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Karl Doghramji, Anna Ivanenko: Chapter 56. Sleep Disorders, in Gabbard’s Treatments of Psychiatric Disorders, 4th

Edition. Edited by Glen O. Gabbard. Copyright ©2009 American Psychiatric Publishing, Inc. DOI:

10.1176/appi.books.9781585622986.264175. Printed 5/10/2009 from www.psychiatryonline.com

Gabbard’s Treatments of Psychiatric Disorders > Part XI. Sleep Disorders >

Chapter 56. Sleep Disorders

INTRODUCTION

This chapter includes disorders subsumed under the broad category of sleep disorders in

DSM-IV-TR (American Psychiatric Association 2000). The category is organized into four sections.

The first section, that of the dyssomnias, includes disorders of the amount, quality, or timing of

sleep, such as primary insomnia, primary hypersomnia, narcolepsy, breathing-related sleep

disorder, dyssomnia not otherwise specified, and circadian rhythm sleep disorder. Treatment

principles for the excessive sleepiness of primary hypersomnia are similar to those for narcolepsy;

therefore, primary hypersomnia will not be discussed separately in this chapter. The second section

is comprised of the parasomnias, disorders involving abnormal behavioral or physiological events

occurring in association with sleep, specific sleep stages, or sleep–wake transitions. The final two

DSM-IV-TR sleep disorder sections pertain to sleep disorders related to another mental disorder

and to a general medical condition, respectively. Disorders falling within these latter two sections

are not addressed in our review, because they comprise a heterogeneous group of disorders

involving sleep-related symptoms secondary to other conditions that are more thoroughly reviewed

in other sections of this volume. This chapter covers disorders encountered during both childhood

and adulthood.

A strong effort has been made to include a broad range of treatments for all of the disorders

mentioned, encompassing various modalities such as behavioral, cognitive, and pharmacological,

among others. However, the focus is understandably on treatments that are most widely accepted,

have the greatest scientific support, and are of greatest clinical relevance. An attempt is made to

emphasize the multimodal approach.

Statement of off-label usages. The use of melatonin and other herbal remedies and dietary supplements is not

regulated by the U.S. Food and Drug Administration (FDA). The authors have determined that, to the best of their

knowledge, the following pharmacological compounds are not approved for the listed uses by the FDA: doxylamine,

diphenhydramine, and all antidepressants for insomnia; all medications discussed for children and adolescents for all

conditions; methylphenidate and mazindol for excessive daytime somnolence in narcolepsy; all antidepressants for

excessive daytime somnolence and auxiliary symptoms of narcolepsy; all agents for restless legs syndrome, with the

exception of ropinirole; all agents for periodic limb movement disorder; theophylline, naloxone, and

medroxyprogesterone acetate with acetazolamide for central sleep apnea; supplemental oxygen for all disorders;

stimulants and hypnotics for circadian rhythm sleep disorders; and all pharmacological agents for the parasomnias.

DYSSOMNIAS

The dyssomnias are disorders of the amount, quality, or timing of sleep. Included in this category

are primary insomnia, primary hypersomnia and narcolepsy (discussed together in our review),

breathing-related sleep disorder, dyssomnia not otherwise specified, and circadian rhythm sleep

disorder.

Primary Insomnia

Primary insomnia involves a complaint of difficulty initiating or maintaining sleep, or of

nonrestorative sleep, that lasts for at least 1 month; causes clinically significant distress or

impairment in social, occupational, or other important areas of functioning; does not occur

exclusively during the course of another disorder; and is not due to the direct physiological effects

of a substance or a general medical condition. In adults, if the determination is made that primary

insomnia is the core issue, the optimal treatment is a combination of behavioral sleep-inducing

strategies and pharmacological agents. Pharmacological agents have the advantage of providing

rapid relief from insomnia and restoring daytime function. Nevertheless, although behavioralPrint: Chapter 56. Sleep Disorders

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measures may take longer to implement, follow-up studies indicate that individuals receiving

cognitive-behavioral therapy (CBT), either alone or in combination with hypnotics, maintain their

gains longer and have better sleep 2 years after the termination of treatment (Morin et al. 1999)

when compared with individuals receiving hypnotic medications alone. The optimal approach,

therefore, appears to be a combination of the two modalities. After CBT techniques are mastered,

hypnotic medications can be gradually withdrawn while CBT is maintained for longer periods if

necessary. Below we discuss some of the more commonly utilized nonpharmacological strategies

(reviewed in Spielman 1987).

Nonpharmacological Interventions for Primary Insomnia

Sleep Hygiene Education

Although the efficacy of sleep hygiene education is not well established by empirical studies, these

measures are often utilized by sleep clinicians and warrant consideration in all insomnia disorders

(Table 56–1).

Table 56–1. Sleep hygiene education

Maintain a regular wake time

Avoid excessive time in bed

Avoid naps, except if shift worker, with narcolepsy, or elderly

Expose yourself to bright light while awake

Use the bed only for sleeping and sex

Avoid nicotine, caffeine, and alcohol

Exercise regularly early in the day

Do something relaxing before bedtime

Don’t watch the clock

Eat a light snack before bedtime if hungry

Relaxation Training

The goal of relaxation training is to reduce tension, stress, or arousal that interferes with sleep.

Interventions used include electromyogram (EMG) biofeedback, abdominal breathing exercises, and

progressive muscle relaxation techniques, among others.

Cognitive Psychotherapy

Cognitive psychotherapy is a “talk therapy” in which therapist and patient work together to identify

and dispel thoughts that are tension producing for the patient and that have a negative effect on his

or her sleep, such as preoccupation with unpleasant work experiences or examinations at school.

Stimulus Control Therapy

Stimulus control therapy is well suited for insomniac patients who spend a great deal of time in bed

brooding over sleeplessness. Patients are asked to use the bed only for sleeping (not for reading or

watching television) and to not remain in bed trying to sleep for more than 10–20 minutes at a

time. Rather, they are urged to go into another room and to return to bed only when they feel

sleepy.

Restriction of Time Spent in Bed

Sleep-restriction therapy is well suited for insomniac patients who wake up repeatedly during the

course of the night, such as the elderly. Sleep is monitored through sleep diaries, and a sleep

efficiency index is calculated by dividing the average daily time spent asleep by the average daily

time spent in bed. The clinician then asks the patient to lie in bed, on a daily basis, for a time that isPrint: Chapter 56. Sleep Disorders

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equivalent to his or her total sleep time. The patient continues to fill out sleep logs and calls the

physician every 5 days with log data. If the sleep efficiency during the prior 5 days is less than

85%, no changes are made. However, if the sleep efficiency is greater than 85%, time in bed is

increased by 15 minutes, by allowing the patient to go bed earlier. No changes are made to the

morning awakening time. Patients avoid napping. Over the course of a few weeks, consolidation of

sleep is usually noted, along with an increase in the quality and the sensation of restorative sleep.

Pharmacological Strategies for Primary Insomnia

Hypnotic Agents

Hypnotic agents commonly used in the treatment of primary insomnia are listed in Table 56–2.

Table 56–2. Hypnotic agents used in the treatment of primary insomnia

Generic Trade name

Half-lifea

Active metabolites DEA Schedule Dose (mg)

Benzodiazepines

Flurazepam Dalmane 2.3–100 Yes 4 15, 30

Quazepam Doral 25–84 Yes 4 7.5, 15

Estazolam Prosom 10–24 No 4 0.5–2.0

Temazepam Restoril 8–22 No 4 7.5, 15

Triazolam Halcion < 6 No 4 0.125–0.5

Benzodiazepine receptor agonists

Eszopiclone Lunesta 6 No 4 1–3

Zolpidem Ambien 2.5 No 4 5, 10

Zolpidem ER Ambien CR 2.8 No 4 6.25, 12.5

Zaleplon Sonata 1 No 4 5–20

Melatonin receptor agonists

Ramelteon Rozerem 1–5 No Not scheduled 8

Note.CR = controlled release; DEA = Drug Enforcement Administration; ER = extended release.

a Parent compound and active metabolites.

Older preparations such as chloral hydrate and the barbiturates have a limited role in primary

insomnia because of side effects such as daytime hangover, lightheadedness, malaise, ataxia, and

nightmares. They are also more dangerous in overdose (Harding and Limbard 1996). The

subsequently introduced benzodiazepine agents have a more favorable side-effect profile and are

distinguished primarily by length of elimination half-life. In general, the potential for daytime

sedation, motor incoordination, amnesia, and slower reflexes is greater for the agents with a longer

elimination half-life (Greenblatt et al. 1981; Thomson Micromedex 2006).

The benzodiazepine receptor agonists (BzRAs) are structurally unrelated to the benzodiazepines

yet share a similarity in receptor activity, in that they are also active at the gamma-aminobutyric

acid (GABAA)–benzodiazepine receptor complex. Animal studies have identified six subunits (1–6)

within the GABAA receptor complex (Möhler et al. 2002). Benzodiazepine hypnotics demonstrate

more or less indiscriminate binding affinities to subunits 1, 2, 3, and 5. The BzRAs, by contrast,

display greater selectivity in binding affinities to specific subunits; for example, zolpidem in vitro

binds preferentially to the 1 receptor. However, the clinical relevance of these differential binding

profiles is still largely a matter of speculation.

As with the benzodiazepines, the most clinically relevant pharmacokinetic parameter for the BzRAs

appears to be elimination half-life. The shortest-half-life agent is zaleplon; thus, this agent is also

the least likely to cause daytime carryover effects when administered at bedtime. Its ultrashortPrint: Chapter 56. Sleep Disorders

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half-life also allows for administration in the middle of the night, as long as the patient is in bed for

a minimum of 4 hours following administration. This same feature is less desirable, however, for a

patient with difficulty in sleep initiation and discontinuous sleep throughout the course of the night.

Zolpidem, zolpidem extended-release (ER), and eszopiclone may be better suited for this purpose.

Zolpidem ER consists of a coated two-layer tablet, one layer that releases its drug content

immediately and another layer that more slowly releases additional drug content; this dual release

provides greater drug concentration during the latter portions of the night. Zolpidem ER and

eszopiclone do not have a limitation imposed regarding duration of use. Although zolpidem ER has

not been investigated in controlled trials lasting longer than 3 weeks, eszopiclone was the subject

of a 6-month study that demonstrated a lack of tolerance during that entire period and a lack of

rebound after rapid discontinuation (Krystal et al. 2003). These positive findings regarding safety

of eszopiclone following long-term use are encouraging for patients who may require longer-term

management. However, periodic reevaluation is still a prudent clinical measure for all hypnotic

agents prescribed for long periods of time. Like the benzodiazepines, the BzRAs are Drug

Enforcement Administration (DEA) Schedule IV agents and carry a risk of dependence and abuse.

As a class, their main adverse effects include daytime drowsiness, dizziness, light-headedness, and

difficulty with coordination. Side effects are greater for the longer-half-life agents and with higher

doses.

Heretofore, all of the marketed hypnotic agents have shared a common mechanism of action, in

that they are all GABAA receptor agonists. A recently introduced medication for insomnia with a

different mechanism of action is ramelteon (Rozerem package insert 2005), which has affinity for

both MT1 and MT2 melatonin receptors in the brain. These receptors, acted upon by endogenous

melatonin, are thought to be involved in sleep–wake and circadian rhythms, although these

properties are still under investigation. The activity of ramelteon at these receptors may also be

important for its clinical properties (Hirai et al. 2005; Kato et al. 2005). The most consistent

sleep-related effect of this agent has been in reducing sleep latency; it is, therefore, indicated for

the treatment of insomnia characterized by difficulty with sleep onset. Although controlled

long-term studies are lacking, ramelteon does not have a limitation regarding duration of use. It

appears to lack abuse liability and is not a DEA controlled substance. Its main adverse effects are

daytime drowsiness and dizziness.

It should be noted that because of space constraints, not all adverse effects of all hypnotic agents

have been thoroughly reviewed here. Readers are referred to the end-of-chapter references for

further information.

Nonhypnotic Agents

Many agents not specifically indicated for insomnia are used for sleep induction. Antihistamines

such as doxylamine and diphenhydramine are available over the counter and are often used as

sleep aids. Although these agents can be sedating, they have unpredictable efficacy and side effects

such as daytime sedation, confusion, delirium, and systemic anticholinergic effects (Agostini et al.

2001; Gengo et al. 1989).

Sedating antidepressants, at low doses, are commonly used for the treatment of insomnias not

associated with depression. However, these agents have not been well explored for this use. The

antidepressant most commonly used for sedation, trazodone, was examined in a controlled trial at a

dosage of 50 mg. Although improvement in subjective sleep latency and duration was demonstrated

during the first week of use, efficacy was lost by the second week of administration (Walsh et al.

1998). Doxepin, another sedating antidepressant, also demonstrated improvement in total sleep

time in a 4-week controlled trial at dosages of 25–50 mg (Hajak et al. 2001). These antidepressants

are also associated with side effects; in the case of trazodone, effects include daytime sedation,

orthostatic hypotension, and priapism. The tricyclic antidepressants are also, as a class, associated

with anticholinergic side effects, such as dry mouth, urinary flow difficulties, and cardiac

dysrhythmias, among others.

Melatonin, considered a dietary supplement, has been used in doses of 0.5–3,000 mg for inductionPrint: Chapter 56. Sleep Disorders

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of sleep, yet studies suffer from methodological pitfalls (Kryger et al. 2005). Anecdotal reports

indicate that melatonin may be efficacious in certain subtypes of insomnia, such as those

associated with shift work, jet lag, blindness, delayed sleep phase syndrome, and the elderly.

However, its efficacy has not been conclusively established. Additionally, concerns have been

expressed both regarding melatonin’s side effects (after the observation of coronary artery tissue

stimulation in animals) and regarding the purity of available preparations. Melatonin’s side effects

may include sleepiness, nausea, and headaches, although these have not been adequately

investigated.

Herbal remedies are also commonly utilized for insomnia; some examples include Valerian,

Chamomilla, kava-kava (Piper methysticum), Passiflora, Avena sativa, and Humulus lupulus

(Ringdahl et al. 2004). These preparations have, at best, shown mild hypnotic ability in limited

studies.

Treatment of Insomnia in Children and Adolescents

In children, nonpharmacological interventions are almost always the first choice of treatment for

insomnia. Behavioral interventions include parental education, sleep hygiene education, extinction,

graduated extinction, scheduled awakenings, and positive bedtime routines (Kuhn and Elliott 2003;

Mindell 1999). Any behavioral intervention for sleep-initiation problems in children should include

education on normal sleep development and establishment of appropriate and realistic parent and

child expectations and treatment goals. School schedules and extracurricular activities should be

taken into consideration when establishing a treatment protocol. It is very important to set and

consistently reinforce fixed bedtimes and rise times. Bedtime should be age appropriate, with an

established bedtime routine to provide behavioral cues for transition to sleep. Morning rise time is

especially important as a powerful environment cue for entrainment of the sleep–wake cycle.

Avoidance of excessive fluids at bedtime and of caffeinated beverages helps with sleep onset and

reduces the likelihood of nocturnal awakenings. Sleeping environment should be controlled to

exclude television, video games, computers, and other such distractions. Children should be

encouraged to sleep in their own bed on a consistent basis. For young children, establishment of

appropriate nap times is very important, given that nap schedules will affect nocturnal sleep onset

and sleep duration. Long and frequent naps will inevitably result in reduced nocturnal sleep periods

and delayed sleep-onset time and may cause nocturnal awakenings.

Extinction has been the most commonly used and researched type of behavioral intervention for

sleep-onset association disorder, night awakenings, and limit-setting sleep disorder. However,

standard extinction strategies can be difficult to implement because of parental problems with

compliance with behavioral protocols and their inability to ignore extinction bursts. Therefore,

graduated extinction is usually better accepted; this involves parental “checks” while ignoring

undesirable child behavior such as crying, temper tantrums, and the like, with longer delays until

the child falls asleep. Various reward systems can be introduced to reinforce positive improvements

and facilitate more rapid development of adaptive sleep-onset associations (Kuhn and Elliott 2003;

Mindell 1999).

Scheduled nocturnal waking is especially useful in children with sleep-maintenance insomnia and

frequent spontaneous awakenings. Parents are instructed to awaken the child 15–30 minutes

before an anticipated spontaneous awakening. This has the result of altering sleep staging and

restarting a new sleep cycle. Sleep restriction is also suited for this purpose; it aims to restrict time

in bed to the actual time of sleep followed by a gradual advancement of bedtime to a more optimal

one. Regardless of the behavioral approach chosen, a key determinant of success is parental

compliance.

There are no well-designed controlled studies of sedative-hypnotics in children, and there are no

U.S. Food and Drug Administration (FDA)–approved pharmacological agents for use in pediatric

insomnia (Owens et al. 2005). Among the antihistamines, diphenhydramine hydrochloride is the

most commonly used agent in children for sleep-initiation problems. Dosages range from 12.5 to 25

mg at bedtime for children ages 2–6 years, and from 25 to 50 mg and above for children 6–12 yearsPrint: Chapter 56. Sleep Disorders

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and older (Reed and Findling 2002). Preliminary studies indicate that this agent reduces sleep

latency and improves sleep continuity in children. Diphenhydramine is usually recommended for

short-term use only. Side effects include drowsiness, behavioral agitation, and occasional

hypertension. There have been reports of life-threatening adverse effects from overdose on

histamine H1 antagonists in younger children, including seizures and death (Baker et al. 2003).

Alpha-adrenergic agonists such as clonidine and guanfacine, indicated for treatment of

hypertension, have been used for sleep difficulties in children with neurological and

neurodevelopmental disorders, as well as attention-deficit/hyperactivity disorder (ADHD).

However, there are no well-designed studies examining the effects of clonidine on sleep

architecture and daytime functioning in children and adolescents. One uncontrolled retrospective

study suggested that clonidine at dosage ranges of 50–800 mcg at bedtime demonstrated a

sustained effect, over a 3-year period, in treating sleep-onset insomnia in children with ADHD

(Prince et al. 1996). However, adverse effects were not systematically collected. This class of

medications should be used with extreme caution, as it is associated with bradycardia, palpitations,

dry mouth, and rebound hypertension on abrupt discontinuation. Therefore, parents should be

instructed to gradually taper the medication dosage prior to discontinuation. Alpha-adrenergic

agonists are also associated with dysphoria and depression following long-term use.

The use of tricyclic antidepressants for insomnia in children is diminishing in popularity. Only two

studies have examined the effects of imipramine on sleep architecture, and both involved small

samples of children with major depression. Imipramine was associated with a suppression in rapid

eye movement (REM) sleep, an increase in stage 2 sleep, and a decrease in stage 4 sleep (Kupfer et

al 1979; Shain et al. 1990). There are no established hypnotic dose recommendations for children.

Similarly, there are no systematic data available on the safety and tolerability of trazodone in

children with insomnia. However, one report suggested that trazodone was associated with a

reduction of sleep-onset insomnia in children after administration of 25–50 mg at bedtime

(Kallepalli et al. 1997).

Benzodiazepine hypnotics are rarely used in children, with the exception of clonazepam 0.25–0.5

mg, which has been employed to treat parasomnias. Little information is available on the use of the

BzRAs in children. If these agents are utilized, dosage adjustment may be warranted, given that the

clearance of zolpidem may be up to three times higher in children than in young adults (Salva and

Costa 1995). The use of adult doses in children has been associated with frightening experiences,

such as hypnagogic hallucinations and paradoxical agitation (Pelayo et al. 2004). The advantage of

the BzRAs over the benzodiazepine hypnotics is their rapid onset of action and shorter half-life.

Clearly, further research is needed before these drugs can be recommended for use in pediatric

insomnia.

The use of melatonin in children has been investigated, especially in the case of sleep-initiation

insomnia caused by circadian factors (Ivanenko et al. 2003a; Palm et al. 1997). A double-blind,

placebo-controlled trial conducted by Smits et al. (2001) in normal healthy elementary school

children suggested that 5 mg of melatonin administered at bedtime may be effective in reducing

sleep-onset latency and in increasing total sleep time. Dosage recommendations for children of

different ages are lacking, as are data on the long-term efficacy and safety of this agent in pediatric

populations.

Primary Hypersomnia

Primary hypersomnia is characterized by excessive sleepiness, as evidenced either by prolonged

sleep episodes or by daytime sleep episodes occurring almost daily, that lasts for at least 1 month;

causes clinically significant distress or impairment in social, occupational, or other important areas

of functioning; does not occur exclusively during the course of another sleep disorder or mental

disorder; and is not due to the direct physiological effects of a substance or a general medical

condition. Treatment principles for the excessive sleepiness of primary hypersomnia are similar to

those for narcolepsy, as discussed below.Print: Chapter 56. Sleep Disorders

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Narcolepsy

Narcolepsy is characterized by a main complaint of excessive daytime sleepiness, variably

accompanied by auxiliary symptoms that may include cataplexy, hypnopompic or hypnagogic

hallucinations, sleep paralysis, and disrupted nocturnal sleep. It is an incurable neurological

disorder that persists for life. Narcolepsy usually develops during childhood, yet it most often does

not come to clinical attention until late adolescence or early adulthood. Prior to treatment, a

thorough diagnostic evaluation is critical, preferably in the context of a sleep disorders center, to

avoid lifelong treatment with highly controlled medications. Behavioral treatment approaches are

important, since they can decrease the magnitude of daytime sleepiness (Rogers et al. 2001).

Behavioral interventions include maintenance of good sleep hygiene habits to ensure that sleep

quality is not further impaired, as sleep quality impairment can contribute to daytime somnolence;

avoidance of sleep deprivation and shift work; use of scheduled naps; avoidance of alcohol and

recreational substances; and avoidance of stimulant substances close to bedtime. Patients with

narcolepsy should be advised to avoid driving and engaging in other potentially dangerous activities

when sleepy. Career counseling for patients, and education for their employers, is often necessary.

Behavioral treatments alone can suffice for some individuals with narcolepsy. However, chronic

treatment with pharmacological agents is often necessary. A dual approach should be considered,

with stimulants for excessive daytime sleepiness (EDS) and REM-suppressing agents for auxiliary

symptoms such as cataplexy, hypnagogic hallucinations, and sleep paralysis (Standards of Practice

Committee 2001). Pharmacological agents used in the treatment of narcolepsy are listed in Table

56–3.

Table 56–3. Pharmacological treatment of narcolepsy

Drug

Usual dosage*

Treatment of excessive daytime sleepiness (EDS)

Stimulants

Modafinil

100–400 mg/day

Methylphenidate 10–60 mg/day

Dextroamphetamine 5–60 mg/day

Methamphetamine 20–25 mg/day

Mazindol

4–8 mg/day (divided dosage)

Other agents

Gamma-hydroxybutyrate (sodium oxybate) 6–9 g/day (divided into two doses)

Adjunct-effect drugs (i.e., improve EDS if associated with stimulant)

Protriptyline

2.5–10 mg/day

Viloxazine

50–200 mg/day

Treatment of auxiliary symptoms

Gamma-hydroxybutyrate (sodium oxybate) 6–9 g/day (divided into two doses)

Antidepressants without atropinic side effects

Fluoxetine

20–60 mg/day

Venlafaxine

75–300 mg/day

Viloxazine

50–200 mg/day

Antidepressants with atropinic side effects

Protriptyline

2.5–20 mg/dayPrint: Chapter 56. Sleep Disorders

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Drug

Usual dosage*

Imipramine

25–200 mg/day

Clomipramine

25–200 mg/day

Desipramine

25–200 mg/day

*

Occasionally, depending on clinical response, the dose may be outside the usual dosage range.

Source. Adapted from Mignot 2005.

The relative efficacy of these agents has not been adequately explored (Mitler et al. 1994).

Longer-acting stimulants (e.g., modafinil, sustained-release amphetamine) can provide all-day

benefit following morning administration. However, stimulants with a short duration of action (e.g.,

methylphenidate) can be used in combination to achieve alertness quickly during the course of

daily activities. Short-acting stimulants can also be administered later in the day with less concern

regarding insomnia. Stimulants with the exception of modafinil can also provide anticataplectic

effects. However, the addition of an REM suppressant is often necessary. Gamma-hydroxybutyrate

(GHB) has positive effects both for cataplexy and for EDS. Because it is a potent sedative, however,

GHB should be administered at bedtime after the patient is already in bed, to avoid mishaps due to

motor impairment. A second dose is administered 2–3 hours later, again while the patient is in bed.

Side effects associated with the stimulants include irritability, talkativeness, sweating, headaches,

irritability, nervousness, tremulousness, anorexia, insomnia, gastrointestinal complaints,

dyskinesias, and palpitations. Psychotic symptoms such as hallucinations may be more common in

individuals with a history of psychiatric disorders. Tolerance to stimulants, although possible, has

not been well described in narcolepsy. Modafinil’s most common side effects are headache, nausea,

and nervousness/anxiety. Most stimulants have a Schedule II DEA designation, whereas modafinil

has a Schedule IV designation. GHB is a DEA Schedule III medication; its most common side effects

are disorientation and sedation if patients awaken during the course of the night. Also reported are

enuresis, nausea, and somnambulism. Because GHB has potent sedative properties, it should not be

used with alcohol or other central nervous system depressants and in untreated obstructive sleep

apnea syndrome. GHB has a high sodium content and thus should not be used by individuals with

compromised renal function, uncontrolled hypertension, or unstable cardiac failure (Micromedex

2006).

There are no double-blind, placebo-controlled studies for children with narcolepsy.

Psychostimulants have been approved for use in children with ADHD, and their safety has been well

established among pediatric populations. Methylphenidate and dextroamphetamine have been

successfully used to treat excessive sleepiness in children with narcolepsy and overall are well

tolerated.

Modafinil at dosages of 200–600 mg/day in two to three divided doses was studied in a small

sample of children with narcolepsy. It was found to be effective in reducing daytime sleepiness

without producing clinically significant side effects (Ivanenko et al. 2003b). Because of its

favorable side-effect profile, modafinil may be considered as a first-line medication for the

treatment of EDS in children with narcolepsy (Pelayo et al. 2004).

Among anticataplexy agents, the antidepressants clomipramine and fluoxetine are the most

commonly used medications. Other tricyclic antidepressants such as imipramine, desipramine, and

protriptyline, as well as other serotonin reuptake inhibitors and mixed-action antidepressants, have

been used in controlling symptoms of cataplexy in children and adolescents.

Breathing-Related Sleep Disorder

Breathing-related sleep disorder is characterized by an impairment in the normal process of

respiration that occurs during sleep. In adults, obstructive sleep apnea syndrome (OSAS) is the

most common of the breathing-related sleep disorders. In this disorder, apneas, or cessations in

ventilation, occur repeatedly during sleep and are due to the closure of the upper airway. ThePrint: Chapter 56. Sleep Disorders

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diagnosis must be established through polysomnography prior to the institution of treatment

(Kushida et al. 2005).

Devices Used to Treat OSAS

The most widely used initial treatment approach for OSAS is the application of nasal continuous

positive airway pressure (CPAP) during sleep (Sullivan et al. 1981). Before beginning treatment,

the optimal air pressure setting must be determined through a titration polysomnographic study.

Although CPAP treatment is highly efficacious, its primary limitation is compliance; the device must

be worn during the entire sleep period to ensure maximal efficacy, yet the proportion of patients

adhering to this guideline may be as low as 20% (Kribbs et al. 1993). Although some patients

discontinue use of the device because of inconvenience, the most common complaints leading to

noncompliance relate to the mask interface (mask tightness, bridge-of-nose pain, facial

indentations, air leakage) (Hoffstein et al. 1992). Other reported adverse experiences include nasal

congestion, dryness, rhinorrhea, claustrophobic air swallowing, and chest discomfort.

Methods of enhancing compliance with CPAP treatment include use of a variety of mask interfaces,

such as oral, intranasal, and full-face masks; use of inline heated humidification; ramping, wherein

pressure is transiently reduced by the patient; use of chin straps to prevent oral air leakage; and

use of bilevel positive airway pressure (BiPAP) devices. By independently adjusting pressure levels

during respiration, BiPAP devices produce lower pressures during the expiratory phase of

respiration, thus permitting the patient to breathe out against a lower positive pressure. Patients

experiencing claustrophobic reactions may benefit from desensitization methods and even

anxiety-reducing medications, although the utility of these approaches has not been adequately

explored.

Other treatment methods include oral appliances (Thorpy et al. 1995), most of which are

mandibular repositioning devices, which achieve a forward motion of the mandible and a slight

opening of the bite area during sleep. The net effect is an enlargement of the airway. Some also

change the posture of the tongue. Efficacy data for oral appliances indicate that although the

respiratory disturbance index improves in the majority of patients, as many as 40% of individuals

treated are left with significantly elevated indexes (Schmidt-Nowara et al. 1995). Therefore, these

devices are generally used only as second-line treatment, for patients who cannot tolerate the

first-line treatment (i.e., CPAP).

Medication Treatment of OSAS

Medications have a limited role in the treatment of OSAS. Supplemental oxygen (Fletcher and

Munafo 1990) also has a limited role; although it can diminish the severity of oxyhemoglobin

desaturation, it also may prolong apneas and diminish ventilatory capacity in patients with

obstructive lung disease and CO2 retention.

Surgical Treatment of OSAS

A variety of surgical methods are also used to treat OSAS. The most efficacious of these is

tracheostomy, which bypasses the entire upper airway. Because of its long-term complications,

however, tracheostomy is not commonly recommended. Upper airway reconstruction surgeries are

more commonly performed; these include uvulopalatopharyngoplasty (UPPP), laser-assisted

uvulopalatopharyngoplasty (LAUP), radiofrequency tissue-volume reduction, genioglossal

advancement (GA), genial bone advancement, maxillomandibular advancement (MMA), nasal

surgery, and tonsillectomy. The less invasive surgical methods are effective in up to 50% of

patients, yet studies examining their efficacy are complicated by methodological pitfalls. More

invasive methods, such as MMA, may be as efficacious as CPAP (Riley et al. 1993) yet are

associated with greater complications. Therefore, surgical treatments are considered only after

CPAP and BiPAP have proven unsuccessful.

Behavioral Strategies for OSAS

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avoidance of sleep deprivation, avoidance of supine sleep positions, and smoking cessation. Devices

that reposition the body to ensure that the supine position is avoided may also be helpful for

individuals whose apneas are most frequent in the supine position. Regardless of treatment method

chosen, OSAS patients should receive long-term follow-up.

Central Sleep Apnea Syndrome

Central sleep apnea (CSA) syndrome is characterized by multiple apneas during sleep that result

from an impairment of inspiratory effort. The treatment of secondary CSA syndrome relies on the

effective management of underlying conditions. These may include nasal and pharyngeal

obstruction; disorders associated with autonomic dysfunction, such as the Shy-Drager syndrome,

familial dysautonomia, and diabetes mellitus; and disorders causing central impairment, such as

postpolio syndrome, congestive heart failure, central alveolar hypoventilation (Ondine’s curse),

obesity-hypoventilation (pickwickian) syndrome, and neuromuscular disorders. Patients may also

require nocturnal ventilation. A variety of treatments have been reported for idiopathic CSA,

including nocturnal oxygen, CPAP, theophylline, naloxone, and medroxyprogesterone acetate with

acetazolamide, yet the database is limited to anecdotal reports (White 2005) and series with small

sample sizes.

Treatment of OSAS in Children

For OSAS in children, identification and management of underlying conditions are important. Such

conditions might include adenotonsillar hypertrophy, obesity, sinus problems, and craniofacial

abnormalities (Redline et al. 1999). For many of these conditions, surgery is the first-line

treatment, primarily adenotonsillectomy (American Academy of Pediatrics 2002). According to

subjective parental reports, adenotonsillectomy is effective in reducing or eliminating symptoms of

OSAS in 97% of cases (American Academy of Pediatrics 2002; Schechter 2002). However, when

objective measures are used, the resolution rate diminishes to 80% (Lipton and Gozal 2003). The

persistence of OSAS in some children emphasizes the importance of polysomnographic testing

following surgical intervention, particularly in children with severe OSAS and associated risk

factors. In severe cases of OSAS, tracheostomy is an alternative when adenotonsillectomy fails or

when the child is insufficiently compliant with CPAP. In children with nasal and craniofacial

abnormalities, specific surgical interventions can be considered, such as septoplasty, inferior

turbinectomy, UPPP, tongue reduction, and mandibular osteotomy (Cohen et al. 1999). Mandibular

retraction has been reported to be useful in children with micrognathia and infants with Pierre

Robin syndrome. Midfacial advancement has shown to be effective in children with severe midfacial

hypoplasia.

CPAP is appropriate for children who have failed to respond to, or who are not candidates for,

surgical treatments (American Academy of Pediatrics 2002). Its efficacy and tolerability have been

reported in a number of studies (Marcus et al. 1995; Waters et al. 1995). The use of CPAP is not

approved for children weighing less than 30 kg. As in adults, a polysomnographic titration study

should be performed before initiation of CPAP treatment. Behavioral desensitization and family

training prior to treatment are keys to the success of CPAP. Parents are typically instructed to

practice desensitization techniques while the child wears the mask at home. Initially, low CPAP

pressures are applied for short periods of time. Gradually, pressures and times of exposure are

increased until the child feels comfortable falling asleep with the mask on. The most common side

effects of CPAP in children are nasal dryness and congestion; dryness and irritation of the eyes; and

facial skin irritation, discoloration, dermatitis, and pressure sores.

Pharmacological interventions for OSAS in children have a limited role. However, there are data

suggesting that nasal steroids may be effective in reducing symptoms of sleep-disordered

breathing. A randomized, placebo-controlled, triple-blind trial of nasal fluticasone in children with

OSAS reported a decrease of the apnea/hypopnea index by approximately 50% (Brouillette et al.

2001), yet did not demonstrate a complete resolution of OSAS in the group. Clearly, this is a

promising area that deserves further investigation (Marcus 2001).Print: Chapter 56. Sleep Disorders

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Because of the risks of developing hypoventilation, supplemental oxygen is not recommended for

routine use in children with OSAS, even though it may improve some respiratory measures in sleep

(Marcus et al. 1995).

Dyssomnia Not Otherwise Specified

The two entities we will consider in this category are restless legs syndrome (RLS) and periodic

limb movement disorder (PLMD).

Restless Legs Syndrome

RLS is a neurological disorder characterized by an irresistible urge to move the legs, arms, or other

body parts, at times accompanied by uncomfortable or unpleasant sensations in these body parts.

Symptoms typically begin or worsen during periods of rest or inactivity, such as lying and sitting,

and are partially or totally relieved by movement, such as walking and stretching. They also

typically worsen in the evening or at night and can be a source of disturbed sleep. In secondary

RLS, the main goal is the effective management of any underlying conditions, including uremia,

neuropathy, and anemia (both iron- and folate-deficiency types). RLS has been found in 33% of

patients with fibromyalgia and rheumatoid arthritis, up to 27% of pregnant women, and in patients

following gastric surgery (Montplaisir et al. 2005). Anecdotal reports have indicated the presence of

RLS symptoms in a wide variety of other disorders, such as diabetes, hypothyroidism and

hyperthyroidism, chronic lung disease, and Parkinson’s disease, and with use of various

medications and substances, such as antidepressants, lithium carbonate, dopamine D2 receptor

blockers (antipsychotics), xanthines, caffeine, and alcohol.

Individuals who meet criteria for idiopathic (primary) RLS (Allen et al. 2003) may benefit from a

variety of nonpharmacological techniques, although studies of these methods are scant and

methodologically inadequate. Clinical wisdom suggests that following sound sleep hygiene

principles can be helpful. Application of pressure to the limbs, hot or cold baths, and distraction

techniques may be useful. Movement of the limbs may ameliorate symptoms temporarily (Hening et

1. 1999). Pharmacotherapy is also often necessary (Table 56–4).

Table 56–4. Management of restless legs syndrome

Step Agent Dosages Side effects Countermeasures

Step

1

Dopamine agonists

Pramipexole

0.125–1 mga

Nausea and orthostatic

hypotension

Slowly increase dosage or use

domperidone if available (10–30 mg)

Ropinirole

Pergolide

0.25–4 mga

0.1–0.5 mga

Insomnia Use small dose of benzodiazepines in

association with dopamine agonists

Daytime fatigue

and somnolence

Reduce dosage or discontinue

dopamine agonists and use levodopa

(if severe and persistent)

Hallucinations Discontinue dopamine agonists

Tolerance Drug holiday for 2 weeks, then return

to lower dosage

Augmentation Use small extra dose during daytime or

discontinue dopamine agonists (if

severe and persistent)

Step

2

Dopamine precursorsPrint: Chapter 56. Sleep Disorders

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Step Agent Dosages Side effects Countermeasures

Levodopa with

benserazide or

carbidopa

100/25 mg,

200/50 mg,b

regular or

slow release

Same as for dopamine

agonists

Morning rebound or

augmentation of

restless legs syndrome

in early evening

See countermeasures for dopamine

agonists (above)

Use small extra dose of levodopa

during daytime or reduce dosage or

combine levodopa with dopamine

agonists or with benzodiazepines or

discontinue levodopa (if severe and

persistent)

Step

3

Benzodiazepines

Clonazepam

0.5–2 mga

Daytime somnolence Reduce dosage

Drug holiday for 2 weeks, then return

to lower dosage

Temazepam

15–30 mga

Tolerance

Nitrazepam

5–10 mga

Step

4

Opiates

Oxycodone

5–20 mgb

Constipation Symptomatic treatment

Codeine

15–120 mga

Dependency Drug holiday or withdrawal

Step

5

Antiepileptic drugs

Carbamazepine

200–400 mga

Nephrotoxicity Monitor blood level regularly and

adjust dosage

Gabapentin

100–1,800 mga

Daytime fatigue

and somnolence

Reduce dosage

aAt bedtime.

bAt bedtime and repeated once during the night.

Source. Reprinted from Montplaisir J, Allen R, Walters A, et al.: “Restless Legs Syndrome and Periodic Limb

Movements in Sleep,” in Principles and Practice of Sleep Medicine, 4th Edition. Edited by Kryger MH, Roth T,

Dement WC. Philadelphia, PA, Elsevier Saunders, 2005, pp. 839–852. Copyright 2005, Elsevier Saunders.

Used with permission.

RLS may have an episodic course and may even undergo long-term remission; therefore, episodic

reductions in medication dosages may be necessary to ensure that treatment continuation is

warranted. Periodic reassessment of the diagnosis is also crucial, to ensure that causes of a

disguised secondary RLS are identified and managed directly. If serum ferritin levels are below 50

micrograms per liter, ferrous sulfate 325 mg with vitamin C 100–200 mg may be helpful; however,

iron levels should be monitored at baseline and over time to avoid toxicity. Side effects of iron

supplementation include gastrointestinal irritation and constipation.

Periodic Limb Movement Disorder

PLMD consists of a complaint of insomnia or daytime sleepiness that is related to rhythmical

movements of the lower extremities (extensions of the big toe and dorsiflexions of the ankle with

occasional flexions of the knee and hip) that occur during sleep. Movements typically last 0.5–5.0

seconds and occur at a frequency of one every 20–40 seconds. The management of PLMD has

received far less attention than has RLS. The apparently close etiological relationship between RLS

and PLMS has led to the assumption, however, that treatment strategies for RLS can also be

considered for PLMD. The most commonly studied pharmacological agents are benzodiazepines,Print: Chapter 56. Sleep Disorders

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dopaminergic agents, and opioids.

In children and adolescents, dopaminergic agents such as levodopa are often used, although no

double-blind, placebo-controlled studies have evaluated this practice (Walters et al. 2000). L-Dopa

dosages of up to 1.5 g/day may provide relief of RLS symptoms in adolescents. Nausea seems to be

a more common side effect in children than in adults. Therefore, a more gradual titration schedule

is warranted in the pediatric population, starting at one-half of a 25/100 levodopa/carbidopa tablet

daily and gradually increasing to a maximum tolerated dosage, usually not exceeding 1.5 g of

levodopa per day (Burg et al. 2002). Some experts recommend use of pramipexole at a starting

dose of as low as one-quarter to one-half of a 0.125-mg tablet, with weekly dose adjustments. A

maximum allowable dose has not been established for pramipexole in children, but it is

recommended that adult dosages not exceed 1.5 mg per day (Pelayo et al. 2004).

As in RLS, supplementation with iron has been shown to be effective in PLMD for reducing the

frequency of periodic limb movements and associated arousals (Simakajornboon et al. 2003). If

serum ferritin concentrations are below 50 micrograms per liter, ferrous sulfate (3 mg/kg/day)

supplementation may be helpful.

Circadian Rhythm Sleep Disorder

Circadian rhythm sleep disorder constitutes a group of sleep disorders in which the timing of sleep

and wake is abnormal relative to the 24-hour rhythm of the internal circadian clock or of the

external environment. Several subtypes of the disorder have been described. Although the

treatments discussed below for this group of conditions have received modest exploration, all—with

the exception of modafinil, which has received approval for the indication of shift work sleep

disorder—await validation in larger methodologically rigorous trials to establish efficacy, dosage,

timing, and side effects.

Delayed Sleep-Phase Type

The first reported treatment for the delayed sleep-phase subtype of circadian rhythm sleep disorder

was chronotherapy (Weitzman et al. 1981). After a 2-week period during which sleep–wake habits

are recorded in a sleep log, sleep times (both bedtime and morning awakening times) are delayed

by approximately 3 hours per day over a period of 1 week or more until the desired sleep times are

achieved. Patients must follow good sleep hygiene principles and refrain from napping during the

course of the day. The primary limitation of chronotherapy is that it requires sleep during the

course of the daytime hours for a limited period of time, which makes it difficult to plan a regular

social schedule. Therefore, phototherapeutic techniques have been developed, which may be more

practical. Phototherapy involves morning exposure to bright light (2,500–10,000 lux), via either

natural sunlight or manufactured light boxes, for 1–2 hours and evening exposure to darkness, via

eye shades, over a period of a few weeks. Patients are instructed to avoid napping during the day,

to adhere to sleep hygiene principles, and to avoid exposure to bright-light sources such as

television and computer monitors at bedtime (Chesson et al. 1999; Rosenthal et al. 1990). Side

effects of phototherapy include jumpiness/jitteriness, headache, nausea, photosensitivity, and

erythema, some of which may be mitigated by the use of ultraviolet shielding (Chesson et al. 1999;

Terman and Terman 1999). Hypomania appears to be a rare complication, most likely to occur in

patients with a history of bipolar disorder (Labbate et al. 1994).

Evening melatonin has also been reported to be of benefit (Nagtegaal et al. 1998), although the

timing, dosage, and side effects of this treatment have yet to be conclusively determined (National

Institutes of Health State of the Science Conference Statement 2005). Following establishment of

the desired schedule, patients should ensure that they adhere to it, since allowing a delay of

sleep–wake schedules even for a day may reset old patterns. Because the delayed sleep-phase type

of circadian rhythm sleep disorder is most common in adolescents, the collaboration of family

members is useful. The patient and family members should be educated regarding the

neurobiological mechanisms of this disorder and should be encouraged to work collaboratively in

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The use of melatonin 1–2 hours before bedtime has also been suggested, at dosages of 1–5 mg in

preadolescent children and up to 10 mg in adolescents and children with neurodevelopmental or

neurological disabilities (Touitou 2001). Parents and children should be encouraged to use

melatonin for several weeks during the sleep-phase shifting process and to discontinue the drug

once the desired sleep-onset time has been achieved.

Jet Lag Type and Shift Work Type

The following two subtypes of circadian rhythm sleep disorder are the products of activities or

pursuits voluntarily undertaken by the patient in response to occupational and social demands.

Clearly, therefore, prior to engaging in treatment, the clinician and patient should weigh the

benefits of continuing these undertakings against the costs incurred by the patient, the family, and

the workplace. Minimizing the aggravating practices is critical not only before initiating treatment

but also following treatment to reduce the need for medications.

Jet Lag Type

Behavioral strategies employed before and during the actual flight play an important role in the

mitigation and prevention of the jet lag type of circadian rhythm sleep disorder. A clockwise or

counterclockwise adjustment of sleep hours gradually prior to the anticipated flight can be helpful

in mitigating postflight symptoms. Sleeping on board may be of benefit, if its time coincides with

the individual’s usual sleep time, and the disruptive effects of light and noise during the flight may

be diminished by the use of eyeshades and earplugs. Other factors that can disrupt sleep on board

the aircraft, such as motion, uncomfortable seats, interruptions by others, and cabin temperature

and pressure, are difficult to control. Alcohol and caffeine should be avoided, as they can disrupt

sleep.

Following arrival at the intended destination, naps can be of value in enhancing alertness at critical

times during the day (Arendt et al. 2005). Exposure to artificial or natural bright light during the

day has been shown to have phase-shifting effects. Therefore, bright-light exposure during the day

following long-distance travel can, presumably, also enhance adaptation to the new light–dark

schedule (Boulos et al. 1995). Melatonin, long considered to be a phase-shifting hormone, has been

examined in a number of short-term studies (Arendt et al. 2005; Claustrat et al. 1992). Although

melatonin’s effects in jet lag have not been well established, administration at bedtime following

travel may help diminish subjective jet lag symptoms. For a discussion of melatonin’s side effects,

refer to “Nonhypnotic agents” under section titled “Pharmacological Strategies for Primary

Insomnia,” earlier in this chapter. Hypnotic agents, taken both on board the flight and following

arrival, may also be helpful. The shorter-half-life agents are desirable in this regard, to minimize

next-day impairment in alertness.

Shift Work Type

As in the case of jet lag type, prevention is of primary importance in the shift work type of circadian

rhythm sleep disorder. Individuals engaged in chronic shift work should ensure that they allow

adequate time to sleep between shifts and adequate time to recover between changes in shift

timing; keep their bedrooms dark and quiet, especially if they sleep during the course of a typical

day; avoid sleep-disruptive substances such as alcohol and caffeine; ensure that shift durations

permit adequate time for sleep and social activities; and design work shifts and social schedules to

facilitate adherence, as much as possible, to a steady sleep–wake schedule, with this schedule

maintained even on days off work (Rosekind 2005). Exposure to bright light during night work can

hasten adaptation to new shifts and enhance sleep time (Czeisler et al. 1990). If sleep–wake

complaints and impairments in performance persist despite these behavioral measures, work

schedules may need to be tailored, in collaboration with patient and employer, to better suit the

individual’s needs; such considerations are best addressed following referral to a specialized sleep

disorders center. Persistent insomnia, disrupted sleep, and daytime somnolence can be addressed

with use of hypnotics at bedtime and of alertness-promoting agents (e.g., stimulants, modafinil)

during the day (Czeisler et al. 2005).Print: Chapter 56. Sleep Disorders

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PARASOMNIAS

The parasomnias comprise disorders involving abnormal behavioral or physiological events

occurring in association with sleep, specific sleep stages, or sleep–wake transitions. The treatment

of the parasomnias has received less attention than has the treatment of any other group of sleep

disorders. There are no methodologically rigorous blinded and controlled studies in this group of

disorders. The behavioral abnormalities in all of the parasomnias can be triggered by factors that

disrupt sleep. Therefore, strict adherence to sleep hygiene principles is necessary.

Nightmare Disorder

Nightmare disorder is characterized by recurrent nightmares, which are disturbing mental

experiences that generally occur during REM sleep. Sleep hygiene education, maintenance of

regular and appropriate sleep schedules, and reduction and minimization of daytime stress are

essential in the management of nightmare disorder. Various psychotherapeutic approaches have

been reported to be effective in reducing the severity and frequency of nightmares, including CBT

and systematic desensitization with relaxation exercises and imagery rehearsal (Krakow et al.

1995). In children, play therapy can be applied, with play rehearsal of new scenarios to reduce the

psychological distress associated with nightmares. In severe cases in which nightmares are

associated with severe nocturnal anxiety, bedtime refusal, and persistent insomnia,

pharmacological intervention may be warranted.

Sleepwalking Disorder

Sleepwalking disorder is most common in children. In cases where self-injury is unlikely and where

parental distress is minimal, parental education and reassurance should be provided, with an

emphasis on preventing injury and helping the child return to bed. The use of alarm systems or

door bells may help to alert parents of a sleepwalking episode. Removing potentially dangerous

objects close to the bedside, such as bedside tables; storing knives and firearms out of the reach of

a child; and locking bedroom doors and windows are examples of safety precautions that parents

can take to maximize safety for the child. Avoidance of sleep deprivation and of stressful situations

close to bedtime should be encouraged. Elimination of caffeine from children’s diet should be

strongly encouraged. Primary sleep disorders, such as sleep apnea syndrome and periodic limb

movement disorder, can diminish the arousal threshold and trigger a sleepwalking episode;

therefore, their detection and treatment are important. In cases of rhythmic movement disorder

with severe head banging, the use of helmets and other protective measures may be helpful in

preventing self-harm.

Nonpharmacological interventions should be attempted for adequate periods of time before

pharmacological methods are considered. For more severe forms of the disorder in which self-injury

is imminent, or when behavioral measures have failed, medications such as clonazepam (0.01

mg/kg; usual starting dose: 0.25 mg once daily at bedtime), diazepam (0.04–0.25 mg/kg), and

lorazepam (0.05 mg/kg) can be considered (Sheldon 2001). Side effects of the benzodiazepines in

children include residual sedation, paradoxical behavioral agitation/disinhibition, rebound insomnia

upon rapid discontinuation, constipation, and dizziness. In refractory cases, carbamazepine and

antihistamines may be tried. Medications should be used only for short periods of time and at the

lowest effective dosages.

Sleep Terror Disorder

Sleep terror disorder is characterized by sudden arousals from slow-wave sleep accompanied by a

cry or piercing scream, with autonomic nervous system and behavioral manifestations of intense

fear. Most of the interventions and treatment principles that apply to sleepwalking also are relevant

for sleep terror disorder.

Parasomnia Not Otherwise Specified

Included in this category are sleep disturbances that are characterized by abnormal behavior or

physiological events during sleep or sleep–wake transitions, but that do not meet criteria for aPrint: Chapter 56. Sleep Disorders

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more specific parasomnia. Examples include REM sleep behavior disorder, sleep paralysis,

sleep-related groaning, and sleep-related eating disorder. Here we will address only one of these

conditions, REM sleep behavior disorder. This disorder is characterized by abnormal behaviors

emerging during REM sleep that cause injury or sleep disruption. When sleep behaviors threaten to

harm the patient or others, or disrupt sleep and result in daytime somnolence, treatment should be

considered. After a diagnosis of REM sleep behavior disorder has been conclusively established

(most likely in the context of a sleep disorders center) and underlying causes have been definitively

ruled out or adequately managed, treatment of the disorder can be initiated.

The most commonly used pharmacological agents are the benzodiazepines, particularly

clonazepam. Because chronic treatment is often necessary, clinicians should be watchful for

tolerance and dose escalation. Other medications reported to be of value in anecdotal cases include

melatonin, tricyclic antidepressants, and antiepileptic drugs. As in sleepwalking, precautions should

be taken to prevent injury, such as sleeping on mattresses that are placed on the floor, removing

pointed objects such as tables from the bedside, removing objects that can be used in an injurious

fashion from the room, and locking windows and doors and providing the key to family members

(Schenck and Mahowald 1990; Schenck et al. 1987). REM sleep behavior disorder has also been

described in children (Sheldon and Jacobsen 1998) and is associated with increased muscle tone

during REM sleep, along with motor movements (often violent) and increased vocalization during

episodes. Children commonly present with injuries related to their violent sleep behavior.

Treatment includes use of benzodiazepines, such as clonazepam 0.5–1.0 mg at bedtime.

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