Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_41_библиотеки_им_акад_М_И_Перельмана
.pdf
286
https://t.me/medicina_free
G. C. Carlson et al.
The choice of pharmacotherapy agent should be made using a shared decisionmaking approach. Factors to consider include type of insomnia (sleep onset, maintenance, or early awakening), consideration of the patients’ age, comorbidities
inclusive of renal and hepatic dysfunction, additional medications including polypharmacy, response to prior therapy, cost and availability of medications, prior history of dependence on controlled substances, and patient and clinician preferences.
Medication alone rarely results in a full remission of insomnia disorder, and over
time increased dosage is needed to obtain the same efcacy. In addition, unlike
CBT-I, where the effects of treatment are long lasting, discontinuation of pharmacotherapy for insomnia results in return of the insomnia symptoms.
Several randomized controlled studies comparing pharmacotherapy vs. CBT-I
have been performed with consistent ndings that behavioral therapies are superior
in treating insomnia when compared to medication and that the effects achieved
with behavioral therapy are long lasting. Morin etal. compared CBT-I with temazepam for an 8-week treatment period and then a 2-year follow-up [88]. In this study,
CBT-I was superior to temazepam in improving sleep time after sleep onset immediately post-treatment, and at 24months follow-up, CBT-I gains in sleep time were
sustained while the temazepam group was similar to the placebo group. Similar
results were noted by Jacobs etal. using CBT-I compared to zolpidem when using
sleep latency as a primary outcome [89]. CBT-I resulted in more sustained benets
than medications in both studies.
Non-Benzodiazepine receptor agonists (non-BZRAs) Non-BZRAs are commonly used to treat insomnia and include eszopiclone, zaleplon, and zolpidem.
Middle of the night formulations (dissolving tablets or spray) of zolpidem are available. The mechanism of action is enhancement of the neurotransmitter gammaaminobutyric acid (GABA) function at the GABA-A receptor within the central
nervous system (CNS). These medications are FDA approved for sleep onset and
sleep maintenance insomnia and, due to their shorter half-life (1–6hours), are considered to have a better safety prole and less daytime impairment when compared
with benzodiazepines. They are all Schedule IV controlled substances although
appear to have less potential for abuse when compared with traditional benzodiazepines. All the non-BZRAs are metabolized by CYP enzymes resulting in potential
drug interactions and in reduced recommended dosages in older patients. For middle of the night awakenings, zolpidem spray and sublingual dissolving tablets offer
a faster onset of action. Zaleplon can also be considered due to its very short halflife (1hour). For middle of night awakening, these medications can be used if there
is remaining 4hours of sleep after the awakening. Zolpidem extended release has
the longest half-life and can be considered in patients where the other non-BZRAs
wane in efcacy over the course of the night. In addition to the usual central nervous
system impairment noted with all insomnia medication, the non-BZRAs carry an
FDA box warning for sleep behaviors such as sleepwalking, sleep driving, sexsomnia, and sleep eating among others. They should not be prescribed in patient with
preexisting parasomnias. According to a meta-analytic review, these medications
13 Management ofInsomnia Disorder
https://t.me/medicina_free
287
decrease sleep latency by 10–20minutes and increase sleep time by 10–30minutes [90].
Benzodiazepine receptor agonists (BZRAs) BZRAs with FDA approval for
insomnia include estazolam, urazepam, quazepam, temazepam, and triazolam. All
are Schedule IV controlled substances and tend to be avoided for treatment of
insomnia due to their longer half-life when compared with non-BZRAs, increased
potential for dependence, and increased risk for side effects with abrupt discontinuation. Benzodiazepines also function by enhancing GABA at the GABA receptor
within the CNS but have less afnity for the GABA-A receptor, and thus tend to
cause more sedation than their non-BZRA counterparts. They are metabolized by
CYP-34A, and like the non-BZRA medications, adjustments must be made for age
and polypharmacy. Due to the long half-life of these sedatives, the FDA has placed
a box warning to avoid with use of narcotics due to the concern for respiratory suppression. Studies on the efcacy of BZRAs use both self-reported and polysomnography data, and the results vary. On average this class of medication reduces sleep
latency by 10–20minutes and increases nighttime sleep by 30–60minutes [90].
Melatonin receptor agonists Ramelteon is a MT1 and MT2 melatonin receptor
agonist which is FDA approved for the treatment of sleep onset insomnia. Ramelteon
is cleared by CYP1A2 and CYP2C9 and should be avoided in individuals with
severe liver disease and those on medications inhibiting these enzymes (i.e., uvoxamine). Effect size of ramelteon is small, but a meta-analysis showed a reduction in
sleep latency of approximately 5 minutes and increase in overall sleep time of
7minutes [91].
Orexin receptor antagonists Lemborexant and suvorexant are dual orexin receptor antagonists (DORAs) which function at the OX1R and OX2R receptors. Both
are FDA approved for sleep onset and sleep maintenance insomnia. The orexin/
hypocretin system initiates at the hypothalamus and communicates with multiple
wake-promoting regions of the brain responsible for secreting acetylcholine, dopamine, histamine, norepinephrine, and serotonin. As with other insomnia medications, DORAs cause somnolence. This class should specically be avoided in
individuals with narcolepsy and individuals on medications which inhibit CYP3A
and those with hepatic impairment. Both medications improve sleep onset latency
and increase sleep time [92].
Antidepressants
Trazadone is one of the most commonly prescribed antidepres-
sants for insomnia, and it improves some sleep parameters over the short-term [93].
Its mechanism of action is via antagonism of 5-HT2A, 5-HT2B, alpha-1A, and 2C
receptors, agonism of 5-HT1, and inhibition of serotonin reuptake. The AASM
clinical practice guidelines recommend against use of trazadone for insomnia as
there is minimal data regarding its efcacy and a very small size effect which was
288
https://t.me/medicina_free
not sustained over time noted in the one randomized trial available for inclusion in
the guidelines [87]. There are many potential side effects of trazadone including QT
prolongation, orthostatic hypotension, priapism, increased suicidal ideation, mania
and hypomania, closed-angle glaucoma, and serotonin syndrome, among others.
Due to the potential side effects at higher doses, it is not recommended to increase
doses over 150mg nightly for the treatment of insomnia. Trazadone also has a long
half-life (10–12 hours) leading to the risk of increased daytime sleepiness in
patients [94].
Low-dose doxepin (3 or 6mg tablets) is FDA approved for the treatment of sleep
maintenance insomnia. Doxepin is a tricyclic antidepressant with primarily antihistamine antagonist (H1 receptor) features at a low dose. As with all other tricyclic
antidepressants, MAOI inhibitors need to be avoided, and it should not be used in
patients with urinary retention or those with untreated closed-angle glaucoma. Due
to the cost of the low-dose tablets, providers may sometimes prescribe the liquid
formulation or the 10 mg tablets, which are signicantly lower priced in the
USA.On average doxepin increases sleep time by 25–40minutes.
Antipsychotics Quetiapine is a commonly prescribed anti-psychotic medication
for insomnia although there is minimal data on its effect on sleep in patients without
psychiatric disease, and it poses signicant side effect risks [87]. Its mechanism of
action is not wholly understood but is known to be a D2 and 5-HT2 antagonist, and
it is metabolized by CYP3A4. It has a high side effect prole including orthostatic
hypotension, dizziness, suicidality in younger patients, and extrapyramidal symptoms, among others. Due to its high side effect prole and the paucity of data on
sleep, it is not recommended for the treatment of insomnia, especially in individuals
without mood disorders or schizophrenia [95].
G. C. Carlson et al.
Nutritional Supplements
Several dietary supplements are marketed for insomnia. Dietary supplements are
not FDA regulated, resulting in variability of concentration and purity of active
ingredients [96]. Although there is scant evidence for the efcacy of supplements
for the treatment of insomnia, overall, the risk for adverse effects is low. Hepatic
failure, however, has been reported with valerian root and kava root.
Melatonin Melatonin is a commonly used dietary supplement for the treatment of
insomnia. It is a melatonin receptor agonist acting at the suprachiasmatic nucleus,
among other areas. As with endogenous melatonin, exogenous melatonin assists
with sleep onset by reducing arousal caused by the suprachiasmatic nucleus. It is
typically dosed between 1 and 5mg for insomnia. Studies of efcacy of melatonin
for the treatment of insomnia show a minimal effect on sleep onset and total sleep
time, which may not be clinically meaningful [97]. Potential side effects include
13 Management ofInsomnia Disorder
https://t.me/medicina_free
headache, nightmares, dizziness, and daytime sleepiness. Exogenous melatonin is
not recommended for use by AASM clinical practice guidelines due to the lack of
efcacy data [87].
289
Medication Treatments forInsomnia: Safety Considerations
All medications for treatment of insomnia can result in depression of the central
nervous system and motor impairment leading to increased risk of falls, motor vehicle accidents, and occupational accidents. This is confounded in individuals with
polypharmacy inclusive of other sedating medications, individuals with cognitive
impairment, individuals with obstructive sleep apnea, and in those who drink alcohol. The benzodiazepines can also suppress respiratory drive. This is enhanced by
addition of opiates and other sedating medications leading to a potential deadly
combination.
Special consideration in the pharmacologic treatment of insomnia needs to occur
in individuals where side effects are particularly problematic or may increase risk
for adverse outcomes. This includes:
• Advanced age
• Cognitive impairment
• Fall risk
• Obstructive sleep apnea or hypoventilation
• Hepatic and renal impairment
• Concomitant medications which induce or inhibit CYP P450 3
• Polypharmacy inclusive of opiates or other sedating medications
• History of dependence on controlled or illicit substances
• History of signicant depression, especially in those with active or historical
suicidal ideation or attempts
• Abnormal sleep behaviors
There is also extensive epidemiological data indicating increased mortality with
hypnotic use. Kripke etal. [98] reviewed 10,529 patients who received hypnotic
prescriptions in the USA (mean age 54) and 23,676 matched controls between 2002
and 2007. After controlling for other co-factors associated with increased mortality
the group prescribed hypnotics had a mortality hazard ratio (HR) from 3.6 to 5.32
compared to controls, with increasing HR in individuals with higher number of
prescriptions for hypnotics. Similar ndings were reported in a later study by Linnet
et al. in multi-morbid and non-multi-morbid patients with increasing mortality
noted in individuals with high numbers of hypnotic prescriptions [99]. Although the
specic cause of death is not delineated in these cohort studies, there is ample evidence to suggest increased mortality with increasing number of prescriptions for
hypnotics.
290
https://t.me/medicina_free
G. C. Carlson et al.
Summary of Key Points
Insomnia is highly prevalent with the population [100]. CBT-I is the rst line
treatment for insomnia disorder, and a large body of research shows that
CBT-I is highly effective for the treatment of insomnia in patients with mul-
tiple medical and psychiatric comorbidities [8, 32]. The strongest research is
for the delivery of CBT-I in an individual treatment format, but there is also
research demonstrating the helpfulness of group-based CBT-I, self-guided
CBT-I, and apps as a supplement to traditional CBT-I treatment [45, 47].
There is also research support for BBT-I and mindfulness-based intervention
for insomnia [51, 62]. The risks associated with behavioral treatments for
insomnia are minimal, though there are circumstances in which some inter-
vention components (e.g., sleep restriction) may be contraindicated [72, 73].
It is important to thoroughly assess daytime activities, comorbid sleep disor-
ders, medical conditions, and mental health conditions, as well as potential
safety concerns prior to initiating behavioral treatments with patients endors-
ing insomnia symptoms. CBT-I has been shown to be superior for the treat-
ment of insomnia when compared with pharmacologic treatment in terms of
immediate effect on sleep and longevity of treatment. Ideally, pharmacother-
apy should not be used without a behavioral component to address factors that
contribute to insomnia maintenance over time; however, pharmacotherapy
can be used in specic situations with emphasis on a time-limited treatment
plan and monitoring of side effects.
Patient preferences are important considerations when providers collaborate with patients to develop a treatment plan. The shared decision-making
model of clinical practice involves presenting evidence-based treatment
options to the patient [101]. In the case of insomnia, this would involve educating patient about the strong recommendation for the use of CBT-I to treat
insomnia disorder and conditional recommendations for behavioral components of CBT-I to treat insomnia disorder. Providers should also describe the
risks associated with CBT-I relative to medication treatments for insomnia
and the impact of CBT-I and/or medications on any comorbid conditions (e.g.,
sleep apnea) and their corresponding treatments (e.g., CPAP). This information will allow patients to make informed choices about their treatment. While
each patient is unique, research suggests that patients prefer non-medication
treatment for insomnia over medication treatment [102]. Additionally, when
patients with comorbid insomnia, depression, and PTSD are presented with
evidence-based treatments for each condition, a study found that patients
report preference for CBT-I [103]. Figure13.1 includes a decision-making
framework for providers to follow after they have educated patients about
evidence-based treatments for insomnia. Through a collaborative and transparent process, providers can connect patients with insomnia symptoms to the
most effective interventions available.
Management ofInsomnia Disorder
https://t.me/medicina_free
13
291
References
1. Buysse DJ, Angst J, Gamma A, Ajdacic V, Eich D, Rössler W.Prevalence, course, and comorbidity of insomnia and depression in young adults. Sleep. 2008;31(4):473–80.
2. Schutte-Rodin S, Broch L, Buysse D, Dorsey C, Sateia M.Clinical guideline for the evaluation and management of chronic insomnia in adults. J Clin Sleep Med. 2008;4(5):487–504.
3. Taylor DJ, Mallory LJ, Lichstein KL, Durrence HH, Riedel BW, Bush AJ.Comorbidity of
chronic insomnia with medical problems. Sleep. 2007;30(2):213–8.
4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders
(DSM-5®). Arlington: American Psychiatric Pub; 2013.
5. American Academy of Sleep Medicine. International classication of sleep disorders,
Diagnostic and coding manual. Darien: American Academy of Sleep Medicine; 2005.
p.51–5.
6. Medic G, Wille M, Hemels ME.Short-and long-term health consequences of sleep disruption. Nat Sci Sleep. 2017;9:151.
7. Qaseem A, Kansagara D, Forciea MA, Cooke M, Denberg TD.Management of chronic
insomnia disorder in adults: a clinical practice guideline from the American College of
Physicians. Ann Intern Med. 2016;165(2):125–33.
8. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for
chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255–62.
9. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for
chronic insomnia disorder in adults: an American Academy of Sleep Medicine systematic
review, meta-analysis and GRADE assessment. J Clin Sleep Med. 2020;0(0):jcsm.8988.
10. Spielman AJ, Caruso LS, Glovinsky PB.A behavioral perspective on insomnia treatment.
Psychiatr Clin. 1987;10(4):541–53.
11. Carlson GC, Kelly MR, Grinberg AM, Mitchell MN, McGowan S, Culver NC, Kay M, Alessi
CA, Washington DL, Yano EM, Martin JL.Insomnia precipitating events among Women
Veterans: the impact of traumatic and nontraumatic events on sleep and mental health symptoms. Behav Sleep Med. 2020;19(5):672–88.
12. Singareddy R, Vgontzas AN, Fernandez-Mendoza J, etal. Risk factors for incident chronic
insomnia: a general population prospective study. Sleep Med. 2012;13(4):346–53.
13. Levenson JC, Benca RM, Rumble ME.Sleep related cognitions in individuals with symptoms of insomnia and depression. J Clin Sleep Med. 2015;11(8):847–54.
14. Morgenthaler T, Kramer M, Alessi C, etal. Amer ican academy of sleep medicine. Practice
parameters for the psychological and behavioral treatment of insomnia: an update. An american academy of sleep medicine report. Sleep. 2006;29(11):1415.
15. Miller CB, Espie CA, Epstein DR, etal. The evidence base of sleep restriction therapy for
treating insomnia disorder. Sleep Med Rev. 2014;18(5):415–24.
16. Embry DD, Biglan A.Evidence-based kernels: fundamental units of behavioral inuence.
Clin Child Fam Psychol Rev. 2008;11(3):75–113.
17. Bootzin RR, Epstein D, Wood JM.Stimulus control instructions. In: Case studies in insomnia. Boston: Springer; 1991. p.19–28.
18. Bootzin RR.Stimulus control treatment for insomnia. Proc Am Psychol Assoc. 1972;7:395–6.
19. Sharma MP, Andrade C.Behavioral interventions for insomnia: theory and practice. Indian J
Psychiatry. 2012;54(4):359.
20. Cohen JS, Edmunds JM, Brodman DM, Benjamin CL, Kendall PC.Using self-monitoring:
implementation of collaborative empiricism in cognitive-behavioral therapy. Cogn Behav
Pract. 2013;20(4):419–28.
21. Spielman AJ, Saskin P, Thorpy MJ.Treatment of chronic insomnia by restriction of time in
bed. Sleep. 1987;10(1):45–56.
22. Manber R.Cognitive behavioral therapy for insomnia guide to overcoming your insomnia.
In: Affairs USDoV, ed. Washington, D.C. 2010.
292
https://t.me/medicina_free
23. Stepanski EJ, Wyatt JK.Use of sleep hygiene in the treatment of insomnia. Sleep Med Rev.
2003;7(3):215–25.
24. Chung K-F, Lee C-T, Yeung W-F, Chan M-S, Chung EW-Y, Lin W-L.Sleep hygiene education as a treatment of insomnia: a systematic review and meta-analysis. Fam Pract.
2018;35(4):365–75.
25. Davison GC.Systematic desensitization as a counterconditioning process. J Abnorm Psychol.
1968;73(2):91.
26. Tsai H, Kuo TB, Lee GS, Yang CC.Efcacy of paced breathing for insomnia: enhances vagal
activity and improves sleep quality. Psychophysiology. 2015;52(3):388–96.
27. Alexandru BV, Róbert B, Viorel L, Vasile B. Treating primary insomnia: a comparative
study of self-help methods and progressive muscle relaxation. J Evid Based Psychother.
2009;9(1):67.
28. Taylor DJ, Pruiksma KE.Cognitive and behavioural therapy for insomnia (CBT-I) in psychiatric populations: a systematic review. Int Rev Psychiatry. 2014;26(2):205–13.
29. Beck AT.Cognitive therapy: past, present, and future. J Consult Clin Psychol. 1993;61(2):194.
30. Carey TA, Mullan RJ. What is Socratic questioning? Psychoth: Theory Res Pract Train.
2004;41(3):217.
31. Beck AT, Haigh EA.Advances in cognitive theory and therapy: the generic cognitive model.
Annu Rev Clin Psychol. 2014;10:1–24.
32. Wu JQ, Appleman ER, Salazar RD, Ong JC. Cognitive behavioral therapy for insomnia
comorbid with psychiatric and medical conditions: a meta-analysis. JAMA Intern Med.
2015;175(9):1461–72.
33. Okajima I, Komada Y, Inoue Y.A meta-analysis on the treatment effectiveness of cognitive
behavioral therapy for primary insomnia. Sleep Biol Rhythms. 2011;9(1):24–34.
34. Gehrman P, Shah MT, Miles A, Kuna S, Godleski L. Feasibility of group cognitivebehavioral treatment of insomnia delivered by clinical video telehealth. Telemed e-Health.
2016;22(12):1041–6.
35. Koffel E, Bramoweth AD, Ulmer CS.Increasing access to and utilization of cognitive behavioral therapy for insomnia (CBT-I): a narrative review. J Gen Intern Med. 2018;33(6):955–62.
36. Koffel EA, Koffel JB, Gehrman PR.A meta-analysis of group cognitive behavioral therapy
for insomnia. Sleep Med Rev. 2015;19:6–16.
37. Espie CA, MacMahon KM, Kelly H-L, etal. Randomized clinical effectiveness trial of nurseadministered small-group cognitive behavior therapy for persistent insomnia in general practice. Sleep. 2007;30(5):574–84.
38. Gehrman P, Gunter P, Findley J, etal. Randomized noninferiority trial of telehealth delivery
of cognitive behavioral treatment of insomnia compared to in-person care. J Clin Psychiatry.
2021;82(5):20m13723.
39. Arnedt JT, Conroy DA, Mooney A, Furgal A, Sen A, Eisenberg D.Telemedicine versus faceto- face delivery of cognitive behavioral therapy for insomnia: a randomized controlled noninferiority trial. Sleep. 2021;44(1):zsaa136.
40. Ulmer C, Bosworth H, Voils C, et al. 0403 Tele-self CBTI: provider supported selfmanagement cognitive behavioral therapy for insomnia. Sleep. 2018;41:A153.
41. Kuhn E, Weiss BJ, Taylor KL, et al. CBT-I coach: a description and clinician perceptions of a mobile app for cognitive behavioral therapy for insomnia. J Clin Sleep Med.
2016;12(4):597–606.
42. Batterham PJ, Christensen H, Mackinnon AJ, et al. Trajectories of change and long-term
outcomes in a randomised controlled trial of internet-based insomnia treatment to prevent
depression. BJPsych Open. 2017;3(5):228–35.
43. Espie CA, Kyle SD, Williams C, etal. A randomized, placebo-controlled trial of online cognitive behavioral therapy for chronic insomnia disorder delivered via an automated mediarich web application. Sleep. 2012;35(6):769–81.
44. Ritterband LM, Thorndike FP, Ingersoll KS, etal. Effect of a web-based cognitive behavior
therapy for insomnia intervention with 1-year follow-up: a randomized clinical trial. JAMA
Psychiat. 2017;74(1):68–75.
G. C. Carlson et al.
13
https://t.me/medicina_free
Management ofInsomnia Disorder
45. Lancee J, van Straten A, Morina N, Kaldo V, Kamphuis JH.Guided online or face-to-face
cognitive behavioral treatment for insomnia: a randomized wait-list controlled trial. Sleep.
2016;39(1):183–91.
46. Miller KE, Kuhn E, Owen JE, etal. Clinician perceptions related to the use of the CBT-I
coach mobile app. Behav Sleep Med. 2019;17(4):481–91.
47. Koffel E, Kuhn E, Petsoulis N, etal. A randomized controlled pilot study of CBT-I Coach:
feasibility, acceptability, and potential impact of a mobile phone application for patients in
cognitive behavioral therapy for insomnia. Health Informatics J. 2018;24(1):3–13.
48. Germain A, Moul DE, Franzen PL, etal. Effects of a brief behavioral treatment for late-life
insomnia: preliminary ndings. J Clin Sleep Med. 2006;2(04):407–8.
49. Buysse DJ, Germain A, Moul DE, etal. Efcacy of brief behavioral treatment for chronic
insomnia in older adults. Arch Intern Med. 2011;171(10):887–95.
50. Troxel WM, Germain A, Buysse DJ.Clinical management of insomnia with brief behavioral
treatment (BBTI). Behav Sleep Med. 2012;10(4):266–79.
51. Bramoweth AD, Lederer LG, Youk AO, Germain A, Chinman MJ.Brief behavioral treatment
for insomnia vs. cognitive behavioral therapy for insomnia: results of a randomized noninferiority clinical trial among veterans. Behav Ther. 2020;51(4):535–47.
52. Lichstein K, Durrence H, Taylor D, Bush A, Riedel B.Quantitative criteria for insomnia.
Behav Res Ther. 2003;41(4):427–45.
53. Morin CM, Jarrin DC, Ivers H, Mérette C, LeBlanc M, Savard J.Incidence, persistence, and
remission rates of insomnia over 5 years. JAMA Netw Open. 2020;3(11):–e2018782.
54. van der Zweerde T, Bisdounis L, Kyle SD, Lancee J, van Straten A.Cognitive behavioral
therapy for insomnia: a meta-analysis of long-term effects in controlled studies. Sleep Med
Rev. 2019;48:101208.
55. Espie CA, Inglis SJ, Tessier S, Harvey L.The clinical effectiveness of cognitive behaviour
therapy for chronic insomnia: implementation and evaluation of a sleep clinic in general
medical practice. Behav Res Ther. 2001;39(1):45–60.
56. Morgan K, Thompson J, Dixon S, Tomeny M, Mathers N.Predicting longer-term outcomes
following psychological treatment for hypnotic-dependent chronic insomnia. J Psychosom
Res. 2003;54(1):21–9.
57. Matthews EE, Arnedt JT, McCarthy MS, Cuddihy LJ, Aloia MS. Adherence to cognitive
behavioral therapy for insomnia: a systematic review. Sleep Med Rev. 2013;17(6):453–64.
58. Kabat-Zinn J. Wherever you go, there you are: mindfulness meditation in everyday life.
Hachette Books; 2009.
59. Keng S-L, Smoski MJ, Robins CJ.Effects of mindfulness on psychological health: a review
of empirical studies. Clin Psychol Rev. 2011;31(6):1041–56.
60. Ong JC, Ulmer CS, Manber R.Improving sleep with mindfulness and acceptance: a metacognitive model of insomnia. Behav Res Ther. 2012;50(11):651–60.
61. Ong JC, Shapiro SL, Manber R.Combining mindfulness meditation with cognitive-behavior
therapy for insomnia: a treatment-development study. Behav Ther. 2008;39(2):171–82.
62. Ong JC, Manber R, Segal Z, Xia Y, Shapiro S, Wyatt JK. A randomized controlled trial of
mindfulness meditation for chronic insomnia. Sleep. 2014;37(9):1553–63.
63. Hayes SC, Strosahl KD, Bunting K, Twohig M, Wilson KG.What is acceptance and commitment therapy? In: A practical guide to acceptance and commitment therapy. NewYork:
Springer; 2004. p.3–29.
64. Hayes SC, Luoma JB, Bond FW, Masuda A, Lillis J.Acceptance and commitment therapy:
model, processes and outcomes. Behav Res Ther. 2006;44(1):1–25.
65. Jiménez FJR. Acceptance and commitment therapy versus traditional cognitive behavioral
therapy: a systematic review and meta-analysis of current empirical evidence. Int J Psychol
Psychol Ther. 2012;12(3):333–58.
66. David D, Cristea I, Hofmann SG.Why cognitive behavioral therapy is the current gold standard of psychotherapy. Front Psych. 2018;9:4.
293
294
https://t.me/medicina_free
67. Ruiz FJ.A review of Acceptance and Commitment Therapy (ACT) empirical evidence: correlational, experimental psychopathology, component and outcome studies. Int J Psychol
Psychol Ther. 2010;10(1):125–62.
68. A-tjak JG, Davis ML, Morina N, Powers MB, Smits JA, Emmelkamp PM.A meta-analysis of
the efcacy of acceptance and commitment therapy for clinically relevant mental and physical health problems. Psychother Psychosom. 2015;84(1):30–6.
69. Salari N, Khazaie H, Hosseinian-Far A, etal. The effect of acceptance and commitment
therapy on insomnia and sleep quality: a systematic review. BMC Neurol. 2020;20(1):1–18.
70. Fiorentino L, Martin JL, Alessi CA.The ABCs of insomnia (ABC-I): an acceptance commitment therapy (ACT)-based insomnia treatment development study: pilot results and future
directions. In: Sleep medicine and mental health. Cham: Springer; 2020. p.85–100.
71. Dalrymple KL, Fiorentino L, Politi MC, Posner D.Incorporating principles from acceptance
and commitment therapy into cognitive-behavioral therapy for insomnia: a case example. J
Contemp Psychother. 2010;40(4):209–17.
72. Barbini B, Bertelli S, Colombo C, Smeraldi E. Sleep loss, a possible factor in augmenting
manic episode. Psychiatry Res. 1996;65(2):121–5.
73. Harvey AG.Sleep and circadian rhythms in bipolar disorder: seeking synchrony, harmony,
and regulation. Am J Psychiatr. 2008;165(7):820–9.
74. Sweetman A, Lack L, Lambert S, Gradisar M, Harris J.Does comorbid obstructive sleep
apnea impair the effectiveness of cognitive and behavioral therapy for insomnia? Sleep Med.
2017;39:38–46.
75. Einollahi B, Izadianmehr N.Restless leg syndrome: a neglected diagnosis. Nephro-urology
Monthly. 2014;6(5):e22009.
76. Sweetman A, Lack L, Catcheside PG, etal. Cognitive and behavioral therapy for insomnia
increases the use of continuous positive airway pressure therapy in obstructive sleep apnea
participants with comorbid insomnia: a randomized clinical trial. Sleep. 2019;42(12):zsz178.
77. Woznica AA, Carney CE, Kuo JR, Moss TG. The insomnia and suicide link: toward an
enhanced understanding of this relationship. Sleep Med Rev. 2015;22:37–46.
78. Pigeon WR, Pinquart M, Conner K.Meta-analysis of sleep disturbance and suicidal thoughts
and behaviors. J Clin Psychiatry. 2012;73(9):0.
79. Bishop TM, Walsh PG, Ashraoun L, Lavigne JE, Pigeon WR.Sleep, suicide behaviors, and
the protective role of sleep medicine. Sleep Med. 2020;66:264–70.
80. Trockel M, Karlin BE, Taylor CB, Brown GK, Manber R. Effects of cognitive behavioral
therapy for insomnia on suicidal ideation in veterans. Sleep. 2015;38(2):259–65.
81. Khurshid KA.Comorbid insomnia and psychiatric disorders: an update. Innov Clin Neurosci.
2018;15(3–4):28.
82. McCurry SM, Song Y, Martin JL.Sleep in caregivers: what we know and what we need to
learn. Curr Opin Psychiatry. 2015;28(6):497–503.
83. Husak AJ, Bair MJ.Chronic pain and sleep disturbances: a pragmatic review of their relationships, comorbidities, and treatments. Pain Med. 2020;21(6):1142–52.
84. Guthrie KA, Larson JC, Ensrud KE, etal. Effects of pharmacologic and nonpharmacologic
interventions on insomnia symptoms and self-reported sleep quality in women with hot
ashes: a pooled analysis of individual participant data from four MsFLASH trials. Sleep.
2018;41(1):zsx190.
85. Miller KE, Brownlow JA, Gehrman PR.Sleep in PTSD: treatment approaches and outcomes.
Curr Opin Psychol. 2020;34:12–7.
86. Mysliwiec V, Martin JL, Ulmer CS, et al. The management of chronic insomnia disorder and obstructive sleep apnea: synopsis of the 2019 U.S. Department of Veterans
Affairs and U.S. Department of Defense Clinical Practice Guidelines. Ann Intern Med.
2020;172(5):325–36.
87. Sateia MJ, Buysse DJ, Krystal AD, Neubauer DN, Heald JL.Clinical practice guideline for
the pharmacologic treatment of chronic insomnia in adults: an American Academy of Sleep
Medicine Clinical Practice Guideline. J Clin Sleep Med. 2017;13(2):307–49.
G. C. Carlson et al.
13 Management ofInsomnia Disorder
https://t.me/medicina_free
88. Morin CM, Colecchi C, Stone J, Sood R, Brink D.Behavioral and pharmacological therapies
for late life insomnia: a randomized controlled trial. JAMA. 1999;281(11):991–9.
89. Jacobs GD, Pace-Schott EF, Stickgold R, Otto MW.Cognitive behavioral therapy and pharmacotherapy for insomnia: a randomized controlled trial and direct comparison. Arch Intern
Med. 2004;164(17):1888–96.
90. Buscemi N, Vandermeer B, Friesen C, et al. The efcacy and safety of drug treatments for
chronic insomnia in adults: a meta-analysis of RCTs. J Gen Intern Med. 2007;22:1335–50.
91. Kuriyama A, Honda M, Hayashino Y.Ramelteon for the treatment of insomnia in adults: a
systematic review and meta-analysis. Sleep Med. 2014;15(4):385–92.
92. Kishi T, Nomura I, Matsuda Y, etal. Lemborexant vs suvorexant for insomnia: a systematic
review and network meta-analysis. J Psychiatr Res. 2020;128:68–74.
93. Yi XY, Ni SF, Ghadami MR, etal. Trazodone for the treatment of insomnia: a meta-analysis
of randomized placebo-controlled trials. Sleep Med. 2018;45:25–32.
94. Rojas-Fernandez CH, Chen Y. Use of ultra-low-dose (≤6 mg) doxepin for treatment of
insomnia in older people. Can Pharm J (Ott). 2014;147(5):281–9.
95. Anderson SL, Vande Griend JP.Quetiapine for insomnia: a review of the literature. Am J
Health Syst Pharm. 2014;71(5):394–402.
96. Leach MJ, Page AT.Herbal medicine for insomnia: a systematic review and meta-analysis.
Sleep Med Rev. 2015;24:1–12.
97. Low TL, Choo FN, Tan SM.The efcacy of melatonin and melatonin agonists in insomnia–
an umbrella review. J Psychiatr Res. 2020;121:10–23.
98. Kripke DF, Langer RD, Kline LE.Hypnotics' association with mortality or cancer: a matched
cohort study. BMJ Open. 2012;2(1):e000850.
99. Linnet K, Sigurdsson JA, Tomasdottir MO, Sigurdsson EL, Gudmundsson LS. Association
between prescription of hypnotics/anxiolytics and mortality in multimorbid and
non- multimorbid patients: a longitudinal cohort study in primary care. BMJ Open.
2019;9(12):e033545.
100. Calhoun SL, Fernandez-Mendoza J, Vgontzas AN, Liao D, Bixler EO.Prevalence of insomnia symptoms in a general population sample of young children and preadolescents: gender
effects. Sleep Med. 2014;15(1):91–5.
101. Elwyn G, Frosch D, Thomson R, etal. Shared decision making: a model for clinical practice.
J Gen Intern Med. 2012;27(10):1361–7.
102. Culver NC, Song Y, McGowan SK, etal. Acceptability of medication and nonmedication
treatment for insomnia among female veterans: effects of age, insomnia severity, and psychiatric symptoms. Clin Ther. 2016;38(11):2373–85.
103. Gutner CA, Pedersen ER, Drummond SP. Going direct to the consumer: examining treatment preferences for veterans with insomnia, PTSD, and depression. Psychiatry Res.
2018;263:108–14.
104. United States Food and Drug Administration. Sleep Disorder (Sedative-Hypnotic) Drug
Information (https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-
providers/sleep-disorder-sedative-hypnotic-druginformation). https://www.fda.gov/drugs/
postmarket-drug-safety-information-patients-and-providers/sleep-disorder-sedativehypnotic-drug-information. Published 2019. Updated 4/30/2019. Accessed 9/8/2021.
295
Соседние файлы в папке Библиотека им академика М.И. Перельмана