Когнитивно поведенческая психотерапия расстройств сна руководство

According to the three-factor (3P) model of insomnia, there
are three primary factors that contribute to the development of chronic
insomnia: (1) predisposing factors — traits or conditions (e.g., high
emotional reactivity) that increase one’s vulnerability to developing insomnia;
(2) precipitating factors — situational conditions (e.g., stressful life
events) that trigger the onset of insomnia; and (3) perpetuating factors
— behaviors and cognitions that contribute to the transition from acute to
chronic insomnia and maintain the disorder long term [36].

One noteworthy aspect of this model is that insomnia can be
maintained long after the life stressor or precipitating event has resolved.
This is thought to be the case because other factors serve to perpetuate
insomnia over time (e.g., going to bed earlier to compensate for sleep loss,
worrying about daytime functioning). In the context of Cognitive Behavioral
Therapy for Insomnia (CBT-I), it is these perpetuating factors that are the
primary focus of treatment [22; 24; 28]. Please note that while sleep problems
and symptoms of insomnia are common in children and adolescents, the present
paper focuses on the application of CBT-I in adult populations. For more
information related to behavioral interventions for pediatric insomnia, please
refer to a prior review and meta-analysis [18].

What is CBT-I?

CBT-I is a multi-component treatment for insomnia that
targets difficulties with initiating and/or maintaining sleep. Standard
treatment is delivered over the course of six to eight sessions (session length
may vary between 30 and 90 minutes). Each session typically has a specific
agenda (e.g., evaluation, rationale, delivery of individual interventions,
adherence management, relapse prevention, etc.). Sessions most often occur in
person or via telehealth on a weekly or bi-weekly schedule and can be delivered
in either individual or group format. Please refer to the Appendix for a list
of treatment manuals that are currently available.

This intervention is typically comprised of two core
components: Sleep Restriction Therapy (SRT) and Stimulus Control Therapy (SCT);
and two adjunctive components: Sleep Hygiene (SH) and Cognitive Therapy (CT).
Most treatment protocols and published manuals [6; 17; 22; 31] deliver SRT and
SCT as complementary therapies. SRT’s primary indication is to increase
homeostatic sleep drive (or the propensity to fall asleep) and to allow for
consolidated sleep. SCT’s primary indication is to manage nocturnal wakefulness
via behavioral modification. Even in the absence of traditional cognitive
therapy exercises (e.g., debunking dysfunctional beliefs and addressing
catastrophization), SRT and SCT still include cognitive work via the
therapist’s explanations and efforts to garner adherence to the prescriptive
aspects of therapy. The art of CBT-I pertains to how successful the therapist
is at garnering patient “buy-in.” This aspect of learning CBT-I is so central
to the process that some treatment manuals provide therapist/patient example
dialogues.

Core Treatment Components

Sleep Restriction Therapy (SRT). SRT is based on the
notion that the most important perpetuating factor for chronic insomnia is
sleep extension [37]. Sleep extension is the tendency for individuals to
compensate for “lost” sleep by increasing their time in bed (e.g., going to bed
earlier, sleeping in later, or napping). A consequence of sleep extension,
however, is the mismatch between sleep ability (i.e., how much time the person
actually sleeps) and sleep opportunity (i.e., how much time the patient spends
in bed). The primary goal of SRT is to address this mismatch by limiting sleep
opportunity to the person’s average sleep ability. SRT is effective because it
increases the homeostatic sleep drive and consequently reduces the time it
takes to fall asleep or the amount of time spent awake at night. According to
the original formulation, SRT can be completed using the following steps: (1)
determine the patient’s baseline sleep ability in terms of average sleep
duration (as assessed with daily sleep diaries gathered over a period of two
weeks), (2) set the patient’s prescribed time in bed (PTIB, i.e., the patient’s
“sleep window”) equal to their average sleep duration during the baseline
period, (3) determine a morning rise time that the patient can closely adhere
to on a daily basis, given their work schedule or other life style constraints,
and (4) set the prescribed time to bed (PTTB) by subtracting PTIB from the
desired wakeup time (e.g., if PTIB is 6 hours and rise time is set to 7:00
a.m., than PTTB equals 1:00 a.m.). This sleep schedule is maintained or altered
based upon how consolidated the patient’s sleep is. For example, if the
patient’s sleep efficiency (SE%; the percent of time in bed spent actually
sleeping) is less than 85%, PTIB is reduced by 15 minutes. If SE% is between
85% and 90%, PTIB remains as prescribed. If SE% is greater than 90%, PTIB is
increased by 15 minutes. Adjustments to the sleep schedule or PTTB are
completed each week after reviewing the patient’s sleep diary from the previous
week.

Stimulus Control Therapy (SCT). SCT is based on
behavioral principles and the idea that one stimulus may lead to a variety of
responses, depending on the conditioning history [2]. In good sleepers, the
stimuli typically associated with sleep (e.g., bed, bedroom, etc.) are paired
with and subsequently elicit the response of sleep. In patients with insomnia,
these same sleep-related stimuli become paired with other activities, such as
reading, watching television, and lying awake in bed while trying to
sleep (also known as sleep “effort”). Engaging in these other behaviors while
in bed contributes to a maladaptive conditioning pattern (or stimulus
dyscontrol) and, therefore, reduces the probability that sleep will occur when
and where the patient wants. Most importantly, these other behaviors strengthen
the association between one’s bed and wakefulness (i.e., the bed and the
bedroom become cues for wakefulness). Stimulus control recommendations are as
follows: (a) lie down to sleep only when sleepy, (b) avoid using the bed for
activities other than sleep or sex, (c) get out of bed if unable to sleep
within 15–20 min and return to bed only when sleepy, (d) repeat this pattern
throughout the night as necessary, (e) get up at the same time every day, and
(f) avoid napping throughout the day [30]. These recommendations form the basis
for the development of good sleeping habits and are to be observed even after
remission is achieved.

Sleep Hygiene (SH). Educating patients about SH
promotes better sleep practices by providing information about behaviors that
influence sleep [24]. Although it shows only minimal treatment effects when
used as a stand-alone intervention [7; 11], SH is considered a necessary part
of CBT-I [23]. SH usually includes a one-page handout that outlines various
lifestyle and environmental factors that can be modified to decrease the risk
of experiencing a sleepless night (e.g., limiting caffeine and alcohol use
before bedtime, napping, creating a comfortable sleeping environment, and
exercising regularly). SH is thought to be most helpful when tailored to the
patient’s own sleep/wake behaviors.

Cognitive Therapy (CT). The primary goal of CT is to
help patients develop realistic sleep expectations by (1) identifying
dysfunctional thoughts about sleep that perpetuate insomnia or contribute to
pre-sleep arousal, (2) examining these thoughts for accuracy, and, if
necessary, (3) modifying them to be more rational and/or realistic [24].
Research on the influence of dysfunctional beliefs about sleep, attentional
biases, and pre-sleep cognitions highlights cognitive restructuring as an
increasingly important component of CBT-I [8]. CBT-I follows the traditional
cognitive therapy approach by identifying maladaptive sleep-related cognitions
and the resulting emotional reactions using thought records. The patient is
then instructed to describe the situation that produced the thought, the
content of the thought, the emotional reaction, and its intensity in detail.
These beliefs are evaluated with cognitive restructuring techniques including,
but not limited to, disputation of dysfunctional beliefs and
decatastrophization, and replacing them with more adaptive sleep-promoting
thoughts [22]. The patient is instructed to apply their revised thought to the
situation and notes the change in emotion. These cognitive therapy techniques
allow the patient to go through a process of guided discovery to realize that
their beliefs may not be accurate or helpful, which in turn helps them to
better manage their problematic sleep beliefs and cognitive responses.

Session-by-Session Outline

CBT-I typically begins with a 60–90-minute pre-treatment
session, during which the therapist collects clinical information from the
patient regarding the presenting sleep concerns, relevant sleep, and
psychiatric history, relevant social and medical history, baseline symptom
measurement (via self-report measures such as the Insomnia Severity Index (ISI)
and a retrospective sleep diary). The primary goal of this initial session is
for the therapist to develop diagnostic impressions and determine whether CBT-I
is appropriate. If the therapist determines that CBT-I is warranted, an
overview of insomnia, CBT-I, the format of treatment sessions, and orientation
to the daily sleep diary is also provided during this initial session.
Following Session 1, baseline sleep data is collected for 1-2 weeks using a
daily sleep diary (while various versions exist, a consensus sleep diary was
published in 2012 [3]). The remaining CBT-I sessions are typically 30–60
minutes and follow the structure outlined in Table 1. 

Relapse Prevention

Prior to treatment termination, relapse prevention
strategies are discussed. The patient is instructed on strategies to maintain
healthy sleep patterns and how to self-administer treatment should they
experience future sleep continuity problems. During this final session, the
therapist discusses how to maintain the gains the patient has made in treatment
and help them to identify the key strategies to manage their insomnia on their
own. This typically includes a review of the strategies that were discussed
during SRT and SCT, such as the 3P Model of Insomnia, the importance of
maintaining a consistent sleep schedule, and what to do when you experience a
bout of acute insomnia (and how to stay mindful of factors or events that may
potentially trigger these future episodes of insomnia).

Table 1

Session-by-session outline

Note. Adopted from Perlis et al. [28] — Cognitive
behavioral treatment of insomnia: A session-by-session guide.

Multicultural Considerations

While the effects of insomnia can be significant for all,
some research suggests that insomnia disproportionately affects those who are
already socially and/or economically disadvantaged, including racial/ethnic
minorities [4; 5; 9; 10; 32]. That is, cultural/racial factors may influence
the likelihood that someone will (1) develop insomnia, (2) identify
sleeplessness as a problem, and (3) seek out or utilize medical or
psychological interventions for sleep-related concerns. For example, racial
minorities are disproportionately represented in lower income populations [33].
Socioeconomically disadvantaged individuals are therefore more likely to engage
in behaviors that precipitate or perpetuate sleep continuity disturbance, such
as having less consistent work/life schedules (e.g., greater proportion of
people working rotating or night shifts), limited access to regular or
comfortable sleeping conditions, or increased stress [1]. Moreover, some
research supports that racial and ethnic minorities are less likely to seek
treatment for their sleep difficulties. Studies have found cultural differences
in what is considered a sleep “problem” [4; 16]. Therefore, it may be the case
that individuals from certain cultural groups are more likely to minimize the
presence of insomnia symptoms [14] or use cognitive appraisal strategies that
minimize the functional impact of sleep/insomnia on their life [13].

These are important multicultural considerations that may
limit the acceptability of interventions such as CBT-I and thus should be the
focus of future research efforts (e.g., how to adapt behavioral interventions
to different racial/ethnic groups).

Adjuvants to Traditional Interventions

In addition to the key components of CBT-I, additional
interventions, such as nighttime grounding/relaxation, deep breathing,
progressive muscle relaxation, or mindfulness meditation, may be beneficial
components as well. For example, one of the most influential changes to CBT-I
was the adoption of mindfulness training. Mindfulness was first introduced in
the context of insomnia to address sleep-related cognitive arousal [26]. The
approach differs from traditional cognitive therapy in that it is not focused
on disputing, derailing, or disengaging worry or intrusive negative thoughts.
Instead, mindfulness is focused on the non-judgmental observation of one’s
cognitions, with the desired goal of changing one’s relationship with their
thoughts as opposed to fighting with them. In this way, the process encourages
more acceptance.

Treatment Adherence Issues

Lack of treatment response can often be explained by
participant non-adherence. Even if adherence does not appear to be an issue
when referencing the sleep diary, the clinician should question each aspect of
the regimen. If an aspect of non-adherence is identified, the clinician may ask
questions to determine reasons for non-adherence, review the basis for the
behavioral prescription, and generate solutions with the participant to promote
better adherence. The most common adherence problems include: not completing
sleep diaries, not adhering to the prescribed bedtime and wake time, not
getting out of bed during the night when unable to sleep, not staying out of
bed long enough during the night for sufficient sleepiness to build, and
napping. During this assessment, the clinician should avoid patronizing or
scolding the participant for non-adherence, as this may worsen the problem. The
participant should feel like a collaborator in this process. General approaches
to the most common issues with adherence are outlined in Table 2.

Table 2

Strategies for managing adherence issues

Note. Adopted from Perlis et al. [28] – Cognitive
behavioral treatment of insomnia: A session-by-session guide.

Efficacy of CBT-I

While a complete review of CBT-I’s overall efficacy is
beyond the scope of the present paper, the evidence is clear: CBT-I works.
According to meta-analytic estimates, the average treatment effect sizes range
from 1.0-1.2, which corresponds to approximately a 50% post-treatment reduction
in individual insomnia symptoms [21; 35; 38]. These treatment effect sizes are
even greater when overall insomnia severity (e.g., as assessed by the ISI) is
assessed [38]. Just as importantly, the effects of CBT-I are stable over time
(i.e., clinical gains can be maintained for up to 24 months post-treatment [23;
25]). Finally, one study showed that CBT-I could even be effective in treating
insomnia among “real world” patients (i.e., those with comorbid medical and
behavioral disorders) [27]. Please also refer to the Appendix for a more
complete list of recommended readings related to the evidence for and efficacy
of CBT-I.

Conclusion and Further Training

There is an overwhelming preponderance of evidence that
CBT-I is an efficacious treatment for chronic insomnia [15; 38]. Specifically,
the literature supports that it is as effective in treating insomnia symptoms
as sedative-hypnotics during acute treatment (4–8 weeks [12; 15; 29]) and is
more effective than sedative-hypnotics in the long term (e.g., 3+ months
following treatment) [19; 20]. For these and other reasons, the American
College of Physicians has recently recommended that CBT-I be considered the
first line treatment for chronic insomnia [34]. The issue that emerges from
this is how to make CBT-I available. Some recommendations include: (1) having
clinicians assess for insomnia; (2) educating clinicians that the first-line
therapy for chronic insomnia is CBT-I; (3) routinely referring patients to
insomnia treatment and allowing clinicians to decide whether to make CBT-I
available in their practice or to refer patients to an outside CBT-I provider.
In the case of the former, one could either hire a CBT-I specialist or learn to
deliver CBT-I within their own practice. One way to accomplish this would be to
buy a treatment manual and read it. While that’s an excellent place to begin
(and it will make the clinician a more informed consumer of CBT-I), practicing
or using this intervention in one’s practice will be more successful if
clinicians engage in a more rigorous training regimen; one that includes CE
courses, observation, and supervision/peer consultation. Resources for such
educational activities can be found via any of the major CBT-I training
programs (i.e., University of Pennsylvania [Perlis/Posner], Oxford University
[Espie/Simon], Ryerson University [Carney], University of Arizona
[Grandner/Taylor], or the VA [Manber]). Such educational opportunities may help
enrich even the most experienced clinician’s foundational knowledge of the
principles and practice of CBT-I. At the end of the day, the prescriptive
components of CBT-I are straightforward, but garnering patient adherence is a
high art form. If the clinician elects to refer for CBT-I, this can be done in
at least one of three ways: (1) prescribe CBT-I as a digital therapeutic (e.g.,
Somryst, Pear therapeutics); (2) recommend the patient use an online
(unattended) internet-based CBT-I (e.g., Sleepio; SHUTi); and (3) refer to
behavioral sleep medicine specialists via the use of provider directories
(https://www.behavioralsleep.org/index.php/united-states-sbsm-members
or https://www.med.upenn.edu/cbti/provder_directory.html).

APPENDIX

List of CBT-I treatment manuals and other recommended
articles that review the theory and evidence for CBT-I

1. Baum A., Garofalo J.P., Yali A.M. Socioeconomic status and chronic stress.
   Does stress account for SES effects on health? Annals of the New York
   Academy of Sciences, 1999, vol. 896, pp. 131–144. DOI:
   10.1111/j.1749-6632.1999.tb08111.x  
2. Bootzin R.R. Stimulus control treatment for insomnia. Reprinted from the
   Proceedings, 80th Annual Convention, APA, 1972. URL:
   https://www.med.upenn.edu/
   cbti/assets/user-content/documents/Bootzin%201972.pdf (Accessed:
   22.05.2022). 
3. Carney C.E., Buysse D.J., Ancoli-Israel S. et al. The consensus sleep
   diary: standardizing prospective sleep self-monitoring. Sleep, 2012,
   vol. 35 (2), pp. 287–302. DOI: 10.5665/ SLEEP.1642 
4. Chen X., Wang R., Zee P. et al. Racial/ethnic differences in sleep
   disturbances: The Multi-Ethnic Study of Atherosclerosis (MESA).
   Sleep, 2015, vol. 38 (6), pp. 877–888. DOI:
   10.5665/SLEEP.4732 
5. Cheng P., Casement M.D., Cuellar R. Sleepless in COVID-19: Racial
   disparities during the pandemic as a consequence of structural inequity.
   Sleep, 2022, vol. 45 (1), zsab242.   DOI:
   10.1093/sleep/zsab242 
6. Edinger J., Carney C. Overcoming insomnia: A cognitive-behavioral therapy
   approach, therapist guide, 2014. URL:

   https://books.google.com/books?hl=en&lr=&id=DPJwBAAAQBAJ&oi=fnd&pg=PP1&dq=Edinger,+J.+D.,+%26+Carney,+C.+E.+(2014).+Overcoming+insomnia:+A+cognitive-behavioral+therapy+approach,+therapist+guide.+Oxford+University
   +Press.&ots=IeTgEZG5hZ&sig=Wv-IZH6iKxHEG4SEr7TDhEquBhU (Accessed:
   22.05.2022) 

7. Engle‐Friedman M., Bootzin R.R., Hazlewood L. et al. An evaluation of
   behavioral treatments for insomnia in the older adult. Journal of Clinical
   Psychology, 1992, vol. 48, pp. 77–90. DOI:
   10.1002/1097-4679(199201)48:1<77::aid-jclp2270480112>3.0.co;2-j
8. Espie C.A. Understanding insomnia through cognitive modeling. Sleep
   Medicine, 2007, vol. 8 (4), pp. 53–58.  DOI:
   10.1016/S1389-9457(08)70002-9
9. Grandner M.A., Ruiter Petrov M.E., Rattanaumpawan P. et al. Sleep symptoms,
   race/ethnicity, and socioeconomic position. Journal of Clinical Sleep
   Medicine, 2013, vol. 9 (9), pp. 897–905. DOI:
   10.5664/jcsm.2990 
10. Grandner M.A., Williams N.J., Knutson K.L. et al. Sleep disparity,
    race/ethnicity, and socioeconomic position. Sleep Medicine, 2016, vol.
    18, pp. 7–18. DOI: 10.1016/ j.sleep.2015.01.020
11. Guilleminault C., Clerk A., Black J. et al. Nondrug treatment trials in
    psychophysiologic insomnia. Archives of Internal Medicine, 1995, vol.
    155 (8), pp. 838–844. DOI: 10.1001/ARCHINTE.1995.00430080076010
12. Irwin M.R., Cole J.C., Nicassio P.M. Comparative meta-analysis of
    behavioral interventions for insomnia and their efficacy in middle-aged adults
    and in older adults 55+ years of age. Health Psychology: Official Journal of
    the Division of Health Psychology, American Psychological Association,
    2006, vol. 25 (1), pp. 3–14. DOI: 10.1037/0278-6133.25.1.3 
13. Jean-Louis G., Magai C., Consedine N.S. et al. Insomnia symptoms and
    repressive coping in a sample of older Black and White women. BMC Women’s
    Health, 2007, vol. 7, article no. 1. DOI: 10.1186/1472-6874-7-1
14. Jean-Louis G., Magai C.M., Cohe C.I. et al. Ethnic differences in
    self-reported sleep problems in older adults. Sleep, 2001, vol. 24 (8),
    pp. 926–933. DOI: 10.1093/sleep/ 24.8.926 
15. Koffel E.A., Koffel J.B., Gehrman P.R. A meta-analysis of group cognitive
    behavioral therapy for insomnia. Sleep Medicine Reviews, 2015,
    vol. 19, pp. 6–16. DOI: 10.1016/ J.SMRV.2014.05.001
16. Lauderdale D.S., Knutson K.L., Yan L.L. et al. Objectively measured sleep
    characteristics among early-middle-aged adults: The CARDIA study. American
    Journal of Epidemiology, 2006, vol. 164 (1), pp. 5–16. DOI:
    10.1093/aje/kwj199
17. Manber R., Carney C. Treatment plans and interventions for insomnia: a case
    formulation approach, 2015. URL:
    https://books.google.com/books?hl=en&lr=&id=
    Rv7OBgAAQBAJ&oi=fnd&pg=PP1&dq=Manber,+R.+%26+Carney,+C.+E.+(2015).+Treatment+plans+and+interventions+for+insomnia:+a+case+formulation+approach.&ots=SCAse7Zs6w&sig=1AVELZaed11W7PE5Avn2lgv9uyw
    (Accessed: 22.05.2022)
18. Meltzer L.J., Mindell J.A. Systematic review and meta-analysis of
    behavioral interventions for pediatric insomnia.  Journal of Pediatric
    Psychology, 2014, vol. 39 (8), pp. 932–948. DOI: 10.1093/jpepsy/jsu041
19. Miller C.B., Espie C.A., Epstein D.R. et al. The evidence base of sleep
    restriction therapy for treating insomnia disorder.  Sleep Medicine
    Reviews, 2014, vol. 18 (5), pp. 415–424. DOI:
    10.1016/J.SMRV.2014.01.006
20. Montgomery P., Dennis J.A. Cognitive behavioural interventions for sleep
    problems in adults aged 60+. Cochrane Database of Systematic Reviews,
    2003. DOI: 10.1002/ 14651858.cd003161
21. Morin C.M., Culbert J.P., Schwartz S.M. Nonpharmacological interventions
    for insomnia: a meta-analysis of treatment efficacy. The American Journal of
    Psychiatry, 1994, vol. 151 (8), pp. 1172–1180. DOI:
    10.1176/AJP.151.8.1172 
22. Morin C.M., Espie C.A. Insomnia: A clinical guide to assessment and
    treatment, 2007. URL:
    https://books.google.com/books?hl=en&lr=&id=nmfjBwAAQBAJ&oi
    =fnd&pg=PA1&dq=Morin,+C.+M.+%26+Espie,+C.+A.+(2003).+Insomnia:+A+clinical+guide+to+assessment+and+treatment.&ots=Fx2LSB1mTM&sig=8-Hrm9ceUbf6viu-F-bg2oHtX5c
    (Accessed: 22.05.2022)
23. Morin C.M., Hauri P.J., Espie C.A. et al. Nonpharmacologic treatment of
    chronic insomnia. Sleep, 1999, vol. 22 (8). pp. 1134–1156. DOI:
    10.1093/SLEEP/22.8.1134 
24. Morin C.M. Insomnia: Psychological Assessment and Management. New York, NY:
    Guilford, 1993.
25. Morin C.M., Vallières A., Guay B. et al. Cognitive behavioral therapy,
    singly and combined with medication, for persistent insomnia: a randomized
    controlled trial. JAMA, 2009, vol. 301 (19), pp. 2005–2015. DOI:
    10.1001/JAMA.2009.682 
26. Ong J.C., Shapiro S.L., Manber R. Combining mindfulness meditation with
    cognitive-behavior therapy for insomnia: a treatment-development study.
    Behavior Therapy, 2008, vol. 39 (2), pp. 171–182. DOI:
    10.1016/J.BETH.2007.07.002
27. Perlis M., Aloia M., Millikan A. et al. Behavioral Treatment of Insomnia: A
    Clinical Case Series Study. Journal of Behavioral Medicine, 2000,
    vol. 23 (2), pp. 149–161. DOI:
    10.1023/a:1005413117932
28. Perlis M.L., Benson-Jungquist C., Smith M.T. et al. Cognitive behavioral
    treatment of insomnia: A session-by-session guide, 2005. 182 p. DOI:
    10.1007/0-387-29180-6
29. Perlis M.L., Morin C.M., Ivers H. et al. Does TST Appreciably Change During
    or After CBT-I? Sleep, 2019, vol. 42 (1). P. A154–A155. 
    DOI:
    10.1093/SLEEP/ZSZ067.379
30. Perlis M., Shaw P.J., Cano G. et al. Models of Insomnia. In M.H. Kryger, T.
    Roth, W.C. Dement (eds.), Principles and Practice of Sleep
    Medicine, St. Louis, MO: Elsevier, 2011, pp. 850–865. DOI:
    10.1016/B978-1-4160-6645-3.00078-5
31. Perlis M.L., Smith L.J., Lyness J.M. et al. Insomnia as a risk factor for
    onset of depression in the elderly. Behavioral Sleep Medicine,
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32. Pigeon W.R., Heffner K., Duberstein P. et al. Elevated sleep disturbance
    among blacks in an urban family medicine practice. Journal of the American
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33. Proctor B.D., Semega J.L., Kollar M.A. Income and poverty in the United
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34. Qaseem A., Kansagara D., Forciea M.A. et al. Management of Chronic Insomnia
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    Physicians. Annals of Internal Medicine, 2016, vol. 165 (2), pp.
    125–133. DOI: 10.7326/M15-2175
35. Smith M.T., Perlis M.L., Park A. et al. Comparative meta-analysis of
    pharmacotherapy and behavior therapy for persistent insomnia. American
    Journal of Psychiatry, 2002, vol. 159 (1), pp. 5–11. DOI:
    10.1176/appi.ajp.159.1.5
36. Spielman A.J. Assessment of insomnia. Clinical Psychology Review,
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37. Spielman A. J., Saskin P., Thorpy M.J. Treatment of Chronic Insomnia by
    Restriction of Time in Bed. Sleep, 1987, vol. 10 (1), pp. 45–56. DOI:
    10.1093/SLEEP/10.1.45 
38. van Straten A., van der Zweerde T., Kleiboer A. et al. Cognitive and
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Уокер Джейми, магистр психологии, аспирант департамента психологических наук, Университет Арканзаса, Фейетвилл, США, ORCID: https://orcid.org/0000-0003-2256-3931, e-mail: jlw110@uark.edu

Мюнч Александрия, доктор психологических наук, Пенсильванский университет, Филадельфия, США, ORCID: https://orcid.org/0000-0003-4826-8498, e-mail: amuench@pennmedicine.upenn.edu

Перлис Майкл Л., PhD, профессор, клинический исследователь департамента психиатрии, Пенсильванский университет, Филадельфия, США, ORCID: https://orcid.org/0000-0002-6806-759X, e-mail: mperlis@upenn.edu

Варгас Айван, PhD, профессор департамента психологических наук, Университет Арканзаса, Фейетвилл, США, ORCID: https://orcid.org/0000-0002-0787-5630, e-mail: ivvargas@uark.edu