Cognitive behaviour therapy for primary insomnia: Can we rest yet?

Sleep Medicine Reviews, Vol. 7, No. 3, pp 237±262, 2003 doi:10.1053/smrv.2002.0266

CLINICAL REVIEW

Cognitive behaviour therapy for primary insomnia: Can we rest yet? Allison G. Harvey1,2 and Nicole K. Y. Tang1 Departments of 1Experimental Psychology and 2Psychiatry, University of Oxford, UK

KEYWORDS cognitive behaviour therapy, insomnia, treatment, randomised controlled trial, review

Summary Cognitive behaviour therapy (CBT) for chronic insomnia has been a topic of interest to researchers and clinicians for over forty years. Investment in this area has paid off. Two meta-analyses and one major review by the Standards of Practice Committee of the American Academy of Sleep Medicine have concluded, beyond doubt, that CBT is effective in the treatment of primary insomnia. In this paper we argue that it is timely to raise new questions of CBT for insomnia: namely, is there still room for improvement? and can we rest yet? Whilst signi®cant progress has been made we argue that the ®eld is not, as yet, at a point where patients can be offered a maximally effective psychological treatment. Two lines of argument are developed to support this conclusion. First, it is noted that whilst the effect size for CBT for insomnia is moderate, it is lower than the effect sizes reported for CBT for a range of other psychological disorders. Second, it is suggested that the large literature outlining optimal procedures for conducting randomised controlled trials (RCTs) need to be more fully adopted by research workers in this ®eld. Directions for future research are outlined including (1) guidelines for improved RCT methodology and (2) suggestions for developing empirically grounded treatments. & 2003 Elsevier Science Ltd. All rights reserved.

Whilst substantial progress has been made toward establishing a psychological treatment for primary insomnia, scope for improvement remains. We argue that investigators in the ®eld cannot rest until the magnitude of change associated with cognitive behaviour therapy (CBT) for insomnia is improved such that patients can be offered a maximally effective psychological treatment. Further, we suggest that the ®eld would bene®t from improving the way in which randomised controlled trials (RCTs) are conducted and reported. This paper begins by outlining forces that have led to sustained interest in CBT for insomnia over the past 40 years. An overview of the components of Correspondence should be addressed to: Allison G. Harvey, Department of Experimental Psychology, University of Oxford, South Parks Rd, Oxford OX1 3UD, UK. E-mail: [email protected]

CBT for insomnia is presented. We then move on to ascertain whether CBT for insomnia is ``good enough'' from two perspectives: the magnitude of change affected as a result of treatment and the RCT methodology employed. It is suggested that further research is required (1) to improve the methodology of RCTs in this ®eld and (2) that employs a scienti®c approach to the development of empirically grounded treatments. We suggest that this two part strategy will markedly increase the possibility of developing an optimal psychological treatment for insomnia.

BACKGROUND Cognitive behavioural approaches to the treatment of insomnia have been of interest for more than forty

1087±0792/03/$ ± see front matter & 2003 Elsevier Science Ltd. All rights reserved.

238

years with the ®rst case study being reported in the late 1950s, followed by more detailed research, including RCTs, a few years later [see 1 for review]. The early 1990s saw an increased emphasis on cognitive interventions with the addition of cognitive restructuring to the treatment [e.g., 2±4]. Currently, there are more than 100 published studies testing the ef®cacy of CBT for insomnia [1]. This high level of interest in CBT for insomnia is likely to be attributable to at least three factors. First, CBT for insomnia is a treatment that works. Two meta-analyses [5, 6] and one major review by the Standards of Practice Committee of the American Academy of Sleep Medicine [7, 8] have concluded, beyond doubt, that CBT has ef®cacy in the treatment of insomnia. Its ef®cacy cannot be accounted for by the passage of time, as established by studies comparing CBT to a waitlist control condition [e.g., 9, 10]. Further, its ef®cacy cannot be attributed to non-speci®c processes such as attention from a therapist, demand characteristics, or patient expectation, as established by studies comparing CBT to an inert but therapist delivered treatment [e.g., 11, 12]. Further, a recent study of the effectiveness1 of CBT has demonstrated that the outcomes obtained under the ideal conditions of ef®cacy studies hold up in the real world [13]. Second, dissatisfaction with pharmacological interventions has also contributed to sustained interest in CBT for insomnia. Benzodiazepines have been shown to provide symptomatic relief in that they hasten sleep onset, reduce wakefulness after sleep onset, and reduce the amount of light (Stage 1) sleep, but only for the duration of the treatment. As benzodiazepines have several drawbacks, including rebound insomnia on cessation of treatment, they have been recommended for transient and short-term insomnia only with nightly use being limited to four weeks or less [see 14 for review]. The early indications from the newer non-benzodiazepine hypnotics, such as zalepon, zopiclone, and zolpidem, are that problems with tolerance and withdrawal are lower if used at the recommended dose and if use is limited to nightly for less than one month [15]. Hence, pharmacotherapy, at this stage, provides treatment for acute insomnia but not for chronic insomnia. 1

A distinction can be drawn between clinical ef®cacy studies and clinical effectiveness studies. In the former, carefully screened patients are treated in ideal, tightly controlled circumstances. Clinical effectiveness studies aim to establish whether the treatment gains observed in ef®cacy studies can be maintained in real world clinical practice [1, 20].

A. G. HARVEY AND N. K. Y. TANG

Third, chronic insomnia is the second most common psychological health problem [16], affecting approximately 33% of the US population, with 9% reporting insomnia on a regular nightly basis [17]. It has serious consequences including functional impairment, work absenteeism, impaired concentration and memory, increased use of medical services [18], increased risk of motor vehicle accident and accident involving the use of machinery [19], and heightened risk of developing depression or an anxiety disorder [see 20 for review]. That is, the large numbers of people affected by insomnia, along with the associated adverse consequences, have contributed to the high level of interest in CBT for insomnia. Taken together, the proven success of CBT, limitations associated with pharmacotherapy, and high prevalence of insomnia has provided the impetus for research on CBT for insomnia. This is an investment that has paid off in that there is agreement that CBT for insomnia is effective [7, 8]. However, whilst signi®cant progress has been made the ®eld is not, as yet, at a point where patients with insomnia can be offered a maximally effective psychological treatment. Accordingly, the aim of the present paper is to ask a new set of questions: namely, is there still room for improvement? and can we rest yet? Before attempting to examine these questions we will brie¯y describe the components that typically constitute CBT for insomnia.

TREATMENT DESCRIPTION It should be noted that most RCTs have compared the ef®cacy of one component to another (e.g., Morin and Azrin [21] compared stimulus control and imagery training). However, more recent studies have examined the ef®cacy of a combination of the components. To give some examples, Edinger and colleagues [22] combined sleep education, stimulus control, and sleep restriction and Morin and colleagues [23] combined stimulus control, sleep restriction, sleep hygiene, and cognitive therapy. Such interventions are typically referred to as multi-component behaviour therapy or multi-component cognitive behaviour therapy. The components that are included under the umbrella of CBT for insomnia are brie¯y described below [see 16, 24 for a more detailed explanation]. Stimulus control involves the person with insomnia being asked to go to bed only when they are tired, to limit their activities in bed to sleep and sex, to get out of bed at the same time every morning, and when sleep-onset does not occur within 10 min, to get up

CBT FOR INSOMNIA

and go to another room. The rationale underlying this treatment is that insomnia is the result of maladaptive conditioning between the environment (bed/bedroom) and sleep incompatible behaviours (e.g., worry/frustration at not being able to sleep). The stimulus control intervention aims to reverse this association by limiting the sleep incompatible behaviours engaged in within the bedroom environment [26]. The sleep restriction component was developed by Spielman, Saskin, and Thorpy [26]. The aim of this intervention is to maximise sleep ef®ciency and the association between the bed and sleep. The treatment begins by restricting the time spent in bed to the person's estimated average amount of nighttime sleep. The aim is to bring the total amount of time in bed as close as possible to the total sleep time. As such, subsequent instructions may involve the time spent in bed being either increased (as the sleep becomes consolidated) or decreased (to further maximise sleep ef®ciency). Sleep hygiene training involves providing education about behaviours known to interfere with sleep such as intake of caffeine, alcohol and nicotine, daytime napping, variable sleep scheduling, exercise within 4 h of bed and reading whilst in bed. After the initial education session, monitoring these ``sleep-unfriendly'' behaviours on a daily basis is conducted to ensure patients improve the compatibility of their lifestyle with sleep. Relaxation training can include progressive muscle relaxation, diaphragmatic breathing, autogenic training, biofeedback, meditation, yoga, and hypnosis. These interventions are designed to reduce psychophysiological arousal. Thought stopping aims to interrupt unwanted pre-sleep cognitive activity by instructing the patient to repeat, subvocally, the word ``the'' every 3 s [articulatory suppression; 27] or to yell ``stop'' subvocally [thought stopping; 28]. Paradoxical intention involves explicitly instructing patients to try to stay awake when they get into bed. The rationale underpinning this intervention is that the paradoxical instruction reduces the anxiety associated with trying to fall asleep causing the patient to relax and fall asleep faster [29]. Cognitive restructuring aims to alter irrational beliefs about sleep and typically involves ``providing accurate information and having the patient identify and rehearse alternative belief statements'' [30, p. 327]. Imagery training involves within session training and between session practice. The RCTs that have employed imagery training have asked patients to

239

image six common objects (candle, hourglass, blackboard, kite, light bulb, fruit) when they can not fall asleep. The instructions emphasise visualising the shape, colour, movement, and texture [e.g., 31, 32]. In a review of the evidence for each component, the Standards of Practice Committee of the American Academy of Sleep Medicine concluded that there was suf®cient evidence to justify the use of stimulus control, progressive muscle relaxation, paradoxical intention and biofeedback, and a moderate amount of evidence associated with sleep restriction and the multi-component behavioral therapy package [7, 8]. Two further issues are perhaps worth mentioning. First, although behavioural theory underpins the stimulus control and relaxation components of the treatment, several authors have suggested that these components operate via a cognitive mechanism in that stimulus control may prevent people lying in bed worrying about not sleeping [33] and relaxation may function by calming pre-sleep cognitive activity [34], reducing concern about the sleep disturbance, and fostering a more positive outlook [12]. Second, there is concern about the utility of the thought stopping component on the basis that it resembles thought suppression [35] that is known to be associated with fuelling of the suppressed thought. That is, some components of CBT for insomnia may not be making a positive contribution and the mechanism of change of others is still debated.

CAN WE REST YET? The question of whether there is room for improvement to CBT for insomnia will now be evaluated from two perspectives: from the perspective of the magnitude of change observed from before to after treatment and from the perspective of the RCT methodology employed.

Magnitude of change In their meta-analysis, Morin et al. [5] included 59 outcome studies involving over 2000 people with insomnia. The patients treated with one or more CBT components were found to be better off compared to 81% of untreated controls for sleep onset and 74% of untreated controls for sleep maintenance. On average, sleep onset latency (SOL) reduced from 64 to 37 min post treatment and time spent awake after sleep onset (WASO) reduced from a mean of 70 to

240

A. G. HARVEY AND N. K. Y. TANG

Table 1 Summary of effect sizes obtained in randomised controlled trials (RCTs) of cognitive therapy (CT), behaviour therapy (BT), or cognitive behaviour therapy (CBT) across a range of psychological disorders Diagnosis Panic disorder

Authors Clark et al. (1999)

Type of study RCT for full CT (12±16 sessions) RCT for brief CT (7 sessions)

Interval Post-treatment 12-month followup Post-treatment 12-month followup

Depression

Dobson (1989)

Post-treatment

2.15

Generalized anxiety disorder

Borkovec and Ruscio (2001)

Meta-analysis of 28 studies of CT Meta-analysis of 13 RCTs of CBT

Post-treatment

1.09

Post-traumatic stress disorder

Van Etten and Taylor (1998) Gillespie et al. (2000)

Meta-analysis of 61 studies of BT Large case series of CT

Post-treatment

1.63±1.93

Post-treatment

2.47

38 min post treatment. In another meta-analysis, Murtagh and Greenwood [6] included 66 outcome studies involving 1538 treated patients with insomnia and 369 no-treatment controls. It was found that CBT for insomnia generally produced considerable and durable improvement to sleep pattern and subjective experience of sleep. Overall, SOL reduced from 61 to 37 min, the number of awakenings reduced from 1.63 to 0.44 times, and total sleep time (TST) increased from 5.65 to 6.18 h post treatment. These effects were maintained, and in most cases enhanced, at followup. Whilst these results are very encouraging, closer examination reveals scope for improvement. First, 19±26% of patients failed to show any response to treatment [5]. Second, the overall average improvement was only 50±60% [5], a degree of change that is likely to be clinically signi®cant but not enough to convincingly move the average patient in to the good sleeper range (an issue discussed in detail below). Third, Morin et al. [5] calculated that the treatment resulted in average effect sizes2 of 0.88 for SOL, 0.65 for WASO, 0.53 for number of awakenings, and 0.42 for TST. The average duration of the followup was 25.9 weeks. The average effect sizes, using the followup data, were 0.92 for SOL, 0.58 for WASO, 0.56 for number of awakenings, and 0.51 for TST. These ®ndings were closely replicated by the Murtagh and Greenwood [6] meta-analysis, although this study also reported an effect size for sleep quality (0.94). Together, these studies clearly endorse the conclusion

2

An effect size is the amount of change associated with a treatment, in standard deviation units.

Effect size 2.9 2.8 2.9 3.2

that CBT for insomnia is effective. However, when compared with the effect sizes obtained for CBT for a range of other psychological disorders the effect sizes obtained for CBT for insomnia are markedly lower. As summarized in Table 1, the effect size of CBT for panic disorder is between 2.80 and 3.20 [36], for depression is 2.15 [37], for generalised anxiety disorder is 1.09 [38], and for posttraumatic stress disorder is between 1.63 and 2.47 [39, 40]. Why the discrepancy in effect size between CBT for insomnia and CBT for other psychological disorders? One possibility is that the effect size may be in¯uenced by the nature of the outcome variables. For example, Dobson's meta-analysis of RCTs of CBT for depression employed a self-report questionnaire of symptoms over the past week (the Beck Depression Inventory) as the primary outcome measure. Whereas the Morin et al. (1994) meta-analysis employed subjective sleep estimates based on daily diary ratings. These outcome measures have in common that they are both subjective, but they differ in that one requires a retrospective judgement to be made spanning one week whereas the other is made immediately on waking each morning. While such a difference is unlikely to provide a full account of the discrepancy there may be other, more subtle differences in outcome measures that require consideration. Second, perhaps there is more comorbidity/heterogeneity in insomnia samples. This seems unlikely, however, given the high rates of comorbidity evident across a wide range of psychological disorders [41]. Another possibility is that perhaps CBT for insomnia is less potent than CBT for other psychological disorders. If so, CBT for insomnia should be a priority for future research.

CBT FOR INSOMNIA

Taken together, a signi®cant group of patients do not respond to CBT for insomnia and many patients who do respond do not improve enough to be classed as good sleepers following treatment. Among those who do respond, the degree of improvement observed is less than that seen for CBT for a range of other psychological disorders. Such data suggest that there is substantial room for improvement in CBT for insomnia and that researchers in this ®eld cannot rest yet.

241

Table 2 summarises, for each of the RCTs of CBT for insomnia reviewed, key aspects of the methodology employed. The ®ndings are discussed below. 1. Clearly de®ned target symptoms. The symptoms that the treatment seeks to reduce must be clearly speci®ed. As evident from the ``target symptoms'' column in Table 2, all RCTs reviewed clearly speci®ed the target symptoms. Further, the ®eld appears to have responded to the recommendation that ``the assessment of ef®cacy is too often limited to self-report measurement'' [47, p. 527]. From Table 2, it is clear that more recent studies have included objective outcome measures such as polysomnography (PSG) and/or actigraphy. However, it is notable that almost without exception, outcome has been evaluated according to sleep parameters (SOL, WASO and TST). It is curious that studies have not included daytime measures as target symptoms given that the de®nition of insomnia requires the presence of ``clinically signi®cant distress or impairment'' [50, p. 557], ``marked personal distress or interference with personal functioning in daily living'' [51, p. 114], or ``decreased functioning during wakefulness'' [52, p. 37]. A ®nal point is that many studies have included sleep ef®ciency as an outcome measure. Sleep ef®ciency is calculated by dividing TST by the total time in bed and multiplying the outcome by 100. Whilst many patients with insomnia spend excessive time in bed, occasionally patients present with reasonable sleep ef®ciency but clearly have severe insomnia (e.g., TST ˆ 3.5 h, total time in bed ˆ 4 h; SE ˆ 88%). Accordingly, sleep ef®ciency may not be a reliable indicator for all individuals with insomnia. 2. Diagnostic criteria. There are three diagnostic schedules that present differing diagnostic criteria for insomnia; the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition [DSM-IV; 48], the International Classi®cation of Sleep Disorders ± Revised [ICSD-R; 51], and the International Classi®cation of Diseases, 10th Edition [ICD-10; 50]. From the ``Diagnostic criteria'' column of Table 2, it is evident that whilst all studies clearly stipulate the criteria employed, a variety of de®nitions of insomnia have been adopted. Five studies employed the ICSD criteria, three studies employed DCSAD5 criteria, one study employed the DSM

RCT methodology The Standards of Practice Committee [7] classi®ed each of 48 RCTs of CBT for insomnia within the following 5 level system; Level 1 was awarded for randomised well-designed trials with low-alpha3 and low-beta4 errors, Level 2 was awarded for randomised trials with high-beta errors, Level 3 for nonrandomised controlled or concurrent cohort studies, Level 4 for nonrandomised historical cohort studies, and Level 5 for a case series. It is of concern that none of the RCTs reviewed by the committee achieved a Level 1 rating. This ®nding suggests that many RCTs of CBT for insomnia fall short of the current standards for RCT methodology. When conducting and reporting RCTs it is crucial to adhere to the highest standards to ensure that if differences between treatments are observed, they are true effects and not a function of biasing processes. With the advent of ``evidence-based medicine'', a large literature outlining optimal RCT procedures has accrued. To ascertain the extent to which RCTs of CBT for insomnia comply with current standards, and to identify areas for improvement, we evaluated published RCTs of CBT for insomnia over the past 15 years (since 1987). The criteria employed to select articles was that established by Morin et al. [8], except that we did not include case series. The RCT standards, by which the selected studies were evaluated, were drawn from a number of sources: recommendations made speci®cally for CBT for insomnia [42], recommendations made for CBT treatments across a range of disorders [43, 44], and recommendations made for RCTs in the medical literature, as summarised by the Consolidated Standards of Reporting Trials [CONSORT; 45, 46].

3

Alpha error ± the probability that a signi®cance difference between treatments is a true difference. 4 Beta error ± the probablity that a non signi®cant difference between treatments is a true non-difference [7].

5

DCSAD criteria ˆ Diagnostic Classi®cation of Sleep and Arousal Disorders (the earlier version of the ICSD criteria).

242

Table 2

Evaluating the method employed by RCTs of CBT for insomnia Target symptoms

Diagnostic criteria

Diagnostic tools

Blind evaluator?

Therapist training?

Treatment Treatment Sample manual? credibility? size

Recruitment Comorbid psychological disorders

Comorbid sleep disorders

Length of follow up

Edinger et al., 2001

Objective (PSG): TST, WASO, SE Subjective (sleep log): TST, WASO, SE Qu'naires: ISQ, SES, BDI

DSM-III-R criteria plus WASO  60 min, insomnia duration  6 mths, insomnia onset after age 10, 1 report of sleep disruptive practice

Structured Interview for Sleep Disorders, 1-wk sleep log, & PSG screening.

Yes

Yes

Yes

Yes (TEQ)

75

Volunteers recruited through media advert, Sleep clinic patients

Yes (SCID) Excluded patients with Axis 1 psychiastric disorders and patients requiring psychotropic medication

Yes (PSG) Excluded patients with PLMS, OSAS & SSM

6 mths

Espie et al., 2001

Subjective (sleep log): SOL, WASO, TST, SQ, sleep medications

ICSD criteria plussleep disturbance 4 nights/wk, insomnia duration  3 mths,  5 PSQI global score

2-wk sleep log, clinician interview, qu'naires, & actigraphy

NR

Yes

*

Yes

139

Patients referred by physicians

* Excluded patients with signi®cant depressive symptoms

Yes (PSG) 12 mths Excluded patients with PLMS, OSAS & parasomnia

Friedman et al., 2000

Objective [PSG (optional) & actigraphy]: SOL, TST, SE, WASO Subjective (sleep log): SOL, TST, SE, WASO

ICSD criteria plus SOL  30 min, SE  80% or TST  6 h or WASO  30 min (on 5 nights during 2 wks of assessment)

Structured interviews, qu'naires, & 2-wk sleep log

Yes

*

*

*

39

Volunteers from community

Yes (SCID & MMSE) Exclude those who scored 526 on MMSE

Yes (PSG) 3 mths Excluded patients with PLMS & OSAS.

Mimeault and Morin, 1999

Subjective (sleep log): SOL, WASO, early morning wakening, TWT, TIB, TST, SE, SQ Qu'naires: PSQI, SII, BAS, BAI, ITEQ

ICSD ‡ DSM-IV criteria plus SOL or WASO  30 min,  3 nights/wk, insomnia duration  1 mth, at least one adverse daytime effect

Diagnostic NR Interview for insomnia (DII), qu'naires, & 2-wk sleep log

Yes

Yes (self-help book)

Yes

58

Volunteers recruited through media advert

Yes (BAI, BDI) Excluded those who scored 430 on BAI, 421 on BDI, and those who were receiving psychological treatment

Yes 3 mths (interview) Excluded those with suspected PLMS or OSAS

A. G. HARVEY AND N. K. Y. TANG

Author(s)

Objective (PSG): SOL, WASO, early morning awakening, TWT, TIB, TST, SE Subjective (sleep log): SOL, WASO, early morning awakening, TWT, TIB, TST, SE Clinical ratings by patients & their signi®cant others Qu'naires: BDI, STAI, POMS, MMSE, BSI ICSD criteria plus WASO  30 min,  3 nights/wk,  1 negative effect complaint, insomnia duration  6 mths,  60 yrs of age

SOL  40 min, WASO  90 min,  3 nights/wk, insomnia duration  6 mths, daytime impairment PSG: SOL  40 min, SE585%

Morin et al., 1993

Objective (PSG & actigraphy): TIB, SOL, TST, WASO, SE Subjective (sleep log): TIB, SOL, TST, WASO, SE, SQ, daytime sleepiness

Hauri, 1997

NR

NR

Clinical NR interviews, 2-wk baseline assessment

Interviews, 1-wk sleep log plus at least 4 actigraphy nights

Interviews, 1-wk sleep log plus actigraphy, & 3 PSG nights

NR

Yes

*

Yes

Yes

Yes

*

*

Yes

*

*

*

*

24

30

26

78

Diagnostic Blind Therapist Treatment Treatment Sample tools evaluator? training? manual? credibility? size

ICSD ‡ DSM-IV Clinician criteria plus interviews, SOL or WASO  PSG 30 min,  3 nights/ wk, insomnia duration  6 mths,  1 negative daytime sequela,  55 yrs of age

SOL  30 min, TST  360 min,  5 night/wk,  1 insomnia complaint, insomnia duration  6 mths

Objective (PSG): WASO, SE, TWT, TST Subjective (sleep log): WASO, SE, TWT, TST Clinical ratings by patients, signi®cant others, & clinicians Qu'naires: SII

Morin et al., 1999

Diagnostic criteria

Guilleminault Objective et al., 1995 (actigraphy): mean nocturnal activity, SOL, WASO, TRT, no. of nocturnal rest periods, duration of nocturnal rest periods Subjective (sleep log): SOL, TST, TIB, WASO, distribution of awakening

Target symptoms

continued

Author(s)

Table 2

Volunteers recruited through media advert

Volunteers recruited through media advert Self-referred patients

Volunteers recruited through media advert Patients referred by physicians

Volunteers recruited through media advert

Yes (clinician interview & qu'naires) Excluded patients with severe psychopathology, scored  23 on BDI, scored  23 on FMSI, receiving psychotherapy, regularly using psychotropic medication

Yes (SCID) Excluded those who had a psychiatric disorder

Yes (SCID) Excluded those who had severe psychological problems using DSM-IIIR criteria

Yes (SCID, BSI & MMSE) Excluded those with major depression symptoms, severe psychopathological conditions, and scored 23 or lower on the MMSE

Recruitment Comorbid psychological disorders

Informal F/U (9±12 mths) for patients with positive response only

10 mths

Yes (clinical 3 mths interview 12 mths and PSG) Excluded patients with PLMS & OSAS

Yes (PSG) Excluded patients with PLMS & OSAS

Yes (PSG) Excluded patients with PLMS & OSAS

Yes (PSG) 3, 12 & 24 mths Excluded patients with PLMS & OSAS

Comorbid Length sleep of disorders follow up

CBT FOR INSOMNIA 243

Subjective (sleep log): SOL, dif®culty falling asleep, SQ, daytime functioning

Objective (PSG): SOL, no. of awakenings, latency to stage 3 sleep Subjective (sleep log & interview): SOL, WASO, total naptime, self-ef®cacy, BDI, feeling refreshed on waking, feeling rested during sleep Subjective (sleep log): SOL, WASO, TST, SE, TIB, TIB after waking

Subjective (qu'naire): SOL, WASO, TST, dif®culty falling asleep, restedness

Jacobs et al.,1993

EngleFriedman et al.,1992

McClusky et al.,1991

Friedman et al.,1991

Target symptoms

continued

Author(s)

Table 2

SOL  60 min,  3 nights/wk, insomnia duration  6 mths

SE  80%

At least 1 of 3 criteria: SOL  45 min for  3 nights/wk;  3 awakenings for  3 nights/ wk;  30 min awakenings for  3 nights/wk

SOL  60 min,  3 nights/wk,  1 daytime sequela, insomnia duration  6 mths

Diagnostic criteria

Yes

Blind evaluator?

Self-report, qu'naires, clinical interview

Modi®ed SQAW

NR

NR

Interviews, NR qu'naires, 2-wk sleep log, 2 PSG nights (for 29 patients only)

Clinical interviews, 2-wk sleep log & SHQ

Diagnostic tools

*

Yes

Yes

*

Therapist training?

*

*

*

*

Yes

*

*

*

30

22

53

20

Treatment Treatment Sample manual? credibility? size

Comorbid psychological disorders

Volunteers recruited through media advert

Volunteers recruited through senior organisation, residences or media advert

Volunteers recruited through media advert, senior clubs, Patients referred by physicians

Yes (self-report & interview) Excluded those with psychiatric disorders using DSM-III criteria

Yes (self-report/ interview) Excluded patients with major depression (scored 45 on GDS)

*

Volunteers * recruited through media advert Patients referred by hospital

Recruitment

Length of follow up

Yes 5 wks (interview/ Qu'naires) Excluded those with RLS, nocturnal myoclonus & OSAS

Yes 3 mths (self-report/ interview) Excluded patients with suspected PLMS or OSAS

Yes 1 mth (interview & hospital screening) Excluded those with suspected organic sleep disorders * 24 mths

Comorbid sleep disorders

244 A. G. HARVEY AND N. K. Y. TANG

NR

SOL  30 min, WASO  30 min, TST  6.5 h, waking before 5 a.m.,  nights/wk,  6 mths, sleep problems affect daily functioning

Morawetz, 1989 Interview, 2-wk baseline sleep log

NR

DCSAD criteria Interview plus SOL  30 min, insomnia duration  1 year

Espie Subjective et al., 1989b (sleep log): SOL

Subjective (sleep log): SOL, WASO, TST, sleep med. usage, daytime functioning

NR

NR

Qu'naires, interview, & 15-day sleep log

Blind evaluator?

Interview

ICSD criteria plus sleep onset/sleep maintenance complaints,  5 yrs of sleep disturbance

Diagnostic tools

DCSAD criteria plus SOL  30 min, insomnia duration  1 year

Subjective (sleep log): SOL, WASO, TST, SQ, tenseness on going to bed, restedness on waking

Sanavio et al., 1990

Diagnostic criteria

Espie Subjective et al., 1989a (sleep log): SOL, TST, SQ (restedness/ enjoyment)

Target symptoms

continued

Author(s)

Table 2

Yes

*

*

Yes

Therapist training?

Yes

*

*

Yes

Yes

Yes

Yes

Yes

141

84

70

40

Treatment Treatment Sample manual? credibility? size

Volunteers recruited through media advert

Patients referred by physicians

Patients referred by physicians

Research volunteers solicited through letters to area physicians

Yes (interview) Excluded those with psychiatric illness

Yes (interview) Excluded those with suspected PLMS or OSAS

Yes (interview) Excluded those with suspected sleep disorders

Yes (interview) Excluded those with suspected sleep disorders

Yes (interview & qu'naire) Excluded patients who were prescribed an antidepressant, those who appeared clinically depressed or scored 460 on ZDS Yes (interview & qu'naire) Excluded patients who were prescribed antidepressants, those clinically depressed or scoring 460 on ZDS

*

Comorbid sleep disorders

Yes (MMPI) Excluded patients with insomnia secondary to anxiety, depression or any other psychopathological conditions

Recruitment Comorbid psychological disorders

4 mths

*

6 wks 3 mths 6 mths 17 mths

12 mths 36 mths

Length of follow up

CBT FOR INSOMNIA 245

Target symptoms

Subjective (sleep log): SOL

Subjective (sleep log): SOL, TST, WASO, sleep med. intake Objective (switch-activated clock): SOL, WASO Clinical ratings by patients & their signi®cant others Qu'naires: BDI, STAI

Subjective (sleep log): WASO, no. of arousal, duration of arousal

Stanton, 1989

Morin and Azrin, 1988

Schoicket et al., 1988

continued

Author(s)

Table 2

Clinical interview, 2-wk sleep log

Self-report, 1-wk baseline sleep log

Diagnostic tools

Sleep Interview, maintenance 2-wk insomnia, sleep log WASO  30 min,  2 nights/wk, insomnia duration  6 mths

DCSAD criteria plus Sleep maintenance insomnia, WASO  30 min,  3 nights/wk, insomnia duration  6 mths,  1 daytime sequela,  55 yrs of age

SOL  30 min, insomnia duration  6 mths

Diagnostic criteria

NR

NR

NR

Blind evaluator?

Yes

Yes

*

Therapist training?

Yes

Yes

*

Yes

Yes

*

65

27

45

Treatment Treatment Sample manual? credibility? size

Patients referred by physicians

Volunteers recruited through media advert

Volunteers recruited through media advert

Yes (clinical interview) Excluded patients with suspected RLS, PLMS & OSAS

*

Comorbid sleep disorders

Yes (MMPI, * qu'naires & interview) Excluded those whose insomnia may have been related to psychopathology

Yes (clinical interviews & qu'naires) Excluded those who had severe psychopath, scored  23 on BDI, was receiving psychotherapy, was regularly using psychotropic medication

* Excluded those who were receiving other professional services

Recruitment Comorbid psychological disorders

CBT for insomnia 42 6 wks

3 mths 12 mths

3 mths 6 mths

Length of follow up

246 A. G. HARVEY AND N. K. Y. TANG

continued

Author(s)

Target symptoms

Diagnostic criteria

Diagnostic tools

Blind evaluator?

Therapist training?

Treatment Treatment Sample manual? credibility? size

Recruitment Comorbid psychological disorders

Comorbid sleep disorders

Length of follow up

Sanavio, 1988

Subjective (sleep log): SOL, TST, SQ, presleep tension

ICSD criteria plus SOL  30 min,  4 nights/wk, insomnia duration  12 mths

Qu'naires, interview, 1-wk sleep log

NR

Yes

Yes

Yes

24

Patients referred by physicians

Yes (MMPI & interviews) Excluded patients with insomnia secondary to anxiety, depression or any other psychopathological conditions

Yes (checked by GP)

3 mths 12 mths

Morin and Azrin, 1987

Subjective (sleep log): WASO Ratings by participants' signi®cant others Qu'naires: BDI STAI

WASO  30 min,  2 nights, no sleep onset insomnia, insomnia duration  6 mths

Interviews

NR

Yes

*

*

21

Volunteers recruited through media advert

Yes (clinical interviews & qu'naires) Excluded those who had severe psychopathology, scored 23 or above on BDI, was receiving psychotherapy, was regularly using psychotropic medication

Yes (clinical interview) Excluded patients with suspected RLS, PLMS & OSAS

3 mths 12 mths

CBT FOR INSOMNIA

Table 2

*No or not reported. NR ˆ Not relevant, No. ˆ number, Min ˆ minutes, Wks ˆ Weeks, Mths ˆ Months, Yrs ˆ Years, F/U ˆ follow-up, Qu'naire ˆ questionnaire. SOL ˆ Sleep onset latency, TST ˆ Total sleep time. WASO ˆ Wake after sleep onset, SE ˆ Sleep ef®ciency, SQ ˆ Sleep quality, TWT ˆ Total wake time, TIB ˆ Time in bed, TRT ˆ Total rest time, ID ˆ Insomnia duration, Sleep Med. ˆ Sleep medication. DCSAD ˆ Diagnostic Classi®cation of Sleep and Arousal Disorders, DSM-III-R ˆ Diagnostic and Statistical Manual for Mental Disorders, 3rd Edition (Revised), DSM-IV ˆ Diagnostic and Statistical Manual for Mental Disorders, 4th Edition, ICSD ˆ International Classi®cation of Sleep Disorders, SCID ˆ Structured Clinical Interview for DSM-III-R/DSM-IV. PSG ˆ Polysomnography, OSAS ˆ Obstructive sleep apnea syndrome, PLMS ˆ Periodic limb movement syndrome, RLS ˆ Restless leg syndrome, SSM ˆ Sleep state misperception. BAI ˆ Beck anxiety inventory, BAS ˆ Beliefs and attitudes about sleep scale, BDI ˆ Beck depression inventory, BSI ˆ Brief symptom inventory, FMSI ˆ Folstein mini-mental state inventory, GDS ˆ Geriatric depression scale. ISQ ˆ Insomnia symptom questionnaire, ITEQ ˆ Insomnia treatment evaluation questionnaire, MMPI ˆ Minnesota multiphasic personality inventory. MMSE ˆ mini-mental status examination, POMS ˆ Pro®le of mood states, PSQI ˆ Pittsburgh sleep quality index, SES ˆ Self ef®cacy scale, SII ˆ Sleep impairment index, SQAW ˆ Sleep questionnaire and assessment of wakefulness, STAI ˆ State trait anxiety inventory, TEQ ˆ Therapy evaluation questionnaire, ZDS ˆ Zung depression scale.

247

248

criteria, two studies employed both the ICSD and DSM criteria. The remainder (n ˆ 10) speci®ed criteria that were not based on any of the current classi®cation systems. It is of concern, for reasons of comparability across studies, that three different classi®cation systems exist and that many researchers choose not to employ any of the standard criteria. 3. Diagnostic tools. At pre-treatment, post-treatment and follow-up it is important to include valid and reliable measures that index the presence of the diagnosis and assess symptom severity. In a review of the medical literature, Marshall et al. [51] found that the use of unpublished scales in outcome trials was a source of signi®cant bias. As is evident in Table 2 (heading ``Diagnostic tools''), many RCTs of CBT for insomnia have relied exclusively on unvalidated measures, particularly clinician interview. Clinician interviews are open to inadvertent bias as the questions one clinician asks may differ to those asked by other clinicians. Further, being unvalidated, the questions may not fully and accurately assess the criteria. Unfortunately, there are currently few widely available psychometrically validated structured interviews for the diagnosis of insomnia. Future research is required to both develop and disseminate fully validated interviews. On a different matter, several studies have employed sleep diaries as an outcome measure. Whilst sleep diaries have the advantage of being inexpensive, non-intrusive, and correlated with objective measures of sleep [52], they have two disadvantages: (1) as sleep is de®ned by the absence of memories, it is dif®cult for some patients to accurately estimate their sleep and (2) sleep diaries may be affected by demand, bias and expectation. We suggest that ideally researchers should combine sleep diary, objective evaluation (PSG or actigraphy), and evaluation with a psychometrically validated structured clinical interview, to index each of the diagnostic criteria for insomnia. 4. Blind evaluators. The person who evaluates the outcome of treatment should be blind to the treatment condition received by the patient and should certainly not be the therapist who treated the patient. Employing blind evaluators is often regarded as less relevant for those studies that have relied exclusively on sleep diaries, PSG or actigraphy. However, as these all involve some judgement on the part of the scorer, we suggest that consideration be given to requiring blinding

A. G. HARVEY AND N. K. Y. TANG

5.

6.

7.

8.

when scoring all outcome measures, including sleep diaries, PSG, or actigraphy. While we found several studies that included blind evaluators for diagnostic status (see Table 2), no studies reported blind scoring of sleep diary, PSG, and actigraphy. The reliability of posttreatment evaluations will be more convincing if all assessment sessions are videotaped and a random sample of independently evaluated tapes used to obtain interrater reliability. Further, consideration should be given to describing how the assessors were trained and the methods employed to monitor their performance and to ensure their judgements remain consistent over time and with other assessors. Therapist training. Morin et al. [5] found that the outcome from CBT for insomnia was better if a professionally trained therapist conducted the treatment compared to treatment administered by a trainee or by self-administration. Accordingly, it is crucial that information be given as to the amount of training and methods of training received by therapists. Most of the studies we reviewed provided information on therapist training (see Table 2). Treatment manual. The treatment should be written in a manual for several reasons: (1) so the treatment is speci®c and can be replicated, (2) to help ensure consistent delivery across patients and therapists, (3) to ensure the treatment can be replicated by other research groups [43], and (4) to aid in the dissemination of a successful treatment. About 50% of the studies reviewed in Table 2 stated that the treatment was based on a manual. Treatment credibility. Checks of the patient's perception of the credibility of the treatment should be carried out after Session 1 or 2. This ensures that the treatment groups are matched for expectation of improvement. From Table 2, this feature has been included in only some of the studies. Sample size. Studies should describe how the sample size was determined and demonstrate that there was suf®cient statistical power to detect group differences. This is especially important for RCTs reporting negative ®ndings. Moher, Dulberg, and Wells [53], in a review of 383 RCTs for a range of disorders, found that of 102 RCTs reporting negative results only 16% of those with dichotomous measures and 36% of those with a continuous measure had suf®cient

CBT FOR INSOMNIA

statistical power to detect differences between groups. Altman et al. [45] suggest that trials reporting negative ®ndings must present a sample size calculation to ensure that the study had enough statistical power to capture the effect. Two studies, often quoted as evidence that matching the treatment to the patient does not work, may not have had suf®cient statistical power to detect differences between groups (Sanavio [3] included 10 patients per group; Espie and colleagues [54] included 14 patients per group). It is likely, therefore, that this question may be worth revisiting. Further, in the recent RCT by Morin and colleagues [23] that compared CBT (n ˆ 18), pharmacotherapy (n ˆ 20), or both (n ˆ 20), with placebo (n ˆ 20), it would be interesting to know whether the trend for the combined treatment to improve sleep more than CBT alone, and for the CBT alone group to improve sleep more than pharmacotherapy alone, would have become signi®cant given more statistical power. In order to avoid a Type 2 error, Kazdin and Bass [55] have recommended a sample size of 27 or more per group to detect a large treatment difference and 70 or more per group to detect smaller differences. 9. Recruitment. Information as to how the sample was recruited assists the reader to determine the generalisability of the ®ndings. From Table 2, most studies provided a detailed description of the recruitment methods. Ideally, recruitment should occur from the population for whom the treatment is intended. In the present context, studies involving treatment seeking patients referred by general practitioners are likely to be the most generalisable to a ``real world'' sample, followed by patients recruited via media adverts which are, in turn, likely to be more generalisable than samples drawn from college or university populations. It should be noted, however, that Morin et al. [5] found no differences between patients who responded to advertisements versus those who were treatment seeking. 10. Comorbid psychological disorders. Insomnia is commonly comorbid with other disorders, especially the depressive and anxiety disorders. It is therefore important for these to be assessed with a structured clinical interview [such as the Structured Clinical Interview for the DSM-IV, SCID; 56]. From Table 2, it is encouraging to see that the more recent studies have included an assessment of comorbid psychological disorders.

249

11. Comorbid sleep disorders. Given that the inclusion of comorbid sleep disorders is likely to reduce treatment effectiveness, many studies have assessed for the presence of comorbid sleep disorders, such as sleep apnea and periodic limb movement disorder (see heading ``Comorbid sleep disorders'' in Table 2). Ideally, this assessment should involve full PSG, as in the more recent RCTs [24, 25]. The risk of basing decisions about patient exclusion, based on interview alone, is that (1) not all patients will be aware of relevant symptoms and (2) it is impossible to make a judgement about whether the severity of symptoms reported justify exclusion. Giving an indication of the number of individuals likely to be affected, Edinger et al. [22] excluded 29 of 192 (15%) patients eligible for screening due to a comorbid sleep disorder. Morin and colleagues [23] excluded 40 of 163 (25%) patients eligible for screening due to a comorbid sleep disorder. Both studies made these judgements on the basis of full PSG. 12. Length of follow-up. An index of the durability of the treatment is, of course, mandatory. As seen in Table 2, the majority of studies have included a followup assessment. Impressively, several studies reported a 12-month followup or longer [e.g., 13, 23]. 13. Treatment adherence. As few of the studies we reviewed mentioned treatment adherence, this aspect of RCT methodology was not included in Table 2. Lichstein et al. [44] have outlined three levels of adherence to treatment. First, the treatment must be delivered in a pure form with no input from other treatment approaches. Methods to ensure delivery include adequate training of therapists, practice cases for therapists, role playing of therapy techniques, viewing taped therapy sessions, and obtaining treatment delivery ratings of taped therapy sessions. The second check is that the treatment was received by the patient (i.e., that the patient understood the treatment). Perhaps one method for doing this would be to obtain, at the end of each session, a verbal description by the patient of the content covered during the session. On the basis that patients with insomnia forget approximately one third of the clinician's instructions, and that for some types of recommendations, recall can be as low as 13% [57], audio taping sessions and asking the patient to review the recording between sessions is likely to assist patients to

250

fully understand the treatment. The third check is for evidence of enactment. That is, has the patient applied the content of the treatment sessions between sessions? One method of checking for enactment would be to set up homework tasks such that the extent to which the patient has applied the treatment to their lives can be quantitatively indexed. 14. Random allocation. It is crucial to ensure that the treatment effects observed are not due to differences between the conditions. Altman et al. [45] highlighted that randomisation involves two parts. First, the sequence of allocating patients to groups must be unpredictable. Second, the sequence must be hidden from the investigator enrolling patients. Although all of the studies reviewed in Table 2 did randomly allocate patients to treatment groups (hence we did not include this variable in the table), the exact procedures were rarely described. To summarise, this section has compared the methodology of RCTs of CBT for insomnia against fourteen aspects of optimal RCT methodology. Several areas that the ®eld could improve have been identi®ed including: evaluating treatment outcome on a broader range of target symptoms, employing standard

A. G. HARVEY AND N. K. Y. TANG

diagnostic criteria evaluated with psychometrically validated instruments, including checks of treatment credibility, and including checks of treatment adherence. Table 3 includes a summary of the key methodological guidelines for conducting RCTs of CBT for insomnia. In the following section we describe the outcome of conducting the same exercise, to that just described, but this time relating to the reporting of the results of RCTs. The importance of clearly describing, in the results section, the ¯ow of patients through an RCT has been emphasised [45, 46]. The number of patients who were randomly assigned, received the treatment, completed the study protocol, and were included in the analysis for the primary outcome should all be clearly speci®ed. Table 4 presents a summary of the data on the reporting of the results by RCTs of CBT for insomnia. The ®ndings are discussed below. 1. Dropouts during treatment. The number of patients who did not complete the treatment must be carefully recorded and reported as these details form an important indicator of the extent to which a treatment is acceptable. Morin and Wooten [48] suggest that ``Even though a particular intervention is ef®cacious, if it produces adverse side effects, is too time consuming, or too costly, adherence is

Table 3 Guidelines for the methodology and reporting of RCTs of CBT for insomnia Methodology 1. Specify clearly de®ned target symptoms 2. Adopt standard diagnostic criteria to de®ne insomnia (DSM, ICSD, ICD) 3. Use valid and reliable diagnostic tools to determine the presence/absence of the diagnostic criteria 4. The evaluators of treatment outcome must be blind to the treatment the patient received 5. Report methods for training of therapists 6. Adopt a treatment manual 7. Include checks of treatment credibility 8. A conduct power analysis to ensure the sample size is large enough to detect differences 9. Describe methods of recruiting the sample 10. Employ a valid and reliable method to assess for comorbid psychological disorders 11. Employ a valid and reliable method to assess for comorbid sleep disorders 12. Include follow-ups to index the durability of the treatment effects 13. Include checks of treatment adherence 14. Randomly allocate patients to groups

Reporting 1. Report the number of dropouts during treatment 2. Report the number of dropouts during followup 3. Report the number of patients who did not respond to the treatment 4. Use intention-to-treat analyses 5. Report statistical signi®cance 6. Report the number of patients to achieve clinically signi®cant change as a result of treatment 7. Report the number of patients to achieve high end state functioning 8. Report the number of patients who refused the treatment 9. Report the effect size of each treatment

Evaluating the reporting of RCTs of CBT for insomnia

Author(s)

Dropouts during treatment (dropout/n) Cognitive behavioural CBT ˆ 2/25 therapy (CBT) RT ˆ 2/25 Relaxation PT ˆ 1/25 training (RT) Placebo therapy (PT)

Dropouts during follow-up (dropout/n) Follow-up questionnaire: CBT ˆ 7/23 PT ˆ 7/23 Follow-up sleep log: CBT ˆ 9/23 RT ˆ 8/23

Espie et al., 2001

Cognitive behavioural 22/161 (over all therapy (CBT) treatment Self-monitoring conditions) control (SMC) Deferred cognitive behavioural therapy (CBT-DEF)

30/139 (over all * treatment conditions)

*

*

Friedman et al., 2000

Sleep restriction therapy (SRT) Nap sleep restriction therapy (NSRT) Sleep hygiene (HYG)

SRT ˆ 1/16 NSRT ˆ 1/12 HYG ˆ 1/11

SRT ˆ 1/15 NSRT ˆ 1/11 HYG ˆ 0/11

*

Yes (Carried forward the baseline value for the end-oftreatment value)

*

Mimeault and Morin, 1999

Cognitive-behavioural BT ˆ 4/22 bibliotherapy (BT) BTPC ˆ 0/18 Cognitive-behavioural WL ˆ 0/18 bibliotherapy with weekly telephone consultation (BTPC) Waiting-list control (WL)

BT ˆ 3/18 BTPC ˆ 4/18

*

*

(1) SE480% (2) Use of sleep aids/nights per week

Edinger et al., 2001

Groups

Nonresponders

Intention-to-treat analysis

*

Yes (ANCOVA with and without dropouts showed similar results so only the more conservative intentionto-treat analyses were presented)

De®nition of clinically signi®cant improvement (1) 450% reduction in pre-treatment WASO (sleep log) (2) scored 41 or less on the Insomnia Symptoms Questionnaire

CBT FOR INSOMNIA

Table 4

251

252

Table 4

continued

Author(s)

Dropouts during treatment (dropout/n) Cognitive behavioural CBT ˆ 0/18 therapy (CBT) PCT ˆ 3/20 Pharmacotherapy Combined ˆ 1/20 (PCT) Placebo ˆ 2/20 Combined CBT & PCT (combined) Placebo medication (placebo)

Dropouts during follow-up (dropout/n) At 3-mth: CBT ˆ 2/18 PCT ˆ 4/17 Combined ˆ 2/19 Placebo ˆ 5/18 At 12-mth: CBT ˆ 0/16 PCT ˆ 1/13 Combined ˆ 1/17 Placebo ˆ 6/13 At 24-mth: CBT ˆ 3/16 PCT ˆ 0/12 Combined ˆ 2/16 Placebo ˆ no dropout

Nonresponders

Intention-to-treat analysis

*

* (Analyses were computed with and without dropouts ± both methods produced similar outcomes. Only the latter method was retained)

Hauri, 1997

Sleep hygiene plus Halcion (SHPH) Sleep hygiene alone (SHA) Waitlist (WL)

SHPH ˆ 1/11 SHA ˆ 2/13

*

*

*

Guilleminault et al., 1995

Structured sleep SH ˆ 0/10 hygiene (SH) Light ˆ 1/10 Structured sleep Exercise ˆ 1/10 hygiene plus moderate late Dropouts were afternoon exercise replaced with (Light) 2 added subjects Structured sleep hygiene plus morning light therapy (Exercise)

*

2

Yes (Dropouts were included in the analyzed data set)

*

Morin et al., 1999

Groups

A. G. HARVEY AND N. K. Y. TANG

SHPH ˆ 0/6 ‡ 5 (from WL) SHA ˆ 0/9 ‡ 4 (from WL) WL ˆ 2/11

De®nition of clinically signi®cant improvement (1) SE485% (2) 515 on sleep impairment index

continued

Author(s)

Groups

Morin et al., 1993

Multifaceted intervention/ immediate treatment (MI) Waiting-list control/ delayed treatment (WLC)

Jacobs et al., 1993

Multifactor behavioral 4/24 (over all intervention (MF) treatment Stimulus control conditions) (SC)

MF ˆ 1/10 SC ˆ 1/10

Engle-Friedman et al., 1992

Support & sleep hygiene Support & sleep hygiene plus progressive relaxation Support & sleep hygiene plus stimulus control Measurement control

Friedman et al., 1991

Sleep restriction (SRT; n ˆ 10) Relaxation (RLT; n ˆ 12)

Dropouts during follow-up (dropout/n) MI ˆ 1/12 WLC ˆ 0/12

Nonresponders

Intention-to-treat analysis

There were * non-responders but the number was not reported

De®nition of clinically signi®cant improvement (1) SE480% (2) WASO560 min (3) No use of sleep medication

*

*

SOL520 min

There was attrition but the number was not reported

11/53 (did not * participate in the follow-up telephone interview) 21/42 (did not return the 1-week sleep diary after the telephone interview)

*

*

4/38 SRT ˆ 3 RLT ˆ 1 Another 4 withdrew because of physical illness SRT ˆ 3 RLT ˆ 1

8/30

*

*

*

BT ˆ 0/15 T ˆ 0/15

BT ˆ 0/15 T ˆ 0/15

*

*

* 253

McClusky et al., Behavior therapy 1991 (BT) Tiazolam (T)

Dropouts during treatment (dropout/n) MI ˆ 0/12 WLC ˆ 0/12

CBT FOR INSOMNIA

Table 4

Groups

Dropouts during treatment (dropout/n)

Dropouts during follow-up (dropout/n)

Nonresponders

Intention-to-treat analysis

De®nition of clinically signi®cant improvement

Sanavio et al., 1990

Biofeedback program (BFB; n ˆ 10) Cognitive program (CT; n ˆ 10) Stimulus control and progressive relaxation (SC; n ˆ 10) Waiting-list control (WL) Relaxation (n ˆ 14) Stimulus control (n ˆ 14) Paradoxical intention (n ˆ 15) Imagery relief placebo (n ˆ 14) No treatment (n ˆ 13)

0/30 (over all treatment conditions)

0/30 (over all treatment conditions)

At 1-yr: 3/30 (10%) BFB ˆ 1/10 CT ˆ 1/10 SC ˆ 1/10 At 3-yr: 7/30 (23%) BFB ˆ 2/10 CT ˆ 3/10 SC ˆ 2/10

*

*

17/101 (Dropouts evenly distributed across conditions)

6 wks ˆ 23% 3 mths ˆ 42% 6 mths ˆ 44% 17 mths ˆ 30% (over all treatment conditions)

*

*

*

Random therapy (RT; n ˆ 43) Tailored therapy (TT; n ˆ 14) Imagery relief placebo (IR; n ˆ 14) No treatment (NT; n ˆ 13)

*

*

At post* treatment: TT ˆ 4/14 (30%) (Rate of other groups were note reported)

Espie et al., 1989a

Espie et al., 1989b

(1) Proportion of patients achieving absolute (i.e., any) reduction in SOL magnitude at post-treatment (2) Proportion of patients achieving SOL reduction of at least 50% (3) Proportion of patients achieving ®nal SOL less than or equal to 30 min

A. G. HARVEY AND N. K. Y. TANG

Author(s)

254

Table 4 continued

continued

Author(s)

Groups

Morawetz, 1989

Self-help tape (Tape; n ˆ 53) No treatment (n ˆ 53) Therapist-led treatment (Therapist-led; n ˆ 53)

Stanton, 1989

Hypnotic relaxation Stimulus control Placebo Stimulus control (n ˆ 9) Imagery training (n ˆ 8) Wait list control (n ˆ 10)

Morin and Azrin, 1988

Schoicket et al., Meditation 1988 (M; n ˆ 22) Stimulus control (SC; n ˆ 22) Sleep hygiene (SH; n ˆ 21)

Dropouts during treatment (dropout/n) 18/159 (over all treatment conditions)

Dropouts during follow-up (dropout/n) *

Nonresponders

Intention-to-treat analysis

*

*

*

*

*

*

*

*

*

*

*

*

7/74 Mˆ1 SC ˆ 2 SH ˆ 4

2/65 (not included * in ®nal analysis) SC ˆ 1 (medical problem) SH ˆ 1 (started taking sleep medication after last treatment session)

*

*

De®nition of clinically signi®cant improvement (1) SOL improved by 50%; sleep maintenance improved by 50%; early morning awakening improved by 20% (2) For subjects using medication: medication use reduced by half

CBT FOR INSOMNIA

Table 4

255

256

Table 4

continued Groups

Dropouts during treatment (dropout/n) H-BFB ˆ 0/6 L-BFB ˆ 0/6 H-CT ˆ 0/6 L-CT ˆ 0/6

Sanavio, 1988

High arousal and biofeedback (H-BFB) Low arousal and biofeedback (L-BFB) High arousal and cognitive therapy (H-CT) Low arousal and cognitive therapy (L-CT)

Morin and Azrin, 1987

Stimulus control (SC) SC ˆ 1/9 ( ‡ 1 Imagery training (IT) due to Wait-list (WL) non-compliance) IT ˆ 2/9 WL ˆ 2/9

Dropouts during follow-up (dropout/n) H-BFB ˆ 0/6 L-BFB ˆ 0/6 H-CT ˆ 0/6 L-CT ˆ 0/6

SC ˆ 1/7 IT ˆ 0/7 WL ˆ 0/7

* ˆ No or not reported in the paper. n ˆ Sample size, No. ˆ Number, ANCOVA ˆ Analysis of covariance. Min ˆ Minute, Wk ˆ Week, Mth ˆ Month, Yr ˆ Year. SOL ˆ Sleep onset latency, SE ˆ Sleep ef®ciency, WASO ˆ Wake after sleep onset.

Nonresponders

Intention-to-treat analysis

(1) Use of sleep * medication at 12-mth: H-BFB ˆ 1/6 L-BFB ˆ 2/6 H-CT ˆ 4/6 H-CT ˆ 2/6 (2) Therapy satisfaction at 12-mths: ``No bene®t at all'' ˆ 2/24 *

*

De®nition of clinically signi®cant improvement *

* A. G. HARVEY AND N. K. Y. TANG

Author(s)

CBT FOR INSOMNIA

likely to be poor. Thus, regardless of how ef®cacious a given treatment is, if it is not acceptable to patients it may be of little clinical use.'' (p. 535). Where the data were available, Table 4 presents the number of dropouts according to treatment condition. Chambers [58] highlighted that stimulus control and sleep restriction may, for reasons of being counterintuitive and unpleasant to complete, be associated with more dropouts. Although the numbers are very small, there is tentative evidence for this suggestion in Table 4 [59]. In addition, bibliotherapy [10] and pharmacotherapy [8] appear to be associated with more dropouts, although again the numbers are too small to be certain. The dropout rates for CBT for other disorders is variable; for the panic disorder trial there were no dropouts [36], whereas for CBT for GAD 8.3% of the sample did not complete the treatment [38]. 2. Dropouts during followup. Dropouts during the followup phase, whilst understandable from the patients perspective (they have been treated, why should they participate in continued assessments?), cause dif®culty in establishing the longterm effectiveness of the treatment. Table 4 indicates that there are signi®cant dropouts during follow-up. This suggests that researchers need to consider creative methods to enhance patient interest in participating in the followup phase. 3. Non-responders. The proportion of patients who do not bene®t at all from treatment are rarely reported (see column ``non-responders'' in Table 4). As the aim is to develop a treatment that bene®ts the maximum number of patients, reporting the number of non-responders is crucial. Lacks and Powlishta [42] point out that group means blur variability and mask information about how many individuals are not helped by the treatment. 4. Intention-to-treat analysis. The rationale of an intention-to-treat analysis is to reduce bias associated with patients not completing the treatment or dropping out during followup. Prior to commencing the study a strategy to deal with loss of patients during treatment or follow-up needs to be formulated [60]. Although still debated, Hollis and Campbell [61] argue that an intention-to-treat analysis should include: (1) those patients who were randomised but ceased treatment before the treatment started or in the early sessions before the treatment could be expected to have begun to take effect, (2) those patients who were noncompliant with the treatment (e.g., did not take

257

the prescribed medication at the prescribed dose), and (3) those patients who dropped out during the treatment or followup phases. They argue that ``the only commonly feasible options are using the last observed response (carry forward) or assuming all missing responses were constant'' [61, p. 673]. Whilst several of the RCTs summarised in Table 4 adopted an intention-totreat analytic strategy, it was often dif®cult to deduce the exact nature of the analysis. Further, where an intention-to-treat analysis was conducted, several studies only included patients who dropped out after the treatment had progressed more than half way and few carried forward the last observed response for dropouts during followup. Future studies of CBT for insomnia should adopt a more conservative intention-to-treat strategy. 5. Statistical signi®cance, clinical signi®cance and high end state functioning. There is currently no universally accepted de®nition of treatment success for insomnia. Accordingly, it is proposed that a distinction be drawn between three different measures of change following treatment. Statistically signi®cant change is change which is statistically reliable and over and above chance ®ndings. Clinically signi®cant change is that which has made a difference to the life of the patient and has moved them out of the sleep disordered range. Several studies in the literature have de®ned clinically signi®cant change as: (1) 50% or greater improvement in an outcome variable (e.g., SOL, WASO, TST) after treatment compared to baseline values and (2) less than 30 min for SOL and WASO [e.g., 13, 47, 62]. It is crucial to note that individuals who achieve clinically signi®cant change can still be subclinically symptomatic. Hence, it is important to also de®ne the number of patients to achieve high end state functioning. That is, that the patient can be declared a good sleeper. As is evident in Table 4, whilst all RCTs have established statistical signi®cance, far fewer have established clinical signi®cance, and none de®ned high end state functioning (hence a column for this variable was not included). We suggest that future RCTs of CBT for insomnia should declare the extent to which the results show statistical signi®cance and clinical signi®cance, along with the proportion of patients who moved in to the high end state range following treatment. 6. Refusers. None of the studies we reviewed reported the number of patients who refused

258

treatment. Accordingly, a column for this variable was not included in Table 4. Such data is important for the reader to determine the representativeness of the sample and the perceived acceptability of the treatment. 7. Effect size. Altman et al. [45] argued that the effect size of treatment should be reported. As we could ®nd no studies where the effect size of the treatment was reported we did not include a column for it in Table 4. To summarise, this section has compared the reporting of results of RCTs of CBT for insomnia against seven aspects of optimal RCT methodology. Several areas that the ®eld could improve were identi®ed including: reporting the number of nonresponders and treatment refusers; adopting a more conservative intention-to-treat analysis; reporting statistically signi®cant, clinically signi®cant, and high end state functioning data; and reporting the effect size of the treatment. Table 3 includes a summary of the key guidelines for reporting the results of RCTs of CBT for insomnia.

Future directions We would like to propose two priorities for future research. First, as already discussed, the methodology and reporting of RCTs needs to become more rigorous so that we can be con®dent that the RCT results reported are not under or over estimates. Second, we suggest that researchers should work to improve CBT for insomnia. Although the reasons for this suggestion have already been outlined in full it is worth brie¯y reiterating: a signi®cant proportion of patients who receive CBT for insomnia do not respond to treatment and for those who do respond, the degree of change (1) does not move the average patient into the good sleeper range and (2) is lower than that observed for CBT for a range of other psychological disorders. This section outlines a proposal for how improvements to the effectiveness of treatment might be achieved. Salkovskis [63] has proposed four steps in the process of developing a highly effective treatment. As summarised in Figure 1, the ®rst step is to fully grasp the phenomenology of the disorder via clinical practice. The aim of clinical practice is to talk to patients and watch for phenomena that are not consistent with existing theory and to then carefully consider whether such phenomena re¯ect maintaining processes that

A. G. HARVEY AND N. K. Y. TANG

Outcome research

Theory Clinical Practice

Experimental studies and related research

Figure 1 Factors involved in empirically grounded clinical interventions. Reprinted from Salkovskis PM. (2002). Empirically grounded clinical interventions: Cognitive-behavioural therapy progresses through a multi-dimensional approach to clinical science. Behavioural and Cognitive Psychotherapy, 30, p. 5. & 2002 by Cambridge University Press. Reprinted with permission. have not yet been recognised [64] These clinical observations should then be used to inform theory and are subjected to experimental investigation. If hypotheses about maintaining processes are con®rmed via experiments, their place in a theory of the maintenance of the disorder is con®rmed. The validated theory can then be used to guide the development of a speci®c targeted treatment in which the maintaining processes are reversed. This process has been applied to the development of CBT for a range of psychological disorders with excellent outcomes (indicated in Table 1). We suggest that previous research in the ®eld of insomnia has focused primarily on testing the ef®cacy of pharmacological and cognitive behavioural treatments. Although the development of psychological theories has also received attention [16, 24, 25, 34, 65±68], experimental investigations have been neglected. The ®eld would bene®t from the completion of experimental studies that test the existing theoretical models with experiments and make use of the ®ndings to re®ne the theories of insomnia with a view to using validated theories to develop new innovative treatment approaches. Interestingly, Salkovskis [63] argues that the results of an RCT is a weak indicator of mechanisms that underpin a disorder. Consider the following reasoning: ``the effectiveness of SSRIs in the treatment of a particular disorder does not (and cannot) indicate that such processes are caused by serotonin de®ciencies'' [64, p. 5]. Instead, the most effective method of delineating mechanisms that underpin a disorder is via experimental studies that are

CBT FOR INSOMNIA

designed to test hypotheses derived from a theory of the disorder [63]. One likely impediment to the completion of experimental studies in this, and other clinical ®elds, is the dif®culty recruiting suf®cient numbers of patients to provide enough statistical power to detect differences. This impediment has been minimised in research on other disorders by adopting a preliminary strategy; the completion of analogue studies; to develop methods and paradigms and assist in re®ning the concepts of interest in a short period of time. One type of analogue study involves employing ``normals'' and manipulating them in to a ``state'' akin to the disorder of interest. A second type of analogue study involves recruiting participants who score high or low on the phenomena of interest. In the context of insomnia, this might be either (1) poor sleepers versus good sleepers or (2) individuals diagnosed with insomnia recruited from the college population versus good sleepers recruited from the college population. Of course, such analogue studies are only the ®rst step. They must be replicated with the exact sample of interest; patients seeking treatment for insomnia. To summarise, we suggest that the ®eld should work toward improving CBT for insomnia via an enhanced emphasis on testing and re®ning existing psychological theories with experiments. A sensible use of resources would involve testing new ideas with experiments based on analogue samples that then, if successful, should be replicated with a treatment seeking sample.

CONCLUSION Whilst progress toward establishing an effective psychological treatment for primary insomnia has been encouraging, we cannot as yet offer a optimally effective psychological treatment that results in a high proportion of patients becoming good sleepers. We have proposed a number of aspects of the method and reporting of RCTs that require improvement to ensure that results presented in the literature are valid and reliable. We have also suggested ideas for developing CBT further. In particular, the emphasis should be on conducting experiments to test and extend existing theories of insomnia (including experiments using analogue samples) and the use of validated theories of insomnia to develop new, empirically derived, treatments.

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Practice Points 1. Whilst CBT is de®nitely effective in the treatment of insomnia, there is substantial room for the growth and development of cognitive behavioural treatments for insomnia. 2. When conducting and reporting randomised controlled trials (RCTs) of CBT for insomnia, researchers should adhere to the guidelines summarised in Table 3. 3. Improvement to CBT for insomnia can be established via a combination of clinical practice, experimental investigations, and theory development.

Research Agenda 1. Work toward compatibility between the DSM, ICSD, and ICD de®nitions of insomnia. 2. Assess daytime impairment in RCTs of CBT for insomnia. 3. Develop and disseminate psychometrically validated structured interviews for the diagnosis of insomnia. These should be employed as outcome measures for CBT for insomnia. 4. Improve the conducting and reporting of RCTs evaluating CBT for insomnia (see Table 4 for summary). 5. Empirically derive novel treatment approaches using a combination of clinical practice, experimental studies and theory development. 6. Make use of analogue samples to conduct experimental studies. 7. This review has focused on primary insomnia. Although the distinction between primary and secondary insomnia is problematic [20], a priority for the future includes the completion of RCTs to test the ef®cacy of CBT for secondary insomnia.

ACKNOWLEDGEMENTS The authors are grateful to Professor Colin A. Espie and the anonymous reviewers of this paper for their helpful comments. This research was supported by the Wellcome Trust (Grant no. 065913).

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