Insomnia and Anxiety (Series in Anxiety and Related Disorders) (15 page)

awake for long periods; (d) avoid reading, watching TV, eating,

worrying and other sleep-incompatible behaviors in the bed/

bedroom; and (e) refrain from daytime napping.

Sleep restriction

Sleep restriction therapy reduces nocturnal sleep disturbance primarily

therapy

by restricting the time allotted for sleep each night so that the

time spent in bed closely matches the individual’s presumed sleep

requirement.

This treatment typically begins by calculating the individual’s average

total sleep time (ATST) from a sleep log that is kept for 1–2 weeks.

An initial time-in-bed (TIB) prescription may either be set at the ATST

or at a value equal to the ATST plus an amount of time that is

deemed to represent normal nocturnal wakefulness (e.g., ATST + 30

min). The initial TIB prescription is seldom set below 5 h per night.

On subsequent visits TIB may be adjusted up or down in 15–30 min

increments dependent upon sleep performance and waking function.

Cognitive Behavior Therapy Model

53

fashioned to target and address a specific and somewhat distinctive subset of

psychological or behavioral factors that is thought to be important in perpetuating

insomnia. This observation, in turn, implies that none of these therapies are likely

to address all of the psychological and behavioral factors presumed to contribute to

chronic insomnia problems.

Given this realization, interest in the development of more omnibus insomnia

therapies emerged in the mid-1980s and in the early 1990s. To address the multitude

of psychological and behavioral factors presumed to sustain insomnia, a multicom-

ponent Cognitive-Behavior Therapy (CBT) for insomnia emerged. The original

renditions of this treatment (Edinger, Hoelscher, Marsh, Lipper, & Ionescu-Pioggia,

1992; Hoelscher & Edinger, 1988; Morin, 1993; Morin, Kowatch, Barry, & Walton,

1993) included a combination of the above-mentioned first generation treatments,

including sleep hygiene education, stimulus control instructions, and sleep restric-

tion therapy. These early protocols also acknowledged the sleep-disruptive role of

cognitive factors (i.e. unhelpful sleep-related beliefs) by incorporating belief-

targeted corrective sleep education or traditional cognitive therapy strategies, such

as cognitive restructuring (Beck, Rush, Shaw, & Emery, 1979; Morin, 1993) to

address these cognitions. Since the emergence of these early protocols, the combi-

nation of stimulus control, sleep restriction therapy, and some form of cognitive

therapy have persisted as the core of current-day CBT insomnia treatment. As dis-

cussed in detail below, this treatment has been widely tested and shown efficacy for

those with chronic insomnia. In fact, CBT is now regarded as a well-established

front-line therapy for the management of chronic insomnia in adults (Morin et al.,

2006; National Institutes of Health State of the Science Conference Statement,

2005). Evidence supporting the efficacy of this treatment is discussed in some

detail later in this chapter. However, before considering the support for such treat-

ments, we first discuss the rationale and theoretical basis for this treatment approach

in the ensuing discussion.

Cognitive Behavior Therapy Model

Most individuals experience a night of poor sleep now and then, but chronic or

persistent insomnia develops in 10–15% of those in the general population who are

the most vulnerable and who are subject to the proper set of sleep-disruptive cir-

cumstances. Perhaps the most popular and useful heuristic for understanding the

evolution of chronic insomnia is the theoretical model proposed by Spielman et al.

(1987). According to the model, the evolution of chronic insomnia is dependent

upon the interplay of predisposing factors, precipitating events, and perpetuating

mechanisms. Some individuals are presumed at relative risk for developing insom-

nia due to predisposing vulnerabilities, such as a weakened or highly sensitive

biological sleep system or a special propensity to sleep poorly when confronted

with stress. Such vulnerabilities alone, however, do not place most such individuals

over an insomnia threshold.

54

4 Cognitive Behavior Therapy for Insomnia: Treatment Considerations

Typically, such individuals only experience the onset of insomnia when confronted

with precipitating events such as a stressful life event, sudden alteration in their

normal sleep-wake schedule, or a major illness. Whereas, insomnia may arise as a

transient condition in some of these individuals, others may manifest psychological

and behavioral characteristics and reactions to their sleep difficulties that ultimately

serve to perpetuate it over time. Thus, although predisposing and precipitating factors

lead to the onset of insomnia, the psychological and behavioral perpetuating factors

that sustain it serve as the treatment targets for insomnia therapy.

The cognitive behavior model of insomnia posits that an array of sleep-disruptive

cognitive factors and behavioral practices act as the key perpetuating mechanisms

for sustaining the sleep difficulties of insomnia patients. Figure 4.1 provides a sche-

matic representation of the role and interplay of these factors in perpetuating sleep

disturbance. Setting the stage for persistent sleep problems is a thinking style that

can include: misattributions about the causes of insomnia, attentional bias for sleep-

related threats, worry and/or rumination about the consequences of poor sleep, and

unhelpful beliefs about sleep promoting practices (Carney & Edinger, 2006;

Carney, Edinger, Manber, Garson, & Segal, 2007; Edinger & Carney, 2008; Espie,

2002; Harvey, 2002; Morin, Stone, Trinkle, Mercer, & Remsberg, 1993). These

cognitions, in turn, promote sleep-disruptive habits and conditioned emotional

Cognitive

Factors

Unhelpful sleep-related beliefs Attention bias

Taking worries to bed

Sleep-disruptive

Behaviors

Napping & too much

time in bed

Sleeping in or

varying sleep

schedule

Anxiety about

not sleeping

Reduced

Disrupted

homeostatic

circadian

Environmental &

Bedtime arousal

drive

timing

behavioral inhibitors

Disturbed Sleep

Fig. 4.1
Cognitive behavioral model of factors that perpetuate insomnia

The Evidence Supporting CBT for Insomnia

55

responses that may alter normal sleep drive, interfere with circadian timing mecha-

nisms, or serve as environmental/ behavioral inhibitors to sleep (Bootzin, 1977;

Morin, 1993; Spielman, Caruso, & Glovinsky, 1987; Webb, 1988). For example,

daytime napping or spending extra time in bed to compensate for a poor night’s

sleep interferes with homeostatic mechanism of the body that operates automati-

cally to increase sleep drive in response to increasing periods of wakefulness (i.e.,

sleep debt). Alternately, the habit of remaining in bed well beyond the normal rising

time following a poor night’s sleep disrupts the body’s circadian or “clock” mecha-

nism that controls the timing of sleep and wakefulness within a 24-h period.

Additionally, the repeated association of the bed and bedroom with unsuccessful

sleep attempts may eventually result in sleep-disruptive conditioned arousal in the

home sleeping environment. Finally, failure to discontinue mentally demanding

work and allot sufficient “wind-down” time before bed may raise bedtime arousal

and serve as a significant sleep inhibitor during the subsequent sleep period. In

sum, all of these factors may contribute to and perpetuate PI (Bootzin & Epstein,

2000; Edinger & Wohlgemuth, 1999; Hauri, 2000; Morin, Savard, & Blais, 2000).

CBT for insomnia was designed to modify the range of cognitive and behavior fac-

tors that ostensibly sustain or add to sleep problems.

The Evidence Supporting CBT for Insomnia

Currently, there is ample evidence supporting the efficacy, effectiveness, and appli-

cability of CBT for a range of insomnia. A variety of studies have shown that CBT

is superior to no treatment (wait list conditions) (Mimeault & Morin, 1999; Morin,

Kowatch et al., 1993; Rybarczyk, Lopez, Benson, Alsten, & Stepanski, 2002) or

such stand-alone therapies such as relaxation training (Edinger, Wohlgemuth, Radtke,

Marsh, & Quillian, 2001a; Edinger et al., 1992; Rybarczyk et al., 2002), sleep

hygiene education (Edinger & Sampson, 2003; Leger, Guilleminault, Bader, Levy,

& Paillard, 2002), and a credible sham (placebo) psychological treatment (Edinger

et al., 2001a) for the management of uncomplicated, primary forms of insomnia. In

addition, several randomized trials (Jacobs, Pace-Schott, Stickgold, & Otto, 2004;

Morin, Colecchi, Stone, Sood, & Brink, 1999; Sivertsen et al., 2006; Wu, Jinfeng,

Chungai, & Chunling, 2006) collectively have shown that CBT and pharmaco-

therapy with common prescription hypnotics (e.g., zolpidem, zolpiclone, temaze-

pam) yield similar sleep improvements during active treatment. However,

improvements obtained with medications tend to disappear after medications are

withdrawn, whereas the improvements obtained during CBT therapy endure long

after active therapy is discontinued. Furthermore, large clinical effectiveness stud-

ies (Espie et al., 2007; Espie, Inglis, Tessier, & Harvey, 2001) as well as clinic-

based case series studies (Morin, Stone, McDonald, & Jones, 1994; Perlis, Sharpe,

Smith, Greenblatt, & Giles, 2001) have shown that multimodal CBT is an effective

treatment for the management of those with primary insomnia.

More recent studies have provided growing evidence that CBT can be effective

for those with more complex forms of insomnia. A number of studies have shown

56

4 Cognitive Behavior Therapy for Insomnia: Treatment Considerations

that CBT leads to sleep improvements in those suffering from insomnia arising

from or associated with chronic peripheral pain syndromes (Currie, Wilson,

Pontefract, & deLaplante, 2000), breast cancer (Savard, Simard, Ivers, & Morin,

2005), fibromyalgia (Edinger, Wohlgemuth, Krystal, & Rice, 2005), mixed medical

conditions (Rybarczyk et al., 2002), and chronic alcohol abuse (Greeff & Conradie,

1998). In addition, case series or clinic-based investigations support the usefulness

of CBT among patients with mixed mental and medical conditions (Kuo, Manber,

& Loewy, 2001; Morawetz, 2003; Morin, Stone et al., 1994; Perlis et al., 2001).

Some of these reports also suggest that CBT may lead to improvements in mood

status or other disease-specific symptoms (Edinger et al., 2005; Kuo et al., 2001;

Manber, Edinger, San Pedro, & Kuo, 2007; Morawetz, 2003; Savard et al., 2005).

These findings coupled with those derived from results obtained in those with pri-

mary insomnia indicate that CBT can be regarded as a well-established or front-line

therapy for ameliorating sleep disturbance in both uncomplicated and complex

forms of persistent insomnia (Morin et al., 2006; National Institutes of Health State

of the Science Conference Statement, 2005).

In addition to the data supporting the efficacy/effectiveness of CBT, there are

some results of mechanistic studies that suggest that this therapy addresses the cog-

nitive and behavioral factors presumed to perpetuate insomnia. Studies designed to

assess therapy effects on cognitive mechanisms have shown that CBT reduces sleep-

interfering beliefs (Carney & Edinger, 2006; Espie, Inglis & Harvey, 2001; Morin,

Blais, & Savard, 2002), enhances sleep-related self-efficacy (e.g., confidence in

one’s ability to produce sleep) (Currie et al., 2000; Edinger et al., 2001a; Edinger &

Sampson, 2003), and lowers bedtime cognitive arousal (Mitchell, 1978; Mitchell &

White, 1977; Sanavio, 1988). Likewise, CBT seemingly reduces sleep-disruptive

behaviors such as spending excessive time in bed (Spielman, Saskin, & Thorpy,

1987), or maintaining erratic sleep/wake schedules (Bootzin, 1972; Edinger et al., 2001a;

Edinger et al., 1992; Edinger & Sampson, 2003; Espie, Inglis, Tessier, et al., 2001;

Monk, Petrie, Hayes, & Kupfer, 1994; Monk, Reynolds III, Buysse, DeGrazia, &

Kupfer, 2003; Morin et al., 1999; Morin, Kowatch et al., 1993). Furthermore,

mechanistic studies have shown that changes in selected CBT-targeted cognitive

(Edinger, Wohlgemuth, Radtke, Marsh, & Quillian, 2001b; Morin et al., 2002), and

behavioral (Edinger et al., 2001a; Vincent & Lionberg, 2001; Vincent & Hameed,

2003) insomnia perpetuating mechanisms mediate improvements in sleep and global

insomnia symptoms. Thus, the improvements achieved with CBT result, at least in

part, from the fact that this therapy effectively addresses the cognitive and behavioral

mechanisms critical to sustaining insomnia problems.