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Chapter

10  

Insomnia
Jack D. Edinger, Meir H. Kryger, and Thomas Roth

OVERVIEW CLASSIFICATION

The term insomnia refers to a condition characterized by dif- Historically, a great deal of controversy and confusion has
ficulties initiating and/or maintaining sleep, accompanied by accompanied the diagnostic classification of insomnia because
clinically significant daytime impairment or distress related to several nosologies use differing approaches to insomnia clas-
the ongoing sleep difficulties. Insomnia may occur as an inde- sification or subtyping. Included among these are the insom-
pendent sleep disorder, or it may evolve as a symptom of a nia classification systems contained in the International
medical condition, psychiatric illness, or other sleep disorder. Classification of Diseases (ICD), the diagnostic and statistical
However, even when insomnia initially arises as a symptom manuals of the American Psychiatric Association (APA;
of another disorder, it often develops partial or total indepen- DSM-III-R, DSM-IV, and DSM-IV-TR), and the previous
dence over time and eventually warrants separate clinical and current versions of the International Classification of
attention. Given this observation, it is best to use the term Sleep Disorders (ICSD, ICSD-R, and ICSD-2, respectively).
comorbid insomnia when prominent, clinically significant These three nosologic systems differ markedly in regard to
insomnia symptoms are observed concurrent to another the numbers and types of insomnia diagnoses they describe.
medical, psychiatric, or sleep disorder. As a consequence, application of these different diagnostic
The sleep and waking symptoms of insomnia are varied schemes to the same insomnia patient population provides
and can change over time. Insomnia sufferers may come to notably discordant diagnostic results.
medical attention solely with sleep onset difficulties or sleep In addition, the putative distinction between primary and
maintenance problems, or they may be seen with a combina- secondary insomnias propagated by many past and current
tion of these. Unrefreshing or nonrestorative sleep may insomnia classification schemes had complicated insomnia
accompany these other symptoms but is relatively rare as an diagnostic practice as well. Historically, the term primary
isolated symptom and may connote another underlying insomnia has been used to connote a form of insomnia that
primary sleep disorder (e.g., obstructive sleep apnea). Isolated exists as an independent sleep disorder, whereas the term
sleep-onset complaints are relatively infrequent but occur secondary insomnia has been used to connote the symptom of
most commonly in younger age groups, whereas sleep main- insomnia that arises from a coexisting medical, psychiatric, or
tenance and mixed onset and maintenance problems are more sleep disorder. However, both research and clinical experience
common presentations of insomnia, particularly in middle- have shown that patients assigned primary and secondary
aged and older adults. Yet insomnia symptoms are not neces- insomnia diagnoses often have myriad overlapping symptoms
sarily stable within individuals but may vary over time, in that make it difficult, if not impossible, to reliably discriminate
that patients who come to medical attention with isolated between them. Furthermore, although some patients may
sleep onset difficulties may later develop sleep maintenance have a true secondary insomnia that results from another
difficulties or a mixture of sleep onset and maintenance prob- coexisting disorder, others may have insomnia that is partially
lems. Common daytime consequences of insomnia include related or unrelated to the putative primary coexisting condi-
impaired cognitive function, fatigue or tiredness, feelings of tion. Unfortunately, we have no reliable methods or assays for
sleepiness, reduced motivation and initiative, and depressed differentiating among these distinctive “secondary” subtypes.
mood or irritability. In addition, adults may display increased Hence, as recommended by the 2005 National Institutes of
proneness for accidents at work or while driving, whereas Health consensus statement concerning the manifestations
poor school performance and behavioral problems, such as and management of insomnia, it seems best to use the more
hyperactivity, are common among school-age children and globally descriptive term, comorbid insomnia for forms of
adolescents. insomnia accompanied by another primary sleep disorder or
Many patients with insomnia come to sleep disorder sleep-disruptive medical or psychiatric condition.
centers for evaluation and management. For a majority of such Considerable collaboration has occurred between the orga-
patients, a clinical interview that includes a thorough sleep nizations developing the insomnia classification scheme
history and mental status along with a medical history and included in subsequent editions of the APA’s Diagnostic and
examination provides sufficient information for case concep- Statistical Manual (i.e., the DSM-5) and the ICSD-3. This
tualization and treatment planning. Polysomnography (PSG) collaboration has resulted in much greater concordance
is not routinely indicated for the evaluation of insomnia com- between the insomnia classification schemes included in these
plaints, unless symptoms suggest another primary sleep dis- two systems, and it has eliminated the primary versus second-
order, such as obstructive sleep apnea (OSA) or periodic limb ary insomnia distinction in favor of the single diagnosis of
movement disorder (PLMD), which requires PSG for diag- insomnia disorder, which can be applied to all insomnia patients
nosis and subsequent management. with and without sleep-disruptive comorbidities. Of course,

148
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Atlas of Clinical Sleep Medicine   149

Prevalence of insomnia by nosology Insomnia across the lifespan


in the general population
40
25
35

% Reporting insomnia
30
20
25
Proportion (%)

15 20
15
10 10
5
5 0
15-19 20-99 30-39 40-49 50-59 60-69 >70
0 Males Females
DSM ICD RDC Any insomnia
FIGURE 10-2.  Percentages of men and women who report insomnia.
FIGURE 10-1.  Prevalence of insomnia by diagnostic nosology. Preva- Insomnia is more common in women than in men in all age groups. (Data
lence estimates of insomnia diagnoses in the general population vary as a from Ohayon MM, Caulet M, Guilleminault C: How a general population perceives
function of the diagnostic criteria and nosology used for ascertainment. DSM, its sleep and how this relates to the complaint of insomnia. Sleep
Diagnostic and Statistical Manual of Mental Disorders, fourth edition; ICD, 1997;20[9]:715–723.)
International Classification of Diseases (version 9); RDC, research diagnostic
criteria. (Mofidied from Roth T, Coulouvrat C, Hajak G, et al: Prevalence and per-
ceived health associated with insomnia based on DSM-IV-TR; International Statisti-
cal Classification of Diseases and Related Health Problems, rev 10; and Research Prevalence of insomnia symptoms
Diagnostic Criteria/International Classification of Sleep Disorders, ed 2 criteria:
results from the America Insomnia Survey. Biol Psychiatry 2011;69[6]:592–600.) 45
40
35
30
both systems advocate the assignment of comorbid diagnoses
Percent

25
when they apply, but they eliminate the need to ascertain 20
cause/effect relationships between insomnia symptoms and 15
coexisting conditions, thus simplifying the overall diagnostic 10
process. 5
0
Long sleep Frequent Early AM Nonrefreshing
EPIDEMIOLOGY latency awaking awakening sleep
FIGURE 10-3.  Of the main insomnia symptoms, the most common is
Approximately 30% to 40% of adults have some degree of sleep maintenance difficulties. Note that the prevalences add up to more
disturbed sleep during any given year. Estimates of the than 100%; therefore many patients have more than one insomnia symptom.
prevalence of those who meet formal criteria for an insomnia (Data from Ancoli-Israel S, Roth T. Characteristics of insomnia in the United
diagnosis vary from between 4% and 22%, depending upon States: results of the 1991 National Sleep Foundation Survey: I. Sleep 22[suppl
the specific diagnostic criteria used (Fig. 10-1). Insomnia is 2]:S347-S353.)
more prevalent in women than in men, but the propensity to
develop insomnia increases in both genders with advancing
age, largely because of the increased occurrence of sleep- explains all forms of insomnia, some theories and models are
disruptive comorbidities that comes with aging (Fig. 10-2). helpful. Spielman’s 3-P model highlights the roles of predis-
Isolated sleep maintenance complaints are more common posing, precipitating, and perpetuating factors and is useful in
than isolated sleep onset complaints, although a sizeable per- helping understand the evolution of insomnia. According to
centage of insomnia sufferers have mixed complaints (Fig. this model, insomnia propensity may exist as a latent trait in
10-3). Insomnia symptoms may vary over time, but a substan- predisposed or vulnerable individuals but typically does not
tial proportion of those who develop insomnia have persistent become manifest until precipitating circumstances, such as a
sleep difficulties that fail to remit without intervention. serious illness or stressful life event, push the individual over
the insomnia threshold. Once the insomnia is present, it
evolves from an acute to a more chronic problem, as the indi-
PATHOPHYSIOLOGY OF INSOMNIA vidual develops maladaptive responses to the sleep-wake dis-
turbance that only serve to perpetuate it (Fig. 10-4). This
Much about the etiology and pathophysiology of insomnia model serves as a useful heuristic for understanding the evolu-
remains unknown. However, it is recognized that various tion of chronic insomnia and has served as the basis for more
factors may contribute to the development of insomnia, complex theoretic models proposed for explaining the devel-
including comorbid sleep disorders, psychiatric and medical opment and nature of insomnia complaints (Fig. 10-5).
illnesses, certain medications and illicit substances, sleep- One of the underlying assumptions of current theories is
disruptive environmental circumstances, and a range of psy- that insomnia patients are in a state of hyperarousal over the
chologic and behavioral factors. Although no single model 24-hour period and that this propensity toward hyperarousal

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150   Insomnia

Spielman’s model for the evolution leads patients to develop sleep disturbances when stressed.
of chronic insomnia This hyperarousal can be viewed as a predisposing factor for
insomnia and may be the basis for some individuals’ develop-
ment of insomnia in response to certain medical conditions,
such as chronic obstructive pulmonary disease (COPD).
However, hyperarousal may also serve a perpetuating role that
Insomnia
makes sleep difficult throughout the 24-hour day. Numerous
Threshold
studies have supported the presence of physiologic hyper-
arousal among insomnia sufferers. For example, imaging
studies conducted with positron emission tomography show
that various brain areas of insomnia patients show less deac-
Premorbid Acute Subacute Chronic tivation during non–rapid eye movement (NREM) sleep than
do similar brain areas in normal sleepers (Fig. 10-6). Other
Predisposing Precipitating Perpetuating
research also supports the notion that the hyperarousal state
FIGURE 10-4.  Spielman’s 3-P model for insomnia. Insomnia develops and results in measurable changes in physiologic systems other
is a function of predisposing and precipitating factors and is sustained over time
by perpetuating factors.
than the central nervous system (Fig. 10-7).

Predisposing factors Sleep state misperception


• Genetics Overestimation of wakefulness
• Hyperarousal Underestimation of sleep
• Depression
• Tendency to worry and ruminate
Perceived wakefulness vs PSG sleep

Insomnia
Precipitating factors Can’t fall asleep
• Acute stress Wake up frequently
• Illness (medical or psychiatric)
• Medications
• Worry and rumination
Neurocognitive factors
Conditioned arousal Cognitive alterations

Perpetuating factors Somatic Sensory processing


• Dysfunctional attitudes about sleep Information processing and
• Staying awake in bed Cortical short-term memory formation
• Increased time in bed
Long-term memory formation
• Worry and rumination about insomnia Cognitive

FIGURE 10-5.  Steps in the evolution of insomnia. PSG, polysomnogram.

Thalamus
Hypothalamus
ARAS ARAS
Mesial
temporal
cortex

Cingulate Insular
cortex

ARAS Mesial
temporal
cortex
Hypothalamus
FIGURE 10-6.  Hyperarousal in insomnia. The red and yellow areas show that regions of the brain that are normally wakefulness-promoting areas do not
decrease their metabolic rate with sleep. Fluorodeoxyglucose positron emission tomography was used to evaluate regional glucose metabolism in the brain.
This suggests that the brains of patients with insomnia are hyperaroused. ARAS, ascending reticular activating system. (From Nofzinger EA, Buysse DJ, Germain A,
et al: Functional neuroimaging evidence for hyperarousal in insomnia. Am J Psychiatry 2004;161[11]:2126–2128.)

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Atlas of Clinical Sleep Medicine   151

Comorbid with
sleep disorders
(10%) Isolated insomnia
Hypothalamic- disorder
Increased
pituitary axis (15%)
metabolic rate
activation

Comorbid with
Hyperarousal other illnesses,
state medications, etc.
(35%)
Comorbid with
psychiatric disorders
Sympathetic Functional (40%)
nervous system neuroanatomic FIGURE 10-8.  Approximate distribution of types of insomnia. Those
activation changes with primary insomnia make up only a small portion of the population of
people with insomnia. (Data from Ford DE, Kamerow DB: Epidemiologic study of
sleep disturbances and psychiatric disorders: An opportunity for prevention? JAMA
1989;262[11]:1479–1484.)
FIGURE 10-7.  Studies have documented a hyperarousal state in insom-
nia patients. Increases in cortisol (hypothalamic-pituitary activation),
increases in heart rate response (sympathetic nervous system activation), an
increased 24-hour metabolic rate, and changes that indicate increased meta- BOX 10-2  Medical Conditions Comorbid with
bolic rate are seen in regions of the brain that promote wakefulness.
Insomnia

• Cardiovascular disease (congestive heart failure and stroke)


• Pulmonary disease (asthma, chronic obstructive pulmonary
BOX 10-1  Criteria for Defining Insomnia disease)
• Gastrointestinal disease (peptic ulcer disease,
• Difficulty falling asleep or gastroesophageal reflux)
• Difficulty staying asleep or • Endocrine disease (diabetes mellitus)
• Early morning awakening or • Renal failure
• Nonrefreshing or nonrestorative sleep • Neurologic disease (Alzheimer and Parkinson diseases)
• Pain from any source (arthritis, fibromyalgia)
The above occur with daytime consequences or distress that lasts at least 1 • Urologic disorders (nocturia)
month despite opportunity and circumstances to sleep. • Perimenopause and menopause
• Cancer

TYPES OF INSOMNIA
BOX 10-3  Psychiatric Conditions Comorbid with
The insomnia features described in Box 10-1 are found in Insomnia
three groups of patients (Fig. 10-8): 1) patients in whom a
medical or psychiatric condition coexists with the insomnia • Anxiety disorder
(comorbid insomnia); 2) patients in whom the primary sleep • Depression
disorder may include symptoms of insomnia (primary sleep • Schizophrenia
disorders); and 3) patients in whom insomnia exists in the • Alcohol and drug abuse
absence of a psychiatric, medical, or other primary sleep dis-
order (isolated insomnia disorder).

Comorbid Insomnia the comorbid disorder. An example is COPD, discussed in


Comorbid insomnia refers to a disorder in patients who have a Chapter 13.4. Figure 10-11 shows that the precipitating
medical or psychiatric condition and also have insomnia factor for insomnia in COPD is a biologic response to the
symptoms (Fig. 10-9). Some of the diseases that frequently disorder (e.g., cough, dyspnea) that disturbs sleep, and that
have comorbid insomnia are listed in Boxes 10-2 and 10-3. with treatment, some of the COPD-perpetuating factors may
As noted earlier, the term secondary insomnia, previously used be resolved, only to be replaced by other perpetuating factors,
to refer to such conditions, is not always accurate. If the such as medications (bronchodilators and corticosteroids) and
insomnia symptoms are indeed secondary, they should resolve some of the psychophysiologic factors mentioned above. Thus
with effective treatment of the presumed primary, or causative in individuals predisposed to insomnia, the COPD-related
medical or psychiatric illness. Typically, that does not happen. arousal will lead to insomnia, whereas in those not so predis-
For example, in patients successfully treated for depression, posed, the COPD will result in only a brief arousal with a
insomnia is the most common residual symptom (Fig. 10-10). rapid return to sleep.
In comorbid insomnia, the precipitating factor is often the Similarly, in congestive heart failure (Fig. 10-12), the
physiologic consequence (typically an arousal from sleep) of abnormal breathing pattern can initiate insomnia. Therapy for

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152   Insomnia

Medical conditions comorbid with insomnia


80

Patients with disease with insomnia (%)


70

60

50

40

30

20

10

0
Hip Obstructive Angina Congestive Myocardial Prostate Diabetes
disease airway pectoris heart infarction disease mellitus
disease failure

Mild insomnia Severe insomnia


FIGURE 10-9.  In a study of 3445 patients with chronic medical conditions, a substantial proportion of patients with common comorbidities had mild
or severe insomnia even in the absence of depression. The mean age of the studied population of patients was 54 years. (Data from Katz DA, McHorney CA:
Clinical correlates of insomnia in patients with chronic illness. Arch Intern Med 1998;158:1099–1107.)

Residual symptoms in remitters to 8 weeks of depression


treatment with fluoxetine 20 mg
50
45

40 37
Patients (%)

30 27
25
22
20
15 15

10 7
4

0
Disturbed Fatigue Interest Guilt Concen- Mood Weight Psycho- Suicidal
sleep tration motor ideation
FIGURE 10-10.  Sleep disturbance/insomnia is the most common residual symptom in patients who remit from depression with treatment. (Data
from Nierenberg AA, Keefe BR, Leslie VC, et al: Residual symptoms in depressed patients who respond acutely to fluoxetine. J Clin Psychiatry 1999;60[4]:221–225.)

heart failure may improve the breathing pattern, but the low fragmentation (Fig. 10-14), and in the electroencephalogram
cardiac output state could still be associated with increased (EEG; Fig. 10-15). At times medications can alter the hyp-
catecholamine levels that could interfere with sleep and cause nogram of a patient with depression by enhancing sleep onset
hyperarousal. difficulties and/or suppressing rapid eye movement (REM)
Sleep difficulties are present in most patients with psychi- sleep (Fig. 10-16).
atric disorders, and it is estimated that approximately 40% of
all patients with insomnia have a coexisting psychiatric
problem (see Box 10-3). These sleep complaints of insomnia PRIMARY SLEEP DISORDERS THAT PRESENT
patients are related to both their disease and the treatment of WITH INSOMNIA
their disease (see Chapter 17). Anxiety and mood disorders
are the most common diseases comorbid with insomnia Several primary sleep disorders often have insomnia as the
among those patients seen in clinical practice (Fig. 10-13). initial complaint (Box 10-4). Insomnia is a classic symptom
In depressed patients and in patients with insomnia that in patients with restless legs syndrome (RLS; see Chapter
occurs in isolation, evidence of hyperarousal may be found in 11.2). Disturbed sleep is a feature of narcolepsy, and many
the sleep hypnogram, primarily in the form of excessive sleep patients, especially women, have insomnia as a manifestation

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Atlas of Clinical Sleep Medicine   153

Excessive mucus
production

Awake Cough Difficulty


initiating and
maintaining
NREM Dyspnea sleep

Effect of
medications

Hypoventilation
Hypoxemia Dyspnea
Reduced FRC Difficulty
REM
maintaining
Chronic Increased sleep
airflow respiratory
Increased V/Q obstruction effort
mismatch

FIGURE 10-11.  Precipitating and perpetuating factors of comorbid insomnia in chronic obstructive pulmonary disease. Coughing, excessive mucus production,
and effects of medications can delay sleep onset and awaken the patient. During rapid eye movement (REM) sleep, a blunting of the drive to breathe and loss
of tone of the accessory respiratory muscles lead to reduced functional residual capacity (FRC) and an increased ventilation/perfusion (V/Q) mismatch, resulting
in hypoventilation and hypoxemia. NREM, non-REM sleep. (Modified from George CF, Bayliff CD: Management of insomnia in patients with chronic obstructive pulmo-
nary disease. Drugs 2003;63:379–387.)

Cursor: 00:14:53, Epoch: 209 - AWAKE 30 sec/page


EMG1-EMG2
1.02 mV
C3-A2
128 V
C4-A1
128 V
Fr3-A2
128 V
Fr4-A1
128 V
O1-A2
128 V
O2-A1
128 V
ROC-A1
128 V
LOC-A2
128 V
ECG1-ECG2
819.2 V
10 min/page
RAT-RAT-
512 V
100

SaO2
%

70

THOR
EFFORT
4.1 mV

ABD EFFORT
4.1 mV

100

Pulse
bpm

40
40

ETCO2
mm Hg

NASAL PRES
500 mV

FIGURE 10-12.  Insomnia in congestive heart failure. An epoch of 30 seconds showing wakefulness (top panel). The bottom is 10 minutes. This patient had
congestive heart failure and awake Cheyne-Stokes breathing episodes with quite significant oxygen desaturations. Note the small blips in the end-tidal CO2
during some of the apneic/hypopneic episodes. These are cardiogenic oscillations. This patient was not able to achieve persistent sleep despite severe sleepiness
because he kept waking up during the hyperpneic episodes.

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154   Insomnia

Psychiatric comorbidities associated with sleep disturbance

60

50

Chronic insomniacs (%)


40

30

20

10

0
No Anxiety Major Dysthymia Alcohol Other Drug
psychiatric disorder depression abuse psychiatric abuse
disorder disorder
FIGURE 10-13.  Psychiatric comorbidities associated with insomnia. Insomnia is found in most psychiatric disorders, and about 40% of chronic insomniacs
have comorbid psychiatric disease. Anxiety disorders are the most common psychiatric comorbidities associated with insomnia, followed by depression.
(Data from Ford DE, Kamerow DB: Epidemiologic study of sleep disturbances and psychiatric disorders: An opportunity for prevention? JAMA 1989;262[11]:
1479–1484.)

Sleep stages

W
R
1
2
3
4

0 1 25 3
6 47 8 9
Hours
FIGURE 10-14.  Hypnogram of sleep onset and sleep maintenance insomnia in a 23-year-old man with untreated depression. Note the long sleep
latency and several prolonged episodes of wakefulness during sleep. Depression cannot be diagnosed from a sleep study. R, rapid eye movement sleep; W,
wakefulness.

BOX 10-4  Primary Sleep Disorders that May Present in phase with their endogenous (delayed) circadian sleep
with Insomnia propensities.
It is also important to note that other circadian rhythm
• Movement disorders (restless legs syndrome, periodic limb disorders, such as phase-advance syndrome and shift-work
movements in sleep) disorder, commonly manifest initially with insomnia symp-
• Obstructive sleep apnea syndrome toms as well. Patients with sleep apnea may come to medical
• Narcolepsy attention with insomnia, giving them the hypnogram and
• Central sleep apnea syndrome overnight oximetry pattern shown in Figure 10-17.
• Cheyne-Stokes respiration
• Delayed sleep-phase syndrome Isolated Insomnia Disorder
Insomnia occurs in the absence of sleep-disruptive comorbidi-
ties in approximately 15% of those patients encountered clini-
cally. Historically such patients have been assigned the
diagnosis of primary insomnia in the DSM nosologies. Within
previous versions of the ICSD, multiple diagnostic labels have
of sleep apnea syndrome; these entities are covered elsewhere been used for these patients, as shown in Table 10-1. However,
in this text. Patients with delayed sleep-phase syndrome do both the DSM-5 and ICSD-3 assign such patients the diag-
not technically fit the criteria for insomnia. Although such nosis of insomnia disorder.
patients may complain of difficulty in falling asleep, they PSGs are not generally performed in cases of isolated
show a normal, undisturbed sleep pattern when sleeping insomnia disorder, except for some cases of patients who are

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Atlas of Clinical Sleep Medicine   155

E2-M1

E1-M2
30s
F4-M1

C4-M1

02-M1

CHIN1

ECG
22:50:11 144 145 145 146 146 147 22:52:11
RLeg
LLeg
SNORE

PTAF
2m

THERM

THOR

ABD
96 96 96 96 96 96 96 96 96 96 96 96 96 97 96 96 96 96 96 97 96 96 96 96 96 96 97 97 96
SaO2 100
92
(%) 85

FIGURE 10-15.  Polysomnogram fragment from the patient in Figure 10-14. Note the high-frequency waves in the alpha range interspersed throughout
the electroencephalogram. Although this finding is not uncommon, it is not specific or diagnostic for depression or other sleep disorders. This may be a mani-
festation of hyperarousal.

Sleep stages

W
R
1
2
3
4

0 1 2 3 4 5 6 7
Hours
FIGURE 10-16.  Hypnogram in a depressed patient complaining of insomnia who is being treated with an antidepressant. Notice that the first rapid
eye movement (REM) episode occurs 4 hours into the night. This is likely related to the REM-suppressing effects of the antidepressant. Note the very long sleep
latency. Once asleep the patient did not have prolonged awakenings. In some patients, antidepressant medications can cause motor restlessness (see Chapter
17). R, REM sleep; W, wakefulness.

suspected of markedly underreporting their actual sleep time.


TABLE 10-1  Primary Insomnia Types For such individuals, conventional scoring of the PSG shows
CATEGORY ESSENTIAL DIAGNOSTIC FEATURES a fairly normal sleep pattern. For the remainder of those with
isolated insomnia disorders, PSG is generally not contributory
Psychophysiologic Hyperarousal and learned sleep-preventing to the assessment and diagnosis of the patient’s sleep-wake
insomnia associations that result in a complaint of complaints. However, if PSG is conducted with such indi-
insomnia viduals, results will typically show a long sleep latency,
Inadequate sleep Insomnia caused by lifestyle and activities that increased wake after sleep onset, frequent awakenings during
hygiene interfere with sleep the night, and evidence of arousal on EEG (see Fig. 10-15).
Idiopathic insomnia Lifelong insomnia often begun during infancy or The hypnogram is useful in getting a snapshot of the entire
early childhood night (Fig. 10-18).
Paradoxic insomnia Complaint of severe insomnia that occurs without
objective evidence of abnormal sleep; such
patients typically have little daytime
impairment; also called sleep state misperception
MANAGEMENT OF INSOMNIA
Adjustment sleep Insomnia related to an identifiable stressor; Most cases of insomnia that require therapy are chronic. Cur-
disorder usually short term
rently the best and most well-established treatments include

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156   Insomnia

Sleep stages
W
R
1
2
3
4

0 1 2 3 4 5 6 7
Hours

Oxygen saturation
100
90
80
70
60
50
Des
0 1 2 3 4 5 6 7
Hours
FIGURE 10-17.  Hypnogram and overnight oximetry in a patient complaining of insomnia who also has obstructive sleep apnea. Notice the very long
sleep latency, during which time oxygen saturation is stable. Once the patient is asleep, the large changes in oxygen saturation caused by back-to-back apneas
are apparent. The oxygen saturation (SaO2) is lowest in the brief episodes of rapid eye movement (REM) sleep. The patient has a prolonged awakening toward
morning. Des, desaturation; R, REM sleep; W, wakefulness.

Sleep stages

W
R
1
2
3
4

0 1 2 3 4 5 6 7 8
Hours
FIGURE 10-18.  Hypnogram in a 34-year-old man complaining of long-standing insomnia. No medical comorbidities or psychopathology are present in
this patient with sleep-onset and middle-of-the-night insomnia, yet many awakenings occur during the night. R, rapid eye movement sleep; W, wakefulness.

pharmacotherapy with benzodiazepine receptor agonists TABLE 10-2  Benzodiazepine Receptor Agonists
(BzRAs), such as those shown in Table 10-2, and the psycho-
logic intervention known as cognitive behavioral therapy for MEDICATION NAME USUAL THERAPEUTIC DOSAGE
insomnia (CBTI; Table 10-3). Studies of pharmacologic inter-
ventions with agents such as zolpidem and eszopiclone have Zolpidem 5 or 10 mg
Eszopiclone 1, 2, or 3 mg
shown sleep improvements with continued use over periods of Zaleplon 5 and 10 mg
6 months to 1 year (Fig. 10-19). Empiric data are insufficient
to demonstrate sustained benefits from pharmacotherapy for
insomnia after medication withdrawal. However, clinical
experience suggests that many patients show a return of insom- sleep-improvement skills that eliminate or minimize the
nia symptoms after they discontinue sleep medications. In myriad factors that perpetuate sleep difficulties. As a conse-
contrast, fairly substantial evidence supports that patients quence, CBTI is often the preferred first-line therapy when
maintain or garner further improvements in their sleep onset available.
latencies, wake times after sleep, or total sleep times long after Some rationale exists for considering the combining of
CBTI is discontinued (Fig. 10-20). This presumably occurs pharmacotherapy and CBTI to optimize insomnia manage-
because CBTI is designed to teach insomnia sufferers ment. Pharmacotherapy generally has immediate first-night

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Atlas of Clinical Sleep Medicine   157

TABLE 10-3  Components of Cognitive Behavioral Therapy for Insomnia


TECHNIQUE INVOLVES ADDRESSES

Sleep hygiene Review of diet, exercise, alcohol, and environmental factors that may help or Lifestyle and behaviors that are hurdles to good
education interfere with sleep; importance of regular bedtime and set time and the quality sleep
negative effects of long naps
Stimulus control Teach patient to go to bed only when sleepy; get out of bed when unable The learned associations of the bed with
to sleep; and when sleepy, stop all sleep-incompatible activities (e.g., wakefulness
television viewing while in bed, using electronic devices before bedtime)
Sleep restriction Emphasize the importance of reducing time in bed to actual sleep time Disrupted and fragmented sleep related to too
much time in bed
Relaxation Teach patient to reduce muscle tension with relaxation techniques and to Increased hyperarousal (physiologic, cognitive,
reduce thoughts that will not shut off by using imagery training and emotional)
meditation
Cognitive Correct inaccurate beliefs and attitudes about insomnia Incorrect information and misconceptions that
are perpetuating the problem

Median wake time after sleep onset in patients Durability of therapeutic benefits of CBTI
treated with eszopiclone or placebo (follow-up: 6 months)
60
FU 435
120 Pre Post
50 420
100
405
40
80
Time (min)

390
Minutes

Minutes
396
30 60 70
64 375
378
40 360
20 *
* * *^ * *
37
33
38 38
349 345
20
10
330
0
0 Sleep onset Wake after Total 0
Month 1 Month 2 Month 3 Month 4 Month 5 Month 6 latency sleep onset sleep time
FIGURE 10-20.  Cognitive behavioral therapy for insomnia (CBTI) pro-
Eszopiclone ITT (n  593) Placebo ITT (n  195) duces durable improvements in sleep-onset latency, wake after sleep
Eszopiclone observed Placebo observed onset, and total sleep time 6 months after treatment is discontinued. FU,
Eszopiclone completers Placebo completers follow-up. (Data from Morin CM, Culbert JP, Schwartz SM: Nonpharmacological
(n  360) (n  109) interventions for insomnia: a meta-analysis of treatment efficacy. Am J Psychiatry
1994;151:1172–1180.)
FIGURE 10-19.  Eszopiclone therapy remains significantly more effec-
tive than placebo for treating sleep maintenance difficulties across 6
months of double-blind treatment. Median sleep maintenance (time
awake after sleep onset) is shown on the x-axis; treatment period is shown
on the y-axis. ITT, intent to treat group. *P < .05 for all comparisons, except The treatment of comorbid insomnia presents a special
^P = .07 for observed cases at month 4. (Modified from Krystal AD, Walsh JK, challenge because comorbid conditions may complicate the
Laska E, et al: Sustained efficacy of eszopiclone over 6 months of nightly treatment: overall management strategy. Moreover, some findings suggest
results of a randomized, double-blind, placebo-controlled study in adults with that comorbid patients may have a more blunted response to
chronic insomnia. Sleep 2003;26[7]:793–799.)
established treatments, particularly patients with comorbid
psychiatric conditions (Fig. 10-21). The best outcomes seem
benefits, whereas the benefits derived from CBTI are some- to occur when we treat the comorbid condition while also
what more delayed. In contrast, the durability of CBTI long providing separate treatment for insomnia. For example,
after therapy is discontinued makes it an important compo- depressed patients with insomnia have greater chances for
nent of insomnia management. With combined pharmaco- both insomnia and depression remission when they receive
therapy and CBTI, the most rapid and durable sleep treatments for both conditions rather than treatment for
improvements might be expected. Unfortunately, studies depression alone (Fig. 10-22). This is the case when the
designed to test such treatment combinations have produced insomnia treatment consists of pharmacotherapy or CBTI. In
mixed results. However, one recent study showed benefits of cases of insomnia that occur comorbid with another sleep
combined zolpidem-CBTI therapy over CBTI alone when a disorder, both an insomnia therapy and a therapy for the
6-week period of combined therapy was followed by a medi- comorbid sleep disorder (e.g., continuous positive airway
cation taper and a continuation of CBTI for an additional pressure for sleep apnea) should be combined to achieve
period. optimal results.

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158   Insomnia

Average effect size for insomnia severity index


total score across patient groups

Large

Moderate

Small

Isolated GAD MDD Perimenopause Rheumatoid


insomnia disorder arthritis
FIGURE 10-21.  Those with comorbid insomnia, and particularly those with comorbid psychiatric illnesses, show a more blunted response to insom-
nia treatment than do those with isolated insomnia disorder. GAD, generalized anxiety disorder; MDD, major depressive disorder.

Depression and insomnia remission:


combined CBTI/escitalopram vs. escitalopram (EsCIT) alone

Depression remission Insomnia remission


70 70

60 60

50 50

40 40

30 30

20 20

10 10

0 0
EsCIT  CBTI EsCIT only EsCIT  CBTI EsCIT only

Remitted Nonremitted Remitted Nonremitted


FIGURE 10-22.  Combined cognitive behavioral therapy for insomnia (CBTI) and antidepressant therapy produces greater changes in insomnia and
depression remission than does antidepressant therapy alone in patients who have comorbid depression and insomnia. EsCIT, escitalopram. (Modified
from Manber R, Edinger JD, Gress JL, et al: Cognitive behavioral therapy for insomnia enhances depression outcome in patients with comorbid major depressive disorder
and insomnia. Sleep 2008;31[4]:489–495.)

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