cognitive-behavioral therapy for chronic insomnia

Curr Treat Options Neurol (2014) 16:321DOI 10.1007/s11940-014-0321-6

Sleep Disorders (S Chokroverty, Section Editor)

Cognitive-Behavioral Therapyfor Chronic InsomniaHeather K. Hood, PhD1

Jenny Rogojanski, PhD2,*

Taryn G. Moss, PhD3

Address1Homewood Health Inc, Guelph, Ontario, Canada*,2Mental Health Program, St. Michael’s Hospital, 193 Yonge Street, Fourth Floor,Toronto, Ontario M5B 1M8, CanadaEmail: [email protected] Psychology, Toronto, Ontario, Canada

Published online: 22 October 2014* Springer Science+Business Media New York 2014

This article is part of the Topical Collection on Sleep Disorders

Keywords Insomnia I Sleep disorder I Cognitive behavioral therapy for insomnia I CBT-I I Insomnia treatment ISleep treatment

Opinion statement

Psychological and behavioral therapies should be considered the first line treatment forchronic insomnia. Although cognitive behavioral therapy for insomnia (CBT-I) is consid-ered the standard of care [1], several monotherapies, including sleep restriction therapy,stimulus control therapy, and relaxation training are also recommended in the treatmentof chronic insomnia [2]. CBT-I is a multimodal intervention comprised of a combination ofbehavioral (eg, sleep restriction, stimulus control) and cognitive therapy strategies, andpsychoeducation delivered in 4 to 10 weekly or biweekly sessions [3]. Given that insomniais thought to be maintained by an interaction between unhelpful sleep-related beliefs andbehaviors, the goal of CBT-I is to modify the maladaptive cognitions (eg, worry about theconsequences of poor sleep), behaviors (eg, extended time in bed), and arousal (ie,physiological and mental hyperarousal) perpetuating the insomnia. CBT-I is efficaciouswhen implemented alone or in combination with a pharmacologic agent. However,because of the potential for relapse upon discontinuation, CBT-I should be extendedthroughout drug tapering [4]. Although the treatment options should be guided by theavailable evidence supporting both psychological therapies and short-term hypnotictreatment, as well as treatment feasibility and availability, treatment selection shouldultimately be guided by patient preference [5]. Despite its widespread use amongtreatment providers [6], the use of sleep hygiene education as a primary interventionfor insomnia should be avoided. Sleep hygiene may be a necessary, but insufficientcondition for promoting good sleep and should be considered an adjunct to anotherempirically supported treatment.

IntroductionInsomnia is defined as the subjective report of persistentimpaired sleep quantity or quality, despite adequate op-portunity for sleep that is associated with daytime impair-ment, such as fatigue, impaired memory, attention, orconcentration. It is one of 18 sleep-wake disorders withinthe DSM-5 [7, 8]; however, it is by far the most commonlyreported sleep problem and one of the most commonpsychiatric disorders among the population [9]. The thirdedition of the International Classification of Sleep Disor-ders [10] uses the termchronic insomniadisorder todenotethe persistent and prolonged nature of the sleep difficulties.

Historically, insomnia was considered a symptom ofother psychiatric and medical conditions and, therefore,symptoms were expected to resolve following adequatetreatment of the primary complaint. However, observa-tions of a bidirectional relationship between insomniaand comorbid conditions have contributed to an increas-ing recognition of insomnia as a primary disorderwarranting clinical attention [11]. As such, the field hasseen a proliferation of research regarding etiologic andtreatment models for primary and secondary insomniain recent years.

There are several models proposed to account for theetiology and pathophysiology of insomnia, includingphysiological, behavioral, cognitive, neurocognitive,and neurobiological perspectives (for a comprehensivereview, see [12]). These models have provided valuableinsights into predisposing (eg, hyperarousal, genetic vul-nerability), precipitating (eg, life stress), and perpetuat-ing factors (eg, worry, rumination, maladaptive sleepbehaviors) that inform our current treatment models.Currently, CBT-I is the empirically supported treatmentof choice for chronic insomnia. In the eight years sincethe publication of themost recent clinical practice guide-lines published by The American Academy of SleepMedicine (AASM) [2], several randomized controlledtrials have added to the evidence supporting CBT-I as

an efficacious treatment for insomnia. Estimates indi-cate that CBT-I and behavioral treatment result in medi-um to large effect size changes in subjective and objec-tive sleep parameters and daytime functioning, evenamong treatment refractory and hypnotic dependentcases [1, 13, 14].

Although a complete description of therapeutic tech-niques is beyond the scope of this review, the followinginterventions are recommended for the treatment ofchronic insomnia [2, 15••]. Recommended behavioraltherapies include sleep restriction therapy, stimulus con-trol therapy, and relaxation. Sleep restriction therapy[16, 17•] involves developing an individualized sleepschedule limiting time in bed to the mean time spentasleep to prevent wakefulness and fragmented sleep.Based on operant and classical conditioning paradigms,stimulus control therapy eliminates sleep-incompatiblebehaviors in the bedroom to promote healthy condi-tioned associations between sleep and the bed/bedroom[18]. Relaxation interventions are intended to reduce thephysiological and mental hyperarousal associated withchronic insomnia through the use of a range of strate-gies, including, but not limited to, progressive musclerelaxation, diaphragmatic breathing, and biofeedback[19].

Although there was insufficient evidence to recom-mend cognitive therapy alone at the time that the mostrecent AASM practice parameters were published [2],more recent evidence indicates that cognitive therapyalone may be an efficacious treatment option. In oneof the only studies to date that sought to dismantle thecomponents of CBT-I, Harvey and colleagues [20••]found that cognitive therapy resulted in slower, butmore sustained, improvements in insomnia symptomscompared with behavior therapy. However, the fullcomplement of CBT-I produced the most robust short-and long-term effects on insomnia severity.

TreatmentCBT for Insomnia

The goal of CBT-I is to directly target cognitive and behavioral variables thatperpetuate insomnia, including factors such as spending an excessive amount oftime in bed, daytime napping, irregular sleep-wake schedules, excessive concernover sleep loss and rumination about the daytime consequences of poor sleep,and performance anxiety [21]. Treatment is generally structured to consist of 4

321, of 9 Curr Treat Options Neurol (2014) 16:321

to 10 sessions that are 50 to 60 minutes in length and spaced out at approxi-mately one session per week, with a 2-week gap prior to the beginning oftreatment to allow for self-monitoring of sleep-related behaviors [22].

The behavioral component of treatment includes stimulus control, wherebythe patient begins to reestablish an association between their sleep environmentand sleep rather than wakeful activities, and establish a routine sleep-wakeschedule. Patients are instructed that they can only use their bed for sleep,and not for other wakeful activities such as eating, reading, and watchingtelevision. The behavioral component also includes sleep restriction therapy,which helps limit the amount of time patients spend in bed to only time that isactually spent sleeping [23]. A standard wake-up time is selected, followingwhich the patient’s earliest bedtime is chosen based on a backward count fromthe wake-time using the average amount of time the patient spends sleeping.The cognitive components of treatment are designed to reverse the cognitiveprocesses that are believed to perpetuate insomnia through the use of thoughtrecords and behavioral experiments [21, 22, 24]. Sleep hygiene instructionsoutlining external factors that may play a role in sleep disturbance (eg, drinkingcaffeine and alcohol in the late evening) are also integrated into treatment;however, sleep hygiene strategies are not sufficient for the treatment of insom-nia in and of themselves.

Currently, CBT-I is the recommended gold-standard treatment in the man-agement of insomnia [2, 5], and efficacy studies suggest that approximately70 %–80 % of patients achieve a therapeutic response with CBT-I, of whichapproximately 40 % achieve full clinical remission [1, 25, 26]. Furthermore,research comparing the unique contributions of behavioral strategies and cog-nitive strategies relative to full CBT-I that integrates both behavioral and cogni-tive interventions found that full CBT-I was associated with the greatest im-provement that is maintained at 6 months post-treatment [20••].

Diet and lifestyle

Diet

& Caffeine is the most frequently used substance to increase wakefulness[27], which is achieved via the blockade of adenosine receptors in thecentral nervous system. Adenosine (a sleep promoting substance) buildsup over extended wakefulness and caffeine acts to counter this process[28], thus, extending this wakefulness.

& Caffeine increases the length of time it takes to fall asleep and reduces slow-wave sleep (ie, deep sleep), which leads to a reduction in the overall totalsleep time and subjective sleep quality [29–32].

& Despite alcohol’s sedative effect, which can help individuals fall asleep[33–35], alcohol is an ineffective sleep aid as it can worsen sleep qualitywhen consumed in large quantities [36]. This is due to a net sympatheticarousal state that occurs after the decline in blood alcohol level afterdrinking. Awakenings from intense dreaming activity with sweating andheadaches are commonly reported as a result of the sympathetic arousal[37].

& Alcohol’s impact on sleep varies and is influenced by a variety of factors,including the total body water, contents of the gastrointestinal tract,

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quantity and speed consumed, the proximity to bedtime, and the bloodalcohol concentration [36, 38].

& Hunger can disrupt sleep [39–41], and it is recommended to eat a lightsnack prior to bedtime. In particular, foods high in the amino acid tryp-tophan (eg, milk, turkey, peanuts, cheese, yogurt) can help to promotesleepiness [42, 43].

& Overall, diet has important implications for sleep quantity and quality andis generally considered as part of CBT-I treatment.

Lifestyle

& Daily routines may be just as important as night-time behaviors whenconsidering sleep [44–49].

& A recent study [50•] examined the regularity and frequency of daytimeactivities in a clinical insomnia population and a good sleeper comparisongroup across a 2-week period. Relative to good sleepers, those with in-somnia were less regular in their daily routines. Findings from this studyadd to the growing number of studies [44–49] that emphasize the relativeimportance of the regularity of daytime activities on sleep.

& Regulating daily routines may be an important target for treatments ofinsomnia. Currently, CBT-I treatments place more emphasis on themorning (ie, regulating rise time) because individuals have better controlover their rise times compared with their sleep onset times. These regularrise times may also be beneficial for sleep as it could increase regularexposure to bright light, which helps to synchronize the internal clock tothe 24-hour day [51]. Sleep difficulties are more than a mere result ofnight-time behaviors, and an individual’s daily lifestyle should be consid-ered when targeting sleep.

Exercise

& Several studies have suggested that poor sleep may relate to inactivity or asedentary lifestyle [44, 52–54]. Medical specialists regard exercise as aneffective nonpharmacologic intervention of preventing or reducing sleepproblems [55–57].

& Sleep and exercise influence each other through complex interactions thatinclude various physiological and psychological pathways [58]. Exerciseleads to physiological changes favorable to homeostatic sleep regulation,which increases slow-wave sleep (deep sleep [55]). Activity also has theability to stabilize the circadian system and to lessen daytime sleepiness [59].

& Self-report data suggests that men and women consider exercise to be themost essential sleep-promoting factors and those who exercise regularlyexperience less daytime tiredness [60]. However, the causality of thisrelationship has been questioned, as those who sleep better and are lessfatigued, may be more likely to engage in physical activity [61].

& Although physical activity is generally considered beneficial for sleep, thereare several moderating factors that can affect this relationship, includingsex, age, fitness level, sleep quality, and the type exercise (intensity, dura-tion, time of day, environment [58]).


Pharmacologic treatmentsConsensus-based recommendations in the AASM clinical guidelines [5]regarding pharmacologic treatments for chronic insomnia indicate thatmedications should be accompanied by behavioral and cognitive therapywhen possible. Although several off-label medications (eg, antidepres-sants, antipsychotics, antiepileptics), nonprescription drugs (eg, antihis-tamines, analgesics), naturopathic (eg, valerian, melatonin), and nutritional(eg, melatonin) supplements are often used to promote sleep, only the follow-ing pharmacologic agents are recommended for the treatment of chronicinsomnia:& Short-intermediate acting benzodiazepine receptor agonists, such as

ezopiclone, zolpidem, zaleplon, triazolam, and temazepam. Despite theirwidespread use, recent meta-analyses revealed relativelymodest effect sizesfor benzodiazepine receptor agonists compared with placebo [62] and lesssustained improvements in insomnia symptoms compared with CBT-I[63].

& Ramelteon, a selective melatonin receptor agonist, has been shown toimprove objective and subjective sleep parameters, and to have a relativelybenign safety profile [64].

& At higher doses, doxepin, a histamine receptor antagonist, is used as anantidepressant medication; however, significantly lower doses have beenFDA- approved for the treatment of sleep maintenance insomnia. Impor-tantly, there is no evidence of rebound insomnia upon discontinuation ofdoxepin [65]. Other sedating low-dose antidepressants, such as trazodone,mirtazapine, and amitriptyline [66] are not FDA-approved for the treat-ment of chronic insomnia and, when used as a sleep-promoting agent, areprescribed at a dose considered inadequate for the treatment of depressionwith comorbid insomnia. In addition, there has been inadequate attentionpaid to the safety, efficacy, side-effect profile (eg, daytime sedation), anddose-response relationship with regards to sleep parameters [67].

& Recently, the FDA approved a novel medication for the treatment ofinsomnia. Suvorexant is an orexin receptor agonist, which has been shownto reduce sleep onset latency and improve sleep maintenance [68]. How-ever, clinical trials have indicated that there is a risk of next day sedationassociated with impaired driving performance when taken at higher ap-proved doses [69].

It is important to note that few studies have compared these medi-cation head to head, so little is known about their relative efficacy, safety, orpatient preference. In addition, although effective in reducing sleep onsetlatency, older approved insomnia medications, such as barbiturates, shouldbe avoided because of the risk for dependence and relapse upon discontinua-tion [62].

Emerging therapies

Mindfulness-based therapy for insomnia (MBT-I)

& Integrates elements of behavioral strategies for insomnia (ie, sleep restric-tion and stimulus control) with mindfulness meditation practices.


& Meditation practices help individuals to learn how to cultivate present-moment awareness and change their relationship to their sleep-relatedthoughts, which tend to be a significant source of anxiety for chronicinsomnia sufferers. Meditation is not used as a relaxation strategy forhelping individual to fall asleep.

& Preliminary findings indicate that combining mindfulness meditationwith CBT-I strategies leads to a significant reductions in self-reported totalwake time and hyperarousal, which has been shown to remain 12-monthspost-treatment [70].

& Further research is necessary to determine whether this treatment may be aviable alternative to CBT-I.

Brief behavioral treatment for insomnia (BBTI)

& A brief, four-session treatment designed to improve dissemination ofcognitive behavioral strategies for insomnia. Two of the four sessions canbe administered over the telephone [71].

& Found to be an effective treatment for chronic insomnia among olderadults [72]; however, no studies have directly compared the efficacy ofBBTI to CBT-I.

Other considerations

& Practitioners should be cautious when using CBT-I with individualswith a diagnosis of bipolar disorder because sleep deprivation canprecipitate manic episodes among these individuals [11, 73]. Be-havioral sleep treatment should be undertaken with care and closeconsultation with other treatment providers with expertise in bipo-lar disorder, such as a psychiatrist. Furthermore, it is recommendedthat treatment for insomnia concurrent with bipolar disorder focusprimarily on stimulus control strategies and establishing a consistent waketime. Sleep should not be restricted to less than 6 hours of total sleep timeper night.

& Other populations for whom sleep restriction should be used with signif-icant caution include individuals with seizure disorders and individualswith excessive daytime sleepiness.

Compliance with Ethics Guidelines

Conflict of InterestHeather K. Hood, Jenny Rogojanski, and Taryn G. Moss declare no conflicts of interest.

Human and Animal Rights and Informed ConsentThis article does not contain any studies with human or animal subjects performed by any of the authors.


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