up a soothing sleep environment: Make sure your childs bedroom is comfortable, dark,
cool, and quiet. A nightlight is f ne; a television, computer, or gaming system is not.
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n Make sleep a priority: As school-aged kids become more and more involved in academic,
social, athletic, and other activities, sleep often becomes less of a priority for families. Parents
work and activity schedules spilling over into the evening hours may also conf ict with time
for sleep, by pushing the dinner hour and homework time later and later. Older school-aged
children may need adult help in managing their time in the evening, so they can get to bed at a
reasonable hour.
n Set limits: If your school-aged child stalls at bedtime, be sure to set clear limits ahead of time,
such as what time lights must be turned off and how many stories you will read together.
n Turn off televisions, computers, and radios: Television viewing, computer game playing,
Internet use, and other stimulating activities just before or at bedtime will often result in sleep
problems. Children also can become dependent upon the TV in order to fall asleep.
n Avoid caffeine: Caffeine can be found in sodas, coffee-based products, iced tea, energy drinks,
and many other substances.
n Contact your childs doctor: Speak to your childs physician if your child has diff culties fall-
ing asleep or staying asleep, snores, experiences unusual awakenings, or has sleep problems
that are causing disruption during the day.
Sleep in a dolescents
(1318 years)
WHAT TO EXPECT
The vast majority of adolescents do not get enough sleep. Research has shown that the average
teenager needs 9 to 9 1/4 hours of sleep a night. This is not all that much less than how much sleep
school-aged children need. However, the average amount of sleep that teenagers get is about 7
hours on school nights. Even on weekends and holidays, when they try to catch up, teenagers
average just 9 hours of sleep. This leads to teenagers missing an average of 2 hours of sleep per
night, and it accumulates over time.
There are a number of reasons why teenagers do not get enough sleep:
n Shift in sleep schedule: After puberty, there is a normal biological shift in an adolescents
internal clock of about 2 hours. This means, for example, that a 14-year-old who used to fall
asleep easily at 9:00 p.m., will have diff culty falling asleep before 11:00 p.m. The time that
teenagers naturally wake up also shifts 2 hours later. This makes it extremely diff cult for them
to get up early (before 7:00 a.m. or 8:00 a.m.).
n Early high school start times: Just at the same time that teenagers internal clocks are shift-
ing later, in most school districts they are switching to high school which starts even earlier in
the morning. Some high schools start as early as 7:00 a.m., which means that some teenagers
have to get up as early as 5:00 a.m. to get ready for and travel to school. Not only does this
result in inadequate sleep, but also requires adolescents to get up for school when they are least
alert (that is, the during the 2 hours just before their natural waketime).
n Social and school obligations: This tendency toward falling asleep later is greatly com-
pounded by homework, sports, after-school activities (often occurring during the evening),
and socializing. These activities also lead to going to bed late. Working after school is another
common cause of not getting enough sleep. In addition, many teens engage in sleep-interfering
activities (computer games, online chat rooms, text messaging) even after lights out. These
activities tend to increase as teens get older, with high school seniors getting the least amount
of sleep just when they need to be at their best academically.
n Erratic sleep schedule: Many teenagers stay up later on non-school nights. They also often
sleep in on weekends until noon or 1:00 p.m., in an attempt to catch up on lost sleep. Al-
though this may seem like a good idea, it can contribute to sleep problems. By going to bed so
much later on Friday and Saturday, it makes it even more diff cult to fall asleep at a reasonable
time on Sunday night. Its like the jet lag you might experience from f ying from the East
Coast to California and back every weekend.
n Caffeine consumption: Teenagers are increasingly turning to caffeine, like coffee and energy
drinks to combat the effects of not getting enough sleep. Some are also buying super-caffein-
ated products, like caffeine pills and gums as well as taking prescription stimulants, such as
Ritalin and Adderall. Not only are these things potentially addictive and physically harmful
(and in some cases, even illegal), but also they may disrupt nighttime sleep.
As a result of all these factors, most adolescents are chronically sleep deprived. Not getting
enough sleep will affect many aspects of your teenagers functioning.
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2 Sl EEp in a Do l ESc En t S (1318 yEa r S)
n Mood: Sleep-deprived teenager are often moody, irritable, and cranky and are more likely to
get frustrated or upset more easily. Not getting enough sleep has also been linked to depression
in teens.
n Behavior: Teenagers who are sleep deprived are often more impulsive and more likely to en-
gage in risk-taking behaviors, such as drinking, driving fast, and engaging in other dangerous
activities.
n Cognitive ability: Not getting enough sleep may result in problems with attention, memory,
decision-making, organization, and creativity, all which are clearly important for success in
school.
n School performance: Many high-achieving, college-bound high school students state that
they have to stay up late in order to get their homework done and participate in extracurricu-
lar and athletic activities. However, studies actually show that students who get better grades
sleep more, not less. Not getting enough sleep in teenagers is also associated with getting to
school late and missing school as well as poor performance on standardized tests. Further-
more, people who are sleep-deprived are less eff cient, thus a cycle develops in which a student
takes longer to complete the same amount of work, leading to her staying up later, and starting
the vicious cycle all over again.
n Drowsy driving: Teenagers, especially older teenage boys, are at the highest risk for falling
asleep at the wheel. The most common drowsy driving accident involves a single vehicle with
a single driver who drives off the road. These accidents most often happen late at night and
in the middle of the afternoon. So dont be fooled that just because it is bright daylight, your
teen wont fall asleep at the wheel. In addition, all teens who are not getting enough sleep are
at risk, especially when a beer or two, marijuana, and relative driving inexperience compound
lack of sleep.
HOW TO HELP TEENAGERS SLEEP WELL

n Maintain a regular sleep schedule: Your teenager should go to bed and wake up at about the
same time (within an hour or so) on weekdays and on weekends. Also, your teenager should
go to bed early enough so that she can get her required 9 hours of sleep.
n Avoid sleeping-in on weekends: Although catching up on some sleep on the weekends can
be helpful, sleeping in until noon on Saturday and Sunday will make it hard for your teenager
to get back on a school schedule in time for Monday morning classes.
n Make sleep a lifestyle priority for the whole family: Keep an eye on potential sleep steal-
ers like late-night activities, after-school employment, and after-hours electronics use. Help
your teenager manage her time better, so that she can get to bed on time.
n Take early afternoon naps: For teens who just cant arrange their schedules to get enough
sleep every night, a brief nap (30 minutes or less) in the afternoon can temporarily help sleepi-
ness. However, this is not a good long-term solution to the problem of chronically not getting
enough sleep.
n Turn off televisions, computers, and radios: Late night television viewing, computer game
playing, Internet use, text messaging, and similar activities at bedtime can result in problems
falling and staying asleep. Even the low light level of a computer or television screen can shift
your teens internal clock even later. Ideally, all electronic devices should be removed from
your teenagers bedroom.
n Avoid caffeine, smoking, alcohol, and drugs: All of these substances may interfere with
sleep. In particular, make sure that your teen understands that caffeine does not counteract or
reverse the effects of alcohol.
n Discuss the dangers of drowsy driving: Do not allow your teenager to drive without getting
enough sleep or to ride in a car with a sleep-deprived driver.
n Contact your teenagers doctor: Speak to your adolescents physician if she has diff culties
falling asleep or staying asleep, snores, or seems excessively sleepy during the day.
Sleep t ips for c hildren
The following recommendations will help your child get the best sleep possible and make it
easier for him to fall asleep and stay asleep.
n Sleep schedule: Your childs bedtime and waketime should be about the same time everyday.
There should not be more than 1 hours difference in bedtime and waketime between school
nights and non-school nights. Make your childs bedtime early so that he can get enough sleep.
n Bedtime routine: Your child should have a 20-minute to 30-minute bedtime routine that is the
same every night. The routine should include calm activities, such as reading a book or talking
about the day, with the last part occurring in the room where your child sleeps.
n Bedroom: Your childs bedroom should be comfortable, quiet, and dark. A nightlight is f ne, as
a completely dark room can be scary for some children. Your child will sleep better in a room
that is cool (less than 75F). Also, avoid using your childs bedroom for time out or other
punishment. You want your child to think of the bedroom as a good place, not a bad one.
n Snack: Your child should not go to bed hungry. A light snack (such as milk and cookies) be-
fore bed is a good idea. Heavy meals within an hour or two of bedtime, however, may interfere
with sleep.
n Caffeine: Your child should avoid caffeine for at least 3 to 4 hours before bedtime, although
its best to avoid it totally. Caffeine can be found in many types of soda, energy drinks, coffee,
iced tea, and chocolate.
n Evening activities: The hour before bed should be a quiet time. Your child should not get in-
volved in high-energy activities, such as rough play or playing outside, or stimulating activities
such as computer games.
n Television: Keep the television set out of your childs bedroom. Children can easily develop
the bad habit of needing the television to fall asleep. It is also much more diff cult to control
your childs television viewing if the set is in the bedroom. Keep all other electronic devices
out of the bedroom too, such as computers, cell phones, and hand-held computer games.
n Naps: Naps should be geared to your childs age and developmental needs. However, very
long naps or too many naps should be avoided, as too much daytime sleep can result in your
child sleeping less at night.
n Exercise: Your child should spend time outside every day and get daily exercise.
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Sleep t ips for a dolescents
The following recommendations will help you get the best sleep possible and make it easier for
you to fall asleep and stay asleep as well as to get enough sleep.
n Sleep schedule: Wake up and go to bed at about the same time on school nights and non-
school nights. Bedtime and wake time should not differ from one day to the next by more than
an hour or so. Also set your bedtime so that you can get enough sleep.
n Weekends: Dont sleep in on weekends to catch up on sleep. This makes it more likely that
you will have problems falling asleep at bedtime.
n Naps: If you are very sleepy during the day, nap for 30 to 45 minutes in the early afternoon.
Dont nap too long or too late in the afternoon or you will have diff culty falling asleep at
bedtime.
n Sunlight: Spend time outside every day, especially in the morning, as exposure to sunlight or
bright light, helps to keep your bodys internal clock on track.
n Exercise: Exercise regularly. Exercising may help you fall asleep and sleep more deeply, al-
though it is best to avoid exercising close to bedtime.
n Bedroom: Make sure your bedroom is comfortable, quiet, and dark. Make sure also that it is
not too warm at night, as sleeping in a room warmer than 75F will make it hard to sleep.
n Turn off televisions, computers, and radios: Late night television watching, computer game
playing, Internet use, text messaging, and similar activities at bedtime can lead to problems
falling and staying asleep. The low light level of a computer or television screen can also shift
your internal clock, making it hard to fall asleep.
n Bedtime: Make the 30 to 60 minutes before bedtime a quiet or wind-down time. Relaxing,
calm, enjoyable activities, such as reading a book or listening to soothing music, help your
body and mind slow down enough to let you sleep. Do not watch television, study, exercise, or
get involved in energizing activities in the 30 minutes before bedtime.
n Snack: Eat regular meals and dont go to bed hungry. A light snack before bed is a good idea;
eating a full meal in the hour before bed is not.
n Caffeine: Avoid eating or drinking products containing caffeine in the late afternoon and eve-
ning. These include caffeinated sodas, energy drinks, coffee, tea, and chocolate.
n Alcohol, drugs, and smoking: All of these things interfere with sleep.
n Sleeping pills: Dont use sleeping pills, melatonin, or other over-the-counter sleep aids. These
may be dangerous, and your sleep problems will probably return when you stop using the
medicine.
n Dont drive drowsy: Teenagers are at the highest risk for falling asleep at the wheel. So dont
drive when you havent gotten enough sleep. Accidents are likely to happen in the middle of
the afternoon as well as at night.
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bedtime problems
Getting a child to go to bed is a common problem that many parents experience. Some children
use stalling and excuses to resist going to bed, whereas others go to bed initially but do not stay
there. Bedtime problems can be one of the most frustrating parts of a parents day. Bedtime prob-
lems can occur at any age but are most prevalent between ages 3 and 6 years.
WHAT CAN YOU DO TO HELP YOUR CHILD GO TO BED?

First of all, it is important to realize that you cannot make a child go to sleep. However, you
can help your child improve his bedtime behavior and help him to get to sleep more easily and
quickly. As with many other skills your child needs to learn, this will take time.
n Stick to f rm bedtime limits: The f rst step is to be convinced that your child needs to change
his bedtime behavior, and that setting and sticking to f rm bedtime limits is in everyones best
interest, especially your childs. Setting limits is an important part of parenting. Children often
do not have a great deal of self-control, and so they benef t from the structure of limits that
you set for them. This helps them to learn self-control. In addition, limits relieve (not cause)
anxiety in children. Finally, prepare yourself for some hard work. Changing behavior is always
diff cult. Your child is probably happy with bedtime the way it is and so will initially have little
motivation to change. You need to be consistent and persistent.
n Explain the new rules to your child: Before you start the new nighttime program, sit down
with your child during the day and let him know what you expect. Do not make your conversa-
tion too long or involved and do not overexplain. Ignore any negative comments by your child
and avoid arguing about the new rules.
n Set bedtime: Once you have decided on your childs bedtime, be consistent about it. Establish
a regular bedtime to help set your childs internal clock. Be sure that your child is ready for
sleep before putting him to bed. This may seem obvious, but sometimes parents set a bedtime
for their own convenience. For example, some childrens biological clocks make them more
likely to be night owls. These children may have diff culty with an earlier bedtime.
n Bedtime fading: Putting children to bed when they are not tired increases the likelihood of
bedtime struggles. Therefore, for some children, it is best to start by setting the bedtime at the
time they usually fall asleep and gradually make the bedtime earlier. When you start, you will
f rst need to determine when your child is naturally falling asleep and set this as his temporary
bedtime. If you would like your child to go to bed at 8:30 p.m., but he usually does not fall
asleep until 10:30 p.m., choose 10:30 p.m. as his temporary bedtime. This will make it easier
to teach your child how to fall asleep within a short time of getting into bed. Once he is fall-
ing asleep easily and quickly at his temporary bedtime, then you can start making his bedtime
earlier by 15 minutes every few days. Be patient. If you move the bedtime back too quickly,
you may have problems with your child not being able to fall asleep.
n Bedtime routine: Be sure to establish a consistent bedtime routine. A bedtime routine should
include calm and enjoyable activities, such as a bath and bedtime stories. Avoid stimulating
high-energy activities, such as playing outside, running around, or watching exciting television
shows or videos. Make a chart of your bedtime routine to help keep your child on track. Also,
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having the last part of the bedtime routine be a favorite activity will help motivate your child
to get ready for bed.
n Ignore complaints or protests: Ignore your childs complaints or protests about bedtime such
as not being tired. Discussing or arguing about bedtime will lead to a struggle with your child,
thus maintaining bedtime problems. Firmly and calmly let your child know it is time for bed
and continue with the routine.
n Putting your child to bed: When the bedtime routine is complete, put your child to bed and
leave the room. It is important that you leave the room while your child is awake, as this helps
your child learn to fall asleep on his own.
n If your child cries or yells: If your child is yelling or calling out to you but remaining in his
bed, remind him one time that it is bedtime. If he continues to be upset, check on your child.
Wait for as long or short a time as you wish. For some children, checking frequently is effec-
tive; for others, checking infrequently works best. Continue returning to check on your child as
long as he is crying or upset. The visits should be brief (1 minute) and non-stimulating. Dont
soothe or comfort your child during these visits and dont get into a discussion. Calmly tell
your child that its time to go to sleep. The purpose of returning to the room is to reassure your
child that you are still present and to reassure yourself that your child is okay.
n What to do if your child gets out of bed or comes out of his room: If your child gets out of
bed or comes out of his room, f rmly and calmly return him to bed. For some children, simply
returning them to bed multiple times works. For others, letting them know that if they gets up
again, you will close the bedroom door, can be effective. If your child gets out of bed, put him
back in bed and close the door for a brief period (1 minute to start). After the allotted time,
open the door. If your child is in bed, praise him and leave the door open. If he is up, put him
back in bed and close the door again but leave it closed for a longer time, increasing the time
by a few minutes each time he gets up.
n Give your child a bedtime pass: Provide your child with one or two bedtime passes, which
can be as simple as index cards that have been decorated. Your child can turn in a card to make
a request (e.g., one more hug, trip to the bathroom). No more passes means no more requests.
This simple system allows children a way to make a reasonable request while maintaining bed-
time rules. To help discourage any requests, you can give your child a reward for any passes
that he still has in the morning.
n Dont lock your child in his room: Locking the door may be scary for your child. The goal is
to teach your child to stay in bed, not punish or scare him.
n Reward your child: Soon after your child awakens in the morning, reward him for what he did
well the night before. Dont dwell on misbehavior from the previous night. Give your attention
to your childs successes. Stickers, praise, and breakfast treats are good ways to reward your
child for even small improvements.
n Be consistent and dont give up: The f rst few nights are likely to be very challenging. You
should start to see major improvements within the f rst few weeks.
n ightwakings
Nightwakings in young children is one of the most common problems that parents face. By 6
months of age, most babies are physiologically capable of sleeping throughout the night and no
longer require nighttime feedings. However, 25% to 50% continue to awaken during the night.
Nightwaking problems can occur at any age but are most common with infants and toddlers.
WHY DOES YOUR CHILD WAKE DURING THE NIGHT?

When it comes to nightwaking, the most important thing for parents to understand is that all
children, no matter the age, wake brief y throughout the night. These arousals occur between
2 to 6 times per night. So the problem is rarely the waking during the night but rather why the
child is unable to return to sleep on her own. Children who are able to soothe themselves back to
sleep (self-soothers) awaken brief y throughout the night, but their parents are unaware of these
arousals. In contrast, signalers are those children who alert their parents by crying or going into
the parents bedroom upon awakening. Many of these signaler children have developed inap-
propriate sleep-onset associations and, thus, have diff culty self-soothing.
WHAT ARE SLEEP ASSOCIATIONS?

Many parents develop the habit of helping their child to fall asleep by rocking, holding, or bring-
ing the child into bed with them. Over time, children may learn to rely on this kind of help from
their parents in order to fall asleep. Although this may not be a problem at bedtime, it may lead
to diff culties with your child failing back to sleep on her own during the night. Thus, sleep as-
sociations are conditions that the child learns to need in order to fall asleep at bedtime (such as
rocking, nursing, or lying next to a parent). These same sleep associations are then needed in
order to fall back to sleep during the night. The bottom line is that your child needs to learn to
fall asleep on her own, so that she can put herself immediately back to sleep when she awakens.
Studies clearly show that infants and toddlers who fall asleep independently fall asleep faster,
wake less often at night, and get over 1 hour more sleep.
WHAT CAN YOU DO TO HELP YOUR CHILD SLEEP THROUGH THE NIGHT?
There are a number of steps that you can take to help your child sleep through the night.
n Develop an appropriate sleep schedule with an early bedtime: Ironically, the more tired
your child is, the more times she will awaken during the night. So be sure to have your child
continue to take naps during the day and set an early bedtime.
n Security object: Try to introduce your child to a transitional or love object. A transitional
object, like a stuffed toy, doll, or blanket, helps a child feel safe and secure when you are not
present. Help your child become attached to a transitional object by including it as part of
the bedtime routine. Try to include this object whenever you are cuddling or comforting your
child. Dont force your child to accept the object, and realize that some children will not accept
one no matter how cute and cuddly the object.
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n Bedtime routine: Establish a consistent bedtime routine that includes calm and enjoyable ac-
tivities, such as a bath and bedtime stories. Avoid exciting high-energy activities, such as play-
ing outside, running around, or watching television shows or videos. The activities occurring
closest to lights out should occur in the room where your child sleeps. Also, avoid making
bedtime feedings part of the bedtime routine after 6 months.
n Consistent bedroom environment: Make sure your childs bedroom environment is the same
at bedtime as it is throughout the night (e.g., lighting).
n Put your child to bed drowsy but awake: After the bedtime routine, put your child in her crib
or bed drowsy but awake and leave the room. Remember, the key to having your child sleep
through the night is to have her learn to fall asleep on her own, so she can put herself back to
sleep when she naturally awakens during the night. Make sure your child is more awake than
drowsy. Some children need to be wide awake to really learn how to fall asleep on their own.
n Checking method: If your child cries or yells, check on her. Wait for as long or as short a time
as you wish. For some children, frequent checking is effective; for others, infrequent checking
works best. Continue returning to check on your child as long as she is crying or upset. The
visits should be brief (1 minute) and nonstimulating. Calmly tell your child its time to go to
sleep. The purpose of returning to the room is to reassure your child that you are still present
and to reassure yourself that your child is okay.
n Respond to your child during the night: In the beginning, respond to your child as you
normally do throughout the night (e.g., nurse, rock). Research indicates that the majority of
children will naturally begin sleeping through the night within 1 to 2 weeks of falling asleep
quickly and easily at bedtime. If your child continues to awaken during the night after several
weeks, then use the same checking method during the night as you did at bedtime.
n A more gradual approach: Some parents feel that not being present when their child falls
asleep feels like too big of a f rst step for them and their child. A more gradual approach is to
teach your child to fall asleep on her own but with you in the room. This approach will take
longer but feels more comfortable to some families. The f rst step is to put your child in her
crib or bed awake and sit on a chair next to it. Once she is able to consistently fall asleep this
way, sit farther and farther away every 3 to 4 nights until you are f nally in the hallway and no
longer in sight. Some parents f nd it easier to pretend that they are asleep rather than sitting in
a chair.
n Be consistent and dont give up: The f rst few nights are likely to be very challenging and
often the second or third night is worse than the f rst night. However, within a few nights to a
week, you will begin to see improvement.
n ighttime f ears
It is normal for children to have nighttime fears, especially at bedtime, and most children have
these at some point. Bedtime fears are normal and part of normal development. Fear of the dark
and other nighttime fears develop as children begin to understand that they can get hurt or be
harmed. Studies f nd that up to 85% of school-aged children and 50% of adolescents have night-
time fears. Children have different fears at different developmental stages; for example, many
young children are afraid of monsters, whereas school-aged children and adolescents often report
fears related to intruders and worrying about daily events.
WHAT TO DO WHEN YOUR CHILD IS AFRAID AT BEDTIME (OR OTHER

TIMES OF THE NIGHT)
Dealing with a child who is afraid of the dark or scared to go to bed at night can be like walking
a tightrope. There is a f ne line between wanting to reassure him and not wanting to reinforce his
fears. If the fears are ignored, the child will not be reassured. If the child is reassured too much,
the parent may be giving the subtle message that there is something to fear. If bedtime fears are
affecting your childs ability to fall asleep and stay asleep, try some of the following.
n Listen and understand: Try to understand your childs fears. Dont dismiss or make fun of
them because fears that seem silly to an adult may be very real to a child.
n Reassure your child: It is important to reassure children who are fearful. When your child
clings to you as he is being tucked in or calls out in fear, you should go back to his bed and
f nd out what is wrong. Say something like, You are safe; we are here to make sure you stay
safe. Be sure to communicate that he is safe over and over again.
n Teach coping skills: Teach your child coping skills and discuss alternative ways to respond to
nighttime fears, such as by being brave and thinking positive thoughts (e.g., monsters are
just pretend, I can take care of myself, and The dark is fun). You can also talk about how
you deal with something that frightens you and read stories about children who are afraid and
conquer their fears.
n Gradually expose your child to fears: Develop a step-wise approach to expose your child
to specif c fears. For example, if your child is afraid of the dark, spend increasing amounts of
time in dark places (starting with 30 seconds and increasing in 1-minute increments) or gradu-
ally diminishing nighttime lighting.
n Use imagination and be creative: You can use your imagination to f ght imaginary fears such
as that of monsters. Many families have found monster spray to be a wonderful way to help
a child cope with bedtime fears. Take a spray bottle and f ll it with water (be sure that it has
not previously had any chemicals in it such as plant food). At bedtime, you or your child can
spray the room to keep the monsters away. In addition to monster spray, there are other ways
in which you can be creative and help your child. For example, consider allowing him to have
a pet for nighttime company. Even a bedside f sh tank might help.
n Introduce a security object: Helping your child become attached to a security object that he
can keep in bed with him may be benef cial. This may help your child to feel more relaxed
throughout the night.
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n Use a night-light: No matter what your child is afraid of, a night-light can help. A night-light
is f ne as long as it does not prevent your child from falling asleep. Another thing to try is leav-
ing the bedroom door open so that your child doesnt feel isolated from the rest of the family.
n Avoid scary television shows: Avoid scary TV shows, videos, or stories that may add to your
childs fears.
n Teach relaxation training: Teaching your child relaxation strategies can help him relax at
bedtime and fall asleep. This will give him something else to think about while lying in bed
and help to distract him from his fearful thoughts. Also, it is impossible to be relaxed and
scared at the same time.
n Discuss your childs fears during the day: Depending on how old your child is and how well
he can talk, try discussing his fears during the day. Talk about how he can be less frightened at
night. In addition, build his self-conf dence during the day. Feeling secure throughout the day
may help him feel more secure at night as well.
n Set limits: At the same time that you are reassuring your child, you need to set limits. Limits
are necessary to prevent your childs being scared behavior from being reinforced. Checking
closets and leaving a low night-light on is reasonable, but sleeping with your child every night
is not.
n Have him stay in his bed: Dont encourage your child to get out of bed. He should stay in bed
and f nd out for himself that he really is safe so that he can learn to overcome his fears. If you
bring your child into your room, or downstairs while f nishing the dinner dishes, the message
is that his bed isnt a safe place to be. It is a much better strategy to stay with him in his room
than to have him join you in yours. If your child is too frightened to stay in his room alone, it is
okay to occasionally stay by his bed until he falls asleep. Dont do this too frequently, or even
for 2 nights in a row, because he may come to depend on your presence. If your child is anxious
about your leaving, check on him frequently. Begin by brief y checking and reassuring him
every 5 minutes, and then every 10 minutes until he is asleep. Similarly, if your child wakes up
in the middle of the night and cant go back to sleep because he is frightened, go and reassure
him. Repeat the message about being safe and tell him that he will be f ne. If he gets up in the
middle of the night and comes into your room, take him right back and gently tuck him into
bed. Reassure him again, but dont let him get up.
n Start a star or sticker chart: Some children receive reinforcement for their fears. They may
be given lots of attention for being afraid or receive special treats. If this is the case, switch
the scenario. Give your child extra attention for dealing with his fears. Tell him how proud
you are of him for being brave. Set up a star system. Have him earn stars for being brave and
sleeping on his own. After earning a certain number of stars, he can turn them in for a treat,
such as watching a favorite video, going to the park, or baking cookies. Be as specif c as pos-
sible as to what is to be rewarded (staying in bed all night, not calling out after lights out), and
set up the reward system so that there is a high likelihood of success. You also can reinforce
progressively appropriate behaviors, such as dimming the lights gradually over a weeks time
or staying in the bedroom for longer periods.
n Address severe or persistent anxiety: If your childs anxiety and fears continue, are severe,
or are present during the day, consider taking him for a psychological evaluation aimed at
identifying and treating anxiety.
n ightmares
WHAT ARE NIGHTMARES?

Nightmares are scary dreams that can wake a child leaving her upset and in need of comfort.
They are very common in children and often a part of normal development. It is rare to f nd a
child or adolescent who has never experienced a nightmare. After a nightmare that results in an
awakening, most children are afraid to go back to sleep and often do not want to be left alone.
Very young children do not know the difference between a dream and reality, so when they wake
up, they may not understand the concept that they were only dreaming and it is now over. They
may keep insisting that something scary is about to occur.
Nightmares are most common between the ages of 6 and 10 years, but both younger and older
children also experience nightmares. Most children experience nightmares infrequently, but oth-
ers do on a frequent basis.
Before the age of 12 years, boys and girls are equally likely to have nightmares. After age 12
years, nightmares are more common in girls.
WHAT DO CHILDREN HAVE NIGHTMARES ABOUT?

Most young toddlers have concerns about being separated from their parents. So they may have
a nightmare about being lost or having something happen to one of their parents. Nightmares in
older children and adolescents often involve some type of imminent harm. Nightmares also typi-
cally include something that is scary or frightening, but can also include other negative feelings
like embarrassment or disgust.
Nightmares also are more likely to happen following some diff cult event. For example, if a
child has just started school or if her parents have gone away overnight, she is more likely to have
a nightmare. For some children, nightmares may also be the reliving of a traumatic event, such as
getting lost or getting shots at the doctors. Older children often have nightmares related to scary
movies or stories, or a frightening daytime experience.
HOW CAN YOU REDUCE THE LIKELIHOOD OF NIGHTMARES?

There are several things that you can do to help reduce the likelihood of nightmares.
n Avoid scary stories, television shows, or movies before bedtime: These will increase the
likelihood of your child having a nightmare. Choose instead a comforting bedtime routine.
n Identify stressors: If there is something in your childs life that you know is distressing, try to
take care of it and reassure your child. If your child suddenly experiences a signif cant increase
in the frequency or intensity of nightmares, try to evaluate why. Look for recurring themes that
could give you a clue as to the cause and then deal with the problem.
n Ensure that your child is getting enough sleep: Children are much more likely to have
nightmares after not getting enough sleep. If your child is having nightmares, make sure that
she is getting enough sleep as this can help decrease both the frequency and the intensity of
nightmares.
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HOW SHOULD YOU RESPOND TO YOUR CHILDS NIGHTMARES?

If your child has a nightmare, there are a few things that you should do.
n Offer reassurance: The best thing that you can do if your child has a nightmare is comfort
her. For babies and young toddlers, merely holding them and providing physical comfort is
enough. For older children, verbal reassurance may also be needed. Following most night-
mares, your child will be reassured by a few minutes of comfort. Stay with her in her room.
Let her know that you are nearby and will make sure that s/he is safe and secure. Most children
are still tired after a nightmare and will be ready to fall back to sleep.
n Give your child a security object: Helping a child become attached to a security object that
she can keep in bed with her can be benef cial. This often helps a child feel more relaxed
throughout the night.
n Leave a light on: If your child insists on having a light on, put it on the dimmest setting pos-
sible so that your child can fall back to sleep.
n Discuss it the next day: The next day, you may want to try and talk to your child about her
nightmare to see if there is anything bothering her. Most of the time nightmares are isolated
events with little meaning, but if your child starts having them on a frequent basis, you should
try and f gure out if anything is disturbing her.
n Draw the nightmare: Have your child imagine different endings to her nightmare and have
her draw the new dream with a good ending. Another way to give your child a sense of control
over her nightmares is to have her draw a picture of the bad dream but then crumple up the
picture and throw it away.
n Encourage the use of imagination: There are other ways to help your child combat a night-
mare by having her use her imagination. For example, have your child f ip her pillow after a
nightmare to change the channel, like on a television set. Hang a dream catcher over her bed,
which will capture the bad dreams while letting the good dreams through.
n Get outside help: If your childs nightmares are severe, meaning that they are interfering
in her life or occurring on a very frequent basis, speak to her physician or a mental health
provider.
Sleepwalking
WHAT IS SLEEPWALKING?
Sleepwalking is a common sleep behavior, especially in preschool and school-aged children.
Although children who are sleepwalking often have their eyes open and appear awake, they are
actually deeply asleep. Thus, they may appear confused or dazed, may mumble or give inap-
propriate answers to questions, and are diff cult to awaken. Some children simply walk into their
parents bedroom, whereas others head to odd places, such as down to the basement or even out-
side. Occasionally, a sleepwalking child may appear agitated. A sleepwalker also is often clumsy
and may perform bizarre or strange actions, such as urinating in a closet. Sleepwalking episodes
typically last from 5 to 20 minutes. Because they are asleep, children will have no memory of
the event the next day. Sleepwalking can occur infrequently, every night, or even several times a
night. Although generally considered benign (not harmful), parents should be aware that children
who sleepwalk could injure themselves. For example, they can fall down stairs or head outside
in the cold.
WHAT CAUSES SLEEPWALKING?

Sleepwalking usually occurs during the deepest stage of sleep (also called slow-wave sleep).
Thus, it is more likely to occur within the f rst 1 to 2 hours after falling asleep, since that is when
deep sleep is most likely to occur. Sleepwalking is also more common in younger children, be-
cause they have much more deep sleep than do teenagers or adults.
Many children sleepwalk once in a while, with about 17% of children (1 in 6) sleepwalking
regularly. Sleepwalking usually starts between 4 and 6 years of age, and peaks between ages 8
and 12 years. Most children outgrow it by adolescence, although some continue to sleepwalk into
adulthood. Sleepwalking often runs in families. Children who sleepwalk are also more likely to
have sleep (night) terrors and vice versa.
Sleepwalking is more likely to happen when your child doesnt get enough sleep. This is
because the body gets more deep sleep after not getting enough sleep. And the more deep sleep,
the more likely a sleepwalking episode will occur. Anything that results in not getting enough
sleep, such as when your child f rst starts giving up her nap or with a change in his schedule (for
example, starting school) may trigger sleepwalking if your child is prone to this behavior. The
likelihood of sleepwalking is also increased by anything that interrupts or disrupts sleep. These
include:
n An irregular sleep schedule (going to bed and getting up at different times from one day to the
next)
n Another sleep disorder, such as snoring or sleep apnea
n Fever, illness
n Some medications
n Sleeping in a different environment, such as at a friends or grandparents home
n Sleeping in a noisy environment
n Stress
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HOW SHOULD YOU RESPOND TO YOUR CHILDS SLEEPWALKING?

n Keep your child safe: Sleepwalkers can injure themselves or leave the house while sleepwalk-
ing. Make sure that all outside doors are secure. Ensure that windows, especially second story
or higher, do not open wide enough that your child can jump out of them. Where your child
sleeps should be made as safe as possible to avoid any accidents. Floors should not be clut-
tered, objects should not be left on the stairs, and hallways should be lit. Tying a bell to your
childs bedroom door can alert you when a sleepwalking episode occurs. Hotel door alarms
(that hang from the doorknob or wedge under the door) can also let you know that your child
is up during the night. Putting gates at the door of your childs bedroom and at the top of stairs
can prevent falls.
n Guide your child back to bed: Guide your child gently back to bed while speaking to him in
a calm and soothing manner. If your child gets upset when you try to guide him, then let him
be and let the event run its course.
n Dont wake your child: Although not harmful to your child, nothing is gained by trying to
wake a sleepwalking child. And, it may even make your child more agitated.
n Make sure your child is getting enough sleep: If your child seems tired in the morning, he
may not be getting enough sleep (sleepwalking itself does not make children tired, because
they are asleep during the episodes). Since sleepwalking is much more likely to happen when
your child does not get enough sleep, you may need to move bedtime earlier.
n Maintain a regular sleep schedule: Sleepwalking is also more likely to happen on nights
when your child goes to sleep at a different time (or place) than usual. If your child is having
a sleep-over at someone elses home, let the parents know that your child is a sleepwalker.
n Look for signs of other sleep problems: If your child takes a long time to fall asleep, fre-
quently wakes during the night, snores, or otherwise doesnt get a good nights sleep, he may
be more likely to sleepwalk. Addressing these sleep issues often decreases or even eliminates
sleepwalking.
n Avoid caffeine: Caffeine can disrupt your childs sleep and increase the likelihood of
sleepwalking.
n Additional treatment: In most cases, sleepwalking requires no specif c treatment. However,
in cases in which a child is at risk for harm or sleepwalking is occurring frequently, treatment
may be necessary. Treatment may include medication or behavior modif cation techniques. Be
sure to speak to your childs doctor if you are concerned.
Sleep t errors
WHAT ARE SLEEP TERRORS?

Sleep terrors, also called night terrors, are sleep behaviors that most often occur in young chil-
dren. They are related to sleepwalking. A child having a sleep terror will often cry out or scream
and appears very agitated, frightened, and even panicked. During the episode, your child may
appear confused and dazed, may mumble or give inappropriate answers to questions, and may be
clumsy. Your child may f ail around, push you away, or behave in other strange ways. As disturb-
ing and frightening as these events appear, children having them usually are totally unaware of
what they are doing. Although your child may appear to be awake, she is actually deeply asleep.
In fact, sleep terrors are much worse to watch than to experience and can understandably be very
distressing for parents.
Although they may seem much longer to a worried parent, sleep terrors typically last for 5 to
10 minutes, occasionally longer. Because they are asleep during the episode, children have no
memory of these events. The hardest part for parents is that most children avoid being comforted
during the episodes. They may even become more agitated if you talk to them and try to calm
them down.
Sleep terrors are not nightmares, and your child is not dreaming during these events. Thus, a
sleep terror is actually much less upsetting for a child than a typical nightmare or bad dream. It
is important to understand that sleep terrors are also not a sign of psychological problems or the
result of a traumatic event. Nor do they cause any psychological harm to a child.
Confusional arousals are another sleep behavior similar to sleepwalking and sleep terrors.
They are also characterized by agitation, disorientation, and crying or moaning (no, no!).
Sometimes a confusional arousal will involve thrashing around in bed. Confusional arousals start
more gradually from sleep compared to sleep terrors. They typically last 5 to 15 minutes, but can
last several hours.
WHAT CAUSES SLEEP TERRORS?

Sleep terrors usually occur during the deepest stage of sleep (also called slow-wave sleep).
Thus, it is more likely to occur within the f rst 1 to 2 hours after falling asleep, since that is when
deep sleep is most likely to occur. Sleep terrors are also more common in younger children, be-
cause they have much more deep sleep than do teenagers or adults. Most children outgrow sleep
terrors by adolescence. Furthermore, sleep terrors often run in families and children who have
sleep terrors are also more likely to sleepwalk and vice versa.
Sleep terrors are more likely to happen when your child doesnt get enough sleep. This is be-
cause the body gets more deep sleep after not getting enough sleep. And the more deep sleep, the
more likely a sleep terror will occur. Anything that results in not getting enough sleep, such as
when a child f rst starts giving up her nap or with a change in his schedule (for example, starting
school) may trigger a sleep terror in a child who is prone to them. The likelihood of sleep terrors
is also increased by anything that interrupts or disrupts sleep. These include:
n An irregular sleep schedule (going to bed and getting up at different times from one day to the
next)
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n Another sleep disorder, such as snoring or sleep apnea

n Fever, illness
n Some medications
n Sleeping in a different environment, such as at a friends or grandparents home
n Sleeping in a noisy environment
n Stress
HOW SHOULD YOU RESPOND TO YOUR CHILDS SLEEP TERRORS?

n Keep your child safe: The most important thing that you can do if your child has sleep terrors
is to keep her safe. Although many children with sleep terrors do not get out of bed, many also
sleepwalk and can injure themselves. Make sure that all outside doors are secure. Ensure that
windows, especially second story or higher, do not open wide enough that your child can jump
out of them. An alarm, such as a simple bell hung on the door, can signal you when your child
is up and about, and help to ensure that she does not leave the house. Some parents attach a
screen or a gate to their childs bedroom door or at the top of stairs. Finally, remove things that
are in the way. If your child may walk or run around during a sleep terror, clear away anything
that he can step on or trip over.
n Dont wake your child: Although not harmful to your child, nothing is gained by trying to
wake your child during a sleep terror. It may even make your child more agitated.
n Try not to interfere: The normal response of parents is to try and comfort their child during
one of these episodes. Try to resist doing this, as most children will just become more agitated.
It is best to walk quietly into your childs room, stand nearby, and let the episode run its course.
The sleep terror is likely to end more quickly if you dont interfere. If your child has gotten out
of bed, guide her gently back to bed, but if she resists, let her be.
n Make sure your child is getting enough sleep: If your child seems tired in the morning, she
may not be getting enough sleep (sleep terrors themselves do not make children tired, because
they are asleep during the episodes). Since sleep terrors are much more likely to happen when
your child does not get enough sleep, you may need to move bedtime earlier.
n Maintain a regular sleep schedule: Sleep terrors are more likely to happen on nights when
your child goes to sleep at a different time (or place) than usual. If your child is having a sleep-
over at someone elses home, let the parents know that your child has sleep terrors.
n Look for signs of other sleep problems: If your child takes a long time to fall asleep, fre-
quently wakes during the night, snores, or otherwise doesnt get a good nights sleep, she may
be more likely to have sleep terrors. Addressing these sleep issues often decreases or even
eliminates sleep terrors.
n Dont discuss sleep terrors the next day: The morning after an event, do not make a point
of discussing the episode with your child unless she brings it up. Making a big deal about the
event may worry or embarrass her. If she does raise a concern, reassure her that this is a normal
sleep behavior in children, it is not harmful, and that you will keep her safe.
n Avoid caffeine: Caffeine can disrupt your childs sleep, and increase the likelihood of a sleep
terror.
n Additional treatment: In most cases, sleep terrors require no specif c treatment. However, in
severe cases, when these behaviors involve injury, violence, or serious disruption to the fam-
ily, treatment may be necessary. Treatment may include medication or behavior modif cation
techniques. Be sure to speak to your childs doctor if your child has frequent or severe sleep
terrors or if you are concerned.
h ead banging, body
r ocking, and h ead r olling
WHAT ARE HEAD BANGING, BODY ROCKING, AND HEAD ROLLING?

Head banging, body rocking, and head rolling are what are known as sleep related rhythmic
movement behaviors. Children who bang their head may do it while lying down and lifting their
head to bang onto a pillow or the mattress, while rocking on their hands or knees and banging
their head into the headboard or wall, or while sitting upright and banging their head backwards
onto the bed or wall. Body rocking consists of moving back and forward, usually while on the
hands and knees. Body rolling involves moving the entire body from side to side. Some children
hum or make repetitive sounds at the same time. These movements are repetititive, and they usu-
ally occur when falling sleep, at naptime and bedtime, or following nighttime awakenings. Some
children also engage in these behaviors while they are actually asleep. These movements seem
to be to help a child fall asleep (or back to sleep) and many children experience them as sooth-
ing. These behaviors are extremely common in young children, with most children starting these
behaviors between ages 9 months and 2 years. It is estimated that 60% of infants have rhythmic
movements at one time or another.
SHOULD YOU BE CONCERNED ABOUT YOUR CHILDS HEAD BANGING OR

BODY ROCKING?
In most instances, rhythmic movement behaviors are meaningless and harmless. In addition,
sleep is not very disrupted as a result of these movements, although it may seem to be. And, al-
though sometimes distressing to parents, signif cant injury is very rare. In addition, these behav-
iors typically occur in normally developing children. In the vast majority of cases their presence
does not indicate that there is some underlying neurological or psychological problem. Children
with conditions such as a developmental delay, autism, or blindness will sometimes rock or bang
their heads, and may even hurt themselves, but the rhythmic movements in these cases are much
more severe, persistent, and sometimes violent. They often occur both during the day and at
night. If your child is healthy and developing normally, banging his head or rocking to fall asleep
should not be a cause for concern.
HOW SHOULD YOU RESPOND TO YOUR CHILDS HEAD BANGING OR

BODY ROCKING?
In the vast majority of children (95%), these behaviors disappear by themselves by age 5 years,
and most of the time by age 3 to 4 years. Rarely, some children continue them into adulthood.
Rhythmic movements are often distressing to parents, however, and may disrupt the sleep of other
family members. So, in the meantime, consider the following.
n Dont worry about trying to protect your child: Even if your child is banging his head hard,
it is very unlikely that he will hurt himself. Thus, there is no need to put extra bumpers on the
crib or place pillows in strategic places, although parents may be reassured by this measure.
You should be advised that most children will f nd a way to continue to head bang or rock, no
matter what creative tricks you try.
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2 h Ea D ba n g in g , bo Dy r o c kin g , a n D h Ea D r o l l in g
n Be careful not to reinforce the behavior: If you go in to your child every time he starts to
rock or bang his head, you may be giving a lot of attention to and thus reinforcing his behavior
without even realizing it. In this case, he may start or continue to head bang just to get your
attention. Make sure that your child gets lots of attention during the day and ignore his head
banging at night.
n Move the crib or bed: Move the crib or the bed away from the wall if the banging or rocking
is making noise and keeping the rest of the family awake. If your child is in a bed rather than
a crib, put guardrails on all sides so he wont fall out of bed. If your child is making his crib
or bed squeak, oil the screws and bolts. Also, be sure to tighten screws and bolts on a regular
basis, as the rocking or head banging can loosen them.
n Look for anything that disrupts your childs sleep: Anything that disrupts your childs sleep
can increase the likelihood of rhythmic movements. So if your child snores or has any other
sleep problems, talk to your childs doctor. In addition, if there is anything in your childs en-
vironment that may wake him up at night, such as household noise or his room being too hot
or cold, try to make some changes. For example, install a white noise make to dampen outside
noise or a fan to cool off the room.
bruxism
WHAT IS BRUXISM?
Bruxism, or teeth grinding, is def ned as repetitive grinding or clenching of the teeth during sleep.
It is quite common in children. Children and adolescents can grind their teeth in any stage of sleep
and at any time of the night. They may also do it while they are falling asleep. In the majority
of cases, teeth grinding doesnt cause any harm and is temporary. However, some children with
bruxism may eventually develop problems, such as jaw and face pain or tooth damage over time.
TEETH GRINDING IN BABIES

Almost 50% of babies grind their teeth. It usually begins at about age 10 months, after a baby has
her deciduous incisors (the two top front teeth and the two bottom front teeth). Some babies only
grind their teeth sporadically. Others can do it throughout the night. In babies, teeth grinding is
not of any concern and eventually goes away on its own. It is also nothing to be alarmed about,
as it is highly unlikely that any dental damage will result. However, if the teeth grinding is worri-
some or if there are any changes in your childs teeth, see a dentist.
TEETH GRINDING IN CHILDREN AND ADOLESCENTS

Teeth grinding also occurs in children and adolescents. It is especially common in young chil-
dren. It usually starts around age 3 years, up until around age 6 years, when adult teeth start
coming in. Teeth grinding becomes less common as a child gets older. Bruxism is also more com-
mon in children with other conditions, such as cerebral palsy, Down syndrome, attention def cit
hyperactivity disorder, and autism.
The most troublesome symptom of bruxism for many families is the annoying noise, which
may disrupt the sleep of other family members. Other more serious, but less common, symptoms
include tooth pain and sensitivity to extreme temperatures, as well as inf ammation of the gums
and dental erosion. Some children may have temporomandibular joint pain and headaches.
WHAT YOU CAN DO ABOUT BRUXISM

Bruxism in infants and occasional teeth grinding in older children does not require any interven-
tion. However, if your child is experiencing headaches, having tooth pain, or is wearing down her
teeth, you should discuss it with your childs dentist. In addition, certain things may increase teeth
grinding, such as stress, allergies, and some medications. Thus, if your child is stressed or anx-
ious, implementing relaxation strategies or seeing a mental health professional may be helpful.
Treatment for teeth grinding can include biofeedback or sleeping on the back with neck sup-
port. Pain relievers or application of heat can help jaw pain. Older children and adolescents may
benef t from being f tted by a dentist with a mouth guard, which prevents dental erosion.
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bedwetting
The medical term for chronic, frequent bedwetting is enuresis. Many young children wet their
bed occasionally at night. It also typically takes a child longer to become dry at night than it does
to be potty-trained during the day. Therefore, enuresis is not diagnosed until after age 5 years and
is usually not treated until after age 7 years. The off cial def nition of enuresis is wetting the
bed at least twice a week. Bedwetting can occur more than once a night. It also can occur in all
stages of sleep, not just in deep sleep.
There are two types of enuresis, primary and secondary. Primary enuresis means that a child
has never been dry at night for at least 6 consecutive months. Primary enuresis is usually a de-
velopmental issue in which the childs control of urination is not yet fully mature. The skills of
waking up in response to a full bladder (which stores the urine before it is passed out of the body)
and being able to control bladder contractions (which force the urine out) during sleep take longer
for some children to achieve. Secondary enuresis means that the child had previously been dry at
night for at least 6 months and the bedwetting restarted. Secondary enuresis is more likely to be
related (although not always) to a medical problem, like a urinary tract infection.
In addition to developmental maturation, there are other things that increase the likelihood
that a child will wet the bed at night. First of all is genetics. Children are more likely to have
enuresis if one or both of their parents wet the bed when they were children. Constipation can
also contribute to bedwetting, as a large amount of stool may press upon the bladder, resulting
in more frequent urination. In addition, there are many other medical problems, such as diabetes
and abnormalities of the urinary system, that can contribute to enuresis. Children who also have
accidents during the day are more likely to have an underlying medical condition.
SHOULD YOU BE CONCERNED ABOUT YOUR CHILDS BEDWETTING?

Bedwetting is very common. It occurs in 10% of 6-year-olds and 5% of 10-year-olds. Infrequent
bedwetting, which occurs less than twice a week, is even more common. Boys are also more
likely to wet the bed than girls. Most of the time, bedwetting stops on its own as a child matures.
Every year that your child gets older, there is a 15% chance that the bedwetting will spontane-
ously go away. However, because bedwetting is a nuisance for families and may cause signif cant
embarrassment or interfere with things your child would like to do, such as sleeping over at a
friends house, treatment may be appropriate.
Secondary enuresis should prompt an evaluation by your childs doctor to check for possible
causes of bedwetting, such as a bladder infection. Snoring and/or sleep apnea, as well as other
disorders that disrupt sleep, also may be associated with secondary enuresis.
HOW SHOULD YOU RESPOND TO YOUR CHILDS BEDWETTING?

First of all, realize that your child has no control over his wetting the bed at night. Thus, there is
no reason to punish your child for wet nights. Also, if your child is under the age of 7 years, in
most cases it is better to wait and see if he outgrows it.
However, if your child is older than age 7 years, if bedwetting is impacting his or your familys
life, or it is distressing to your child, there are a number of things that you can try to temporarily
stop or decrease the likelihood of bedwetting:
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n Good bladder health during the day can make a difference at night. Make sure your child
goes to the bathroom every 2 to 3 hours during the day, and doesnt avoid going to the bath-
room while at school, as many children do. Increasing f uids during the day is also good, as it
helps a child learn to hold his urine during the day.
n Minimize f uids in the evening especially after dinnertime.
n Avoid caffeinated products because they tend to increase urination.
n Avoid constipation by increasing f ber in your childs diet, having your child drink plenty of
f uids, and encouraging your child to take the time needed to pass a stool every day (usually
soon after a meal).
n Try awakening your child from sleep to use the bathroom before you go to bed for the night
or at the time when he usually wets the bed. Some children, however, are hard to awaken and
resist any attempts to have them use the bathroom once theyve been asleep.
n Sticker charts and reward systems can help encourage your child to stay dry at night, but
again realize that your child is not being deliberately diff cult or belligerent if he continues to
wet the bed.
n Bladder training in which you have your child drink increasing amounts of f uid and progres-
sively waiting longer to urinate, can help with nighttime wetting.
n Bedwetting alarms are the most effective behavioral treatment because they help teach a
child to respond to the sensation of a full bladder when asleep. Enuresis alarms come in many
different types, including a pad that goes on the bed or a sensor that attaches to your childs
underwear. These trigger an alarm when they sense moisture. Treatment can take 6 to 16 weeks
and requires signif cant motivation on behalf of your child and you (the parents).
n Medications are also available that can reduce bedwetting. Some medications supplement the
hormone naturally produced by the body to decreased urination during sleep. Others work by
affecting nervous system control of wetting. And still others directly affect bladder muscle
spasms (overactive bladder). Some children take medication just on nights that they are not
sleeping at home, such as for sleep-overs or at overnight camp, whereas other children take it
every night. Your childs doctor can talk to you about the medications available and possible
benef ts and risks.
o bstructive Sleep
a pnea in c hildren
WHAT IS OBSTRUCTIVE SLEEP APNEA?

Obstructive sleep apnea (OSA) is a breathing problem that occurs only during sleep. Both chil-
dren and adults can have sleep apnea. Sleep apnea involves brief (typically lasting 1020 sec-
onds) breathing pauses (or apneas) that occur frequently throughout the night. These breathing
pauses are caused by some type of airway blockage (or obstruction). In children, enlarged tonsils
and adenoids are the most common cause. These breathing pauses can lead to a temporary de-
crease in oxygen levels. These changes in oxygen levels alert the brain that there is a problem.
The brain then jump starts breathing again by waking up the sleeping person. Although breath-
ing resumes, these brief wakings disrupt and fragment sleep. Its just like being poked by some-
one 30 or 40 times a night while you are trying to sleep. Both the frequent dips in oxygen and the
multiple wakings negatively affect normal daytime functioning. This is because adequate oxygen
is necessary for optimal brain function and brief y waking frequently throughout the night can
lead to signif cant daytime sleepiness.
WHAT CAUSES OBSTRUCTIVE SLEEP APNEA?

In most children, large tonsils and/or adenoids cause sleep apnea. Large tonsils can block airf ow
through the mouth. Large tonsils reduce airf ow through the nose. Being overweight or obese
can also affect breathing. It is an increasingly common risk factor for sleep apnea in children.
Allergies, asthma, frequent sinus infections, and gastroesophageal ref ux (frequent heartburn,
sour taste) are also risk factors for sleep apnea. Having one or more close family members with
sleep apnea or loud snoring also increases your childs likelihood of having sleep apnea. Other
children who are at risk for sleep apnea are those with a narrow facial bone structure or a small
jaw. Children with neuromuscular disorders such as cerebral palsy, and some genetic conditions,
such as Down syndrome and Prader-Willi syndrome, are also more likely to have sleep apnea.
WHAT ARE THE SYMPTOMS OF OBSTRUCTIVE SLEEP APNEA?

n Snoring, especially if it is loud and occurs every night
n Breathing pauses during sleep or frequently choking or gasping when asleep
n Nasal congestion, nasal voice, and diff culty breathing through the nose
n Restless sleep
n Frequent nightwakings
n Sweating during sleep
n Morning headaches
n Diff culty waking and/or being irritable in the morning
Children with OSA also frequently have symptoms during the day, as a result of not sleeping
well at night. They may appear sleepy during the day, doze off on short car rides or in front of
the TV, or fall asleep in school. Other children with sleep apnea have more subtle symptoms of
sleepiness. For example, they may be moody, irritable, or have behavior problems, such as hy-
peractivity, aggressiveness, def ance, or poor impulse control. Some children with sleep apnea
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have problems paying attention and focusing in school. And some may even be diagnosed with
attention def cit hyperactivity disorder. Many children with sleep apnea have problems in school.
HOW IS OBSTRUCTIVE SLEEP APNEA DIAGNOSED?

Children with symptoms of OSA may require an overnight sleep study to conf rm the diagno-
sis. The overnight sleep study, which is done in a specialized sleep laboratory, uses a variety of
sensors to monitor snoring, breathing, heart rate, oxygen levels, sleep stages, body movements,
and sleep disruptions. A parent typically sleeps in the same room with the child during the sleep
study. (For more information on preparing your child for a sleep study see Appendix D11.) Your
doctor will review the results of the sleep study with you and recommend the best treatment for
your child.
HOW IS OBSTRUCTIVE SLEEP APNEA TREATED?

Because most children with sleep apnea have large tonsils and/or adenoids, an operation to re-
move the tonsils and adenoids is typically the recommended treatment. This surgery generally
takes care of the problem. A referral to an ear, nose, and throat specialist (otolaryngologist) is
required for such surgery. Most of the time, the surgery can be done on an outpatient basis. Some
children may require another sleep study after the surgery to conf rm that the sleep apnea has
improved.
For other children, such as those whose tonsils and adenoids have already been removed or are
not enlarged or in children with very mild sleep apnea, other treatments may be recommended.
For example, children who are overweight should be counseled about nutrition and exercise to
help them lose weight. Those with allergies or asthma may be treated with medications. Reduc-
ing exposure to allergens, such as tobacco smoke and dust mites, can help. Plastic coverings on
bedding and air f lters can also improve breathing during the night. Sometimes allergy shots may
even be recommended. In addition, sleep apnea is typically worse when a child sleeps on his
back. Therefore, sewing a hard ball into a pajama or t-shirt pocket and then wearing this back-
wards to bed may help keep your child from rolling over onto his back during the night. Body
pillows can also help.
Finally, some children with sleep apnea will require a treatment called continuous (or bi-level)
positive airway pressure. This is a portable breathing machine that is used at night to relieve
blocked breathing. This treatment requires another overnight sleep study to f nd the best f tting
mask and pressure settings.
your c hilds Sleep Study
An overnight sleep study is a special test that your doctor may recommend to help evaluate your
childs sleep problem. A sleep study involves monitoring a number of different body functions
overnight. It measures how much and how well your child sleeps. It also measures breathing,
heart rate, oxygen levels, and body movements during sleep. Children with symptoms of some
sleep disorders (obstructive sleep apnea, periodic limb movement disorder, narcolepsy) require
an overnight sleep study to make the diagnosis. A sleep study will also determine the severity of
your childs sleep problem. Sometimes a sleep study also is recommended if a child or adolescent
is extremely sleepy during the day to check for an underlying sleep disorder. Occasionally, a sleep
study is done to conf rm the diagnosis of sleepwalking or sleep terrors. However, children with
bedtime struggles, diff culty falling asleep, or nightwakings do not routinely need a sleep study
unless there are symptoms of other sleep disorders (snoring, very restless sleep).
If your doctor recommends an overnight sleep study for your child, there are some things that
are helpful to know ahead of time. Sleep studies are typically done in a sleep lab. Most sleep
labs do studies on both adults and children, while some see only children. It is important, in either
case, that the sleep technicians working with your child have experience in doing sleep studies
on children. The sleep lab should be child-friendly. Sleep labs typically require a parent to stay
with a child overnight; however, labs vary as to whether adolescents also need a parent with them.
Most of the time, a fold-out bed or chair for parents is available in the childs room.
Most labs ask you and your child to arrive for the sleep study early in the evening. You will
be told what to bring, and any questions you (or your child) may have will be answered. Some
labs allow families to visit the lab ahead of time. This may be helpful, especially if your child
is anxious or has special needs. Make sure your child has whatever he needs to be comfortable.
Bring things like special pajamas, his own pillow, a stuffed toy, a favorite bedtime snack, and a
storybook.
Once you arrive at the lab and get settled, a specially trained sleep technician will hook up
your child to the different monitors and sensors that are part of the sleep study. None of these are
painful, and there are no needles involved. Typically, the sensors include EEG (electroencepha-
logram or brain wave) and EMG (electromyogram) monitors attached to the head and face.
These give information about sleep stages and whether sleep is disrupted or fragmented. Sensors
at the nose and mouth measure the f ow of air in and out of the lungs. Belts around the chest
determine breathing effort. EKG (electrocardiogram) measures heart rate. A sensor attached to a
f nger or toe (pulse oximeter) measures oxygen levels. There will likely be another EMG moni-
tor attached to your childs legs to measure leg movements. A microphone is also placed to detect
snoring. A video camera allows the sleep technician to watch your child while he sleeps without
disturbing him. It will record any unusual behaviors during sleep. Sometimes younger children
or those with special needs have diff culty tolerating all the monitors and wires (especially those
at the nose and mouth). In that case, the sleep technician may attach some of these monitors after
your child has fallen asleep.
You can help greatly by explaining the process to your child in words that he will understand.
Encourage your child to cooperate and remain calm. You can distract your child by playing with
a favorite toy, reading a story, singing a lullaby, or chatting. Younger children may be more com-
fortable sitting in their parents lap during the hook up process. Also encourage your child to
ask questions (Will it hurt?, What if I have to go to the bathroom?, Can you see what I am
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dreaming?). It is also helpful for children to feel that they have some control so let them decide
what monitor goes on f rst or place a sensor on a doll (or a parent) f rst. Some children like it
when the different monitors are compared to things that are familiar (the pulse oximeter makes
you look like ET, this is a plastic moustache for you to wear, these are special stickers that go
on your legs). Also let the sleep technician know about any special issues with your child (e.g.,
hypersensitivity to certain sounds or textures, anxiety about needles).
Most sleep labs end the overnight study early in the morning (6:00 a.m. or 7:00 a.m.). This
allows you to shower and get out in time for school or work. Some labs will allow you to sleep
in a little longer if you make a request ahead of time. Be sure to share any feedback about your
and your childs experience, good or bad, with the sleep lab personnel.
Generally the results of a study will be available within 1 or 2 weeks. Your childs doctor will
discuss the results with you and decide on a treatment plan.
WHAT IS RESTLESS LEGS SYNDROME?

Restless legs syndrome (RLS) is a neurological disorder in which a child or adolescent experi-
ences a need or urge to move the legs. These feelings are typically worse in the evening and
at bedtime. They can also occur during periods of inactivity such as sitting still for a long time.
This urge to move is often accompanied by uncomfortable feelings in the legs. These sensations
may be described by children as creepy-crawly or tingling. Some parents interpret their childs
complaints as growing pains or simply believe that their child is f dgety. These uncomfortable
feelings are often partially or completely relieved by movement, such as stretching or jiggling the
legs, getting up and walking or running around, or simply tossing and turning. For some children,
rubbing the legs may make them feel better. Because of the leg discomfort and increased leg
movements, it often takes a long time for a child or adolescent with RLS to fall asleep at bedtime.
This results in not getting enough sleep.
In addition, children with RLS often kick their legs or twitch when they are asleep, which are
called periodic limb movements. These movements may disrupt sleep, resulting in feeling tired
the next day. Unlike restless legs symptoms, a child with periodic limb movements is typically
not aware of the problem, although a parent may observe kicking and restless sleep.
WHAT CAUSES RESTLESS LEGS SYNDROME?

RLS appears to be genetic, as it often run in families. The majority of children with RLS have a
parent or grandparent with similar symptoms. In addition, certain factors may make RLS worse.
These include iron def ciency (with or without anemia), caffeine, and certain medications (anti-
depressants such as Prozac). In addition, some children with a chronic illness, such as diabetes,
cancer, and kidney disease, are at increased risk for RLS.
WHAT ARE THE SYMPTOMS OF RESTLESS LEGS SYNDROME?

The symptoms of RLS include the following.
n Leg discomfort: Children or adolescents often describe these uncomfortable leg sensations
as creepy-crawly, itching, burning, popping, tingling, or sometimes as painful. They may also
use more colorful descriptions, such as ants crawling on my legs or soda bubbling through
my veins. These sensations usually occur only at bedtime or are much worse at bedtime. They
can, though, also occur at other times of inactivity, such as while sitting still in school or on
long car rides.
n Leg movements: Children and adolescents with RLS often have an irresistible urge or feel-
ing that they have to move their legs. These movements can relieve the uncomfortable feel-
ings. These movements can be shaking or kicking the legs, tossing and turning while lying in
bed, or even walking or running about.
n Diff culty falling asleep: Children and adolescents with RLS often take a long time to fall
asleep because of the leg discomfort and need to move. They not only have problems falling
asleep, but may also have diff culty staying asleep.
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n Bedtime behavior problems: Because of the diff culty falling asleep caused by RLS, some
children may resist or struggle at bedtime.
n Daytime problems: The diff culties falling asleep and staying asleep can result in signif -
cant daytime sleepiness. In addition, problems with mood, behavior, and school are com-
mon in children with RLS. They may also be hyperactive, impulsive, irritable, and have poor
concentration.
HOW IS RESTLESS LEGS SYNDROME DIAGNOSED?

There is no def nitive test for RLS. So the diagnosis is made based on the description of symp-
toms. A medical history and physical examination will also be done to make sure there are no
other problems. Your doctor may order a blood test for low iron called a serum ferritin level.
Finally, an overnight sleep study may be recommended to evaluate for other sleep disorders, es-
pecially periodic limb movements, which can only be def nitively diagnosed with a sleep study.
HOW IS RESTLESS LEGS SYNDROME TREATED?

Treatment for RLS may involve any of the following.
n Good sleep hygiene: It is especially important that children and adolescents with RLS main-
tain good sleep hygiene. This includes keeping a regular sleep schedule and having a consis-
tent bedtime routine. An earlier bedtime may also help, especially if the symptoms are worse
when your child is overtired.
n Change bedtime habits: Given that the leg discomfort gets worse the longer the child or
adolescent lies in bed, it is usually better for your child to wait to get into bed until she is ready
to turn out the light. Therefore, the bedtime routine, such as reading stories, should all occur
before getting into bed.
n Exercise: Exercising at least a few hours before bedtime can be benef cial.
n Reduce the discomfort: Massage, cold compresses, or a heating pad may provide temporary
relief.
n Avoid caffeine: Caffeine can make RLS symptoms worse, so all caffeine should be avoided.
Caffeine can be found in many sodas, tea, and coffee. Some antihistamines and cold or sinus
preparations can also make symptoms worse.
n Treat iron def ciency: If a blood test shows low iron (ferritin level <50), then iron supple-
ments are usually recommended. The amount of iron in these supplements is typically more
than that in a regular multivitamin, and several months of treatment are often needed to in-
crease the ferritin level. Your doctor may recommend an iron supplement that also includes
vitamin C. Vitamin C will increase the iron absorption. Some children develop constipation
with iron supplements. Pay attention to your childs diet, including increasing high f ber foods
and increasing f uids. The addition of a stool softener is occasionally needed.
n Consider medication: For children and adolescents with RLS who have signif cant sleep
disruption, medication may be recommended. There are a number of different types of medi-
cations that can help. Your doctor can discuss these with you.
periodic l imb
movement Disorder
WHAT IS PERIODIC LIMB MOVEMENT DISORDER?

Periodic limb movement disorder (PLMD) is a neurological disorder that occurs during sleep. It
involves episodes of repetitive movements, usually in the legs. They occur approximately every
20 to 40 seconds. The movements may appear as brief muscle twitches, jerking movements, leg
kicks, or an upward f exing of the feet. These movements occur in clusters, lasting from a few
minutes to a few hours. Most children and adolescents with PLMD are not aware of the move-
ments. However, PLMD can result in frequent brief arousals throughout the night, leading to
daytime sleepiness.
Children and adolescents with PLMD also often have restless legs syndrome (RLS). RLS is
a related disorder and involves an urge to move the legs, which is typically worse at bedtime and
sometimes when sitting still for a long time. It is accompanied by uncomfortable sensations in the
legs (tingling, burning, creepy-crawly), which are relieved by movement. Children with RLS
often have diff culty falling asleep at bedtime.
WHAT CAUSES PERIODIC LIMB MOVEMENTS?

Periodic limb movements may run in families. PLMD is often related to low iron (with or without
anemia). In addition, some children with a chronic illness, such as diabetes, cancer, and kidney
disease, are at increased risk for developing PLMD.
WHAT ARE THE SYMPTOMS OF PERIODIC LIMB MOVEMENT DISORDER?

The symptoms of PLMD may include any of the following, although many children and adoles-
cents do not report any symptoms.
n Leg movements: Repetitive leg movements in sleep characterize PLMD. The child or adoles-
cent is usually not aware of these movements, but leg movements may be seen by parents.
n Restless sleep and sleep disruption: Children and adolescents with PLMD are often de-
scribed as restless sleepers. This is because of the leg movements and frequent arousals. Some
children also wake up multiple times at night. Children with both RLS and PLMD often have
diff culty falling asleep as well.
n Daytime sleepiness: The sleep disruption associated with PLMD can result in being sleepy
the next day. In addition, problems with mood, behavior, and school are common in children
with PLMD. They may also be hyperactive, impulsive, irritable, and have poor concentration.
HOW IS PERIODIC LIMB MOVEMENT DISORDER DIAGNOSED?

An overnight sleep study is required to conf rm the diagnosis of PLMD. In addition, a medical
history and physical examination will be conducted. Your childs doctor may order a blood test,
called a serum ferritin level, for low iron.
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HOW IS PERIODIC LIMB MOVEMENT DISORDER TREATED?

Treatment for PLMD may involve any of the following.
n Good sleep hygiene: It is especially important that children and adolescents with PLMD
maintain good sleep hygiene. This includes getting enough sleep and keeping a regular sleep
schedule.
n Treat RLS: If restless legs symptoms are also present, treatment of the RLS may improve
sleep.
n Avoid caffeine: Caffeine can make PLMD symptoms worse. Caffeine can be found in many
sodas, tea, and coffee, as well as some medicines such as Excedrin.
n Treat iron def ciency: If a blood test shows low iron (ferritin level <50), then iron supple-
ments are usually recommended. The amount of iron in these supplements is typically more
than that in a regular multivitamin, and several months of treatment are often needed to in-
crease the ferritin level. Your doctor may recommend an iron supplement that also includes
vitamin C. Vitamin C will increase the iron absorption. Some children develop constipation
with iron supplements. Pay attention to your childs diet, including increasing high f ber foods
and increasing f uids. The addition of a stool softener is occasionally needed.
n Consider medication: For children and adolescents with PLMD whose sleep is very dis-
rupted, medication may be recommended. There are a number of different types of medica-
tions that can help. Your doctor can discuss these with you.
n arcolepsy
WHAT IS NARCOLEPSY?
Narcolepsy is a chronic (lifelong) neurologic disorder. It is characterized by severe and persistent
daytime sleepiness, even despite getting enough sleep at night. Narcolepsy affects about 200,000
people in the United States. However, most cases go undiagnosed and untreated for many years.
Although it is relatively uncommon, its impact on a childs life can be dramatic. It affects boys
and girls equally, and usually develops during adolescence. Most people have the f rst symptoms
of narcolepsy between the ages of 15 and 30 years.
WHAT ARE THE SYMPTOMS OF NARCOLEPSY?

The symptoms of narcolepsy can appear all at once, or they can develop over many years. The
primary symptom is severe daytime sleepiness. The daytime sleepiness is often the only symptom
in children and adolescents. Other symptoms include cataplexy, sleep paralysis, hypnagogic hal-
lucinations, automatic behaviors, and disrupted nighttime sleep.
n Excessive daytime sleepiness is the main symptom of narcolepsy. People with narcolepsy of-
ten report feeling sleepy all the time. They have great diff culty f ghting the urge to fall asleep,
even when they are very motivated to stay awake. The sleepiness occurs not only in situations
in which many normal people feel sleepy (after meals or during a dull lecture), but also dur-
ing activities that are ordinarily stimulating, such as eating a meal or during a conversation.
The sleep periods may be so brief (several seconds) that sometimes neither the person with
narcolepsy nor observers realize that the person is asleep. But these can nonetheless result in
signif cant problems, such as zoning out in school or falling asleep at the wheel.
n Cataplexy is a sudden, brief, temporary loss of muscle control. It may involve the whole body
(collapsing to the f oor). But it more typically involves just specif c muscles (drooping of the
head or arm, weakness of the knees). Cataplexy is most often triggered by a strong positive
emotion, such as laughter or surprise. It can also be triggered by stress or other emotions, such
as anger. Cataplexy can be the f rst symptom of narcolepsy but it usually develops after the
daytime sleepiness.
n Sleep paralysis is a feeling of not being able to talk or move for a brief period either when
falling asleep or just after waking up. Touching the person usually causes the paralysis to dis-
appear, although it usually just ends on its own.
n Hypnagogic hallucinations are vivid, dream-like experiences that are diff cult to distinguish
from reality, occurring when falling asleep or just after waking up. The hallucinations may
involve images that are seen, heard, or felt. The images can be scary, such as of strange animals
or prowlers. These hallucinations often occur at the same time as sleep paralysis, so they are
particularly frightening because a child has no means of escape from the scary images.
n Automatic behaviors involve continuing a familiar, routine, or boring task without being
fully aware or later remembering doing it. A person is actually asleep during the activity. An
example of automatic behavior is writing a page of nonsense while doing homework.
1
2 n a r c o l EpSy
n Disturbed nighttime sleep frequently occurs in children and adolescents with narcolepsy.
Although they have diff culty staying awake during the day, they may also wake frequently
during the night. These multiple wakings make the daytime sleepiness even worse.
n Other symptoms of narcolepsy may include lethargy, low motivation, depression, poor con-
centration, and school failure. Children and adolescents with narcolepsy may be diagnosed at
f rst with depression, attention def cit hyperactivity disorder, and other mental health disorders
before the true condition is recognized. In addition, children and adolescents with narcolepsy
may have migraines and be overweight.
WHAT CAUSES NARCOLEPSY?

Narcolepsy is a disorder of the central nervous system. It affects the part of the brain that controls
sleep and wakefulness. The underlying cause of narcolepsy seems to be a decrease in specif c
brain chemicals (hypocretin/orexin) that help keep us awake. Many symptoms of narcolepsy
(cataplexy, sleep paralysis, and hypnagogic hallucinations) are features of rapid eye movement
(REM) or dream sleep, but instead occur when a person is awake. For example, hypnagogic
hallucinations look like awake dreams. Sleep paralysis is similar to the loss of muscle tone that
normally occurs during REM sleep (and prevents us from acting out our dreams). Narcolepsy
sometimes runs in families. However, most children do not have any relatives with narcolepsy.
HOW IS NARCOLEPSY DIAGNOSED?

Narcolepsy is diagnosed by (1) taking a medical history; (2) performing a physical exam to rule
out other potential causes of severe sleepiness; and (3) conducting an overnight sleep study (to
assess for other possible causes of sleep disruption) followed by a multiple sleep latency test
(MSLT). The MSLT is a diagnostic test that measures sleepiness. It involves a series of four or
f ve 20-minute opportunities (naps) to fall asleep. These are scheduled 2 hours apart on the day
following a sleep study. The MSLT documents whether the person falls asleep and how long it
takes to fall asleep. It also indicates whether there are other sleep abnormalities suggestive of
narcolepsy.
HOW IS NARCOLEPSY TREATED?

At the present time, there is no cure for narcolepsy. But the symptoms can usually be adequately
controlled so that a child or adolescent with narcolepsy can lead a normal life. Treatment usually
involves a combination of medication, lifestyle changes, and educating others.
n Medication: One or more medications are usually prescribed to control the symptoms of
narcolepsy. The excessive daytime sleepiness is often treated with stimulants (like Ritalin,
Dexedrine, or Modaf nil). Cataplexy may be treated with antidepressants (like Prozac). Caf-
feine, though, should be avoided, especially in the late afternoon and evening, so that sleep at
night is not disturbed.
n Lifestyle changes: The effective treatment of narcolepsy requires not only medication but also
adjustments in lifestyle. The following recommendations can help with the daytime sleepiness.
n Follow a strict sleepwake schedule that ensures adequate sleep. Your child should go to bed
and get up at the same time each day.

n Take regular scheduled short naps once or twice each day, as needed.
n Increase physical activity; avoid boring or repetitive tasks.
n Avoid activities that can be dangerous, such as swimming or cooking, except during times
when you know your child will be alert. Driving is a particularly important issue for adoles-
cents with narcolepsy. Your teen should not drive until the daytime sleepiness is well treated.
n a r c o l EpSy 3
n Education: Narcolepsy is a chronic disorder that affects every aspect of a childs life. There-
fore, education of everyone in your childs life, like family, friends, teachers, school nurses,
and coaches is essential. Daytime sleepiness may be mistaken for laziness, boredom, or lack of
ability. Cataplexy may be misinterpreted as a psychiatric problem. So be sure to educate fam-
ily members and help your childs friends and their parents understand narcolepsy. Most im-
portantly, make sure your childs teachers and other school personnel understand the disorder.
Small changes in class, such as allowing a child to get up and walk around the room to reduce
sleepiness or providing the opportunity to take an afternoon nap, can make a tremendous dif-
ference in a childs quality of life and academic performance.
Delayed Sleep phase Disorder
WHAT IS DELAYED SLEEP PHASE DISORDER?

Delayed sleep phase disorder (DSPD) is a common sleep problem in teenagers and young adults.
It is caused by a shift, or delay, in the normal sleepwake pattern (internal clock) by 2 or more
hours. For example, rather than falling asleep at 10:00 p.m. and waking up at 7:00 a.m., an
adolescent with DSPD will not be able fall asleep until midnight or later. He also will have a
built-in morning wake time of 9:00 or 10:00 a.m. (or later). If a child or adolescent is allowed
to sleep on his own natural schedule (like on school vacations), sleep is normal. Your child will
then feel rested and can function well. However, because most teens have schedules that require
them to get up early, adolescents with DSPD have great diff culty waking up in the morning for
school. Also, because they fall asleep so late, they usually do not get enough sleep. This leads to
them being chronically sleep deprived. On weekends or holidays, when they can sleep in, they
get enough sleep. Most children and adolescents with DSPD describe themselves as night owls
and usually feel and function their best in the late evening.
Especially for children and adolescents who go to school, DSPD can cause signif cant prob-
lems, as they are unable to get up for school. This often results in multiple school absences and
tardiness.
WHAT CAUSES DELAYED SLEEP PHASE DISORDER?

DSPD usually develops during adolescence but can start in childhood. It affects about 7% to
16% of teens and seldom occurs after the age of 30 years. Although the cause of DSPD is not
completely known, it likely is an exaggerated form of the normal shift in sleep and wake times
that occurs in all adolescents around the time of puberty. While all adolescents experience a delay
in their internal clock of about 2 hours, in those with DSPD they may shift even more. Children
who are natural night owls are also more at risk to develop DSPD. There also may be a genetic
contribution, as DSPD sometimes runs in families.
It is important to realize that DSPD involves a biological shift in sleep. This is different from
a teen that is able to fall asleep at a reasonable bedtime, but chooses to stay up later to do things
like socialize or f nish homework. A teen with DSPD wants to fall asleep earlier, but cannot. Un-
fortunately, many adolescents with DSPD end up getting labeled as noncompliant, lazy, or truant.
WHAT ARE THE SYMPTOMS OF DELAYED SLEEP PHASE DISORDER?

A child or adolescent with DSPD often experiences the following.
n Daytime sleepiness: Because of falling asleep so late and the need to get up early for school,
children and adolescents with DSPD often experience daytime sleepiness as a result of not
getting enough sleep.
n Inability to fall asleep at the desired time: On nights that children or adolescents with DSPD
try to go to sleep at a normal time, they are unable to do so. This often leads to a complaint
of insomnia. However, if they were to go to bed at their usual fall-asleep time, they would
have no problems falling asleep.
1
2 DEl ayED Sl EEp ph a SE DiSo r DEr
n Inability to wake up at the desired time: As a result of falling asleep so late, many children
and adolescents with DSPD have extreme diff culty getting up in the morning for school or
other activities. This leads to them being frequently late for or missing school.
n No other sleep complaints: Once asleep, children and adolescents with DSPD sleep well with
few or no awakenings. In addition, on days that they are able to sleep as long as they wish,
especially on weekends or holidays, sleep is normal and daytime sleepiness is not experienced.
n Other daytime symptoms: Some children and adolescents with DSPD experience problems
with irritability, depression, poor concentration, and academic and behavior problems. These
are the result of daytime sleepiness and the effects of missing school and social activities.
While some adolescents with DSPD manage, others cannot and fall further and further behind
in school. These teens may become very discouraged, which can lead to a vicious cycle in
which they become less and less motivated to get up in time for school. In some cases, school
refusal or depression is also a problem. These can complicate both diagnosis and treatment,
and often requires more intensive mental health involvement.
HOW IS DELAYED SLEEP PHASE DISORDER DIAGNOSED?

There is no def nitive test for DSPD, so the diagnosis is made based on a description of the
problem. Keeping a sleep diary over several weeks can be very helpful in identifying DSPD. The
typical pattern is a much later bedtime and wake time on weekends, with no diff culty falling
asleep. An overnight sleep study may be recommended to be sure that there are no other sleep
problems, such as obstructive sleep apnea or restless legs syndrome, but a study is not necessary
to diagnosis DSPD.
HOW IS DELAYED SLEEP PHASE DISORDER TREATED?

DSPD can be a challenge to successfully treat. It requires signif cant effort and commitment on
the part of the child or adolescent. Thus, for treatment to be successful, the child or adolescent has
to be very motivated to f x the problem. The goal of treatment is to reset the internal clock to a
more normal schedule that is more compatible with the demands of school or work.
There are usually several phases of treatment. These include an initial period in which the
sleepwake cycle is moved gradually earlier, followed by a longer maintenance phase in which
the change in sleep schedule needs to be maintained. Making the initial shift is often easier than
maintaining that change because it is easy to slip back to a later sleep schedule. Thus, an im-
portant part of the maintenance phase involves recognizing this tendency to drift to a later bed
and wake time.
Treatment of DSPD may involve some or all of the following.
n Sleep hygiene: Good sleep habits are especially important for children and adolescents with
DSPD. These include:
n A regular sleep schedule, including going to bed and waking up at the same time every day,
both on school and non-school days.

n Avoiding caffeine, smoking, and other stimulant drugs.
n A bedroom that is cool, quiet, and comfortable.
n A bedtime routine that is calm and sleep inducing.
n Avoiding stimulating activities before bed, such as using a computer and watching televi-
sion.
n It is also very important to avoid attempting to catch up on sleep either on weekends or by
napping during the day. This will only make things worse.
n Shifting the internal clock: Treatment for DSPD often involves systematically advancing or
delaying bedtime on successive nights.
n Advancing the sleepwake schedule: Advancing the sleep schedule involves moving bed-
DEl ayED Sl EEp ph a SE DiSo r DEr 3
time earlier by 15 minutes or so every few nights. For example, if your child usually falls
asleep at 12:30 a.m., then bedtime is set for 12:15 a.m. for several nights until your child
is able to fall asleep easily at the new earlier time. Bedtime is then is moved to 12:00 a.m.,
then to 11:45 p.m., and so on, until the target bedtime (such as 10:30 p.m.) is reached. A key
factor in being successful is also shifting the waketime earlier. This will help your child fall
asleep earlier the next night.
Delaying the sleepwake schedule: Delaying the sleep schedule (also called chronother-
apy) is typically used to reset bedtime and waketime in those with a very delayed natural
fall asleep time (for example, 2:00 or 3:00 a.m.). Chronotherapy involves going to bed 2 to
3 hours later each successive night. For example, if your child usually falls asleep at 2:00
a.m. and naturally wakes at 11:00 a.m., delay bedtime until 4:00 a.m. and waketime until
1:00 p.m. on day one. On day two, shift to a 6:00 a.m. bedtime and 3:00 p.m. waketime, and
so on until the desired bedtime is reached (e.g., 10:30 p.m.). This process generally takes 7
to 10 days to accomplish. This strategy works because it is easier to make yourself stay up
later than to try and fall asleep earlier. However, chronotherapy obviously involves a period
of several days during which your child is sleeping during the day and is up at night. This is
ideally done over a school or summer vacation.
Sticking with it: Once the desired bedtime and wake time are reached, your child must be
strict about keeping the same schedule, weekdays and weekends, for at least several months.
Even one night of late night studying or socializing can shift the internal clock back. Even-
tually, the schedule can become a bit more f exible.
Adjusting the daytime and evening schedule: Many teens with DSPD also have a delayed
daytime schedule. For example, they eat breakfast at lunchtime and do activities like play-
ing computer games late at night. To help reinforce the new bedtime and waketime, it is also
important to shift daytime activities early, such as eating meals and doing homework earlier.
n Melatonin: The body normally produces a hormone called melatonin, which is very impor-
tant in setting the internal clock. Melatonin is normally released in the brain in the evening, in
response to darkness, and is shut off in the morning by exposure to light. In individuals with
DSPD, this pattern of melatonin release is also delayed. Taking synthetic (artif cial) melatonin
in the evening may help shift the fall-asleep time earlier. The dose of melatonin and the time
that it is taken are both important, so it is important to discuss these with your childs doctor.
Melatonin is available without a prescription. Because the concentration and purity of differ-
ent brands may vary, some patients prefer to order pharmaceutical grade melatonin online.
Side effects of melatonin are generally minimal, but may include morning grogginess and
headache.
n Light therapy: Since a persons internal clock is controlled by light exposure, it is best for
individuals with DSPD to avoid bright light in the evening before bedtime (e.g., only have
dim lights on, avoid bright television and computer screens). This helps turn on melatonin.
They should also be exposed to bright light in the morning, such as eating breakfast in a sunny
eastern-facing spot. Sometimes treatment with a light box, which delivers intense light, is
recommended. This involves sitting in front of a light box for 20 to 30 minutes right after get-
ting up in the morning. The light box should be positioned 16 to 20 inches away at head or
chest level. Staring directly at the light box is not necessary, and, in fact, should be avoided, as
eye irritation can occur. This is especially the case in individuals with fair skin and light eye
color. Also, some antibiotics and acne creams may increase light sensitivity. Light boxes or
visors are portable and can be obtained online at such sites as www.litebook.com, www.apol-
lolight.com, and www.lighttherapyproducts.com.
insomnia
WHAT IS INSOMNIA?
Insomnia refers to diff culties falling asleep or staying asleep, including the problem of waking
too early in the morning. Chronic insomnia is experienced by approximately 10% of adolescents,
and is much less common in children. Insomnia can be a short-term problem, usually related to a
stressful event, or it can be long term and chronic.
Many times, insomnia is a symptom that is caused by something else. Just like pain, which can
be a symptom of many things, problems with falling asleep or staying asleep may be the result
of another sleep disorder or other problem (e.g., anxiety). When the insomnia is not related to
another sleep disturbance, psychiatric problem, or medical problem, it is referred to as primary
insomnia or psychophysiological insomnia.
WHAT CAUSES INSOMNIA?

Primary insomnia almost always involves A., poor sleep habits, such as spending too much time
in bed, napping during the day, or not going to bed and waking up at the same time every day, B.,
negative thoughts about sleep, such as Ill never be able to fall asleep tonight, and C., tension
and worry about sleeping.
WHAT ARE THE SYMPTOMS OF INSOMNIA?

A child or adolescent with insomnia may have the following symptoms.
n Diff culty sleeping: A child or adolescent with insomnia has diff culty falling asleep or stay-
ing asleep, or may wake too early in the morning.
n Behaviors that interfere with sleep: Such behaviors may include worrying during the day
about falling asleep at night and trying too hard to fall asleep. (But adolescents with insomnia
usually can fall asleep at other times, such as while watching television.)
n Tension about sleep: A child or adolescent with insomnia is usually tense about going to bed
and about being able to sleep.
n Daytime problems: A child or adolescent with insomnia may complain about having diff -
culty functioning during the day, is often tired, and may be moody or irritable.
HOW IS INSOMNIA DIAGNOSED?

There is no def nitive test for insomnia, so a diagnosis is made based on the description of symp-
toms. A medical history should also be done to exclude other problems, such as another sleep
disorder, a medical problem, or a psychiatric problem.
HOW IS INSOMNIA TREATED?

Treatment of insomnia, because it is a learned habit, requires effort and patience. Treatment can
involve the following.
1
2 in So mn ia
n Sleep hygiene: Good sleep habits are essential for children and adolescents with insomnia.
These habits should include a regular sleep schedule that involves going to bed and waking up
at the same time every day; avoiding caffeine, tobacco, and other drugs; sleeping in a room that
is cool, dark, quiet, and comfortable; establishing a bedtime routine that is calm and sleep in-
ducing; and avoiding all stimulating activities at or close to bedtime, such as computer games
and television.
n Relaxation: Teaching a child or adolescent relaxation strategies, such as deep breathing, posi-
tive imagery (e.g., being on a beach), or meditation, can help her to relax at bedtime. It will
also give her something pleasant to think about while lying in bed.
n Change thoughts about sleep: Since most children or adolescents with insomnia have nega-
tive thoughts about sleep, such thoughts should be replaced by positive ones. For example,
rather than saying, I wont be able to sleep tonight, it is better to think, Tonight Ill just relax
and rest at bedtime.
n Dont be a clock watcher: Remove the clock from the bedroom, as watching a clock during
the night may feed your childs anxiety, thus making it harder for her to fall asleep.
n Restrict the time in bed: Set bedtime so that the time in bed is equal to the usual amount of
sleep each night, such as 7 or 8 hours. Being extra sleepy will help a child or adolescent to
fall asleep right away and stay asleep. Once that happens, bedtime can be moved earlier by 15
minutes every few nights until the desired bedtime is reached.
n Get out of bed: Rather than lying in bed tossing and turning, its better to get out of bed and
do another activity, which will also help prevent the bedroom from being associated with
sleeplessness. After 20 minutes of trying to fall asleep, get out of bed for 20 minutes and do
something relaxing (such as readingnot watching television!). Then try again, repeating the
20-minutes-in-bed, 20-minutes-out-of-bed cycle.
n Medication: Medications are usually not recommended for children and adolescents with
insomnia.
Seven Rules for Beating Insomnia

1. Choose a set wake-up time: Wake up at the same time every day, no matter how much or
how little sleep you got the night before.
2. Choose a bedtime: Choose the earliest possible bedtime that is late enough that you are
sleepy but is not so early that it doesnt let you be in bed too long. You only want to spend
the amount of time in bed that you actually need for sleep.
3. Go to bed when you are sleepy, but not before your chosen bedtime: Dont go to bed
until you are sleepy. So, if you are still wide awake at your chosen bedtime, wait a while
longer until you are sleepy enough to fall asleep quickly.
4. Get out of bed when you cant sleep: If you are lying in bed and cant sleep, get out of
bed and do something relaxing out of the bedroom such as reading a book. Go back to bed
when you feel sleepy enough to fall asleep quickly. Again, if you do not fall asleep quickly,
get up. Keep repeating this cycle until you fall asleep. You need to get out of bed when you
cant sleep both at bedtime and in the middle of the night.
5. Dont worry or plan in bed: When lying in bed at night, dont spend the time worrying
or planning for the next day. Set aside another time of the day to do these things. If you
automatically start thinking and worrying when you get in bed, get up and dont head back
to bed until your thoughts wont interfere with falling asleep. Thinking in bed is a habit, and
one that you can break.
6. Only use your bed for sleep: Dont do anything but sleep in your bed. That is, dont do
other activities, such as watch television or do homework.
7. Avoid naps: Naps will interfere with your ability to fall asleep at bedtime, so no naps.
Adapted from Owens, J. A., & Mindell, J. A. (2005). Take Charge of Your Childs Sleep. New
York: Marlowe.

A Clinical Guide To Pediatric Sleep

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A Clinical Guide To Pediatric Sleep

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A Clinical Guide to

Judith A. Owens, M.D., M.P.H.

2010 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business

Library of Congress Cataloging-in-Publication Data

Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi

Section i: introduction to Pediatric Sleep

Section ii: Pediatric Sleep Disorders

Section iii: Sleep and Medications

Section iV: Sleep in Special Populations

Suggested Readings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211

The following appendices can be found online on the books website:

Def nition of Sleep

Insuff cient Sleep

in SuFFic ien t Sl eeP

n Risk-taking behaviors, especially in adolescents.

Functions of Sleep: Cognition

30 seconds to 5 minutes. Recall of fragmented visual imagery (hypnogogic hallucinations)

Sleep Stage Percentages in Healthy Young Adults

t ABl e 1.1. Normal developmental changes in childrens sleep architecture

Age Category Sleep Physiology

n eur o An At o My An D Ph ySio l o g y o F Sl eeP

The Importance of Morning Light Exposure

Sl eeP AS An in t r in Sic Bio l o g ic Al Pr o c eSS An D Sl eeP AS A

Nature vs. Nurture

What Is Enough Sleep?

Developmental issues t hat May impact Sleep

c ommon Sleep issues

Safe Sleep Practices for Infants

Prevalence of Sleep Problems

o ther important c oncepts

n Naps: average is 3 to 4 hours

times during infancy)

Developmental issues t hat May impact Sleep

Sleep as a Social Behavior

c ommon Sleep issues

Prevalence of Sleep Problems

c ommon Sleep Disorders

o ther important c oncepts

To Co-sleep or Not to Co-sleep

t o DDl er S (12 Mo n t h S t o 3 yeAr S)

n Naps: average is 2 to 3 hours

Developmental issues t hat May impact Sleep

c ommon Sleep issues

Prevalence of Sleep Problems

c ommon Sleep Disorders

o ther important c oncepts

Cultural and Family Context of Sleep

Developmental issues t hat May impact Sleep

Macro Sleep Micro Sleep

Sleep Practices Health Issues

c ommon Sleep issues

Los casos de Prevalence of Sleep Problems

o ther important c oncepts

Developmental issues t hat May impact Sleep

Healthy Sleep/Healthy Child

The Electronic Sandman

c ommon Sleep issues

Prevalence of Sleep Problems

c ommon Sleep Disorders

o ther important c oncepts

Owls and Larks

ADo l eSc en t S (12 t o 18 yeAr S)

Developmental issues t hat May impact Sleep