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Psychiatry Board Review Manual
Statement of
Editorial Purpose
The Hospital Physician Psychiatry Board Review
Manual is a study guide for residents and
practicing physicians preparing for board
examinations in psychiatry. Each manual
reviews a topic essential to the current
practice of psychiatry.
PUBLISHING STAFF
PRESIDENT, Group PUBLISHER
Bruce M. White
editorial director
Debra Dreger
SENIOR EDITOR
Bobbie Lewis
Primary Sleep Disorders:
The Dyssomnias
Editor:
Jerald Kay, MD
Professor and Chair, Department of Psychiatry, Wright State University
School of Medicine, Dayton, OH
Contributor:
Michael Ignatowski, DO
Psychiatry Resident, Department of Psychiatry, Wright State University
School of Medicine, Dayton, OH
EDITOR
Tricia Faggioli
assistant EDITOR
Farrawh Charles
executive vice president
Barbara T. White
executive director
of operations
Table of Contents
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
General Approach to the Patient
with Dyssomnia. . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Jean M. Gaul
Primary Insomnia. . . . . . . . . . . . . . . . . . . . . . . . . 2
PRODUCTION Director
Primary Hypersomnia. . . . . . . . . . . . . . . . . . . . . . 5
Suzanne S. Banish
PRODUCTION Associate
Nadja V. Frist
ADVERTISING/PROJECT Director
Narcolepsy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5
Breathing-Related Sleep Disorders. . . . . . . . . . . . 7
Patricia Payne Castle
Circadian Rhythm Disorder . . . . . . . . . . . . . . . . . 7
sales & marketing manager
Dyssomnia Not Otherwise Specified. . . . . . . . . . 8
Deborah D. Chavis
Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
NOTE FROM THE PUBLISHER:
This publication has been developed with­
out involvement of or review by the Amer­
ican Board of Psychiatry and Neurology.
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
Cover Illustration by Kathryn K . Johnson
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Psychiatry Volume 11, Part 6 Psychiatry Board Review Manual
Primary Sleep Disorders: The Dyssomnias
Michael Ignatowski, DO
INTRODUCTION
A dyssomnia is a primary disorder of sleep or wakefulness characterized by inability to sleep (ie, insomnia) or
excessive sleepiness (ie, hypersomnia). Dyssomnias are
disorders of duration, quality, and timing of sleep. The
prevalence of sleep-related problems in the general
population is estimated to be around 30%, affecting
between 50 and 70 million Americans of all ages.1 The
incidence and prevalence of sleep disorders are even
higher in the psychiatric population. Ford and Kamerow2 revealed that 40% of patients with insomnia and
46.5% of patients with hypersomnia had a psychiatric
disorder compared with only 16.4% of patients with no
sleep complaints.
Normal sleep is divided between rapid eye movement (REM) and non-REM cycles. Non-REM sleep is
separated into 4 stages based on increasing depth of
sleep, which can be observed through polysomnography (PSG). Sleep latency (ie, the time spent trying
to fall asleep) is normally 10 to 20 minutes. In stage 1
sleep, the occipital dominant rhythm decreases, and
the 8 to 13 Hz alpha waves seen in the awake state
diminish. Alpha waves are replaced by 3 to 7 Hz theta
waves, and larger vertex transients can be seen. In
stage 2, bursts of 12 to 15 Hz waves known as sleep
spindles occur, along with high voltage waves of positive
and negative polarity known as K complexes. In stage 3,
slow wave activity of 1 to 3 Hz known as delta waves are
observed, which comprise 20% to 49% of the stage 3
sleep period. Stage 4 consists of over 50% delta waves.
Stages 3 and 4 of non-REM sleep are more prominent
in the first half of normal sleep (Figure 1).3
REM accounts for 20% to 25% of sleep and is associated with vivid dreaming. All muscles except for ocular
and respiratory muscles are paralyzed during REM to
prevent acting out dreams. REM normally starts around
60 to 90 minutes after sleep onset and is most prominent in the latter half of sleep. REM and non-REM
usually occur in 90- to 110-minute cycles.4 Age-related
degenerative changes occur in the sleep cycles that lead
to a reduction of sleep efficiency (Table 1); however,
the overall need for sleep does not decrease with age.5
Hospital Physician Board Review Manual
GENERAL APPROACH TO THE PATIENT WITH
DYSSOMNIA
Evaluation of the dyssomnias should include an
in-depth sleep history (ie, onset, frequency, duration,
and severity of sleep complaints), mental status examination, and physical examination. Initial interviews
should include a review of illicit and prescription drugs
as well as alcohol and caffeine use. These interviews are
often aided by spouses, bed partners, or parents of children with sleep disorders. A mental status examination
is necessary to rule out an insomnia or hypersomnia
secondary to mental illness. A physical examination
should be performed to rule out general medical
causes of dyssomnia, such as neurologic, cardiac, respiratory, rheumatologic, or endocrine disorders. Laboratory tests may be useful in cases where illnesses such as
hyperthyroidism or pheochromocytoma are suspected.
Instruments such as the Epworth Sleepiness Scale or the
Sleep Disorders Questionnaire are used to differentiate
the dyssomnias. PSG may be used if a patient has symptoms suggestive of sleep apnea, periodic limb movement,
narcolepsy, or violent behavior in sleep (Table 2).
PRIMARY INSOMNIA
DIAGNOSTIC AND ASSOCIATED FEATURES
Insomnia is the complaint of poor sleep quality
with daytime functional impairment or distress for at
least 1 month (Table 3).6 The prevalence of insomnia
is believed to be approximately 10% in the general
population.1 To meet criteria for sleep-onset insomnia,
a patient must have a sleep latency of greater than
30 minutes. Patients with sleep maintenance insomnia
have difficulty staying asleep, with frequent and extended awakenings totaling 30 minutes or premature
awakenings with less than 6.5 hours of total sleep.7 A
patient with a psychophysiologic primary insomnia
often has anxiety about getting sleep when attempting
to fall asleep, thus preventing him or her from doing so.
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Primary Sleep Disorders: The Dyssomnias
Awake - low voltage - random fast
50 µV
1 sec
Drowsy - 8–12 cps - alpha waves
Stage 1 - 3–7 cps - theta waves
Theta waves
Stage 2 - 12–14 cps - sleep spindles and K complexes
Sleep spindle
K complex
Delta sleep - 1/2–2 cps - delta waves > 75 µV
REM sleep - low voltage - random, fast with sawtooth waves
Sawtooth waves
Sawtooth waves
Figure 1. Stages of sleep. (Adapted with permission from Hauri P. The sleep disorders [current concepts]. Kalamazoo [MI]: Upjohn;
1982:7.)
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Psychiatry Volume 11, Part 6 Primary Sleep Disorders: The Dyssomnias
Table 1. Age-Related Changes in Sleep in the Elderly
Table 2. Common Components of Polysomnography
Decreased sleep efficiency (time asleep/time spent in bed)
Component
Function
Decreased non–rapid eye movement stages 3–4
Electroencephalogram
Measures brain activity and stages of
sleep
Electrooculogram
Measures eye movements and rapid
eye movement sleep
Electromyogram
Measures limb and body movement
Pulse oximetry
Measures oxygen saturation and extent
of apneas
Decreased rapid eye movement latency
Small decrease in rapid eye movement
Increase in arousals and awakenings
Phase advancement in circadian rhythm
Respiratory movement of None present in central sleep apnea
chest and abdomen
during hypoxic event
Idiopathic insomnia begins in childhood and is chronic
without an associated cause. Adjustment sleep disorder
is the term given to loss of sleep secondary to an acute
emotional stressor. Sleep-state misperception (paradoxical insomnia) is a form of primary insomnia in which
a patient may complain of nonrestorative, inadequate
sleep, but findings on PSG are within normal limits.
EVALUATION AND MANAGEMENT
Primary insomnia is a clinical diagnosis that can be
made with a complete history, along with a mental status and physical examination to rule out other causes.
PSG is not necessary for routine evaluation of primary
insomnia unless other causes are suspected.8
Treatment of primary insomnia is multifaceted and
includes both cognitive behavioral therapy (CBT) and
pharmacologic treatment. CBT approaches have been
shown to be as effective, if not more effective, than
pharmacologic therapy.9,10 A variety of modalities are
used in CBT, including stimulus control, muscle relaxation, paradoxical intention, biofeedback, and sleep
restriction (Table 4); all have been shown to be efficacious in individual treatment.7,11
Pharmacologic treatment of primary insomnia often
includes the use of sedative hypnotics, which act on
benzodiaz­epine receptors to control inhibitory activity of
γ-aminobutyric acid (GABA) at GABAA receptors. Shortterm (3–6 wk) use of benzodiazepines has been shown to
be effective in initiating and maintaining sleep; however,
the side effect profile limits their use to a maximum of
6 weeks and varies based on the duration of action of
the medications.12 Hypnotics with long half-lives, such as
temazepam, tend to cause daytime sedation and hangover symptoms and also may accumulate in the body
with repeated use, especially in the elderly. Short halflife hypnotics, such as triazolam, produce less daytime
sleepiness; however, they are associated with a higher risk
of tolerance and withdrawal insomnia.12 Furthermore,
nighttime amnesia upon awakening may be more common with short-acting hypnotics as compared with longacting hypnotics.
Hospital Physician Board Review Manual
Electrocardiogram
Monitors for arrhythmias
The newer hypnotics act selectively on the α1 subunit
of GABAA and have a faster onset of action. Zolpidem
and zaleplon have similar side effect profiles to shortacting benzodiazepines and tend to decrease sleep
latency.13 Eszopiclone has been approved for long-term
treatment of insomnia and works both to decrease sleep
latency and improve sleep maintenance.14 Overall, the
hypnotics are generally contraindicated in patients with
sleep apnea, those who are pregnant, substance abusers, and those who need to be alert at night. Caution
should be used when prescribing hypnotic medications
to patients with renal, hepatic, or pulmonary disease;
the elderly; and patients who snore loudly.15
The efficacy of antihistamines (eg, diphenhydra­mine
and hydroxyzine) in chronic insomnia has not been
shown to offset their side effects (eg, confusion, delirium, drowsiness) the following day.16 Melatonin, which
promotes sleepiness and reduces sleep latency in some
circadian rhythm disorders, has not been shown to be
effective in treating primary insomnia compared with
placebo.17,18 Ramelteon is a selective melatonin receptor
agonist that acts on melatonin 1 (MT1) and MT2 receptors and is far more potent at targeting these receptors
as compared with melatonin, which nonselectively acts
on MT1, MT2, and MT3 receptors. A randomized,
double-blind, placebo-controlled study of ramelteon in
patients with chronic primary insomnia demonstrated
reduced sleep latency and increased total sleep time.19
Antidepressants used by psychiatrists to treat insomnia often include amitriptyline, doxepin, trimipramine,
mirtazapine, and trazodone. The sedating properties
combined with the antidepressant effect appear to be
helpful for insomnia associated with comorbid depression20; however, the risks tend to outweigh the benefits
for patients without a depressed mood.21,22 Although antidepressants are widely used, evidence does not support
the use of antidepressants for primary insomnia alone.
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Primary Sleep Disorders: The Dyssomnias
Table 3. DSM-IV-TR Criteria for Primary Insomnia
A.The predominant complaint is difficulty initiating or maintaining
sleep, or nonrestorative sleep, for at least 1 month
B.The sleep disturbance (or associated daytime fatigue) causes
clinically significant distress or impairment 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
Table 4. Treatment Modalities Used in Cognitive Behavioral
Therapy
Sleep hygiene
Techniques include avoiding caffeine,
alcohol, and nicotine in the evening and
night, exercising in the late afternoon,
minimizing environmental stimulus, and
waking up at the same time
Relaxation therapy
Progressive relaxation techniques are
taught, as well as EMG biofeedback, in
order to decrease somatic muscle ten­
sion; meditation and imagery training
may reduce cognitive tension
Sleep restriction
Wake at the same time everyday, and
allow only the amount of time in bed
you think you are getting plus 15 min;
when sleep efficiency improves, go to
bed 15 min earlier each night
Cognitive strategies
Identifying and replacing fears of sleep
loss, and helping the patient develop
realistic expectations of sleep
Stimulus control
Associating the bedroom with sleep by
eliminating the use of the bedroom for
anything besides sleep or sex. Also, the
patient is instructed to go in the bed­
room only when sleepy
Paradoxical intention
Involves having patient remain passively
awake and avoiding falling asleep; this
may eliminate performance anxiety and
is only useful in sleep-onset insomnia
D.The disturbance does not occur exclusively during the course of
another mental disorder (eg, major depressive disorder, general­
ized anxiety disorder, a delirium)
E.The disturbance is not due to the direct physiologic effects of a
substance (eg, a drug of abuse, a medication) or a general medical
condition
Adapted with permission from American Psychiatric Association.
Diagnostic and statistical manual of mental disorders. 4th ed., text
revision. Washington (DC): The Association; 2000:604. Copyright 2000,
American Psychiatric Association.
Barbiturates and antipsychotic medications should not
be used in primary insomnia due to the lack of efficacy
and risks involved.23
PRIMARY HYPERSOMNIA
Hypersomnia is the complaint of excessive sleepiness with daytime functional impairment or distress for
at least 1 month (Table 5).6 Individuals who have hypersomnia lack the distinguishable feature of narcolepsy,
such as catatonia and immediate-onset REM. Hypersomniacs experience long periods of nonrefreshing sleep
with difficulty awakening. The etiology is often idiopathic,
but depression is associated with primary hypersomnia
15% to 25% of the time. Headache and Raynaud’s phenomena have also been seen with this condition.24
Recurrent primary hypersomnia, or Kleine-Levin
syndrome (KLS), is defined as excessive sleepiness lasting for at least 3 days, several times per year, for at least
2 years. KLS manifests as hyperphagia, hypersexuality,
aggression, and hypersomnia lasting up to 18 hours
per day. In a systematic review of 186 cases, KLS was
found most often in males (median age, 15 yr) and
occurred after viral infections in 38% of cases.25 Similar
episodes of hypersomnia have been documented in
young females, known as menstrual cycle–associated
hypersomnia syndrome.26
Diagnosis of hypersomnia is made clinically. If PSG
is performed, findings include a prolonged sleep
period and short sleep latency with normal REM latency. Medications used to treat primary hypersomnia
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EMG = electromyography.
include activating selective serotonin reuptake inhibitors (SSRIs) and stimulants, but evidence for their use
is lacking. Modafinil, a wake-promoting agent without
the addictive properties of other stimulants, appears
to be useful as a first-line treatment.27 Only lithium reduces the frequency and severity of KLS.25
NARCOLEPSY
DIAGNOSTIC AND ASSOCIATED FEATURES
Narcolepsy presents as excessive sleepiness and
REM intrusion into the wakeful state, occurring daily
for at least 3 months (Table 6).6 The classic tetrad of
narcolepsy consists of sleep attacks, cataplexy, sleep
paralysis, and hypnagogic/hypnopompic hallucinations. Sleep attacks are irresistible urges to sleep that
occur throughout the day at inappropriate times. A
typical patient with narcolepsy will nap approximately
15 minutes and feel refreshed afterwards. Total sleep
time is usually not significantly increased. Cataplexy is a
Psychiatry Volume 11, Part 6 Primary Sleep Disorders: The Dyssomnias
Table 5. DSM-IV-TR Criteria for Primary Hypersomnia
Table 6. DSM-IV-TR Diagnostic Criteria for Narcolepsy
A.The predominant complaint is excessive sleepiness for at least
1 month (or less if recurrent) as evidenced by either prolonged
sleep episodes or daytime sleep episodes that occur almost daily
A.Irresistible attacks of refreshing sleep that occurs daily for at
least 3 months
B.The excessive sleepiness causes clinically significant distress or
impairment in social, occupational, or other important areas of
functioning
(1)Cataplexy (ie, brief episodes of sudden bilateral loss of mus­
cle tone, most often in association with intense emotion)
C.The excessive sleepiness is not better accounted for by insomnia
and does not occur exclusively during the course of another
sleep disorder (eg, narcolepsy, breathing-related sleep disorder,
circadian rhythm sleep disorder, or a parasomnia) and cannot be
accounted for by an inadequate amount of sleep
D.The disturbance does not occur exclusively during the course of
another mental disorder
E.The disturbance is not due to the direct physiologic effects of a
substance (eg, a drug of abuse, a medication) or a general medical
condition
Adapted with permission from American Psychiatric Association.
Diagnostic and statistical manual of mental disorders. 4th ed., text
revision. Washington (DC): The Association; 2000:609. Copyright 2000,
American Psychiatric Association.
brief bilateral loss of muscle tone that causes a fall to the
ground and is commonly triggered by strong emotions.
Sleep paralysis is the inability to move voluntary muscles
moments before sleep or upon awakening. Although
not as patho­gnomonic of narcolepsy as cataplexy, the
mechanism of sleep paralysis may be similarly associated
with REM paralysis of voluntary muscle that intrudes into
the wake cycle. Finally, a patient with narcolepsy may
experience hypnagogic or hypnopompic hallucinations.
The detailed visual hallucinations may be the result of the
vivid dreams of REM presenting in the wake cycle.6
Prevalence of narcolepsy in the United States is less
than 1%. Symptoms usually begin between the ages
of 15 and 25 years, and a strong genetic component
exists.28 More than 85% of narcoleptic patients with
cataplexy share the HLA DQB1*0602 allele, often in
combination with HLA DR2, compared with 12% to
38% of the general population across diverse ethnicities.29 Recent studies have shown decreased levels of the
highly excitatory neuropeptide hypocretin (orexin) in
the cerebrospinal fluid of narcoleptics.30
EVALUATION AND MANAGEMENT
Diagnosis of narcolepsy is made by PSG, followed
immediately by a Multiple Sleep Latency Test, which
measures sleep latency and REM latency during 4 to
5 scheduled nap times.31 A narcoleptic has a sleep
latency of less than 5 minutes and an REM latency of
less than 10 minutes. PSG also may show slight reductions in sleep efficiency and increases in REM and
Hospital Physician Board Review Manual
B. The presence of one or both of the following:
(2)Recurrent intrusions of elements of rapid eye movement
sleep into the transition between sleep and wakefulness, as
manifested by either hypnopompic or hypnagogic hallucina­
tions or sleep paralysis at the beginning or end of sleep
episodes
C.The disturbance is not due to the direct physiologic effects of a
substance (eg, a drug of abuse, a medication) or another general
medical condition
Adapted with permission from American Psychiatric Association.
Diagnostic and statistical manual of mental disorders. 4th ed., text
revision. Washington (DC): The Association; 2000:615. Copyright 2000,
American Psychiatric Association.
non-REM stage 1 sleep.6 Another test used to determine
excessive sleepiness is the Maintenance of Wakefulness
Test, which measures the ability to stay awake under
soporific conditions.31
Treatment of narcolepsy includes the use of stimulants, such as dextroamphetamine, methylphenidate,
and amphetamine, which are associated with a high risk
of rebound insomnia, tolerance, and abuse. Modafinil,
an α1 adrenergic agonist, does not cause these troublesome adverse effects and should be considered first-line
treatment of narcolepsy. Pemoline, a stimulant used to
treat narcolepsy, has been discontinued in the United
States due to cases of hepatic failure.32 Patients who do
not respond to adequate doses of any stimulant should
be reassessed for other sleep disorders.31 Selegiline, a
monoamine oxidase inhibitor, is effective for treatment
of narcolepsy at high doses, but its use is limited because
of diet restrictions and hypertension.31
While effective for sleep attacks, the aforementioned
medications do not treat cataplexy, sleep paralysis,
or REM-associated hallucinations. These conditions
have been successfully treated with SSRIs and tricyc­
lic anti­depressants, as the serotonergic properties of
these medications suppress REM.31 Sodium oxybate
(γ-hydroxybutyric acid; GHB) is a central nervous system depressant useful in treating cataplexy. The exact
mechanism of action is unknown, but the drug may
work through the GABAB and GHB receptors. Unlike
as with an SSRI, abrupt discontinuation does not cause
rebound cataplexy. Like others in its class, sodium oxybate carries a high risk of diversion and abuse.33 Recent
studies have shown that sodium oxybate is effective as
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Primary Sleep Disorders: The Dyssomnias
monotherapy in treating daytime sleepiness and works
as an adjunct to modafinil.34
Scheduled nap times may be helpful as adjunctive
behavioral therapy. Finally, patients should be advised
not to operate vehicles and avoid potentially dangerous
situations until the symptoms are well controlled.31
BREATHING-RELATED SLEEP DISORDERS
Breathing-related sleep disorders occur as a result of sleep apnea or alveolar hypoventilation and
cause nighttime arousals leading to daytime sleepiness
(Table 7).6 Obstructive sleep apnea (OSA) is the most
common breathing-related sleep disorder, affecting
more than 5% of adults.35 Other less common breathingrelated sleep disorders include central sleep apnea syndrome and central alveolar hypoventilation syndrome.
The population most often affected by OSA is overweight middle-aged males who have short, thick necks
and decreased airway size.35 Furthermore, there is an
increased prevalence of OSA in the psychiatric population.36 Because patients with bipolar disorder and schizophrenia may be taking medications that cause weight
gain and therefore may lead to OSA, a psychiatrist
should be aware of the signs and symptoms.37
Decreased muscle tone during sleep and the pull of
gravity while supine further obstruct a narrow airflow,
causing snoring, gasping, and apneas. The Mallampati score of airway classification is a useful predictor
of OSA (Figure 2).38 An apnea is defined as complete
cessation of breathing for at least 10 seconds, whereas
a hypopnea is a partial cessation of respiration. Arousal
increases tone and alleviates the airway obstruction but
leads to fragmented sleep, which in turn leads to daytime sleepiness. Many patients are unaware of arousals,
and those affected will wake in the morning and from
naps unrefreshed. Also, the cessation of breathing can
cause hypoxia, which can lead to complications, such
as morning headache, hypertension, arrhythmia, and
further weight gain.6
Diagnosis of OSA starts with a patient history, which
includes complaints of excessive sleepiness and snoring
or gasping for breath. The history often can be better
obtained by interviewing a patient’s bed partner. PSG
must confirm the diagnosis by showing 5 or more apneas per hour (apnea index) or 10 or more apneas and
hypopneas per hour (respiratory index). Apneas and
hypopneas cause a decrease in oxygen saturation of 4%
or more by pulse oximetry, and arousals can be seen
on electroencephalography. If no respiratory muscle
effort is observed during an apneic event, central apnea
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Table 7. DSM-IV-TR Diagnostic Criteria for BreathingRelated Sleep Disorder
A.Sleep disruption, leading to excessive sleepiness or insomnia, that
is judged to be due to a sleep-related breathing condition (eg,
obstructive or central sleep apnea syndrome or central alveolar
hypoventilation syndrome)
B.The disturbance is not better accounted for by another mental
disorder and is not due to the direct physiologic effects of a
substance (eg, a drug of abuse, a medication) or another general
medical condition (other than a breathing-related disorder)
Coding note: Also code sleep-related breathing disorder on Axis III.
Adapted with permission from American Psychiatric Association.
Diagnostic and statistical manual of mental disorders. 4th ed., text
revision. Washington (DC): The Association; 2000:622. Copyright 2000,
American Psychiatric Association.
should be suspected, which is associated with neurologic and cardiac disorders that affect ventilation.
First-line treatment of OSA consists of weight reduction as well as continuous positive airway pressure
(CPAP) devices. After PSG demonstrates sleep apnea,
CPAP titration can either be performed the following
day or the same day as a split study. CPAP increases
quality of life, has few side effects, and is only limited by
comfort and compliance.39 Bilevel positive airway pressure can be used in patients who require high pressure
and have difficulty breathing against a fixed continuous
pressure or when a patient has a central hypoventilation syndrome. Because the majority of apneas occur
in REM sleep, protriptyline (a tricyclic antidepressant)
is sometimes used as an adjunct because it suppresses
REM. Positional therapy to keep a patient nonsupine is
also an effective supplement, as most apneas occur in the
supine position.40 Surgical techniques may be helpful for
anatomic abnormalities that cause obstruction. Palatal
surgery and oral appliances can be used if a patient does
not tolerate CPAP; however, these therapies are often
more helpful in eliminating snoring than in eliminating
apneas. Tracheotomy is the only surgical procedure consistently successful in treating OSA but should be used
only when all other options have been exhausted.41,42
CIRCADIAN RHYTHM DISORDER
Circadian rhythm disorder occurs when events in
a patient’s life interfere with their sleep-wake pattern
(Table 8).6 Circadian rhythms are initiated by the
suprachiasmatic nuclei in the hypothalamus, which is
synchronized by sunlight to about 24 hours. A light
response causes a reduction in melatonin production
Psychiatry Volume 11, Part 6 Primary Sleep Disorders: The Dyssomnias
Class I
Class II
Class III
Class IV
Figure 2. Mallampati airway classification. A higher score is an independent predictor for the presence and severity of obstructive sleep
apnea. (Used with permission, copyright © www.thomasnowacki.com.)
in the pineal gland (Figure 3) and an increase in core
body temperature.43 Nighttime darkness leads to increased melatonin production and a decrease in core
body temperature, which promotes sleepiness. Circadian rhythm disorders are classified into 4 subtypes based
on characteristics of a patient’s sleep phase: delayed
sleep phase type, unspecified type (includes advanced
sleep phase, non–24-hour sleep-wake pattern, or irregular sleep-wake pattern), jet lag type, or shift work type.
A delayed sleep phase occurs when actual sleep is
delayed in relation to a desired time, leading to difficulty awakening and sleep-onset insomnia.6 Melatonin
production and core body temperature are shifted to
a later time. Also, delayed sleep often is first seen in
adolescents and may result in missed classes or work.
Delayed sleep is associated with unipolar depression.44
Treatment includes bright light therapy from 6 am to
9 am and avoiding evening light exposure.45 Melatonin
has also been shown to advance a delayed sleep phase
when given in late afternoon hours.46
An advanced sleep phase occurs when actual sleep
occurs earlier than when is desired, resulting in excessive evening sleepiness and awakening at hours earlier
than ideal to the patient.6 Melatonin production and
core body temperature are shifted to an earlier time.
Advanced sleep phase disorder is often seen in the
elderly and may be part of the normal aging process.
Treatment for an advanced sleep phase syndrome that
does not resolve includes bright light therapy between
8 pm and 11 pm and avoiding morning light exposure.45
Individuals with non–24-hour sleep-wake patterns have
free-running circadian cycles that do not follow time
clues. Instead, cycles adhere to the endogenous rhythm
that is slightly longer than 24 hours. Thus, patients’
sleep complaints change as time goes on due to the
Hospital Physician Board Review Manual
progressing delay in the sleep cycle. Melatonin has
been shown to be helpful in setting a circadian rhythm
in completely blind individuals with non–24-hour sleepwake patterns.47 Individuals with irregular sleep-wake
patterns have a lack of identifiable cycles of sleep and
wakefulness. Like non–24-hour patterns, sleep complaints may vary. A patient may need to keep a detailed
sleep log to assist with the diagnosis.
Jet lag from traveling across time zones from west
to east results in a sleep phase delay. Similarly, jet lag
from traveling across time zones from east to west results in sleep phase advancement. The course is usually
self-limiting, and treatment with light and melatonin
has shown little efficacy.46 Sedative hypnotics, such as
triazolam, may aid with westward travel when crossing
several time zones by facilitating the adaptation of the
circadian rhythm through sleep induction.48
Shift work (rotating, night, or early morning shifts)
may also cause sleep disruption, which results from conflict between the pattern of sleep and wakefulness and
the desired pattern of sleep and wakefulness required
by shift work. Evidence does not support the use of
melatonin for this diagnosis.46 Light therapy prior to
work and avoidance of light exposure after work may be
somewhat helpful in managing sleep disorders caused by
shift work.45 Modafinil is approved for shift workers to decrease excessive sleepiness and improve performance.49
DYSSOMNIA NOT OTHERWISE SPECIFIED
Dyssomnia not otherwise specified includes dyssomnias caused by an environmental disturbance, such as
noise or light. This may result from the cry of an infant
to snoring or movement of a bed partner. Also included
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Primary Sleep Disorders: The Dyssomnias
Table 8. DSM-IV-TR Diagnostic Criteria for Circadian
Rhythm Sleep Disorder
A.A persistent or recurrent pattern of sleep disruption leading
to excessive sleepiness or insomnia that is due to a mismatch
between the sleep-wake schedule required by a person's environ­
ment and his or her circadian sleep-wake pattern
Retino­
hypothalamic
tract
Pineal gland
Supra­
chiasmatic
nucleus
– GABA
B.The sleep disturbance causes clinically significant distress or
impairment in social, occupational, or other important areas of
functioning
Para­
ventricular
nucleus
C. T
he disturbance does not occur exclusively during the course of
another sleep disorder or other mental disorder
Superior
cervical
ganglion
D.The disturbance is not due to the direct physiologic effects of a
substance (eg, a drug of abuse, a medication) or a general medical
condition
Figure 3. The melatonin production pathway. GABA = γ-aminobutyric
acid. (Used with permission, copyright © www.thomasnowacki.com.)
Specify type:
and carbamazepine are efficacious for RLS as well.52 Gabapentin and clonidine may be helpful for treating RLS
symptoms, and supplemental iron should be considered
for patients who are iron-deficient.52 Newer evidence suggests that ropinirole and other dopamine agonists as well
as dopaminergic agents (eg, amantadine and selegiline)
also may be effective for managing RLS.51
Delayed sleep phase type: a persistent pattern of late sleep onset
and late awakening times, with an inability to fall asleep and awaken
at a desired earlier time
Jet lag type: sleepiness and alertness that occur at an inappropriate
time of day relative to local time, occurring after repeated travel
across more than one time zone
Shift work type: insomnia during the major sleep period or exces­
sive sleepiness during the major awake period associated with
night shift work or frequently changing shift work
Unspecified type
Adapted with permission from American Psychiatric Association.
Diagnostic and statistical manual of mental disorders. 4th ed., text
revision. Washington (DC): The Association; 2000:629. Copyright 2000,
American Psychiatric Association.
in this category are restless leg syndrome (RLS) and
periodic limb movement syndrome (PLMS).
RESTLESS LEGS SYNDROME
Features of RLS include an intense urge to move one’s
legs associated with sensory complaints and motor restlessness. RLS occurs while awake, but symptoms worsen
at rest and at night, often resulting in sleep-onset insomnia.6 Prevalence of RLS in the general population is estimated to be between 2% and 10%.6,50 The pathophysiology involves the dopamine system and depletion of iron
stores.51 Iron-deficiency anemia, uremia, neuropathy,
rheumatoid arthritis, and pregnancy are all associated
with RLS (ie, secondary RLS).15 Also, some studies have
shown that SSRI medications can exacerbate RLS.50
Diagnosis is made by patient history and a bed
partner’s observations, once other medical causes have
been ruled out. First-line treatment includes levadopa/
carbidopa or pergolide. Oxycodone, propoxyphene,
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PERIODIC LIMB MOVEMENT SYNDROME
Features of PLMS include brief, repetitive stereotyped limb movement that occurs while asleep, causing
arousals that can lead to daytime sleepiness. The movements occur mostly in non-REM stages 1 and 26 and
typically involve the leg with extension of the great toe
and flexion at the ankle, knee, and hip.52 Prevalence
of PLMS in the general population is estimated at approximately 3% to 4%.50 More than 80% of individuals
with RLS also have PLMS, and both are associated with
dopamine deficiency.53 Medical conditions, such as ure­
mia, must be ruled out (as in RLS).
Diagnosis of PLMS includes patient history and an
interview with the bed partner as well as PSG. Treatment
is similar to that used for RLS and includes levadopa with
a decarboxylase inhibitor or pergolide as first-line treatment. Opioids are more successful in RLS, but clonazepam may be more helpful in PLMS.52 Dopamine agonists
and dopaminergics may be efficacious as well.51
CONCLUSION
Psychiatrists play a key role in sleep medicine. The
connection between sleep disturbance and mental
health is profound and must not be overlooked. Regardless of whether a sleep disorder leads to a psychiatric disorder or is a component of a psychiatric pathology, understanding dyssomnias is crucial to the health
of a psychiatrist’s patients.
Psychiatry Volume 11, Part 6 Primary Sleep Disorders: The Dyssomnias
Psychiatry. 2nd ed. Hoboken (NJ): Wiley; 2003.
REFERENCES
1. National Center on Sleep Disorders Research. 2003 National Sleep Disorders Research Plan. Available at www.
nhlbi.nih.gov/health/prof/sleep/res_plan/sleep-rplan.
pdf. Accessed 27 Dec 2006.
2. Ford DE, Kamerow DB. Epidemiologic study of sleep
disturbances and psychiatric disorders. An opportunity
for prevention? JAMA 1989;262:1479–84.
3. Hauri P. The sleep disorders (current concepts). 2nd ed.
Kalamazoo (MI): Upjohn; 1982:7.
4. Carskadon MA, Dement WC. Normal human sleep: an
overview. In: Kryger MH, Roth T, Dement WC, editors.
Principles and practice of sleep medicine. 4th ed. Philadelphia: Elsevier/Saunders; 2005:13–25.
16. Gengo F, Gabos C, Miller JK. The pharmacodynamics
of diphenhydramine-induced drowsiness and changes
in mental performance. Clin Pharmacol Ther 1989;45:
15–21.
17. Buscemi N, Vandermeer B, Hooton N, et al. The efficacy
and safety of exogenous melatonin for primary sleep
disorders. A meta-analysis. J Gen Intern Med 2005;20:
1151–8.
18. Almeida Montes LG, Ontiveros Uribe MP, Cortes
Sotres J, Heinze Martin G. Treatment of primary insomnia with melatonin: a double-blind, placebo-controlled,
crossover study. J Psychiatry Neurosci 2003;28:191–6.
19. Erman M, Seiden D, Zammit G, et al. An efficacy, safety,
and dose-response study of Ramelteon in patients with
chronic primary insomnia. Sleep Med 2006;7:17–24.
5. Bliwise DL. Normal aging. In: Kryger MH, Roth T, Dement
WC, editors. Principles and practice of sleep medicine. 4th
ed. Philadelphia: Elsevier/Saunders; 2005:26–38.
20. Sharpley AL, Cowen PJ. Effect of pharmacologic treatments on the sleep of depressed patients. Biol Psychiatry
1995;37:85–98.
6. American Psychiatric Association. Diagnostic and statistical manual of mental disorders: (DSM-IV-TR). 4th ed.,
text revision. Washington (DC): The Association; 2000:
597–630.
21. Mendelson WB. A review of the evidence for the efficacy
and safety of trazodone in insomnia. J Clin Psychiatry
2005;66:469–76.
7. Morgenthaler T, Kramer M, Alessi C, et al. Practice parameters for the psychological and behavioral treatment
of insomnia: an update. An American Academy of Sleep
Medicine report. American Academy of Sleep Medicine.
Sleep 2006;29:1415–9.
8. Chesson A Jr, Hartse K, Anderson WM, et al. Practice
parameters for the evaluation of chronic insomnia. An
American Academy of Sleep Medicine report. Standards
of Practice Committee of the American Academy of
Sleep Medicine. Sleep 2000;23:237–41.
9. Sivertsen B, Omvik S, Pallesen S, et al. Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled
trial. JAMA 2006;295:2851–8.
10. Jacobs GD, Pace-Schott EF, Stickgold R, Otto MW.
Cognitive behavior therapy and pharmacotherapy for
insomnia: a randomized controlled trial and direct comparison. Arch Intern Med 2004;164:1888–96.
11. Morin CM, Culbert JP, Schwartz SM. Nonpharmacological interventions for insomnia: a meta-analysis of treatment efficacy. Am J Psychiatry 1994;151:1172–80.
12. Gillin JC. The long and the short of sleeping pills. N Engl
J Med 1991;324:1735–7.
13. Mitler MM. Non-selective and selective benzodiazepine
receptor agonists—where are we today? Sleep 2000;23
Suppl 1:S39–47.
14. Melton ST, Wood JM, Kirkwood CK. Eszopiclone for
insomnia. Ann Pharmacother 2005;39:1659–66.
15. Gillin JC, Ancoli-Israel S, Erman M. Sleep and sleep-wake
disorders. In: Tasman A, Kay J, Lieberman J, editors.
10 Hospital Physician Board Review Manual
22. Ware JC. Tricyclic antidepressants in the treatment of
insomnia. J Clin Psychiatry 1983;44(9 Pt 2):25–8.
23. NIH Consensus Development Program. State-of-thescience conference statement on manifestations and
management of chronic insomnia in adults. June 13–
15, 2005. Available at http://consensus.nih.gov/2005/
2005InsomniaSOS026html.htm. Accessed 28 Dec 2006.
24. Bassetti CL, Pelayo R, Guilleminault C. Idiopathic hypersomnia. In: Kryger MH, Roth T, Dement WC, editors.
Principles and practice of sleep medicine. 4th ed. Philadelphia: Elsevier/Saunders; 2005:791–800.
25. Arnulf I, Zeitzer JM, File J, et al. Kleine-Levin syndrome:
a systematic review of 186 cases in the literature. Brain
2005;128(Pt 12):2763–76.
26. Kesler A, Gadoth N, Vainstein G, et al. Kleine Levin syndrome (KLS) in young females. Sleep 2000;23:563–7.
27. Bastuji H, Jouvet M. Successful treatment of idiopathic
hypersomnia and narcolepsy with modafinil. Prog Neuropsychopharmacol Biol Psychiatry 1988;12:695–700.
28. Thorpy M. Current concepts in the etiology, diagnosis
and treatment of narcolepsy. Sleep Med 2001;2:5–17.
29. Mignot E. Genetic and familial aspects of narcolepsy.
Neurology 1998;50(2 Suppl 1):S16–22.
30. Nishino S, Ripley B, Overeem S, et al. Hypocretin (orexin) deficiency in human narcolepsy [letter]. Lancet 2000;
355:39–40.
31. Littner M, Johnson SF, McCall WV, et al. Practice parameters for the treatment of narcolepsy: an update for
2000. Standards of Practice Committee. Sleep 2001;24:
451–66.
32. U.S. Food and Drug Administration. Center for Drug
www.turner-white.com
Primary Sleep Disorders: The Dyssomnias
Evaluation and Research. Drug discontinuations: letter from Abbott. Available at www.fda.gov/cder/drug/
shortages/Cylert_Disc.pdf. Accessed 4 Jan 2007.
44. Regestein QR, Monk TH. Delayed sleep phase syndrome:
a review of its clinical aspects. Am J Psychiatry 1995;
152:602–8.
33. Lemon MD, Strain JD, Farver DK. Sodium oxybate for
cataplexy. Ann Pharmacother 2006;40:433–40.
45. Chesson AL Jr, Littner M, Davila D, et al. Practice parameters for the use of light therapy in the treatment of sleep
disorders. Standards of Practice Committee, American
Academy of Sleep Medicine. Sleep 1999;22:641–60.
34. Black J, Houghton WC. Sodium oxybate improves excessive daytime sleepiness in narcolepsy. Sleep 2006;29:
939–46.
35. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective.
Am J Respir Crit Care Med 2002;165:1217–39.
46. Buscemi N, Vandermeer B, Hooton N, et al. Efficacy and
safety of exogenous melatonin for secondary sleep disorders and sleep disorders accompanying sleep restriction:
meta-analysis. BMJ 2006;332:385–93.
36. Sharafkhaneh A, Giray N, Richardson P, et al. Association of psychiatric disorders and sleep apnea in a large
cohort. Sleep 2005;28:1405–11.
47. Sack RL, Lewy AJ, Blood ML, et al. Melatonin administration to blind people: phase advances and entrainment. J Biol Rhythms 1991;6:249–61.
37. Winkelman JW. Schizophrenia, obesity, and obstructive
sleep apnea. J Clin Psychiatry 2001;62:8–11.
48. Buxton OM, Copinschi G, Van Onderbergen A, et al.
A benzodiazepine hypnotic facilitates adaptation of
circadian rhythms and sleep-wake homeostasis to an
eight hour delay shift simulating westward jet lag. Sleep
2000;23:915–27.
38. Nuckton TJ, Glidden DV, Browner WS, Claman DM.
Physical examination: Mallampati score as an independent predictor of obstructive sleep apnea. Sleep 2006;29:
903–8.
39. Kushida CA, Littner MR, Hirshkowitz M, et al. Practice
parameters for the use of continuous and bilevel positive
airway pressure devices to treat adult patients with sleeprelated breathing disorders. American Academy of Sleep
Medicine. Sleep 2006;29:375–80.
40. Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice
parameters for the medical therapy of obstructive sleep
apnea. American Academy of Sleep Medicine. Sleep
2006;29:1031–5.
41. Kushida CA, Morgenthaler TI, Littner MR, et al. Practice
parameters for the treatment of snoring and obstructive
sleep apnea with oral appliances: an update for 2005.
American Academy of Sleep Medicine. Sleep 2006;29:
240–3.
49. Czeisler CA, Walsh JK, Roth T, et al. Modafinil for excessive sleepiness associated with shift-work sleep disorder.
U.S. Modafinil in Shift Work Sleep Disorder Study Group
[published erratum appears in N Engl J Med 2005;
353:1078]. N Engl J Med 2005;353:476–86.
50. Ohayon MM, Roth T. Prevalence of restless legs syndrome and periodic limb movement disorder in the
general population. J Psychosom Res 2002;53:547–54.
51. Littner MR, Kushida C, Anderson WM, et al. Practice
parameters for the dopaminergic treatment of restless
legs syndrome and periodic limb movement disorder.
Standards of Practice Committee of the American Academy of Sleep Medicine. Sleep 2004;27:557–9.
42. Practice parameters for the treatment of obstructive
sleep apnea in adults: the efficacy of surgical modifications of the upper airway. Report of the American Sleep
Disorders Association. Sleep 1996;19:152–5.
52. Chesson AL Jr, Wise M, Davila D, et al. Practice parameters for the treatment of restless legs syndrome and
periodic limb movement disorder. An American Academy of Sleep Medicine Report. Standards of Practice
Committee of the American Academy of Sleep Medicine.
Sleep 1999;22:961–8.
43. Richter HG, Torres-Farfan C, Rojas-Garcia PP, et al. The
circadian timing system: making sense of day/night gene
expression [published erratum appears in Biol Res 2004;
37:357–8]. Biol Res 2004;37:11–28.
53. Montplaisir J, Boucher S, Poirier G, et al. Clinical, polysomnographic, and genetic characteristics of restless legs
syndrome: a study of 133 patients diagnosed with new
standard criteria. Mov Disord 1997;12:61–5.
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Psychiatry Volume 11, Part 6 11